Something very cool is happening in emergency medicine, specifically low risk chest pain. What I mean by that is figuring out who is low risk and what to do about it. This is one of the biggest areas of CYA, for the uninitiated, cover your ass, medicine. And for good reason, it’s a big cause of lawsuits and if we get it wrong, people can die. We just had two episodes on cardiac CT addressing this very topic and one thing that came up in the last show with Rory Spiegel, was that the Cardiac CT did not perform any better than just using risk assessment and cardiac enzymes. But what does that mean? What is risk assessment in the ED? Is it, “Holy moly, that sounds like cardiac chest pain for sure, bang, you’re admitted.” Or is it, “C’mon, that’s not cardiac chest pain.” Well, that’s indeed a small part of it, but there has been improvement on assessing risk using enzymes and risk scores. The TIMI score has been out there for a while but it’s not as nuanced an instrument as we’d like. The HEART score may be a better and more usable tool in the ED.

Links for this episode

Amal Mattu's full explanation of Chest Pain ADP, Low risk chest pain, medico-legal aspects of chest pain, chest pain guidelines

University of Maryland Low Risk Chest Pain ADP

Shared Decision Making Graphic

Heart Score Calculator 

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We are hungry for a sensible, safe and consistent pathway for evaluating chest pain. A new chest pain ADP has emerged from from the primordial soup, and it comes from none other Dr. Amal Mattu. Here is a link to Amal’s full explanation of the ADP and chest pain risk assessment and I recommend you to listen to it to get the full flavor of what he’s talking about. But for now, a  recap….

Many chest pain pathways have relied on the TIMI score, but that is a somewhat cumbersome tool for our needs. The HEART score shows promise as a decision instrument with more utility in the emergency department. The HEART score uses 5 criteria: history, EKG, age, risk factors, and troponin to determine risk of a 6 week major adverse cardiac event. Each one of these pieces has three parts. For example, risk factors: no risk factors, zero points; 1-2 risk factors, 1 point; 3 or more risk factors, 2 points. If a patient has everything, everything positive in the heart score, that’s 10 points -high risk. Low risk is 3 points or less. A low risk score gives a 1.7% 30 day risk of major adverse event. Add in a second negative (delta) troponin, and the risk goes down to under 1%.

Guest post by Rory Spiegel, A.K.A Captain Basil, A.K.A EM NERD

In today’s age of Modern Medicine, we consistently favor the objective findings provided by medical technology over the more subjective judgments of the experienced clinician. Yet the precision of these tools has rarely demonstrated superiority when compared to the experience and wisdom of the practicing physician.  Nowhere is this more evident than with the recent introduction of CT coronary angiogram (CTCA) for the work-up of chest pain in the Emergency Department. The lure of CTCA is rooted in our fear of uncertainty and the promise that this test may provide a safe non-invasive measure to quell these doubts.  Despite the overwhelming lack of evidence demonstrating CTCA’s efficacy over the more traditional risk stratification methods of history, physical, EKG and biomarkers, CTCA continues to make a push into the hearts and minds of Emergency Physicians.

The claims of CTCA’s successes are based off the negative predictive ability demonstrated in a number of cohorts of low-risk chest pain patients. In four large prospective trials, authors found that following a negative CTCA a diminutively low number of patients had an MI within the next 30 days (1,2,3,4). What proponents of this test fail to mention is that none of the patients in these cohorts, independent of the type of downstream testing they received, had a bad outcome during the 30-day follow up period. In the ACRIN-PA trial, the largest of these cohorts, only 2 of the 1357 patients who did not rule in for MI during their initial presentation experienced an MI within the next 30 days, independent of what was found on their CTCA (4). Seemingly just by meeting entry criteria to be enrolled in these trials, patients identified themselves as being at such a low-risk that they were destined for a good outcome independent of the testing strategy they received.

