The Hot Stove League of EM/Tox

First in a series of presentations for medical students going into Emergency Medicine and interns starting out on the cardinal presentations. A must study before your rotation!!

Download the PDF show notes here!

Abdominal Pain outline

Here are the articles – at the end is the study by Jerry Hoffman (okay so it was an abstract) that showed that buffered lidocaine was not worth much to the patient.

Chinnock, Brian et al. Irrigation of Cutaneous Abscesses Does Not Improve Treatment Success Annals of Emergency Medicine , Volume 67 , Issue 3 , 379 – 383

O’Malley et al Routine Packing of Simple Cutaneous Abscesses Is Painful and Probably Unnecessary Academic Emergency Medicine 2009; 16:470–473

Talan DA et al. Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess N Engl J Med. 2016 Mar 3;374(9):823-832.
Alsaawi et al. Ultrasonography for the diagnosis of patients with clinically suspected skin and soft tissue infections: a systematic review of the literature. Eur J Emerg Med 2015

Bourne et al Injectable lidocaine provides similar analgesia compared to transdermal lidocaine/tetracaine patch for the incision & drainage of skin abscesses: A randomized, controlled trial J Emerg Med. 2014 Sep;47(3):367-71

Tornay et al Heated versus buffered lidocaine and the pain on local injection: A comparative study Annals of Emergency Medicine 1994 , Vol. 23, Issue 3, p629
Small study that showed most patients would not pay $2 for buffered lidocaine.  “Heating a solution of lidocaine with epinephrine reduces the pain of local injection, but buffering with bicarbonate is more effective in this regard. The value of this difference to the patient may be minimal”

Great Prezi today at conference by Drexel EM3 Dr. Rachel Wenzel – shows how this media tool can be used to mind map a complex  topic. 

Tips on EM presentations skills

Michael Pasirstein MD

Why

Students have already had a few years of being taught by other departments how to do an oral presentation, but it may not be applicable to EM.

Majority of the student and resident educational interactions with attending physicians in EM occur during oral presentation.

Student evaluation is directly linked to how well the student presents.

About the article

The authors are using their success to assist learners present all pertinent information in under 4 minutes

History of the Oral presentation

Earliest mention of the oral presentation is from the dean of the New Orleans Medical School, Erasmus Fenner, in 1846, though it seems intuitive that doctors and learners have been communicating with oral presentations much longer than about 200 years.

In 2003, the SNAPPS format of presentations was developed at Case Western Reserve University School of Medicine. This format was designed for outpatient oral presentations. The SNAPPS method focuses on

• brief patient summaries
• Narrowing DDx of 2-3 etiologies
• Analyzing information to determine the most likely cause of chief complaint
• Probing the attending for knowledge
• Planning pt management
• Selecting an issue for self-directed learning

Students noted that:

Effective presenters alter the way they present but had difficulty describing how, making it difficult for novices to mimic

EM

The origins of the oral presentation and the recent studies noted previously are not EM specific

In EM we:

• Assume every patient has an emergent condition
• Have multiple undifferentiated patients at once
• Prioritize patients
• Have incomplete patient data

EM Oral Presentations – How are we different?

• CC
• HPI
• Meds/allergies
• PE
• Summary statement
• Assessment and plan

What is minimized are

• PMHx,
• PSHx
• Soc Hx
• FmHx
• ROS

Essentially, the HPI should include all the pertinent information from those areas that are minimized.

Earlier learners will still have items that are positive in the ROS, as they may not be aware of what is pertinent and what is not.

To further improve speed, the student should include only pertinent positives and negatives on physical exam.

The 3 Minute Emergency Medicine Medical Student Presentation: A variation on a theme.

the-3-minute-emergency-medicine-medical-student-presentation-a-variation-on-a-theme-pdf-

K2 Krash – what to do?

What is the K2 Krash – it’s the phenomenon of hypotension and bradycardia after a synthetic cannabinoid overdose. Typically an overdose with hypotension and bradycardia is a life-threatening phenomenon, for example calcium channel blockers and beta blockers. K2 crash seems to be less life-threatening and responds well to fluid resuscitation unlike other poisonings with the same cardiovascular effect.

I suggest you follow Leon Gussow’s tip on managing hypotension in overdoses – scan the IVC and fill up the tank until the respiratory collapse of the IVC is replaced with a plump IVC and then add pressors if needed or wait out the metabolism of the synthetic cannabinoid. Typically the clinical course of hypotension is less than six hours.

http://journals.lww.com/em-news/Fulltext/2014/07000/Toxicology_Rounds__An_Idea_Whose_Time_Has_Come__.10.aspx

We do know that the K2 Krash is the result of stimulus of the CB1 receptor. We also know that endogenous cannabinoids are released by platelets and macrophages during sepsis. Whether they in fact have a protective effect remains to be seen, but they appear to result in vasodilation of the brain and coronary vasculature. Perhaps that’s why K2 Krash appears to be a relatively benign event once it resolves.

Here’s a great article on cannabinoid induced hypotension.

Cannabinoid-Induced Hypotension and Bradycardia J Pharmacol Exp Ther-1997-Lake-1030-7

A nice case series on synthetic cannabinoid overdoses – about half of which demonstrated bradycardia and hypotension. Synthetic Cannabinoid Abuse in Adolescents: A Case Series

Also a discussion on how synthetic cannabinoids play a role in sepsis. Platelet- and macrophage-derived endogenous cannabinoids are involved in endotoxin-induced hypotension

Enjoy and let me know what you think!

