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 email@example.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.
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.
Tue, 21 October 2014
Legal analyst Gunnar Schwartzbaum (nom de plume) joins the show to talk about the legal ramifications of quarantine and isolation orders.
In this episode
Thu, 2 October 2014
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.
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
Swami's practice changers
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.
Mon, 1 September 2014
How often do you see patients who tell you they are having a sinus headache need antibiotics. There are so many things wrong with that, not the least of which is the antibiotics part, but ….what about the cause of the headache in the first place?
Is this headache a migraine?
If you have a patient who has some scomoata, maybe shimmering lights that start small, get bigger, a little nausea followed by headache- what is that? it’s a migraine. Done. But it’s not always so clear cut.
The POUNDing mnemonic can help sort this out.
If the patient answers “yes” to 4 or more of the 5 ques- tions, the LR is 24. We like to see a positive likelihood ration of at least 10 to indicate something is useful. Twenty four: is very useful. For 3 criteria, the LR is 3.5, not too impressive. For 1 or 2 criteria, the LR is 0.41, weak.
What about photophobia, the absence of photophobia makes migraine less likely, we know that migraines can cause debilitating photosensitiy, but interestinly, the presence f photophobia doesn’t make migraines MORE likely because in the great headache ven diagram, there is tremendous overlap in symtoms, and photophobia is one of those symptoms that many headaches share.
Sinus headaches. What's in a name?
Sinus headache, so easy to say, it just rolls off the tongue. We say it, patients say it, but is it really a sinus headache?
Study Bottom Line: About 3000 patients, most carrying a diagnosis of sinus headaches. The overwhelming majority of patients met International Headache Society migraine headache criteria.
We’re not talking about patients with fever and purulent discharge. This is the patient with sinus pressure, sinus pain, even nasal congestion. So that sinus headache may not be a sinus headache after all, but a migraine with pain localized to a sinus area. But, you say, there’s overlap between sinus and migraine headaches,. That is true, but a 2008 study from Laryngoscpoe of patients seen at an ENT clinic with a previous diagnosis of sinus headache (either from a physician or themselves) suggests that many sinus headaches do not have objective evidence of sinusitis AND get better with migraine treatment. Patients with a negative workup by exam, nasal endoscopy and CT scan were treated with triptans and the majority, over 80%, got better. Migraine treatment made what was previously diagnosed as sinus headache better.
Maybe triptans help with sinus headaches, but maybe, and the evidence suggests this, many of what we and our patients call sinus headaches are actually migraines.
Fri, 27 June 2014
An unruly, intoxicated and violent patient rolls into the ED. The situation and the patient are both in need of control. How do you go about it? Redirection? Calming words? Sometimes those things aren't quite enough and chemical sedation is in order. When it comes to choice of sedating agent, everyone seems to have their secret formula. We canvassed the planet to see how chemical takedowns are done across the globe.
ZdoggMD Art of the chemical takedown FOAMed World Premier
Scott Weingart 5mg of droperidol and 2mg of midazolam mixed together in a syringe with 11⁄2 inch needle and jabbed into whatever large muscle is available. Wait a few minutes. If necessary, will repeat once. Then establish IV
Minh Le Cong Ketamine IV, IM, or IO.
Cliff Reid Ketamine
Chris Nickson Benzo, olanzipine or droperidol
Sean Nordt The B-52. 5mg Haldol, 2mg Ativan and 50mg of benadryl mixed together in a single syringe and given IM
Katrin Hruska abusive patients are asked to leave the emergency department
Amit Maini 5mg of IM droperidol. Repeat in 5-10 minutes if needed
Sa'ad Lahri: lorazepam (4 to 8 mg IV) and haloperidol (5mg IV)
Yosef Leibman midazolam, droperidol. Starting to use clotiapine - a dibenzothiazepine anti-psychotic and a phenothiazine with anti-anxiety properties.
Gerry O'Malley Burly security guards and a show of force. If that doesn't work- benzodiazepine
Ray Moreno: Toxin related or sympathomimetic: midazolam 5 - 10mg IM. Psychiatric related- olanzipine. No idea what's causing the agitation- midazolam
Chris Richards- The B-52. 5mg Haldol, 2mg Ativan and 50mg of benadryl mixed together in a single syringe and given IM
Droperidol, QTc prolongation, and the Black Box with toxicologist Sean Nordt....
When droperidol was 'black boxed' in the US, it sent shockwaves across the emergency medicine community because this drug was, for many of us, the go to agent for sedation of combative and agitated patients. Over the past several years, the pendulum has swung away from the black box and toward increasing use of droperidol. Why is that? Have we all gone mad? Are we putting patients in danger?
The history (or the conspiracy, depending on how you look at it) is expertly explained in the below article. It involves big pharma, outlier case reports of patients given much higher doses than are used in the ED for either nausea or sedation, and suspicious timing. There is no doubt that butyrophenones can influence the QTc, but so can a lot of other meds we use (that are not black boxed).
Sean Nordt's approach to giving droperidol in the agitated patient
Interested in checking out the best emergency medicine CME and CNE on the planet?