Question Of The Day #55

question of the day
~ Joseph Ciano, USA ~ Leave a comment
738.2 - STEMI
Which of the following is the most likely cause for this patient’s condition?  
  • A) Hypovolemia
  • B) Systemic infection
  • C) Pulmonary embolism
  • D) Poor cardiac output

This patient presents with chest pressure at rest and an anterior ST segment elevation myocardial infraction (STEMI) seen on 12-lead EKG.  This patient should be given aspirin, IV fluids to increase the preload status, and receive immediate coronary reperfusion therapy.  This patient’s hypotension is likely due to infarction of the left ventricle causing poor cardiac output (Choice D).  This is known as cardiogenic shock.  The patient has been vomiting, but the acute onset of symptoms and STEMI on EKG make poor cardiac output (Choice D) more likely than hypovolemia (Choice A) as the cause for the patient’s condition.  Systemic infection (Choice B) and pulmonary embolism (Choice C) are also less likely given the clinical information in the case and the STEMI on EKG.  The best answer is Choice D.  Please see the chart below for further detailing of the different types of shock.   

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References

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Welcome from GEMS LP!

~ Global EM Student Leadership Program ~ Leave a comment

Hello and welcome to the first blog post from ACEP’s International Section’s Global Emergency Medicine Student Leadership Program. We are thrilled to partner with iEM in the hosting of this blog, and we thank them for their collaboration and enthusiasm.

Global EM is a young, quickly growing field in the world of health care, but there remains much work to be done. The GEMS LP program was designed to involve students in this exciting and fulfilling specialty. The program itself falls under ACEP’s International Section in conjunction with the International Ambassador Program. All of these entities share a common goal: the advancement of the emergency medicine specialty worldwide.

Through this blog, we hope to educate, inspire, update, and collaborate on all things global EM.  Every couple of weeks, you can expect to read the ‘key points’  from our journal clubs. In each meeting, we review fundamental global health topics through a book chapter and a research paper, followed by a dynamic discussion with a diverse group ranging from medical students to attendings, working both in the US and abroad. Additionally, you can look forward to interviews with some of ACEP’s International Ambassador team members, interesting case discussions, GEMS LP project highlights and other fun commentaries from our mentees and team! 

We look forward to providing you relevant content that will encourage discussion, contemplation, and promotion of the field of global emergency medicine. Thank you for joining us on this new adventure! Please visit our page (https://iem-student.org/gems-lp/) for more information about our leadership team, awesome mentors, and upcoming events and meetings. 

Comments, suggestions, additions? Please reach out to us!

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Acute Atrial Fibrillation in the ED: Almost all goes home

~ Israa M Salih, UAE ~ Leave a comment

Atrial fibrillation (AF) is the most common dysrhythmia presenting to ED. The management options depend on patient stability, presence of underlying causes and factors in the patient history. In stable patients presenting in AF with a rapid ventricular response, both rate and rhythm control are acceptable approaches. Physicians often tend toward rate control because evidence has shown no mortality benefit between the two approaches. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial contributed to this trend when it concluded no survival advantage and higher risk of adverse drug effects with rhythm control. However, rhythm control is the preferred approach for the management of acute stable AF in Canadian guidelines. The advantages are a higher rate of symptom resolution, restoration of sinus rhythm and avoiding the need for rate control prescriptions, decreased ED length of stay, and hospital admissions.

In the electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2) trial, it was found that both drug–shock and shock-only strategies were effective, rapid, and safe with 96% of patients discharged home in sinus rhythm. The drug infusion worked for 50% of patients avoiding procedural sedation.

The evidence that supports the management of acute AF in the ED without hospital admission is increasing. Implementing practices to achieve that will markedly decrease the burden on the health care system.

ED Management

Approach of Atrial fibrillation

AF might be secondary to variable causes, including ACS, Heart failure, PE, sepsis and bleeding. In patients with secondary AF, cardioversion might be harmful, and the mainstay of treatment is tackling the underlying cause. Those patients will require hospital admission. For primary AF, if the patient is unstable, electrical cardioversion should be done without delay. Stable primary AF may be managed with rate or rhythm control.

