Cardiology, Improving Outcomes, Mythbusting

SVT: treat, wait, re-evaluate

What do you *really* need to do with your SVT patients? Well, this is a retrospective observational study of 633 consecutive SVT patients over 10 years seen in a single ED. This was more hypothesis generating than anything – they basically provide patient characteristics and try to tease out if labs / imaging were necessary.

Their mean age was 55, 62% of patients were female, 55% had prior SVT history, 31% had at least one cardiovascular risk factors (dyslipidemia, hypertension, diabetes, CHF, or vascular disease), and 9% had ischemic heart disease.

Some interesting lab nuggets:

-0.4% had a hemoglobin < 8g/L

-1.5% had a sodium >150 mmol/L, none <126

-no patient with severe hyperthyroidism

Chest Xray was obtained 30% of the time, and while it was abnormal 21.6% of the time (41 of 190), none of the time did it alter ED treatment – despite showing 14 cases of pulmonary edema, 4 cases of pneumonia, and 3 pleural effusions.

The authors conclude that patients with uncomplicated SVT are over-investigated, and that most have normal or near-normal results. While I tend to agree – for the 25 year old in SVT without a concerning story – the 55 year old diaphoretic (14% were diaphoretic) female with ischemic heart disease I’m going to work up. Chest films were only ordered on 30% of these patients – frankly in a US hospital, I’m thankful its not higher.

I know Billy Mallon loves his TSH, but why not get a better history to see if there are other concerning symptoms before sending off TSH… Speaking of which, maybe we could decrease those Chest films if we fixed the patient a bit, then reassessed to see if imaging is wanted. (ie, are you still short of breath?).

Finally, I think this study is plagued by premature closure, as they only searched for cases with a discharge diagnosis of paroxysmal supraventricular tachycardia. They’re likely missing at least a few patients who came in with SVT and were found to have actually have another diagnosis.

Ultimately, while this study should not change practice by any means, it should give us pause before shotgunning labs & chest films until after we treat the patient, re-evaluate, and get a better history. This could probably be said for many other diagnoses besides SVT.

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Cardiology, Cardiology, Critical Care, Improving Outcomes, Improving Throughput, Mythbusting, Pulmonary, Radiology, Radiology

Probing the dyspneic patient.

For undifferentiated dyspnea, how would you like to have an accurate diagnosis in 24 minutes?

I love this study.

Basically, for all dyspneic patients (not trauma related, and over age 18), 10 EP’s were given an H&P, vital signs, and an EKG, as well as access to a Chest X-Ray, Chest CT, cardiologist performed echo, and labs including an ABG.

These same 2,683 patients, in tandem, had point of care ultrasound testing (lung, IVC, echo). Here’s the catch – the ultrasonographers were only provided the H&P, vital signs, and EKG then asked to make a diagnosis. The treating provider was blinded to POCUS diagnosis.

These numbers for diagnostic accuracy of POCUS are astounding.

+LR for acute HF? 22 (-LR 0.12)

+LR for ACS? 105 !!!

+LR for pneumonia? 10.5 (-LR 0.13)

+LR for pleural effusion? 95 (-LR 0.23)

+LR for pericardial effusion? 325!!! (-LR 0.14)

+LR for COPD/asthma? 22 (-LR 0.14)

+LR for PE? 345!!!

+LR for pneumothorax? 4635!!! (-LR 0.12)

+LR for ARDS? 90

Yes, for certain things like pneumonia, the difference in p-values between tradition means and POCUS diagnosis was not significantly different, but what about volume status? I cant imagine blindly giving 30 cc/kg would benefit the patient with a plethoric IVC and pleural effusion. There is some elegance a play here.

Additionally, sure, ED diagnosis for ACS had a higher LR, but they also had a cardiologist performing and interpreting echos in the ED (a rather rare siting in a US ED I would imagine) – without much improvement in their -LR (0.53 vs 0.48). For PE, the -LR of POCUS was predictably mediocre if not outright bad (0.6), while the -LR for ED diagnosis of PE, with the benefit of chest CT, was -0.10.

Now look, I get that these EP’s were quite sono-savvy. They all had 2+ years of experience, over 80 hours of ultrasound lessons & training, with at least 150 lung and 150 ED echo’s under their belt. The diagnosis was made in 24 minutes with POCUS in comparison to 186 minutes for traditional means. And while most of us can not do a year+ ultrasound fellowship, and neither can we all be as savvy with the probe as these authors (or Matt, Mike, Jacob, Resa, Laleh, etc) – it does not mean we shouldnt try. You can still greatly increase your yield just by practicing. To boot, the cognitive offload you experience by saving yourself a few hours by (correctly!) knowing which direction you are heading with a patient is an immense boon to both your mental heath & your patients well being.

