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.

Cardiology, Cardiology, Improving Throughput, Mythbusting

Surprise! You still do not need to treat asymptomatic hypertension in the ED!

Surprise! We have yet another paper, in addition to the ones mentioned here that demonstrates acutely managing hypertension without end organ damage is unnecessary.


This multicenter study retrospectively looks at 1,016 patients, age 18 years or older, with an initial blood pressure greater than or equal to 180/100, with no evidence of target organ damage, that were discharged with a primary diagnosis of hypertension.  435 patients (42.8%) received antihypertensive therapy (88.5% received clonidine!), while the rest did not receive antihypertensive treatment in the ED.   Those who received antihypertensives often had a higher mean initial systolic and diastolic BP (systolic 202 vs 185, and diastolic 115 vs 106). Otherwise, all other measures were similar & not statistically significant- this includes repeat ED visits within 24 hours (4.4% vs 2.4% antihypertensives vs none), repeat visit within 30 days (18.9% vs 15.2%), mortality at 30 days (0.2% for both groups), as well as mortality at one year (2.1% vs 1.6%).

Unfortunately, this is a retrospective study, so perhaps they are not catching the patients with a chief complaint of hypertension, and perhaps ultimately diagnosed as a bleed.  It is reassuring to see that 30 day and mortality and 1 year mortality are similar.  However, with 94.5% of the total patient population being African American, these results may not necessarily be broadly applicable to all ED patients.  It would have been nice to see them analyze all patients over a 12 month period who presented with a triage BP > 180/100, and blind reviewers to disposition and outcomes.  With only ~500 patients in each arm, I am not certain this adequately screens for rare events, but I still think that this is one of the better attempts to date to back up ACEP policy on asymptomatic hypertension

(1) Initiating treatment for asymptomatic hypertension in the ED is not necessary when patients have follow-up; (2) Rapidly lowering blood pressure in asymptomatic patients in the ED is unnecessary and may be harmful in some patients; (3) When ED treatment for asymptomatic hypertension is initiated, blood pressure management should attempt to gradually lower blood pressure and should not be expected to be normalized during the initial ED visit.

Cardiology, Cardiology, Improving Outcomes, Improving Throughput, Mythbusting

Chest Pain Statistics That’ll Make Obs Bump Trops

I have been lucky enough to attend ACEP over the last few years, and even luckier to watch David Newman speak. Specifically, I have attended his “Is One Troponin Enough?” lecture, which was practice changing for me.  It also encouraged me to drench both my patient discussions and MDM’s in evidence prior to discharging patients. Among others, Newman is at it again in today’s article, found here.

At 3 institutions over 5 years, from July 1, 2008 to June 30, 2013, encompassing over a million ED visits in total at these three institutions combined, the authors sought to determine the incidence of clinically relevant adverse cardiac events in patients hospitalized for chest pain with two negative troponins, normal vital signs at time of arrival to the ED, and nonischemic EKGs throughout their stay.  Clinically relevant events were defined as life-threatening arrythmia, inpatient STEMI, cardiac or respiratory arrest, or death during hospitalization.

Essentially, during the 5 year study period, over one million ED visits, and over 11,000 patients admitted with two negative troponins, only 20 patients had an adverse outcome (0.18%). When you exclude abnormal vitals at presentation, ischemic EKG findings, left bundle branch block or a paced rhythm, only 4 events were seen out of 7266 patients (0.06%), with two being non-cardiac, and two (possibly) being iatrogenic.


Let’s process this for a minute.  When taking all-comers – not just the low risk observation patient- with two negative troponins (drawn between 60-240 minutes in this study) your risk is quite low at 0.18%, now exclude non-ischemic EKGs, patients with abnormal vitals, a paced rhythm, or a left bundle branch block, and your risk is 0.06% of an adverse outcome – and more likely to be iatrogenic than cardiac!