Rate control can be achieved with the following:

CCB: Diltiazim 0.25 mg/kg over ten mins, repeat q15-20 mins, up to three doses (avoid in heart failure)

BB: Metoprolol 2.5-5 mg q15-20 mins

Digoxin: 0.25-0.5 mg loading dose then 0.25 mg q4-6 hs (if hypotension or acute HF occur)

Target is HR <100 at rest or <110 walking

Rhythm control is safe with the following according to The CAEP AF best practice guidelines:

  1. Anticoagulated for three or more weeks.
  2. No valvular heart disease, prior stroke or TIA plus: 
  • Onset in 12 hours or less
  • Onset more than 12 hours but less than 48 hours plus less than two of :
    • Age less than 65, DM, HTN, HF.
  • Cleared by TOE

Methods:

  • Procainamide 15mg/kg in 500 ml of NS over an hour.

Other agents: Amiodarone, Ibutilide, flecainide, etc.

  • Electrical: 150-200 J synchronized. Requires sedation.

Anticoagulation:

If CHADS positive then discharge on DOAC or Warfarin.

Disposition:

Almost all patients can be discharged home after cardioversion or effective rate control with appropriate follow up: within a week if warfarin or rate control agent prescribed, otherwise in 4 weeks.

Patients will require admission if one of the following:

  • Highly symptomatic after treatment.
  • ACS
  • Acute heart failure not improved in the ED

References and Further Reading

  1. Stiell, I. G., Macle, L., & CCS Atrial Fibrillation Guidelines Committee (2011). Canadian Cardiovascular Society atrial fibrillation guidelines 2010: management of recent-onset atrial fibrillation and flutter in the emergency department. The Canadian journal of cardiology, 27(1), 38–46. https://doi.org/10.1016/j.cjca.2010.11.014
  2. Wyse, D. G., Waldo, A. L., DiMarco, J. P., Domanski, M. J., Rosenberg, Y., Schron, E. B., Kellen, J. C., Greene, H. L., Mickel, M. C., Dalquist, J. E., Corley, S. D., & Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. The New England journal of medicine, 347(23), 1825–1833. https://doi.org/10.1056/NEJMoa021328
  3. Baymon, D. E., & Baugh, C. E. (2020). Patients with Atrial Fibrillation in the Emergency Department: Strategies to Achieve Best Outcomes. https://www.hmpgloballearningnetwork.com/site/eplab/patients-atrial-fibrillation-emergency-department-strategies-achieve-best-outcomes
  4. Martín, A., Coll-Vinent, B., Suero, C., Fernández-Simón, A., Sánchez, J., Varona, M., Cancio, M., Sánchez, S., Carbajosa, J., Malagón, F., Montull, E., Del Arco, C., & HERMES-AF investigators (2019). Benefits of Rhythm Control and Rate Control in Recent-onset Atrial Fibrillation: The HERMES-AF Study. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 26(9), 1034–1043. https://doi.org/10.1111/acem.13703
  5. Stiell, I. G., Sivilotti, M., Taljaard, M., Birnie, D., Vadeboncoeur, A., Hohl, C. M., McRae, A. D., Rowe, B. H., Brison, R. J., Thiruganasambandamoorthy, V., Macle, L., Borgundvaag, B., Morris, J., Mercier, E., Clement, C. M., Brinkhurst, J., Sheehan, C., Brown, E., Nemnom, M. J., Wells, G. A., … Perry, J. J. (2020). Electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2): a partial factorial randomised trial. Lancet (London, England), 395(10221), 339–349. https://doi.org/10.1016/S0140-6736(19)32994-0
  6. Ian G. Stiell, et al. (2021). 2021 CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist.https://caep.ca/wp-content/uploads/2021/06/2021-CAEP-AAF-Checklist-FINAL-6-June-2021.pdf
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Question Of The Day #54

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most likely cause for this patient’s condition?
  • A) Hypovolemic shock
  • B) Distributive shock
  • C) Obstructive shock
  • D) Cardiogenic shock

This patient sustained significant blunt trauma to the chest, presents to the Emergency Department with hypotension, tachycardia, a large chest ecchymosis, and palpable sternal crepitus.  The ultrasound image provided shows a subxiphoid view of the heart with a large pericardial effusion.  In the setting of trauma, this should be assumed to be a hemopericardium.  This patient has cardiac tamponade, which is considered a type of obstructive shock (Choice C).  Treatment includes IV hydration to increase preload, bedside pericardiocentesis, and ultimately, a surgical cardiac window performed by cardiothoracic surgery.  The other shock types (Choices A, B, D) do not describe this patient’s presentation.  Please see the chart below for further description of the different shock types and therapies.

