Topics in this EM Quick Hits podcast

Paul Dorion on immediate cardioversion vs rate control/delayed cardioversion for atrial fibrillation (00:32)

Justin Morgenstern & Justin Hensley on emergency management of snake bites (10:24)

Brit Long on reliability of clinical features in the diagnosis of ovarian torsion (21:35)

Michelle Klaiman on emergency management of crystal methamphetamine use disorder (26:48)

Hans Rosenberg & Rob Ohle on workup of suspected aortic dissection (32:16)

Anand Swaminathan on epinephrine and magnesium sulphate in severe asthma (38:05)

Podcast production, editing and sound design by Anton Helman

Podcast content, written summary & blog post by Sucheta Sinha, Michelle Klaiman & Brit Long, edited by Anton Helman

Cite this podcast as: Helman, A. Dorion, P.  Swaminathan, A. Long, B.  Klaiman, M. Rosenberg, H, Hensley, J. Ohle, R. Morgenstern J. EM Quick Hits 12 – AFib Early vs Delayed Cardioversion, Snake Bites, Ovarian Torsion Myths, Crystal Meth, Aortic Dissection, Severe Asthma Meds. Emergency Medicine Cases. January, 2020. https://emergencymedicinecases.com/em-quick-hits-january-2020/Accessed [date].

Immediate cardioversion vs rate control and delayed cardioversion for acute atrial fibrillation

  1. For stable patients who present to the ED with the primary diagnosis of rapid atrial fibrillation with moderate to severe symptoms and no complications mandating immediate cardioversion (heart failure, cardiac ischemia, shock) options include electrical or chemical cardioversion or rate control with delayed cardioversion.
  2. Arguments for immediate electrical cardioversion include high success rate and prompt resolution of symptoms.
  3. Support for immediate ED cardioversion comes from the recent RAF2 trial which compared two strategies for cardioversion (rhythm control) in acute-onset atrial fibrillation: 1) procainamide infusion + shock vs 2) placebo fluid infusion + shock. Both were similarly effective (>93%) in converting to sinus rhythm and 95% of patients remained in sinus rhythm even 2 weeks afterwards.
  4. It is unclear whether or not the risk of stroke is reduced, increased or uneffected with cardioversion in the ED compared to rate control.
  5. Arguments against immediate cardioversion include high ED resource utilization, potential rare complications associated with procedural sedation and that most patients spontaneously convert without intervention within 36hrs (about 70%).
  6. Our expert believes that encouraging patients with uncomplicated primary atrial fibrillation to return to the ED for cardioversion whenever they have symptoms of atrial fibrillation results many unnecessary ED visits and be an unnecessary burden on the system.
  7. Support for withholding immediate cardioversion comes from a 2019 NEJM study which compared immediate ED cardioversion to rate control and reassessment within 36hrs for consideration of delayed cardioversion (going home with a rate control agent) if still in atrial fibrillation. 91% of patients in the delayed cardioversion group were in sinus rhythm at 1 month and 94% in the immediate cardioversion group,  showing non-inferiority. There was no differences in potential risks or patient-reported quality of life between the two strategies.
  8. Practical considerations such as availability of follow up within 36hrs limits the “delayed” cardioversion strategy.

Ian Stiell’s take on immediate vs delayed cardioversion of atrial fibrillation in EM Cases Quick Hit 7 

  1. Pluymaekers NAHA, Dudink EAMP, Luermans JGLM, et al. Early or Delayed Cardioversion in Recent-Onset Atrial Fibrillation. N Engl J Med. 2019;380(16):1499-1508.
  2. Stiell, Ian G. et al. Safe Cardioversion for Patients with Acute-Onset Atrial Fibrillation and Flutter: Practical Concerns and Considerations. Canadian Journal of Cardiology. Published online June 13, 2019.
  3. Andrade JG, Verma A, Mitchell LB, et al. 2018 Focused Update of the Canadian Cardiovascular Society Guidelines for the Management of Atrial Fibrillation. Can J Cardiol. 2018;34(11):1371-1392.
  4. Stiell, I et al. CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist. CJEM 2018;20(3):334-342.