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Improving Outcomes, Improving Throughput, Radiology

Ultrasound MiniFellowship, eh?

Are you looking for a bridge after taking an ultrasound course at a conference?  Do you feel like you need a bit more oversight until you get comfortable with probe in hand?  Are you having trouble conceptualizing what it means to have ultrasound guide your practice in the critically ill?… Read on.

I recently had the pleasure of attending a CCUS POCUS mini-fellowship –  it was everything I was hoping for & more- and has pushed me to be a better clinician.

First, a blurb about ultrasound fellowships.  As a PA, there isn’t really any hands on US training during our programs.  There likely is some POCUS for PA EM residents – but most practicing EM PA’s are not residency trained.  Therefore, we’re at the mercy of our co-workers who may (or may not) have any US training.  It’s hard to learn POCUS when you don’t have someone over your shoulder to guide you!

I had done a few ultrasound courses, but was struggling to really implement it into my practice regularly.  Ultimately, this was my own fault.  I was repeatedly told to pick up the probe and practice.  Literally, every sono-savvy person has told me this.  A large part of my problem was that I did not pick up the probe immediately after courses to drill down on fundamentals – and scan every person regardless of their complaint.  This is not meant to disrespect those that I took courses with before – they were *extremely* helpful and I’m incredibly thankful for their expertise! – the fact that I continued to seek out ultrasound training is a testament to prior courses showing me the importance of developing this tool set.  Now, onto Canada.

I ended up taking a 2 day course with Philippe Rola in Montreal.  Philippe is extremely responsive via email, we had spoken on the phone a few times prior to my arrival as well.  He’s friendly, approachable, and has been doing mini-fellowships since 2009 (!).

I was looking to optimizing views, particularly on patients with challenging anatomy (I mean, have you seen the average American BMI recently?), and what started with, “where the hell is the IVC” turned into, “This is a plethoric IVC.”  While it might be that the 3rd (or is it 4th?) time is the charm for courses for me, and that I would get it eventually via spaced repetition, but there is something about practicing on patients with acute illness and watching Rola make decisions based on POCUS in real time that helps put the pieces together a bit faster.

I believe the main advantage of this US course is the real time feedback on real patients… and if you are there for more than one day, you get to watch the ICU story unfold.  You see about 10-12 patients in their ICU, and a handful of ICU consults on the floors or in the ED.  You may or may not go to a rapid response, and see how it really makes a difference in the heat of the moment.  Fortunately, this is not reminiscent of your student days when the mentor says, “You’ll have to sit this out, this one’s mine, sorry.”  Philippe was extremely patient with me in the hypotensive altered patient while I scanned.  He’s excellent at questioning at just the right time to help tie it together- “ok, what are you seeing? A plump IVC and some pleural effusions in this hypotensive patient?  So whats your next step?”

To maximize your experience, I would strongly encourage you to have 1-2 specific goals in mind like, “I want be able to consistently visualize the IVC and have a few back up views just in case.” Expecting more than 1-2 things is probably spreading yourself thin.  You’re not going to become a pro overnight.  Be upfront & honest with Rola – he can tailor to your skill level- whether it be an assessment of valvular function or just wanting to visualize the heart.  Philippe had recommended 2-3 days at a time, which I agree with – I think after 2-3 days you reach the point of diminishing returns and “get full.”  You need some time to process what you’ve learned, and to practice on your own (before going back!).

Upon my return home, I made it a point to utilize the probe on my next shift.  If at all possible, I would recommend arranging shifts to be “main ED” shifts when you get back home such that you see the belly pain, shortness of breath, and chest pain patients so that you can apply what you learned immediately.  I did this on my first shift back with the hope of scanning 5 patients or more – I literally brought the machine with me when I walked into the room.  Surprisingly, I thought it would slow me down.  This was not the case at all.  I also realized a major benefit that I was not expecting.  The cognitive offloading of using the probe and eliminating some of the guess work kept me fresher longer. I saw more patients than average, with sicker than average patients, and it did not feel like taxing shift at all.  I didnt have to task switch to check on that xray or CT nearly as much as I usually do (though I was still ordering what I usually would to confirm suspicions since I’m still early in POCUS training)…. I would be interested to see the throughput of docs using POCUS vs those not, and I’d also like to see the level of “decision fatigue” at the end of a shift – I’m convinced that POCUS provides a significant cognitive offload to the EM provider, and the POCUS’ers are less fatigued at the end of their shift.