We now have four trials randomizing low-risk chest pain patients to either a standard work up or CTCA following a negative Emergency Department work up. Each study demonstrated that CTCA adds no additional prognostic value to our standard risk stratification strategies and likely leads to increased invasive procedures. In a meta-analysis of these four trials published in JACC in 2013, Hulten et al found a significant increase in the number of invasive angiographies, PCIs and revascularizations performed in the patients randomized to the CTCA arm (5). The only arguable benefit these trials were able to identify, in patients randomized to receive CTCA, was a moderate reduction in the length of stay. Even these temporal benefits are an illusion though, as many patients in the traditional care arm experienced a prolonged length of stay because they were subjected to unnecessary provocative testing that required admission to observation units (4).

The concept that CTCA adds diagnostic utility to the traditional ED chest pain work-up has been consistently disproven. Proponents continue to argue for the utilization of CTCA in the Emergency Department, suggesting that CTCA will provide additional risk stratification of patients with CAD, and allow us to determine which patients will benefit from more aggressive medical therapy. Until the FACTOR-64 Trial, published in in JAMA in 2014, this concept had not been validated in a prospective fashion (6).  Muhlestein et al enrolled 1000 high-risk patients and randomized them into traditional management of CAD or the use of CTCA to guide medical management. The authors found no difference in the primary endpoint: rate of death, MI or unstable angina (UA) between the groups (7.6% vs 6.2%). Additionally the patients randomized to the CTCA group received far more diagnostic caths (5.1% vs 13.3%), PCIs (1.8% vs 6.0%), and CABGs ( 1.3% vs 2.9%) than patients in the traditional management group. Even the concept that CTCA will allow for a reduction in patients receiving aggressive medical management is flawed. In the FACTOR-64 cohort, patients randomized to the CTCA group were upgraded to more aggressive management far more frequently than patients in the control group(6). Clearly in patients at high risk for CAD, CTCA adds little to the downstream management and likely will lead to overdiagnosis and overtreatment.

CTCA in the low risk patient who has already been ruled out for ACS using history, physical exam, EKG and biomarkers, fails to add further diagnostic utility. Additionally its use to help guide medical management of CAD seems to lead to increased testing and treatment without decreasing the rate of MI or death. The next question becomes, “How does CTCA perform in the high-risk patient in whom we suspect ACS?” Though the data on this question is certainly not as robust as that for the low-risk patient, there are a number of trials to guide us.

The first of these trials is a secondary analysis of the ROMCAT II cohort published in JACC in August 2014. In this analysis, Puchner et al examined how effective CTCA was in identifying ACS independent of other diagnostic tools (EKG, biomarkers) (7). The authors found that when using the traditional threshold for positive study (> 50% stenosis), CTCA was only 78.4% sensitive for ruling out ACS. In order for CTCA to reach a clinically acceptable sensitivity, the test threshold had to be lowered to the point where no obstructive CAD was visualized on CTCA (7). What these findings suggest, though the authors do not state, was in a number of patients who were diagnosed with ACS during their initial Emergency Department visit detected by EKG or biomarkers, were actually missed by the CTCA. Thus in the high-risk patient with either EKG changes or elevated troponin values, a negative CTCA is not sufficient to exclude ACS.

The next trial examining the diagnostic accuracy of CTCA in high-risk patients is the NXT Trial, which was published in JACC in late 2014 (8). In this trial, CTCA was used as a straw man comparator to another non-invasive tool for the diagnosis of CAD, CT fractional flow reserve (FFR). This trial compared both CTCA and CT-FFR to the gold standard of angiographic calculated FFR in patients with at least a 30% stenosis. At the typical threshold of 50% stenosis, CTCA was only 94% sensitive for identifying hemodynamically important stenosis (FFR< 0.80). Additionally when this threshold of 50% stenosis is employed, the specificity is equally clinically unacceptable at 34% (8).

Essentially the diagnostic characteristics are not unlike those of a D-Dimer assay. In the high-risk patients, the ones we are truly concerned with in the diagnosis of ACS, its sensitivity is not acceptable to safely rule out the disease process in question. In the low risk patients its poor specificity will lead to overtesting, overdiagnosis and overtreatment.

