Ditch the steroids for urticaria

Summer is here. People are going out and eating strange food, getting stung by strange things, and in general, coming into the ED for interesting rashes.

Contrary to a previous post suggesting a longer taper for contact dermatitis, this paper suggests that steroids are well, quite bunk for urticarial rashes.

This French, two-center, randomized, double-blinded study look at 5mg of levocetirizine vs 5mg of levocetirizine plus 4 days of 40mg prednisone for acute urticaria of under 24 hours duration. Patients were excluded if they had angioedema or anaphylaxis – among a multitude of other things, such that only 100 of 710 potentially eligible patients were enrolled (exclusion criteria comprised of: a history of diabetes, peptic ulcer disease, pregnancy, and chronic kidney disease, among many others).

The authors note that in Italy (strangely, why not in France?) , 93% of patients presenting to the ED for urticaria received steroids in 2011 – which I imagine is probably slightly higher than what I would expect for US EDs. So they reasonably suggest that, hey, maybe we can lower steroid-related ADR’s if we find a way to decrease the number of times we prescribe them.

Basically, after 1 hour, 2 days, and 5 days, there was no difference in itch control or rash resolution between the two groups, and if anything, a trend towards better outcomes with levocitirizine alone (For instance, 62% with an itch score of zero for steroids + levocitirizine vs 76% in levocitirizine only at 2 days). Relapse rates were 30% vs 24% (steroids+levo vs levo only) during the first 5 days, which was not statistically significant.

Sadly, and oddly, they report that “one patient in the placebo group had vomiting and abdominal pain in the ED 1 hour after initiation of treatment. These symptoms were related to anaphylaxis, and the patient rapidly improved after a steroid injection.” … which as we know, probably was not anaphylaxis if it improved “rapidly” after steroids (and without adrenaline). But I digress…

Previously, there have only been two studies looking at steroid use for urticaria; This one showing earlier resolution with 3 days of prednisolene (unsure if this is prednisolone, prednisone, or something else) against 10mg of loratadine (94% vs 66% resolution at 3 days), and this one showing lower itch scores with 4 days of 40mg prednisone plus 25mg of hydroxyzine every 4-8 hours than hydroxyzine treatment alone.

I think this particular study lends some credibility to those of us that are steroid-averse, and probably lends to a reasonable discussion with patients that are concerned about getting steroids. Likewise, it is probably reasonable to do a single dose dexamethasone treatement and chase it with a short course of levocitirizine.

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.


TXA’s post-partum fragility

Warning: An American on TXA.

The WOMAN trial was an international randomized double-blind placebo controlled trial across 193 hospitals in 21 countries looking at TXA use for morbidity and mortality for post-partum hemorrhage.

First off, this was a massive undertaking as this was an enormous trial – about 10,000 patients in each treatment arm, with fantastic follow up- only 31 of about 20,060 total patients were lost to follow up. If the treating provider was unclear as to the utility of TXA for post-partum hemorrhage control, the patient was randomized 1:1 to placebo or 1g of TXA, and if the bleeding continued after 30 min or stopped and restarted within 24 hours of the first dose, a second dose (1g TXA) or placebo was given. Baseline characteristics were quite similar between the placebo and TXA arms.

So since social media is clamoring, and since this is published in the Lancet, there must be a mortality benefit, right?

This is where I point out three things:

1) there was no difference in mortality (2.3% vs 2.6% – favoring placebo)

2) TXA had 0.4% fewer patients who experienced death due to post-partum hemorrhage

3) this was accompanied by a p value of 0.045, and a fragility index of…..

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A study of 20,000+ patients, and a p-value of 0.045, and a fragility index of zero.  And again, the most patient-centered outcome possible- mortality – favored placebo.

TXA is not the magic bullet in this instance.  There is a weak signal of benefit if you are proceeding to laparotomy for bleeding – particularly for caesaean delivery (1.5% vs 2.4% mortality benefit, fragility index of 4), but that is an exploratory analysis needing further review, otherwise, this is a flimsy trial.  While TXA remains inexpensive, it is worth a go- particularly in low-resource areas after laparotomy (provided TXA is still inexpensive there), but by no means does a clinician not giving it deserve to be chided – the evidence is incredibly fragile and not worthy of social media’s  “life-saving” claims – at least for post-partum hemorrhage.

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.


Let’s stop the sepsis high-five.

82 y/o F from SNF, AMS, “foul smelling urine.”

80/50, 103.1 PR, 120HR 98%.

An initial POCUS showed a collapsing IVC, you give 30 cc/kg LR, 650 Tylenol PR, vancomycin loading dose, and 3.375g Zosyn. BP is now 110/74, HR is 80 bpm, labs show an obvious UTI, and you call to admit the patient.