Bottom line, I think I needed other courses to whet my appetite and open the door, and I needed Montreal to push me through the door and get me to start practicing more.  If you work in an environment where you don’t have much POCUS backup and want to learn with one of the best and don’t want to break the bank, come to Montreal!

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Critical Care

Who ya gonna call? #VancZosyn!

If there’s some strange cough in your resus room,

Who you gonna call? Vanc-ZoSyn!
If something’s fevered… and it don’t look good,
Who you gonna call? Vanc-ZoSyn!

I ain’t afraid of no Staph.
I ain’t afraid of no Strep.

If high lactates are running through your EMR,
Who you gonna call? Vanc-ZoSyn!

 

There’s been some FOAM rumblings about Vanc/ZoSyn causing AKI, but this was the first time it has been compared directly head to head with Vancomycin-Cefepime. This was a retrospective matched cohort study with 279 patients in each arm – one received combination therapy with vancomycin-cefepime (VC), the other received vancomycin-piptazobactam (VPT) for > 48 hours. Patients were excluded if their baseline serum creatinine was >1.2mg/dl or they were receiving RRT. Patients receiving VC were matched to patients receiving VPT based on severity of illness, ICU status, duration of combination therapy, vancomycin dose and number of concomitant nephrotoxins. The primary outcome was the incidence of RIFLE criteria-defined AKI, with a slew of secondary outcomes performed as well.

So, wait, what’s so special about RIFLE anyway? Glad you asked: In general, the worse the acute kidney injury, the higher the mortality.

Since this study shows an 11% AKI rate with VC and 29% AKI rate with VPT, maybe we can improve our mortality if we simply switch from zosyn to cefepime?

Except that this group reports mortality was actually worse in the VC group (though not statistically significant – 8.6% vs 5.7%). That’s right – the group with more AKI had less mortality. In other news, ICU stay was decreased (6 vs 8 days), which was statistically significant., and only ~1% of patients in both arms required long term hemodialysis.

While I was getting ready to click submit on this blog post, I found a second paper (published Nov 28, 2016) that looked at a matched cohort of 1633 VPT vs 578 VC patients, with essentially similar results – 21.4% AKI in VPT vs 12.5% VC.  This second paper found similar LoS, but also a similar trend in mortality-  6.9% for the VPT arm and 9.2 for VC.

So… I’m not certain what to make of this – but it seems more than fair to question whether drug induced AKI is a meaningful surrogate marker for sepsis mortality.  We need a long term look at mortality between VC vs VPT to see if VPT induced AKI follows the same trends. Maybe we’re trading a slight bump short term mortality for improved long term mortality with VC (or maybe not).  In the meantime, I think we need to pump the brakes on shouting about Vanc/Zosyn AKI until we sort this out a bit more.

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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.

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Mythbusting

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.

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Critical Care, Improving Outcomes, Mythbusting, Neurology

Compazine… for infectious disease?

Today’s article’s (1, 23 ) are a break from the usual trials that are typically discussed and a bit more “benchside medicine” than bedside medicine.  In fact, let’s look at this as an early request for one of the 12 trials of Christmas.

Phenothiazines have demonstrated in vitro (as well as some in vivo) activity for gram positive cocci, mycobacteria, amoeba (4; 5), and some gram negative rods.

It should be noted that Klebsiellae, pseudomonads and acenetobacters were highly resistant to almost all of these drugs.

The MIC for phenothiazines are usually not reached with conventionally used doses, but these compounds do enhance the activity of various antibiotics to which various bacteria are susceptible (including vancomycin), and even decrease the MIC of resistant organisms.

So where am I going with all of this? For starters, lets look at some common causes of meningitis, in no specific order:

Strep pneumo (gram positive); group B strep (gram positive); staph aureus (gram positive); Listeria (gram positive); Neisseria meningitidis (gram neg diplococci); H flu (gram neg)

All things phenothiazines are thought to have activity against.

You’re likely to be giving patients with potential meningitis something for pain (I hope?), so why not go with compazine?  Likewise, patients whom you may suspect bacteremia from a cellulitis, why not give compazine to, ummm, “counteract the nausea” associated with the opiates you gave for pain control?

I think this falls into the unlikely to harm, might help category, and is seemingly a ripe area for research.  Is this practice changing?  Nope, not at all.  Food for thought, but until compazine is proven unsafe in an infectious process, I will continue my love affair with compazine for headaches, nausea, and vomiting (regardless of suspected etiology).

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