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?
Thu, 24 April 2014
Rich Levitan, pioneer in airway management, talks about operator stress response in the difficult airway. Referenced in this discussion: The laryngeal handshake, books On Combat and Warrior Mindset. Rich offers several courses including the one of a kind Practical Emergency Airway Management Course and the Advanced Airway Endoscopy Course in Yellowstone.
Interested in a truly unique CME experience? Join Rich Levitan, Scott Weingart, Matt Dawson, Mike Mallin, Andy Sloas and me December 6-8, 2014 for a 5 star, all inclusive vacation in Cabo San Lucas and earn your CME credits in style. The 2014 Cabo CME Retreat will focus on the newest emergency medical practices and technologies in the areas of ultrasound and airway medicine. Our lineup of leading emergency doctors and medical speakers will present at Secret’s Resort, the newest all inclusive luxury resort in San Jose del Cabo. Secrets Puerto Los Cabos Golf & Spa Resort boasts five gourmet restaurants, incredible views, infinity pools, and world renowned golf courses designed by Greg Norman and Jack Nicklaus. At this limited-access retreat, you will experience a CME conference unlike any other.
To register and/or find out more, go to the Cabo CME homepage
Tue, 18 February 2014
Cardiac arrest. It seems so easy. Just follow the algorithm on the reference card, and all cardiac arrest issues will be solved. The truth is that codes can be messy, chaotic and scattered. On this episode of ERcast, we hear from the RAGE podcast experts on how to take control of the room and run an effective resuscitation.
The medicine isn't always the hard part. Being an effective leader, communicating well, and making things happen are often the bigger challenges. And speaking of Making things happen. Click that link for one of the greatest medical lectures. Ever.
Adenosine vs Verapamil Articles
Adenosine versus Verapamil for termination of SVT (AVNRT)
Sat, 8 February 2014
Which is more effective for pain and fever control: Acetaminophen or Ibuprofen? Should a patient in the emergency department with upper GI pain be started on an H2 blocker or a proton pump inhibitor? Special guest Anand 'The Swami' Swaminathan joins ERCast to explore these and many more medical quagmires.
Bonus segment: How can a medical students present themselves well during critical rotations? In this case, we are talking about emergency medicine rotations.
Acetaminophen versus Ibuprofen
Perrott DA et al. Efficacy and safety of acetaminophen vs ibuprofen for treating children’s pain and fever: a meta-analysis. Arch Pediatr Adolesc Med 2004; 158(6): 521-6.
2004 meta-analysis - summarized the findings from 17 randomized, controlled trials comparing the two drugs in children <18 years of age. Three studies involved pain, 10 involved fever, and all 17 involved safety.
1. Pain – no difference between ibuprofen 4-10 mg/kg vs. APAP 7-15 mg/kg
2. Fever – ibuprofen 5-10 mg/kg superior to APAP 10-15 mg/kg (at 2 hours and more pronounced at 4-6 hours)
15% more children were likely to have reduced fever with ibuprofen compared to acetaminophen.
When selecting for studies using only the 10mg/kg dose of ibuprofen, there was a doubling of the effect in support of ibuprofen.
Safety: there was no evidence that one drug was less safe than the other (or placebo). The authors determined that this data was inconclusive and that more large studies would be needed to identify small differences in safety
Pierce CA et al. Efficacy and safety of ibuprofen and acetaminophen in children and adults: a meta-analysis and qualitative review. Ann Pharmacother 2010; 44(3): 489-506.
First meta-analysis looking at the question in adults.
Qualitative review revealed that ibuprofen was more effective than acetaminophen for pain and fever reduction, and that the two were equally safe.
From the quantitative data, the authors found that for pain, ibuprofen was superior in children and adults. For fever, ibuprofen was superior in children, but conclusions could not be made for adults due to insufficient data.
What about alternating acetaminophen and ibuprofen?
Malya RR. Does combination treatment with ibuprofen and acetaminophen improve fever control? Ann Emerg Med 2013; 61(5): 569-70.
1. Identified 4 studies that the author deemed high-quality and relevant to emergency practitioners.
2. Three of the four studies found that the combination was more effective at reducing fever than either alone.
One study that looked at alternating regimens over 24 hours found that 6-13% of parents exceeded the maximum number of recommended doses (Hay, 2008).
There is suggestion that the two drugs could act synergistically to cause renal tubular injury; however, acetaminophen and ibuprofen have different pathways of metabolism, and adverse effects in patients taking both have only been described in rare case reports.
EM Lyceum Review of APAP (acetaminophen) vs NSAIDS (ibuprofen). This review also includes a breakdown of PPIs vs H2 blockers, medical treatment for vertigo, and calcium channel blockers versus beta blockers for atrial fibrillation with rapid ventricular response (RVR)
Check out the RAGE podcast. In this episode of ercast, we discuss a recent round table on managing SVT (AVNRT) with verapamil versus adenosine.
Mon, 20 January 2014
Interview with hematologist Dr. Tom Deloughery about a smattering of clotting quagmires...Superficial Thrombophlebitis, Recurrent Pulmonary Embolism, Calf Vein DVT, Clotted PICC Lines, Starting (loading) dose of warfarin, low molecular weight heparin, widowmaker clots.
Quandary 1. Recurrent pulmonary embolism
Your patient is on warfarin, INR is therapeutic and has another PE. What do you do?