Now let’s couple the above study with this study, where they examined almost 700,000 private-insurance ED patients in 2011 presenting with chest pain. They followed patients that both did and did not receive additional diagnostic testing (exercise stress test, stress ECHO, myocardial perfusion scintigraphy, or coronary CTA). Essentially, the rate of MI at 7 days and 190 days was low overall (0.11% and 0.33% respectively). Most importantly – patients who did not undergo initial non-invasive testing were no more likely to experience a myocardial infarction than those who did not receive additional testing. Compared to no testing, additional testing was associated with significantly higher odds of cardiac catheterization and revascularization procedures without a concomitant improvement in the odds of experiencing an MI.

So why are we consulting cardiology for observation patients with two negative troponins? Why are we ordering stress testing for inpatient or observation patients? This is yet another example of why it is important to provide well-informed consent for your patient, and a great example of a well-intentioned hospitalization and consultation providing (potentially) more harm than good.

It is high time we cease and desist the scare tactics we employ to patients to strong arm them into either an AMA or admission, rather than providing them a look at the current data before making their decision.

Cardiology, Improving Outcomes, Mythbusting

Crazy Gets Sick Too.

This paper examines 57,000 patients who had a a new diagnosis of schizophrenia, dementia, or “mood disorders” who were initiated on antipsychotics within 120 days of Acute Myocardial Infarction (AMI) – defined by receiving PCI, fibrinolytics, CABG, and/or antiplatelet therapy. Those with known comorbid cardiomyopathy, or a diagnosis of pericarditis, aortic dissection, or coronary aneurysm were excluded.

Essentially, the risk of having an MI was increased in the first month of initiation of first or second generation anti-psychotics, as well as with an increased antipsychotic dose within 4 months from initial psychiatric diagnosis. Males, elderly patients, and those with dementia had an increased risk, and those that were healthier, without diabetes, hypertension, or high cholesterol were also at an increased risk – all in comparison to a similar spectrum of patients who were started on benzodiazepenes or non-benzodiazepene hypnotics. The OR for AMI with first generation anti-psychotics was 2.32, and 2.74 for second-generation anti-psychotics. The OR for AMI after initiation of anti-psychotics within one month? 5.46!

For the most part, I like this study – it examines a large number of patients, and has a reasonable comparison (anti-psychotics vs benzos vs non-benzo hypnotics). I don’t like that they don’t provide a breakdown of interventions – if 95% of the patients were only initiated on anti-platelet therapy, then I’m not so sure of the validity of the article. Also, it is a Taiwan study, and the authors acknowledge that they may metabolize drugs differently than other ethnic groups, so they caution that their results may not be applicable to all populations.

Regardless, I think the message is clear and broadly applicable: crazy gets sick too, sometimes more than the general population.

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

Day Five of Christmas- where’s the Obs EBM?

Welcome to the Twelve Trials of Christmas series on EMinFocus!  This is the fifth 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.

I believe that the longer a patient stays in the hospital, the more likely they are to develop new and exciting pathology (pulmonary emboli, VRE, general deconditioning, an unhealthy affinity for tuna sandwiches, etc).  t’s not that I want to throw people out so to so to speak, it’s that their risk of developing hospital acquired badness is higher than their risk of adverse outcome from their diagnosis (like, say, low / no risk chest pain).  As such, I’ve recently taken an affinity towards our observation unit to see which, if any, of the classically admitted COPD’ers / CHF’ers, etc, can be placed in observation for <24 hours (actually need to be there), and do well.

We need to see some studies for who is a candidate for observation – and perhaps some data on why ED providers put no risk chest pain and other similar low yield findings in observation. There is little to no data on observation units, despite over a third of hospitals in the US having them.  Despite guidelines for observation, there are few evidence based guidelines.  We know that increasing age is associated with an increased rate of admission from observation status (about 26% vs 18 %); and there are also cellulitis guidelines for observation units, but that is about it.  While there are Ottawa guidelines for admission for CHF and COPD, and the famous PORT scores, these rules were designed to identify low risk patients, not necessarily those that needed a day or two in the hospital.