 

Emergency management of snake bites envenomation

  1. North American venomous snakes include the Massasauga rattlesnake and the Prairie rattlesnake and are crotalids which have necrotoxic venom. This venom has more local effects and less rapid toxicity (as opposed to the more immediate life threat of neurotoxic snake bites of some Australian and Asian snakes).
  2. First Aid for crotalid bites includes moving calmly away from the snake, calling 911, removing constricting items on the limb that is bitten, and immobilizing the limb in a neutral position at or above the level of the heart to minimize swelling. Do not use a tourniquet, attempt to “suck out the venom”, or put ice on the wound.
  3. Lab tests include INR, platelets, Cr, CK, electrolytes as some snake bite envenomations result in DIC, thrombocytopenia, rhabdomyolysis and renal failure.
  4. Measure and mark out the extent of swelling and pain q1-2hrs to monitor progression of disease. Monitor for progression for up to 24hrs.
  5. Treatment algorithm for pit viper snake bites (which includes crotalids) divides patients into minor and major envenomation. Major envenomantion involves systemic systemic signs and symptoms including angioedema.
  6. All patients with major envenomations should have a consult with the local poison control center to guide treatments.
  7. The antivenom treatment for crotalids is Crotaline Fab. 4-6 vials is the initial dose reserved for patients with major envenomations. For immediate life-threatening envenomations 8-12 vials is the recommended dose.
  8. Outside of North America there are more dangerous neurotoxic snake bites that involve different management. For neurotoxic snake bites (e.g. cobra, Australian brown snake) first aid includes pressure immobilisation bandaging with adequate compression to limit lymphatic spread of the neurotoxin. Avoid pressure immobilisation bandaging in crotalid snakebites.

Unified Treatment Algorithm for the Management of Pit Viper Snakebite in the United States.

  1. Life in the Fast Lane approach to snakebites: https://litfl.com/approach-to-snakebite/
  2. Lavonas EJ, Ruha AM, Banner W, et al. Unified treatment algorithm for the management of crotaline snakebite in the United States: results of an evidence-informed consensus workshop. BMC Emerg Med. 2011;11:2.
  3. Isbister GK, Brown SG, Page CB, Mccoubrie DL, Greene SL, Buckley NA. Snakebite in Australia: a practical approach to diagnosis and treatment. Med J Aust. 2013;199(11):763-8.

 

Myths in the utility of clinical features in diagnosis of ovarian torsion

  1. Myth: Ovarian torsion only occurs in women of reproductive age. Ovarian torsion affects women of all ages including children, postmenopausal and pregnant women.
  2. Myth: My patient’s pain is mild, and she has had it off and on for a few days. This cannot possibly be torsion, right? The classic presentation of ovarian torsion is not always present; patients may have intermittent pain or no pain at all. Intermittent torsion can occur. Only 50% of patients have acute, severe pain.
  3. Myth: My patient is minimally tender, and no mass can be palpated on bimanual examination. Therefore, torsion can be ruled out. Do not rely on a normal abdominal, pelvic, or bimanual examination to rule out torsion. Literature suggests the abdominal and bimanual exams, whether conducted by emergency clinicians or obstetricians, do not have adequate sensitivity (23-26%). Our bimanual exam often fails to detect ovarian masses < 5 cm in diameter.

If your patient has lower quadrant pain but an otherwise unrevealing evaluation, keep torsion on the differential.

  1. Robertson JJLong BKoyfman A. Myths in the Evaluation and Management of Ovarian Torsion. J Emerg Med. 2017 Apr;52(4):449-456.
  2. EmDOCs deep dive on ovarian torsion: ttp://www.emdocs.net/em3am-ovarian-torsion/
  3. EmDOCs pearls and pitfalls on ovarian torsion: http://www.emdocs.net/ovarian-torsion-pearls-and-pitfalls/

 

Emergency management of crystal methamphetamine use disorder

  1. Crystal methamphetamine is smokable crystals composed of the highly purified d-isomer of methamphetamine. It is easy to make, cheap and has five times more CNS potency than regular meth.
  2. Crystal methamphetamine use disorder is an epidemic problem in North America that has largely been ignored because of the opioid epidemic. It is often associated with repeat visits and medical admissions for complications such as rhabdomyolysis.
  3. Onset is seconds when smoked, and the duration of effect is 10-12 hours. The large dopamine surge can cause agitated psychosis often requiring chemical sedation. Auditory or tactile hallucinations are common including formication (the sensation of insects crawling on the skin) that causes skin picking and excoriation.
  4. Evidence based treatment includes psychosocial interventions such as Cognitive Behavioural Therapy and contingency management (cash or voucher rewards for positive behavior change). Motivational interviewing in the ED after the patient has been stabilized is advised to assess readiness for change and suitability of referral for psychosocial counselling.
  5. Weak and controversial evidence exists for stimulation substitution therapy with modafinil and bupropion. Consider a prescription for olanzapine in those patients with chronic hallucinations so they are then able to participate in psychosocial interventions.
  6. Online resources include himynameistina.com and checkhimout.ca/highlife.

