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.


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, Improving Throughput, Mythbusting

Albuterol: Sepsis Mimic

In today’s day and age of overtesting, some providers will not send home a patient with an abnormal lactic acid at all, regardless of etiology. So let’s examine what can possibly cause abnormalities of the current apple of our sepsis eye.

Here, 28 healthy subjects were randomized to placebo or 10 mg of nebulized albuterol over an hour. This is what many of us would consider “an hour long treatment” – or about 4 of those plastic neb vials. Serum lactate (and serum potassium as well) was measured prior to treatment, and at 30 minutes and 70 minutes after the start of treatment.

In the 14 patients receiving albuterol, their lactate went up on average 0.77 mmol/L vs a decrease of 0.15 mmol/L for the placebo group, while serum potassium levels went down by 0.5 mEq/L in the treatment arm vs no change in the placebo arm.

In our current overdiagnosis induced sepsis frenzy, if you must order a lactic acid, do it before giving albuterol, or better yet, if there is clearly some other reason for dyspnea aside from an infectious etiology (asthma or COPD that require immediate albuterol) – don’t order a lactic at all and document that an infectious etiology is not the cause of today’s abnormal vital signs.

Critical Care, Improving Outcomes, Improving Throughput, Mythbusting, Pediatrics, Pediatrics, Pediatrics, Pulmonary

Do we need to give (alot) more Magnesium to asthmatics?

Some of us have quirky things we like to do that not everyone else does– dexamethasone for sore throats, ketamine for the agitated patient (or anything really), et cetera… This paper looks at one of those things – Magnesium in asthmatics. 

This was a prospective, randomized open-label study of patients between 6 and 18 years of age over a two year period who presented to an ED in Asuncion, Paraguay and were admitted for a severe asthma exacerbation.  Patients were excluded if given antibiotics before or during the ED visit, febrile, or if there was suspicion for infectious etiology.  All patients enrolled had no relief despite 2 hours of treatment which included dexamethasone 0.2mg/kg IV, nebulized salbutamol every 20 minutes up to 5mg and nebulized albuterol every 2 hours.  There were two treatment arms, each with 19 patients: one received a 50mg/kg bolus of MgSO4, while the other group received 50mg/kg/hr/4 hrs (ie, up to 2g / hr for 4 hours – up to 8g total).  Physicians in charge of patient disposition, after the initial 8 hours, were not part of the study group and blinded to the treatment received.  Primary outcome was discharge at 24 hours, with secondary outcomes total LOS and cost implications.  The two groups were similar in terms of age, sex, initial Wood-Downes asthma score, and peak flows.

Despite the numerous downfalls to this study (single center, open-label, prospective, small sample size…), the results are intriguing- bolus magnesium had an average LOS of 48 hours vs 34 hours for high dose prolonged infusions, had a higher cost ($834 vs $603), and fewer patients with a LOS <24 hrs (10.5% vs 47.4%).  It took almost two years to get under 40 patients in this single-center study,  but still, there were no adverse events and no bounceback visits within a week from discharge.  Interestingly, there were no obese patients in the study – so how applicable this study is to the US patient population, I do not know (plus, salbutamol is not widely used for acute asthma in the US).   That, and even for this mag-o-phile 8g per hour for 4 hours seems like alot!

Should this change your practice?  Not quite yet – unless you’re not giving magnesium.  In the meantime, I’ll add another one to the list of trials I’d love to see.

Critical Care, Improving Outcomes, Improving Throughput, Mythbusting, Pulmonary, Twelve Trials of Christmas!

Day 7 of Christmas- NAC for COPD.

Welcome to the Twelve Trials of Christmas series on EMinFocus! This is the seventh of twelve posts in a series where I ramble on various topics for which I would love to see an EM study done. I’ve taken morsels of prior studies (case series, small trials, etc) and highlight reasons on why I believe this study would benefit EM. Some may pan out, some may not. All of them I would be highly interested in assisting with in any way possible to continue to advance our fine specialty.

The next ED study I would like to see is Nacetylcysteine (NAC) for COPD.  Initially, the BRONCHUS trial in 2005 looked at 523 patients using once daily 600mg NAC for prevention of flares and mproving FEV1. They found no benefit.  Two studies in the last two years have looked at twice daily dosing of NAC, finding decreased exacerbations, and a third showing NAC potentiated the bronchodilatory effect of ipratropium.