 So, perhaps, much like we have recently begun to risk stratify PE’s into going home and being lysed, so we will have to do the same for utilization of observation & inpatient resources.  What delineates which patients in the grey area between obvious discharge home and ICU admission can go to observation – not just the ED provider saying “yeah, they look ok for observation” – some actual evidence that suggests the patient can be turned around in under 24-36 hours.  I suspect for CHF, we’ll see that most of these patients, once properly cared for in the ED (cough, nitro nitro nitro, cough), can go to observation, which will likely surprise most ED & inpatient providers – thus, hopefully decreasing the risk of hospital acquired badness for these patients.

Cardiology, Cardiology, Improving Outcomes, Improving Throughput, Mythbusting

“So Doc, what are we doing about this patients blood pressure?”


The next patient in the rack was sent by WebMD after their new iHealth Wireless Wrist Blood Pressure Monitor told them to come to the ED because their blood pressure was at “stroke level.”

While indeed, this patient has a blood pressure on initial evaluation of 205/115, but they have not had any chest pain.  They are clearly not altered on eval, and they deny any vision changes or headaches and have a non-focal neurological exam.  When asked why they even checked their blood pressure, it was because all their friends who have doctors were told to check their blood pressure at home.  

So what does this patient need?

If the patient offers some vague complaints that were persistent, I guess you could argue for electrolytes, maybe an EKG / troponin (if dyspneic, diaphoretic, or nausea after exertion then perhaps go the ACS workup route).  If the patient is completely asymptomatic or with fleeting vague symptoms, the first step – if any (after an H&P) – should be a urinalysis.  In June 2010, AJEM published an important study on this.  They screened 5,416 patients just like the ones above.  Essentially, if the patient has neither hematuria nor proteinuria, there is a 98.3% chance that they will not have a serum creatinine above 2.0.  For Creatinine above 1.3 and 1.5, the lack of both proteinuria and hematuria has a negative predictive value of 92.4% and 95.3% respectively. 

What does ACEP say? ACEP recommends, with a level C recommendation, that screening for acute end-organ injury is not required. As long as the patient is not altered, has a normal neurological exam, no vision changes, and no crushing chest pain, you essentially already screened them without doing a single test! A UA will do a great job at ruling out AKI. If a UA is positive for either hematuria or proteinuria, then send a serum creatinine – if at that point you have an elevated creatinine >25% from baseline, then consider admission. With a benign history and exam, the patient does not need electrolytes, troponins, a BNP, an EKG, Chest XRay, and certainly not a brain CT. Here is the data ACEP provides on this:

A Class III study, the VA Cooperative Trial of 1967, was a randomized placebo-controlled trial of 143 male patients with diastolic blood pressure of 115 mm Hg to 130 mm Hg. No adverse outcomes in either group were demonstrated during the initial 3 months of enrollment. Four of 70 patients in the placebo group (6%; 95% CI 2% to 14%) versus 0 of 73 patients in the treatment group (0%; 95% CI 0% to 5%) developed significant complications within 4 months of enrollment, including sudden death, ruptured aortic aneurysm and death, severely elevated blood urea nitrogen level, and congestive heart failure. However, within 20 months, 27 of 70 patients (39%; 95% CI 27% to 51%) treated with placebo and 2 of 73 patients (3%; 95% CI 0.3% to 9.5%) treated with antihypertensive drugs experienced adverse events (absolute risk reduction 36%; number needed to treat = 3.″

So at 3 months, no worries. At 4 months, trouble may start. At 20 months, big trouble. So what are we supposed to do about it in the ED? For the patient who has no symptoms, a normal UA, and isolated hypertension treat based on the locale you’re in. If follow up is easy, leave it alone. If getting into clinic is impossible, consider starting an oral medication in the ED.

Now, what does the legal side of this look like?  Well, I attempted to peruse Google Scholar, using the terms “Emergency Department” “malpractice” and “hypertension.”  I’m far from good at browsing the medico-legal literature, but of the 97 results, I can not find a single case of an asymptomatic hypertensive that was sent home and the provider was later sued.  Of the vaguely pertinent cases where the patient presented with significantly elevated blood pressure (email or tweet me for links), all the patients had some other symptoms that were alarming- “cold symptoms” – ie, misdiagnosed CHF;  chest pain and weakness that was given Ramipril, Bisoprolol / HCTZ that later stroked; syncopal elderly patient that fell twice in the ED and was usually ambulatory; “slow, unsteady, hot & sweat with double vision,” ; severe headache, off balance, blurred vision, dizziness.  Bottom line, you’ve got time to work with outside the ED walls, so there is no need to “buff the chart” and give IV hydralazine prior to discharge.  As ACEP policy notes, you are more likely to do harm than good.