Finally, a brief comment regarding the patient’s expectations and desires. Champions of this test have noted that when given the option, patients choose CTCA over other testing strategies, said to desire the definitive answers it provides. This general endorsement speaks less to the efficacy of the test itself and more to our misinterpretation of the data when communicating the benefits of CTCA to our patients. We have clear evidence demonstrating that CTCA does not add any further risk stratification to the traditional Emergency Department workup. Patients only think it provides an additional level of security because of how it is presented to them. The evidence suggests that in the low-risk patient, CTCA adds no diagnostic value and will only lead to needless downstream interventions.

Certainly a more honest shared decision making moment would be similar to the one proposed by Dr. Jeremiah Schuur and Dr. Joshua Kosowsky in their letter to the editor (9) in response to Lit et al’s paper examining the use of CTCA in an Emergency Department population 4). In this letter they suggest the use of a more evidence-based consent when discussing the risks and benefits of CTCA. It goes as follows:

Sir, although you only have a 1 in 100 chance of having a heart attack in the next month, I do not feel safe sending you home. So, I ordered an expensive test that will not reduce your risk of a heart attack, but it could cause kidney damage or cancer.

Goldstein JA, Gallagher MJ, O’Neill WW, Ross MA, O’Neil BJ, Raff GL. A randomized controlled trial of multi-slice coronary computed tomography for evaluation of acute chest pain. J Am Coll Cardiol 2007;49:863–71.

1. Goldstein JA, Chinnaiyan KM, Abidov A, et al. The CT-STAT (Coronary Computed Tomographic Angiography for Systematic Tri- age of Acute Chest Pain Patients to Treatment) trial. J Am Coll Cardiol 2011;58:1414–22.
2. Hoffmann U, Truong QA, Schoenfeld DA, et al. Coronary CT angiography versus standard evaluation in acute chest pain. N Engl J Med 2012;367:299–308.
3. Litt HI, Gatsonis C, Snyder B, et al. CT Angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med 2012;366:1393–403.
4. Hulten E, Pickett C, Bittencourt MS, et al. Outcomes after coronary computed tomography angiography in the emergency department: a systematic review and meta-analysis of randomized, controlled trials. J Am Coll Cardiol. 2013;61:(8)880-92.
5. Muhlestein JB, Lappé DL, Lima JA, et al. Effect of screening for coronary artery disease using CT angiography on mortality and cardiac events in high-risk patients with diabetes: the FACTOR-64 randomized clinical trial. JAMA. 2014;312:(21)2234-43.
6. Puchner SB, Liu T, Mayrhofer T, et al. High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial. J Am Coll Cardiol. 2014;64:(7)684-92
7. Nørgaard BL, Leipsic J, Gaur S, et al. Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial (Analysis of Coronary Blood Flow Using CT Angiography: Next Steps). J Am Coll Cardiol. 2014;63:(12)1145-55.
8. Schuur et al. CT Angiography for Possible Acute Coronary Syndrome. N Engl J Med 2012; 367:83-86 July 5, 2012

Use of CT scans for the evaluation of renal colic increased 10 fold between 1996 to 2007. Is this good for patients? Have they benefitted from the detailed information that CT scanning? The answer is no. Several studies have revealed that we are not only irradiatiting patients at an increasingly alarming rate, their outcomes are not improving because of it. In this episode, recorded at the Cabo CME retreat, ERCast meets up with Matt Dawson and Mike Mallin from The Ultrasound Podcast to discuss the article Ultrasonography versus computed tomography for suspected nephrolithiasis.

Study Breakdown

• About 3ooo patients with suspected renal colic divided into 3 groups defined by initial diagnostic study
  • CT scan
  • Radiology Ultrasound
  • Point of Care Ultrasound
  • Results: Using CT as the initial study increased radiation exposure but did not reduce adverse outcomes.
  • ERCast editorial: Another way to look at: Starting with ultrasound as the initial imaging modality decreased radiation exposure and did not increase adverse outcomes. Whether you see the cup as half full or half empty, starting with US in an uncomplicated case of suspected renal colic seems like the right call. If you start with CT on everybody, then everybody gets irradiated.

For a more detailed discussion on this topic, check out the Broomedocs Podcast.