Given the above, a trial of NAC in the ED may provide some benefit in helping patients get over the initial hump, and perhaps, lead to an early discharge. (Perhaps akin to early systemic steroids in addition to the patients inhaled steroid regimen during exacerbations).  At the least, it may cause pulmonology to reconsider giving NAC to their patients on the outside world and help it come standard of care.

Improving Outcomes, Mythbusting, Pulmonary, Twelve Trials of Christmas!

Day six of Christmas – curing the bronchitis!

Welcome to the Twelve Trials of Christmas series on EMinFocus! This is the sixth of twelve posts in a series where I ramble on various topics for which I would love to see an EM study done. I’ve taken morsels of prior studies (case series, small trials, etc) and highlight reasons on why I believe this study would benefit EM. Some may pan out, some may not. All of them I would be highly interested in assisting with in any way possible to continue to advance our fine specialty.

Essentially, there are about 4 things to do for a cough.  Dextromethorphan (robitussin), anything with Benadryl/codeine/phenergan/hydrocodone, tessalon, and honey.  For pediatrics at least, honey seems to be the preferred method for parents and seems work better than Dextromethorphan and Benadryl in head to head trials.  I’ve yet to find data on Tessalon, Phenergan, or codeine suggesting it is useful for a cough when compared to placebo.  I’d like to add another medication to the toolkit for an intractable cough: nebulized lidocaine.

The studies are not of the best quality, but here is what I can find:

– 21 patients with obstructive, restrictive, or infective disease who received 10-20mg of nebulized lidocaine Q4-6hrs seemed to improve and/or resolve the cough when compared to standard of care (hycodan, Robitussin).

– A case series of 3 pts treated with a single dose 10mg lidocaine and 5mg bupivacaine (both nebulized) and had no recurrence of cough.

– A case series of 3 patients with a chronic cough secondary to lung cancer treated with higher doses of nebulized lidocaine  (up to 400mg!) along  with 2-5mg albuterol.  Resolution of cough persisted for >1week in all patients.

– A case report of a pediatric patient treated with 30mg nebulized lidocaine for a cough refractory to cough suppressants, beta agonists, steroids, and antibiotics.  The cough completely resolved.


There are multiple studies looking at nebulized lidocaine for endoscopy and laryngoscopy, but no reports of systemic toxicity from nebulized lidocaine as there appears to be less systemic uptake when administered via nebulizer.  So, it appears safe in that regard.   The asthma literature is a mixed bag, as some say it cause harm during asthma exacerbations as it may decrease FEV, but others show benefit.  However, for COPD flares, it appears beneficial.

For those hacking coughs that truly feel bad for, I’d love to see an ED trial of nebulized lidocaine as a one time dose – or even perhaps in an observation unit for your COPD’ers / pneumonia/bronchitis patients.  Easy trial to perform, and one that would significantly improve patient satisfaction – and perhaps then something other than a z-pack would get credit for improving the cough!  

Improving Outcomes, Improving Throughput, Mythbusting, Pulmonary, Pulmonary, Radiology, Radiology

Good thing you caught that Chest Cold early.

There has been recent discussion in the #FOAM world in regards to labeling otherwise benign conditions (such as GERD in pediatrics) and the patient & family perception requiring medications for this.
Seth Trueger (@mdaware), at ACEP13, brought to my attention an interesting paper in regards to another common labeling of a benign condition, acute bronchitis.

In 2005, 459 patients were presented with a written scenario describing a typical acute respiratory infection in which they were labeled either to have a “chest cold”, “viral infection” or “acute bronchitis” and also were provided with a treatment plan that excluded antibiotic treatment. There is no changes in satisfaction or dissatisfaction with the diagnostic label however, 26% of patients were dissatisfied with treatment 1 provided with the label “bronchitis”and not provided a prescription for antibiotics compared to 13% for a chest cold and 17% for a viral illness respectively. There was no differences in regards to patient’s satisfaction based on age, sex, or education level.

The authors also note that patient pressure is a significant role in antibiotic overprescribing. They note that 54% pediatricians feel parental pressure to inappropriately prescribe antibiotics. For adults, 77% of the time when providers were questioned about antibiotics, they were prescribed first 29% of the time when providers were not asked.

So, to want to decrease your patient dissatisfaction, might I suggest, in the words of Hoffman & Bukata:

“It seems to be a chest cold. Good thing you caught it early before it turned into bronchitis!”