Make sure it’s truly recurrent. If it is...
First dose of warfarin
1. How long to you need to wait to start warfarin after the first shot of LMWH? You can start both meds at the same time.
2. Is there a need for a loading dose of warfarin? Sort of....Dosing and effect are unpredictable. As a general rule, Tom gives young and otherwise healthy patients 10mg as a first dose. Over 65 or young and frail, first dose 5mg.
3. If your patient needs to restart warfarin after being off it for a while, do you need to bridge with LMWH until the INR is therapeutic? In the setting of DVT and PE, yes. In atrial fibrillation, you probably don’t .
Can clot in the saphenous vein progress to DVT? Yes. 5-10%. Non saphenous vein clots progress to DVT at a rate of about 1%. As saphenous vein clot gets closer to the femoral vein, risk rises of it becoming a deep clot, but there are also perforator veins all along the saphenous vein that connect it to the deep system. Clot can connect from the superficial (saphenous) vein to deep vein through a perforator at any point, but it’s less of a worry than deep propagation directly into the femoral vein near the groin.
Treating superficial thrombophlebitis needs to take into account the ‘thrombo’ (clot) and ‘itis’ (inflammation)
NSAIDS decrease rate of inflammation and clot extension
Therapeutic vs prophylactic LMWH: both decrease rate of inflammation and clot extension - outcomes are equal, so prophylactic LMWH is preferred (once a day, lower dose)
Small, under 5-7cm and not proximal (not upper half of thigh) NSAIDS
Larger than 5- 7cm or proximal, prophylactic dose of LMWH or fondaparinux (40mg daily)
Duration of therapy
There is uncertainty as to the optimal duration of therapy. Tom treats for two weeks. If patients are still symptomatic, treat for another two weeks.
Upper extremity thrombophlebitis
It is thought that upper extremity superficial thrombophlebitis has a more benign course. Treat with NSAIDS and hot packs. If this isn’t working, transition to LMWH.
What should you do with a PICC line clot?
Anticoagulation does not help with recannalization. Pull the line.
Putting in a new PICC right away - high rethrombosis rate.
Calf vein DVT
15-30% will grown and cause PE. Follow up ultrasound to check for extension is an option.
Unless there is a contraindication, treat with anticoagulation. ACCP recommends 3 months of treatment, Tom treats for 6 weeks.
Factor V Leiden mutation
9% prevalence in Portland, OR. Mostly a caucasion disease. Raises risk of first clot 3 fold (more DVTs than PE). Having this mutation does not increase risk of DVT recurrence.
Bonus point of the day
The SUPERFICIAL femoral vein is a DEEP vein. Perhaps the worst anatomic name ever. If you get a report that your patient has clot in the superficial femoral vein, that is a DVT, not superficial thrombophlebitis.
Mon, 20 January 2014
The 4th anniversary of ERcast recognizes some of the luminaries who have helped and inspired me since the show's inception.
Tue, 17 December 2013
We learn about the MUD PILES, the causes of anion gap acidosis, as medical students. And it gets even further drilled into us in residency. But sorting out a gap acidosis can be real challenge, even with a nifty mnemonic. To help us get smarter in understanding some of the nuance of gap acidosis, Sean Nordt, MD, PharmD.
Case: Alcoholic, diabetic with a blood glucose of 295, bicarbonate of 12, and an anion gap 28. Is this alcoholic ketoacidosis (AKA), diabetic ketoacidosis (DKA), toxic alcohol, something else? What is the cognitive process for sorting out this anion gap acidosis?
Nordt: Without additional history, send...
Case continues: The patient has a normal mental status. Heart rhythm is sinus tachycardia in the low 100s. To treat this sinus tachycardia, he gets the sinus tachycardia antidote - 3 liters of normal saline. Since AKA (a starvation and volume depletion ketosis) is high on the differential diagnosis, he also gets a hamburger and apple juice. His labs are rechecked and few hours later and his bicarbonate is unchanged at 12 and anion gap drops slightly from 28 to 24.
How fast should the anion gap and serum bicarbonate to correct in AKA?
Nordt: It should start to improve in 1-2 hours and takes about 5-7 hours to reverse. If the anion gap and bicarbonate aren’t improving (or getting worse) in an hour or two, think about an alternate diagnosis.
Case continues: Since there’s not much improvement in the gap acidosis after several hours of re-feeding and fluid resuscitation, maybe this is not a case of AKA. Could it be DKA? Probably, but it could also be one of the many other causes of anion gap acidosis. With a persistent gap acidosis, or maybe one that’s hard to figure out, are there clues to look for or other tests that can help?
Let’s go through the different things that we use, or tests we order, to sort out the gap.
Working through the MUD PILES on this patient...
Methanol - Still possible
Uremia- No. Renal function normal
DKA- Still possible
P- Propylene Glycol. Possibly. Propylene glycol gets metabolized to lactic acid. Excessive propylene glycol from medications is unlikely in the ED (unlike the ICU where patients get many injectable meds), but can be found in pet friendly antifreeze.
INH- No Iron- No Infection-No evidence of this
Lactic acidosis- Still possible. He takes metformin but renal function is normal
Ethylene Glycol - Still possible
Salicylates- Salicylate level negative
The remaining MUD PILES...
How do we figure out the answer? We don’t always have to have the right answer in emergency medicine, but we shouldn’t be wrong.