References

Smith-Bindman, Rebecca, et al. "Ultrasonography versus computed tomography for suspected nephrolithiasis." New England Journal of Medicine371.12 (2014): 1100-1110.

Westphalen, Antonio C., et al. "Radiological imaging of patients with suspected urinary tract stones: national trends, diagnoses, and predictors." Academic Emergency Medicine 18.7 (2011): 699-707.

Moore, Christopher L., and Leslie Scoutt. "Sonography first for acute flank pain?." Journal of Ultrasound in Medicine 31.11 (2012): 1703-1711.

Interested in trying your hand at medical podcasting for Primary Care RAP? Listen to the show and then send me a note rob@hippoeducation.com 

Enteral contrast for CT diagnosis of appendicitis

Sanjay Arora MD and Michael Menchine MD

Written summary courtesty of EMRAP. Author: Marlowe Majoewski

Drake FT et al. Enteral Contrast in the Computed Tomography Diagno- sis of Appendicitis: Comparative Effectiveness in a Prospective Surgical Cohort. Ann Surg. 2013 Oct 10. PMID: 24598250.

Bottom line: This study confirms that the addition of oral and/or rectal contrast does not increase the accuracy of CT scanning in patients with suspected appendicitis.

The Review: Appendicitis is very common with a lifetime risk estimated at 8.6% for men and 6.7% for females. The clinical imperative has been to miss zero cases. The traditional approach has led to acceptance of a high rate of negative appendectomies. CT imaging can reduce the rate of negative appendecto- mies without increasing the rate of perforation. Previously, patients were given oral, rectal, and IV contrast prior to CT scanning. Contrast agents add time, discomfort, and the potential for contrast-related complications. CT technology has advanced.

There have been three trials of IV and oral contrast versus IV contrast alone, which have found similar diagnostic accuracy. Some centers are adopting IV-only protocols.

The Study: The authors looked at a large database of CT scans performed in Washington. The registry captures about 85% of non-elective appendectomies. They collect all imaging and lab data. The data is abstracted and includes 56 hospitals in Washington, which represents nearly all of them.

The outcome of interest in this study was the concordance of radiology imaging and final radiology interpretation. The results were analyzed by the type of contrast used: no contrast, IV contrast, IV and enteral contrast, or enteral contrast only.

9,047 patients underwent appendectomy in the two years included in the study. 8,089 underwent CT scan first. 55% had IV only, 25% had IV and enteral contrast, and 12% had no contrast. The patients were evenly distributed across the groups. There did not appear to be a selection bias. This may have been a location-specific protocol.

The addition of enteral contrast added another hour to the patient’s emergency department stay.

What did they find? Concordance was 90% between the CT to the OR findings in the IV-only group. This was not changed with the addition of enteral contrast. Scans without contrast had 85.7% agreement. Scans with enteral contrast only also had a high agreement.

The authors found that the negative appendectomy rate was higher in the patients with enteral plus IV contrast than the group with IV contrast alone (3.5% versus 2.7%). They theorized that this was because one of the soft signs of appendicitis on CT scan is an appendix that doesn’t fill with enteral contrast, and there are other reasons the appendix may not fill with contrast.

Conclusion: There is no added value of enteral contrast even in a big wide vari- ety of cases, urban versus rural. There is no difference in diagnostic accuracy between IV and oral contrast versus IV contrast alone.

Should we be CAT scanning hearts in the emergency department?

Scenario: A patient presents to the emergency department with chest pain. EKG and enzymes are OK. Then it's off to get a cardiac CT - coronary arteries look clean and off they go. No admission needed, you see their anatomy right there on the scan and it looks fan-freaking-tastic. With all of the energy and money we spend on chest pain workups, admissions, and lawsuits, why is this a bad idea? There are two camps when it comes to Coronary CT Angiography (CCTA).

Camp one says

• CCTA can get patients out of the hospital faster with a clear idea of their coronary anatomy
• A CCTA approach has a similar outcome compared to using just EKG and cardiac enzymes

Camp two says, "Wait a sec, why change what we’re doing if using CCTA doesn’t improve outcome over old school EKG and enzymes. CCTA is expensive, there’s radiation, contrast exposure and, if it doesn’t improve outcome, why should we be doing it?

