Mythbusting, Improving Outcomes, Radiology, Radiology

Spinal Abscess: The Baystate Review

This is a review of all spinal abscesses at Baystate (total 162), from 2005 – 2015.  They compare 88 randomly selected controls whom had similar ICD-codes less the spinal abscess plus an MRI that was negative for acute infectious process. 

Interesting take home points, much of which is consistent with prior (albeit scant) literature:

-73% of patients are over age 50.

-more likely to have their second visit (50.6% vs 29.6% of controls) – though this 50.6% of patients with a second visit is surprisingly low for me – no word on how many were sent home from the ED, and had an MRI as an outpatient that were not included in this calculation.; or maybe we’re getting better at finding the needle in the haystack?  Or maybe we’re MRI’ing everyone?

-Many received antibiotics within the month: (35.2% vs 6.8% of controls) – this signifies a huge red flag for me.  If a patient revisits the ED and recently had pyelo (or anything infectious really), and now presents with back pain, probe a bit more for the possibility of vertebral osteo or discitis. 

-percentage of patients with history of IVDA: 20.4% vs 4.6% … this number seems low, but also is somewhat in line with prior studies – thus making me wonder how many I’ve missed…

– percentage of patients with alcoholism with a spinal abscess: 19% vs 8% – the more I get interested in ID, the more I realize that alcoholism is basically a form of immunosuppression.

-percentage of spinal abscess patients with obesity 21.6% vs 2.3%; I’m surprised only 2.3% of controls were obese.  Not sure what role this plays as being a diabetic in and of itself was not associated with a higher increased risk in this study.

-fever was present 62.4% in those with a spinal abscess vs 13.6% of those without; this includes self reported fever, which I have to wonder how often we sweep this aside when the patient is afebrile in the ED.

-16% had no identifiable risk factors; a third of the patients  presented with back pain, fever, neurologic deficits vs 6%

-Other symptoms and signs related to potential spinal cord impingement were seen with similar frequencies and of similar durations among cases and controls- meaning, focal deficits seen in both groups.

-noncontiguous co-infection: 53.7% of time (pneumonia, distant osteo, endocarditis… of those with a co-infection, 20% had more than one).

-blood cultures were positive 63.4% of the time, and >75% of the time it was staph Aureus. 

-Majority of lesions were found in the L-spine at 56.2%  – which means almost half are elsewhere!

-while “admits” for spinal abscess were up from 2.5 to 8 in 10,000 admissions from 2005 to 2015, I have to believe that number is somewhat inflated as admits like chest pain, pneumonia and renal colic probably decreased, while MRI became more readily available. 

All in all, this paper is pretty much in line with others on this topic, and strengthens the signal a bit for certain key points: a good number of spinal abscesses are not in the L-spine; many patients are older than you think, and, among other things: its more than just IVDA. 

Critical Care, Improving Outcomes, Mythbusting

Procalcitonin: Holy Grail, or Holy Sh*t ?

Procalcitonin is marketed as, “a marker of broad routine use, both for differential diagnosis of bacterial infection as well as for antibiotic stewardship.

But is it?  This study looks at 107 ICUs that had >25 sepsis cases in 2012, and had an ability to perform procalcitonin (PCT) levels on their septic patients, and essentially looked to compare the outcomes of those that had PCT ordered and those that did not.  All in all, there were about 17,000 septic patients without a PCT ordered, and about 3800 patients with a slightly lighter wallet and slightly more anemic after their admission than their comparators.

There was little difference in baseline characteristics – save for those having PCT ordered more likely hailing from the West (27.9% of PCT orders vs 12.7% of those not getting PCT ordered) and the opposite holding true for the South (55.3% without vs 49% with PCT).  PCT was slightly less ordered at teaching facilities (37.8% of septic patients without PCT orders vs 31.9% of those with a PCT ordered).  All other OR were <1.25.

There was no difference in length of stay and no differences in mortality.

There was an increase in days of antibiotic treatment for those in whom a PCT was ordered (relative risk increase 1.17), and with that an accompanying increase in Cdiff (OR 1.42) .  Of course, 1 PCT begets another (33% of the time, and about 3 days later).  Patients with serial PCT orders had higher rates of antibiotic use, higher Cdiff, and again, no mortality benefit.

Stop the madness.  Indiscriminately ordering tests that will not change management should not be done.  And they certainly should not be repeated.

Improving Outcomes, Pediatrics

They think tractors are sexy.

This is more of a fun read with summer coming up and provides an interesting glimpse into America.

They looked at all pediatric related lawnmower accidents from 1990-2014 from a 100-hospital sample they felt to be representative of US ED’s.  Overall, lawn-mower related injuries have gone down by almost 60% since 1990 – hooray for Darwin! Interestingly, there is a bimodal distribution of injuries, with ~15,000 total visits over the study period for 2 year olds, ~7,500 for those ages 7-9, and steadily rises after age 9 until accidents peak at about 20,000 total visits over the study period for 15-17 year olds.

In comparing the <5 year old age group to those 13-17 years old, the youngin’s were more often injured via contact with a hot surface (40% vs 5%), and fell off more (13% vs 4%).  This makes intuitive sense as they young tykes like to touch things they shouldn’t (particularly unsupervised), and some folks just HAVE to capture the moment with junior on their lap.

Also filed under WTF, is a 7.5% rate of injury for those under 5 years as the OPERATOR (vs 37% as bystander and 21% as passenger).  I mean, a four year old as an operator of a lawn mower?  Who possibly thinks this is a good idea?  Likewise, with 40% injuries for those under 4 caused by burns – this is something that could be easily fixed by not letting the wee ones around the mower as it cools.

10.6% of those under 4 years old with lawn-mower related injuries are admitted – many of these are probably preventable by common sense.  I guess they’re learning from Kenny Chesney at a young age.

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.

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.

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!

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.