Or as I like to call this, the “sepsis-high five.”


This is a single center study of 828 patients looking at time delay between first and second antibiotic. They broke it down to 6, 8, 12, and 24 hour drugs, and considered a delay of 25% significant (90 minutes for a q6 hour drug, 180 minutes for a BID drug, etc). The primary outcome being in-hospital mortality.

So what’d they find? Well, unsurprisingly, they found that 72% of patients had a delay with 6hr dosing between their first dose and second dose compared to 47% for Q8hr antibiotics, and 25% for Q12hr antibiotics. (<5% for Q24hr drugs- but they had 6 hours to hang the dang drug!)… They acknowledge several issues: we often order a one time dose in the ED, but the upstairs care only knows Q6hr drugs at 12-6-12-6 dosing. I think this is most likely the case in this study, since the next dose for a 6, 8, and 12 hour drug were 9.55, 9.6, and 10.6hr respectively. They also acknowledge that it is possible that delayed second antibiotics are not inherently contributory to adverse patient outcomes, but simply a surrogate for patients who generally received less attention and care overall, particularly given 43% of delays occurred in ED boarding in their institute.

Paradoxically, those that received the q6hour antibiotic (cough, ZoSyn, cough), had high rates of adherence to the sepsis bundle (fluid loading, early pressors, early abx, etc) – but also high rates of >25% delays to second doses. True, it only took an hour and a half to have a delay for zosyn, but that is the point here: while yes, you provided solid care up front, are your system failures (preset administration times from your inpatient order sets) hurting your patients? Or is it a sign that those getting tighter adherence to everything (Q6hr drugs, early pressors, etc), and that those patients are getting better care with better adherence to second dose antibiotics as merely a proxy?

Regardless, there was a 1.6x increased odds of mortality for those with >25% delay, and a 2.4x high rate of mechanical ventilation, with an OR of 72 for a missed second dose of a q 6hr drug, 24 for a q 8hr drug, and 7 for a q 12hr drug.

Call it better care. Call it a reason to do a ZoSyn continuous infusion. Call it an inpatient problem. Regardless, it should not be ignored.

Me? I maintain that if the patient is still in my emergency department, its still my patient no matter how long they have been there. Hence, I’ve been known to periodically order a second dose of ZoSyn – especially for the critically ill and those being transferred. So, much like after a successful intubation post-arrest there is much work to do, there is much work to do post resuscitation for a septic patient.


Dedicated post-arrest services? meh.

Should we regionalize post-arrest care?  Well, if your facility does not have a cath lab, then the answer is yes.  But Academic Hospital A, which sees >100 arrests a year, just started advertising a fancy post-cardiac-arrest service.  Academic Hospital B also sees >100 arrests a year, but does not have a post-arrest service aside from their MICU.

You, being at hospital C without a cath lab, have just achieved ROSC in a witnessed arrest. Who do you transfer to?

This study looks at 987 post-arrest patients that survived to admission at 7 hospitals in and around Southwestern Pennsylvania. One of them is a regional referral center with post cardiac arrest services consulted on OHCA with ROSC, accepts sudden cardiac arrests from outside facilities, and is consulted on in-hospital arrests with ROSC. There are two additional tertiary care centers that see >100 SCA annually, and 4 “low volume” centers. They look at multiple variables, and evaluate discharge disposition, discharge CPC, and length of survival post-discharge.

They improved numbers of discharge CPC – the post arrest service center with a discharge CPC of 1 or 2 32% of the time vs 37% of the time for the other 6 facilities. More patients were discharged to home (41% vs 32%) from the post-arrest service center and survived for longer if they were treated with the post-arrest service.


While the authors claim similar patient characteristics between the post-arrest service center and the other 6 hospitals…. 46% of patients were transferred to the post-arrest service center vs 16% at hospitals 2-7 – perhaps skimming a healthier patient that made it through the transfer (remember- you had to survive to discharge to be counted) – the authors even acknowledge that their transferred patients did better than their other arrests.

Add in that the initial rhythm 51% of the time was VT/VF for the post-arrest service center vs 41% in the other six hospitals, and you’ve got plenty of confounders. Frankly, given all of this, it’s a bit strange that the proportion of patients surviving to discharge did not differ at all. One would think if you have a post arrest service and the scales are tipped in your favor to begin with, that you’d have a higher percentage of patients surviving.

Ultimately, patients lived longer post-arrest when treated at a facility with a post-arrest service, and the authors are touting this as reason to (further) regionalize post-arrest care.  Sure, there are slightly better neurologic outcomes, but the scales were tipped in their favor to begin with. I don’t trust this conclusion, especially when the post-arrest service had an advantageous patient population to begin with that should have led to a measurable increase in improved survival, in addition to an increase in length of survival.

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.