In this podcast I review “Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess” Talan et al NEJM 2016;374:823-32 and see what the clinical advantage to adding TM-SMX to simple I&D. Then we take a quick turn to some Tox and look at “Extracorporeal membrane oxygenation in the treatment of poisoned patients” deLange et al in Clinical Toxicology 2013;51:385-393.

ECMO in poisoned patient

4XTRIM SULFA BID and MRSA Abscess

Okay so – so it’s a little weird to have those two – but hey that’s what I am reading…

Enjoy and let me know what you think

In this interview I am excited to introduce Ernie as the new Program Director for our incoming class of interns in June. I talk with Ernie about his new position, what motivates him to teach, and we entertain deep thoughts on autonomy, mastery, and purpose. Special shout out to all our fantastic EM Program Candidates listening in podcast land. Get in touch for any questions you might have for Ernie (or anyone here at Drexel EM) and good luck in the Match! See you in June!

Journal Club PodCast: Flipped classroom!

Assignment is to read the articles, listen to the podcast, and be prepared to apply your knowledge to clinical scenarios when you come to Journal Club.

Articles are:
Acute stroke intervention: A systematic review JAMA April 14, 2015

Endovascular Therapy after IV TPA versus TPA alone for stroke NEJM March 7 2013

Comparative efficacy of different acute reperfusion therapies for acute ischemic stroke: a comprehensive benefit-risk analysis of clinical trials Brain and Behavior 2014

A review of decision support, risk communication and patient information tools for thrombolytic treatment in acute stroke: lessons for tools developers BMC Health Services Research 2013

Tool for describing stroke risk from AAEM tpaedtool-AAEM

See you at Journal Club!

Opinions are of course our own…! Music is “Heartbeats” by Cat Hamilton created exclusively for this podcast – how cool is that!

Recommendations for reversal of antithrombotic agents in patients with intracranial hemorrhage

Finally put this together in a PDF – download at the link below. Put it to good use and let me know if it works for decision support! Also lots of good podcasts on the way – Rita McKeever and I will finally put more TOX in emtoxcast and Ed Ramoska will join me for a flipped journal club podcast on CVA interventions! Stay tuned…

Recommendations for reversal of antithrombotic agents in patients with intracranial hemorrhage

Neurocritical Care Society and Society for Critical Care Medicine recommendations for reversal of antithrombotic agents in patients with intracranial hemorrhage

Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage : A Statement for Healthcare Professionals from the Neurocritical Care Society… – PubMed – NCBI http://www.ncbi.nlm.nih.gov/pubmed/26714677

Here’s my breakdown of Table V from that article – I will try to find a way to post a downloadable PDF of this!

Antithrombotic: Timing, Antidote, Factor Replacement, antifibrinolytics

Vitamin K antagonists (warfarin) If INR > 1.3 then Vitamin K 10 mg IV, plus 3 or 4 factor PCC IV

(dosing based on weight, INR and PCC type) OR FFP 10–15 ml/kg IV if PCC not available

Direct factor Xa inhibitors: activated charcoal (50 g) within 2 h of ingestion, activated PCC (FEIBA) 50 units/kg IV OR 4 factor PCC 50 units/kg IV

Direct thrombin inhibitors (dabigatran): Activated charcoal (50 g) within 2 h of ingestion, AND Activated PCC (FEIBA) 50 units/kg IV OR 4 factor PCC 50 units/kg IV                                                                Idarucizumab 5 g IV (in two 2.5 g/50 mL vials) consider hemodialysis or idarucizumab redosing for refractory bleeding after initial administration if 1) dabigatran was taken with 3-5 half lives and NO evidence of renal insufficiency or 2) dabigatran was taken beyond 3-5 half lives WITH renal insufficiency

For other DTIs: Activated PCC (FEIBA) 50 units/kg IV OR 4 factor PCC 50 units/kg IV

Unfractionated heparin: Protamine 1 mg IV for every 100 units of heparin administered in the previous 2–3 h (up to 50 mg in a single dose)

LMWH

Enoxaparin: Dosed within 8 h: Protamine 1 mg IV per 1 mg enoxaparin (up to 50 mg in a single dose) Dosed within 8–12 h: Protamine 0.5 mg IV per 1 mg enoxaparin (up to 50 mg in a single dose)       Minimal utility in reversal >12 h from dosing

Dalteparin, Nadroparin and Tinzaparin: Dosed within 3–5 half-lives of LMWH: Protamine 1 mg IV per 100 anti-Xa units of LMWH (up to 50 mg in a single dose) OR rFVIIa 90 mcg/kg IV if protamine is contraindicated

Danaparoid: rFVIIa 90 mcg/kg IV

Pentasaccharides: Activated PCC (FEIBA) 20 units/kg IV or rFVIIa 90 mcg/kg IV

Thrombolytic agents (plasminogen activators): Cryoprecipitate 10 units IV OR antifibrinolytics (tranexamic acid 10–15 mg/kg IV over 20 min or e-aminocaproic acid 4–5 g IV) if cryoprecipitate is contraindicated

Antiplatelet agents: DDAVP 0.4 mcg/kg x 1, if neurosurgical intervention, transfuse one apheresis unit