Judd Hollander, one of the world's experts on CCTA use in the emergency department chest pain workup joins the show to give his point of view.

A History of CCTA in the emergency department

An unexpected podcast with Dr. Dike Drummond, otherwise known as The Happy MD.

Dike coaches physicians through the stressful aspects of medical practice and has written a book on working though BURNOUT: Burnout Prevention Matrix

In this show

• How to be an effective educator.
  • Effective teaching isn't about disgorging information while the Powerpoint slides flow by. It's about giving your listeners new skills to be better at what they do.
• The secret to dealing with hospital administrators by acting like Columbo
• Recognizing and overcoming burnout

The way we learn to manage pulseless electrical activity (PEA) from the Advanced Cardiac Life Support course is a mockery wrapped up in a sham. The mnemonic is cumbersome and the treatment (such as CPR for all, empiric epinephrine) is not always appropriate for a patient with normal electrical activity and a pulse. Fear not, because there is a way out of this madness. Joe Bellezzo from the ED ECMO project joins the show to talk about his thoughts on PEA and what I think is a revolutionary approach to evaluating and treating PEA. Instead of lumping all patients with electrical activity and no palpable pulse in to one group, the authors make use of ultrasound and common sense.

PEA made easy

Step one. Look at the QRS. Is it wide or narrow?

Narrow QRS is often from some sort of right side of the heart inflow or outflow problem. The electricity is working just fine. There’s either not enough blood coming in or not enough blood going out. What are some things that can cause that? Cardiac tamponade, tension pneumothorax, mechanical hyperinflation and pulmonary embolism, severe hypovolemia.

Wide QRS. What are some things that cause PEA and impaired conduction? Hyperkalemia, sodium channel blocker toxicity such as you would see in an OD, ischemia, massive pulmonary embolism.

Myocardial infarction can cause PEA in both the narrow and wide complex groups and these patients usually do poorly. In the setting of MI, think myocardial rupture.

Step two. Look at the heart with ultrasound

Narrow QRS. If you see a collapsing RV and an effusion, that's tamponade. Collapsed RV could also be from a pneumothorax or hyperinflation. A dilated right ventricle may indicate pulmonary embolism.

Wide QRS. Ultrasound will usually show a hypo kinetic heart or it may not be beating at all.

Step three. Empiric Treatment

Narrow QRS. This is often a flow problem so unleash the wide open fluids. Then focus on specific treatment if you have identified a cause by ultrasound. Cardiac tamponade- pericardiocentesis, Tension pneumothroax-decompress the chest, massive pulmonary embolism- thrombolytics, hyperinflation- adjust the vent settings

Wide QRS. There's a fair chance that your patient has some sort of metabolic problem (hyperkamemia or sodium channel OD) so push an amp of sodium bicarbonate and an amp of calcium.

Littmann, Laszlo, Devin J. Bustin, and Michael W. Haley. "A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity." Medical Principles and Practice 23.1 (2013): 1-6.

What's it like to be an emergency physician? Take a look inside the psyches of ED docs from around the planet.

So, you want to be an ER doctor. What does that mean? Is it even possible to understand the reality of life as a full time emergency physician when you make the leap of faith on Match day? Because that's what it is, isn't it? The match, a leap of faith? You spend, at best, a few months in medical school doing all of the fun stuff in a specialty and then you need to decide the course of the rest of your life as a physician. It's analogous to emergency medicine in a way, making a monumental and critical decision based on insufficient information.