Deep dive into management of agitated patient with Reuben Strayer & Marg Thompson: Episode 115 

  1. Alharbi, F. F., & el-Guebaly, N. (2016). Cannabis and amphetamine-type stimulant-induced psychoses: A systematic overview. Addictive Disorders & Their Treatment, 15(4), 190-200.
  2. Hart CL, Gunderson EW, Perez A, et al. Acute physiological and behavioral effects of intranasal methamphetamine in humans. Neuropsychopharmacology. 2007;33(8):1847.
  3. Richards, J.R., et al., Treatment of toxicity from amphetamines, related derivatives, and analogues: A systematic clinical review. Drug Alcohol Depend. (2015).
  4. Schep LJ, Slaughter RJ, Beasley DM. The clinical toxicology of methamphetamine. Clin.Toxicol. (Phila.) 2010; 48: 675–94.
  5. Wodarz N, Krampe-Scheidler A, Christ,Met al. Evidence-Based Guidelines for the Pharmacological Management of Acute Methamphetamine-Related Disorders and Toxicity Pharmacopsychiatry. (2017). 50. 87-95.

 

 

Aortic dissection challenges in diagnosis

  1. While the miss rate of aortic dissection has been reported to be as high as 14-38%, the 2018 ADvISED Study reported a miss rate of only 0.7% based on clinical features alone. A likely alternative diagnosis or low clinical suspicion rules out >99% of cases.
  2. High risk features of aortic dissection include risk factors (connective tissue disease, bicuspid aortic valve, personal or family history of aortic disease), recent aortic manipulation, acute onset pain, severe pain, tearing/ripping pain, migratory pain, hypotension, pulse deficit/blood pressure differential, murmur of aortic insufficiency and neurological deficit. The absence of any high-risk feature for acute aortic dissection makes the diagnosis unlikely.
  3. The role of D-dimer in the workup of aortic dissection is controversial. In the absence of a proven diagnostic algorithm, it is difficult to know whether D-dimer will improve the miss rate or just increase the number of imaging studies performed.

Other EM Cases aortic dissection resources:

  1. Episode 92: Aortic Dissection Live from the EM Cases Course
  2. Journal Jam: D-Dimer to Rule out Aortic Dissection

  1. Roncon L, Zuin M, Zonzin P. Letter by Roncon et al Regarding Article, “Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus D-Dimer for Acute Aortic Syndromes: The ADvISED Prospective Multicenter Study”. Circulation. 2018;138(4):445-446.
  2. Ohle R, Mcisaac S, Atkinson P. How do I rule out aortic dissection?. CJEM. 2019;21(1):34-36.

 

Epinephrine and magnesium sulphate for severe asthma exacerbation

  1. In the patient with a severe asthma exacerbation, although robust RCTs are lacking, consider epinephrine 10-15 micrograms IV over 1 minute, repeat x1 prn then if clinical response start infusion of epinephrine 5-10 micrograms/min.
  2. If there is no IV access consider anaphylaxis dosing of epinephrine 0.3-0.5mg IM.
  3. IV magnesium sulphate has been shown to reduce hospital admission in patients with severe and life-threatening acute exacerbations unresponsive to initial treatments, whereas the evidence has been weaker for nebulized magnesium. There is no evidence of benefit of magnesium sulphate in asthma for patient-oriented outcomes, however this may be due to the low dose of 2g IV used in most studies.
  4. High dose Magnesium sulphate infusion [Magnesium sulphate 50mg/kg over 1hr then 50mg/kg/hr x 4hrs (max 8g total)] has also been shown in pediatric patients in a small single center study to increase the proportion of patients discharged at 24hrs by 37% (NNT=3).
  5. Our expert recommends considering MgSO4 2g IV over 20 mins repeated x 3 doses (total 8g), then infusion 2-4g/hr x 2-3hrs in patients with severe and life-threatening asthma exacerbation.

Easy epinephrine drip: put 1 mg of epinephrine in a 1L bag of NS (concentration of 1mcg/mL). Run at 300ml/hr (5 mcg/min).

  1. Cydulka R, Davison R, Grammer L, Parker M, Mathews J. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med. 1988;17:(4)322-6.
  2. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CA. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Database Syst Rev. 2000;(2):CD001490.
  3. Irazuzta JE, Paredes F, Pavlicich V, Domínguez SL. High-Dose Magnesium Sulfate Infusion for Severe Asthma in the Emergency Department: Efficacy Study. Pediatr Crit Care Med. 2016;17(2):e29-33.
  4. Goodacre S, Cohen J, Bradburn M, et al. Intravenous or nebulised magnesium sulphate versus standard therapy for severe acute asthma (3Mg trial): a double-blind, randomised controlled trial. Lancet Respir Med. 2013;1(4):293-300.

 

None of the authors have any conflicts of interest to declare