PMID: 16322409

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

NIV for Pneumonia

It is by and large a foregone conclusion that non-invasive ventilation (NIV) saves intubations (and lives) in COPD and CHF. There has not been too much #FOAM specifically for pneumonia and NIV, so let’s dive in.

Recently, there was a publication stating that NIV treatment failure was significantly higher for pneumonia vs COPD (49% vs 12%). This was a small study (under 80 patients), but does this mean we should not try NIV for pneumonia? More importantly, do pneumonia patients have worse outcomes than they otherwise would if they were intubated sooner? Is it worthwhile to give a NIV trial in pneumonia?

To start, 127 patients with respiratory failure secondary to community-acquired pneumonia (CAP) were examined prospectively. 25% of these patients failed NIV. Those that failed NIV were more likely to have confusion at presentation, were >65 years old, had worsening chest films over time, and lack of improvement at 1 hour on NIV.  A second study of similar ilk (CAP placed on NIV) examined 64 patients in which 43% of patients successfully avoided intubation (ie, 57% failed NIV). Success was associated with a lower APACHE II score, higher pH at the end of NIV trial (7.34 vs 7.44), and lower respiratory rate (28 vs 23 breaths/minute).

Now that flu season is upon us, let’s examine the 685 patients with confirmed influenza A that were studied in Barcelona in a prospective observational registry.  489 patients were intubated in the ED and 177 received NIV.  NIV was effective 40.6% of the time, and associated with shorter LOS.  Key details in this study were that not requiring vasopressors, the absence of renal failure, and fewer than one lobe involvement on CXR were all significantly associated with successful NIV. Most importantly, the delay in intubation did not affect mortality (26.5% for ETT, 24.2% for NIV).  Thus, for every 100 NIV patients in whom the decision to intubate was made, there was ~25% mortality – roughly the same rate as those that were intubated without a NIV trial – so the delay does not worsen outcomes.

For the immunocompromised, an evaluation of 120 patients came to similar conclusions: higher APACHE II scores and a need for vasopressors were associated with failure of NIV.  Underlying disease did not affect NIV duration rates or outcomes.  Again, the authors found that the mortality rate of failed NIV patients that required intubation was similar to those that were intubated from the start.

Conclusions?  If you need to start pressors, or have new onset renal insufficiency, you may want to skip NIV and reach for the intubation kit first.  Otherwise, with 40-75% success rate of NIV, and without an adverse outcome for delayed intubation in pneumonia patients, it seems reasonable for the patient to first have a trial of non-invasive ventilation.





PMID: 24814916

PMID: 25043135

PMID: 20435435

PMID: 22404211

PMID: 22944604

Mythbusting, Pulmonary

Being Color Blind to Bronchitis.

An October 2013 BMJ study compared patients aged 18-70 without underlying lung disease or immunosuppression, with an acute cough of less than one weeks duration. Cough with “discolored” sputum was a requirement of all patients, and they required at least one other symptom of lower respiratory tract infection (dyspnea, wheezing, chest pain or chest discomfort). Patients were excluded if they had previously used NSAIDs or antibiotics within the last 2 weeks, greater than 7 days of cough, allergies to NSAIDs or Augmentin, or had pneumonia on chest film. The three arms were as follows for ten days:

Ibuprofen 600mg TID (136 patients)
Augmentin 500-125 TID (137 patients)
Placebo TID (143 patients)

Patients had follow up at 2-4 days, 11-13 days, and again at 30 days if symptoms were not resolved by the second visit. Patients kept a diary of disease severity, daytime cough, night time cough, limitations of ADLs, and fever. There was essentially no difference in the number of days with cough, regardless of treatment, and 12 % of Augmentin patients having an adverse drug reaction, compared to 3% of placebo and 5% of ibuprofen. The authors point out a previous Cochrane review found antibiotics to have a slight advantage over placebo in controlling cough, but that review came from a total of 275 patients – more than a hundred fewer than this trial. The authors are also quick to point out that COPDers have been shown to benefit from antibiotic treatment with a change in sputum color.

The next time a patient states, “but I’m coughing up green stuff,” you’ll have the evidence in hand to either refute the prescription request, or give a risk benefit discussion about the 400% increased rate of side effects from antibiotics over placebo in this setting (12% vs 3%).

PMID: 24097128

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

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 .



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