I graduated from medical school in the mid 90s. I was certain, CERTAIN, that I was going to be an orthopedic surgeon. That idea was locked in until I actually rotated in ortho. The comraderie was great, the OR was fun, clinic always interesting, but it didn't feel like it fit my personality. As I rotated through each medical specialty in the third year of med school, there was always time spent in the ED. Whenever I was there, in the emergency department, I loved it. The pathology, the pace, procedures, and the challenge of diagnosing and managing undifferentiated complaints and…. the people who worked in the ED were my sort of folk: A) Smartasses B) Short attention spans C) Excited at the uncertainty of what was lying behind curtain number one and D) What I hoped would be part of my persona some day- taking care of business in the critically ill patient, getting it done like there was nothing to it. Caring for patients in the ED, I  felt like I was making a difference. But, as I said, the downsides aren't as apparent when you're in the infatuation stage. I later leaned what stressed me out, and believe me, even if you think you're invincible, you too have a stress point. For me, it was task saturation. Too much to do all at once. When you get out of training and it's just you with a fully loaded ED with lots of sick patients,  phone calls to make, procedures to do, conversations, charting, and on and on... task saturation. It's one of the skills you learn in residency but nothing can fully prepare you for your first day at the captains helm. That was something I had to learn, not only to live with, but how to manage. Task saturation happens at least once every shift.

This episode is intended to give you a peek inside the mind of the workaday ED doc. The lessons they've learned  and what can they pass on to you. Don't get me wrong, it's still the best job in the world, at least I think so, but it's also not easy. If you're thinking about emergency medicine as a career, you should go into it with open eyes and understand  the highs, the lows, the sexy resuscitation, burnout, all of it, warts and all.

Legal analyst Gunnar Schwartzbaum (nom de plume) joins the show to talk about the legal ramifications of quarantine and isolation orders.

In this episode

• What to do if a patient with suspected Ebola wants to leave the hospital against medical advice.
• What is the difference between isolation and quarantine?
• How do you enforce an isolation order?
• What is home quarantine?
• Can you refuse to care for a patient with suspected Ebola?

CDC Ebola Reference Page

It’s well accepted that the window for acute atrial fibrillation cardioversion of atrial fibrillation ends at  48 hours post onset. We did a whole episode on that very point.  The 48 hour window is now being challenged by the biggest study to date looking on  this topic.

Time to Cardioversion for Acute Atrial Fibrillation and Thromboembolic Complications was published as a letter to JAMA on August 13, 2014. Ryan Radecki sent the first FOAMed shot across the bow with this review.  You can stop now and check out Ryan's review; he's far more erudite than I. If you need more info, read on...

Study in a nugget: This was a retrospective study from Finland that looked at around 2500 patients with a primary diagnosis of atrial fibrillation (AF), aged 18 years or older, with successful cardioversion in the emergency department within the first 48 hours of AF onset.  The primary outcome, a thromboembolic event, was defined as a clinical stroke or systemic embolism confirmed by computerized tomography or magnetic resonance imaging, surgery, or autopsy. Time to cardioversion was determined as the difference between the beginning of arrhythmic symptoms to the exact time of cardioversion. There were 3 groups: less than 12 hours, 12 hours to less than 24 hours, and 24 hours to less than 48 hours.

Thromboembolism Rates

Overall:0.7%.

Under 12 hours: 0.3%

24 to 48 hours: 1.1%.

It seems like 12 hours is the inflection point when risk went up and a CHADS VASC score of greater than 1 increased risk.

I’m not sure where this leaves us, maybe risk stratification in ED cardioversion? This was observational, retrospective, and did not include post cardioversion anticoagulation as an intervention. There is no definitive answer or management change from this letter. It does raise the question of whether we should anticoagulate cardioverted AF patients with over 12 hours of symptoms, or those with a CHADS VASC over 1. However, there is no evidence that a post cardioversion anticoagulation strategy would decrease thromboembolic event rate. Also, the incidence of post cardioversion thromboembolic events in this letter is far higher than reported in other literature.

Rob's practice changers

Cunningham Technique

Loop Abscess Drain Technique

Delayed Sequence Oxygenation

Swami's  practice changers

Nasal Cannula Apneic Oxygenation

Tranexamic Acid for Mucosal Bleeds

Nuotio, Ilpo, et al. "Time to cardioversion for acute atrial fibrillation and thromboembolic complications." JAMA 312.6 (2014): 647-649.

CABO CME Retreat December 5-9, 2014

Primary Care RAP