PMID: 20579559

PMID: 24352797

Cardiology, Cardiology, Improving Outcomes, Mythbusting

So did you pass out, or almost pass out?

Recently, @EBMGoneWild brought up this great article on Twitter.  @EMSwami hit the nail on the head:  It’s time we thought about pre-syncope in the same way we think of syncope.

The above referenced paper reviews 780 presyncopal patients over age 16 presenting within 24 hours of “a feeling of impending loss of consciousness and (did not lose) consciousness.”  Patients were excluded if they had a loss of consciousness, a seizure, or trauma. 4.7% of patients were admitted (41 total patients), and there were 40 “serious outcomes,” with 13 of them happening outside of the hospital.  Since those are the ones that keep us up at night, let’s look at those.

1) 76 year old male, bounces back 1 day later and admitted for orthostatic hypotension.

2) 75 year old male, bounces back 3 days later with complete heart block.

3) 84 year old male, bounces back 3 days later in SVT with aberrancy.

4) 74 year old female, bounces back 3 days later, now with dyspnea, diagnosed with PE.

5) 88 year old male, bounces back 4 days later with complete heart block.

6) 55 year old female, bounces back 11 days later with complete heart block.

7) 85 year old male bounces back 11 days later, two days later found to be in complete heart block.

8) 63 year old male bounces back 17 days later, originally with urinary retention, now with AMI.

9) 57 year old female bounces back 18 days later, persistent dizziness and ataxia, worsening, found to have cerebral metastasis.

10) 59 year old female bounces back 20 days later, DOA, history of breast cancer, though not thought to be terminal.

11) 66 year old male bounces back 27 days later, had Afib on stress testing.

12) 49 year old male bounces back 30 days later, several syncopal episodes in past, had VFib at outpatient cardiology follow up.

13) 91 year old nursing home patient with history of dementia and prior stroke, died at SNF, unknown cause, unknown date, but within 30 days.

Of these, I’m not certain orthostatic hypotension should be considered a serious adverse event, nor the stress-test induced Afib. Take out number 13- 91 years old, history of dementia- and that leaves us at a 1.3% adverse outcome rate.   Exactly one adverse outcome was under age 55.  For comparison, the landmark SF Syncope Criteria paper exclusively looked at those over age 65 and it has a 98% sensitivity.

So what is the take home?  To me, there are three.  First, is to order – AND DOCUMENT!-  telemetry strips on your near syncope (and syncope!) patients.  There were a few near misses that were caught because someone actually looked at the cardiac monitor rhythm strips when the sirens were going off.  Please, before discharging a patient, if you ordered a cardiac monitor – or if the patient happened to be placed on one – REVIEW AND DOCUMENT IT.  This brings me to the second point.  It is better to be lucky than good.  One of the “serious adverse events” was admitted 11 days after the initial near syncopal event, only to happen to catch an intermittent complete heart block on day 13.  The patient was admitted and monitored for two days before his concerning symptoms manifested.  The inpatient team had several more hours than the ED to diagnosis this patient and happened to call a consult to Lady Luck for final diagnosis.  It’s better to be lucky than good, but sometimes luck favors those well prepared who review the rhythm strips and follows the evidence.  Thirdly, if you see enough near syncopal patients, eventually, you’ll get a bounceback in complete heart block.  You’ll recall it took the inpatient team two days to find a complete heart block on a patient that bounced back to the ED.  To reduce risk, feel free to refer to cardiology, but the reality is that medicine is not a zero risk game.  Every time you admit for arrhythmia concerns, this actually means you are certain that there is a higher risk of arrhythmia than the inherent risk of PE or HAI from hospitalization. Let that sink in for a moment, then consider discharging for holter monitor / loop recorder placement instead.

There is risk at every turn no matter the intersection, so choose wisely my friends!