Fri, 3 April 2015
Can a fever get so high that it causes brain damage? That question was posed to us by a listen with a recent patient whose temperature reached 106.9 Fahrenheit. Andy Sloas from the PEM ED podcast returns to ERCast to gives his take on cooling, workup, and the difference between heat exposure and infectious fever.
Upcoming 2015 conferences
June: SMACC Chicago
December: Atlantis CME Retreat
Tue, 10 March 2015
In October 2013, Scotty Weingart was on the show and suggested that closed chest CPR has no role in traumatic cardiac arrest. It made sense because, after all, the things that cause a traumatic arrest won't be helped by closed chest compressions. Tension pneumothorax, pericardial tamponade, hypovolemia from exsanguination - pushing on the chest isn't going to reverse any of those. But where is the evidence to support that claim? Don't we always compress the chest when the heart has stopped?
There is, unfortunately, a dearth of data on this topic. Swami and I scoured the known literature and here's what we found...
Lockey DJ et al. Development of a simple algorithm to guide the effective management of traumatic cardiac arrest. Resuscitation 2013; 84: 738-42.
The authors' algorithm states that in all traumatic arrests, you should look for a penetrating injury to the chest or epigastrium. If you find one, crack the chest ASAP.
If you don’t see a penetrating injury, consider a medical cause for the arrest.
There are a few key procedures in trauma arrest and the study recommends using the HOT mnemonic.
If these three things are addressed and there’s no ROSC, you should consider stopping resuscitation. This simple list emphasizes a systematic approach so that you open the chest when it’s indicated without thinking about it too much.
Leis CC et al. Traumatic Cardiac Arrest: Should Advanced Life Support Be Initiated? Acute Care Surgery 2013; 74: 634-8.
Advanced life support in this article means advanced procedures, not ACLS and CPR. The authors argue that we should resuscitate patients in traumatic arrest stating that 49.1% attain ROSC and 6.6% have a good neurologic outcome, including 23.1% of children.
ALS here included IV fluids, intubation, chest tube insertion, pericardiocentesis and FAST in the field. There was no mention of chest compressions.
Bottom Line: The question as to whether or not closed chest CPR in traumatic cardiac arrest has not been well studied. In the literature we found, chest compressions were rarely mentioned (if at all). Logistically, compressions can get in the way of life saving procedures and haven't been shown to help (nor have they been shown not to help). Considering the pathophysiology of traumatic arrest, compressions don’t make a lot of sense in the emergency department, since pumping on a closed chest in a patient with no volume (hemorrhagic shock), a hole (pericardial effusion), or obstructed outflow (tension PTX) isn’t going to help.
Links mentioned at the end of the show
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Thu, 19 February 2015
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
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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%.
Sun, 15 February 2015
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:
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.
Fri, 23 January 2015
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.
For a more detailed discussion on this topic, check out the Broomedocs Podcast.
Sat, 10 January 2015
Interested in trying your hand at medical podcasting for Primary Care RAP? Listen to the show and then send me a note firstname.lastname@example.org
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.
Tue, 6 January 2015
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
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
2001 Coronary CT vs stress testing
de Filippi et al. Randomized comparison of a strategy of pre discharge coronary angiography versus exercise testing in low-risk patients in a chest pain unit: In hospital and long-term outcomes. JACC 2001
2012 ACRIN-PA Trial
Litt, Harold I., et al. "CT angiography for safe discharge of patients with possible acute coronary syndromes." New England Journal of Medicine 366.15 (2012): 1393-1403.
• 1,370 patients, Age > 30 years
Inclusion criteria: TIMI score of 0–2, EKG without ischemic changes, and negative first set of cardiac biomarkers
2012 ROMICAT II Trial
Hoffmann, Udo, et al. "Coronary CT angiography versus standard evaluation in acute chest pain." New England Journal of Medicine 367.4 (2012): 299-308.
2012 Two year CCTA follow up
Coronary artery disease progression in patients without significant stenosis on coronary computed tomographic angiography. Chang, et al. American Journal of Emergency Medicine. Nov 2012.
2013 Long term outcome and downstream effects
• No deaths and no difference in MI, repeat ED visits or re-hospitalizations
• All studies showed decreased ED length of stay
• 8.4% of CCTA and 6.3% of UC patients had invasive angiography and 4.6% of CCTA and 2.6% of UC patients underwent re-vascularization
2013 Pushback against use of CCTA in the emergency department
Radecki, Ryan Patrick. "CT coronary angiography: new risks for low-risk chest pain." Emergency Medicine Journal 30.10 (2013): 856-857.
Special thanks: ROMICAT II and ACRIN-PA breakdown by Salim Rezaie of rebelem.com
Sat, 6 December 2014
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
Sat, 29 November 2014
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.
Thu, 6 November 2014
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.