 

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References

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The dose makes the poison: Coffee consumption, physiology and health impact

~ Brenda Varriano, Canada ~ Leave a comment

Introduction

As my alarm goes off at 4 am, I dread the day ahead. However, after countless sleepless nights since moving into a new city, I need to wake up early for my M3 orientation. Fortunately, I have caffeine at my disposal. So, reaching for my cup, I became inspired for my next wellness article, “Oh Sweet, Sweet nectar of the Gods.” For this article, I will start by sharing some statistics about coffee, followed by coffee processing, physiology, and, lastly, effects on the body.

In 2020, data from the national coffee association revealed that coffee consumption is up by 5% in the USA since 2015. The average American coffee drinker drinks over 3 cups of coffee a day. With coffee being a stimulant, it is no surprise that it is a favorite among physicians and medical students. Interestingly, one study reported that in-patient physicians were more likely to drink coffee and energy drinks than out-patient-based physicians. During orientation, the surgery director gave a piece of wisdom to the class of 2023. “Drink espresso. Less volume, more caffeine, less need to use the washroom after scrubbing in.”

Coffee Processing and Physiology

Given the high consumption rates of coffee, I want to start by appreciating the tremendous processing it must go through before we consume it. Coffee is derived from the Coffea (genus) shrub; the two most common species being canephora and arabica. First, coffee berries are handpicked, where the flesh is removed, and the seeds are left to ferment and dry. At this stage, the coffee is known as green coffee. Starbucks and other chains have started serving cold brews of coffee at this stage.

Interestingly, green coffee has the highest caffeine content. Second, comes the roasting stage, which impacts the amount of caffeine content and taste of coffee. The longer that coffee is roasted, the more moisture is lost and the less dense it becomes. As coffee is roasted, starches are broken down to simple sugars, high heat causes the breakdown of caffeine, and oils begin to develop. The oils contribute to coffee’s famous aroma. Finally, these beans are ground and brewed as they make their way into our cups. (Note: this is a very brief description, which does not cover decaf coffee)

Coffee is a stimulant, which has unique effects on the human body. Much of this content regarding coffee physiology shall be derived from a review by McLellan et al. 2016 and a sports podcast for those ortho heads: https://www.strongerbyscience.com/caffeine/#Adenosine_antagonism. First, coffee is considered a xanthine derivative with three methyl groups attached (scientific name-1,3,7-trimethylxanthine). This structure is similar to adenosine, explaining coffee’s action as an adenosine antagonist, meaning to inhibit the actions of adenosine at an adenosine receptor (figure 1). There are four adenosine receptors. By inhibiting different subtypes of adenosine receptors, caffeine can cause different effects. For example, adenosine receptors in the brain block the release of serotonin, dopamine, glutamate, and other neurotransmitters (less in the synapse). Caffeine blocks adenosine’s actions, thus increasing the amount of neurotransmitters in the synapse, explaining caffeine’s effects. For example, increased dopamine leads to an increased perception of reward. By altering glutamate levels, caffeine can even alter the seizure threshold. However, it is less straightforward than I am making it to sound since neurotransmitters can cause different effects in different brain regions.

Figure 1: The structure of caffeine vs. adenosine https://www.strongerbyscience.com/caffeine/#Adenosine_antagonism

Peripherally, coffee mainly acts as a sympathetic stimulant, see Figure 2. One mechanism is by stimulating your adrenal glands to secrete catecholamines which act on various organs in the body. Finally, the effects of caffeine vary, depending on individual caffeine metabolism. For example, metabolism differs between naïve or experienced caffeine consumers. Finally, the dose/timing of caffeine intake impacts metabolism. Literature suggests that absorption takes approximately 45 minutes, peak serum caffeine occurs after 15 minutes to 2 hours following ingestion, and finally, half-life ranges from 2.5-4.5 hours.

Figure 2: Impact of Coffee on the body (Van Dam et al., 2020)

Specific Effects

Coffee, while used as a stimulant, impacts our health more than we realize. A recent umbrella review by Poole et al. (2017) looked at the risks and benefits of coffee consumption based on the findings of over 200 meta-analyses. Coffee consumption was analyzed in the following conditions: high vs. Low consumption, any vs. none, and having an extra cup of coffee per day. Overall, coffee consumptions appeared to reduce the risk of all-cause mortality, cardiovascular mortality, and cardiovascular disease. Coffee consumption was also suggested to correlate with a reduced risk of cancer. These findings have been echoed in other studies. For example, a study in 2016 by Liebeskind et al. described the “coffee paradox.” In this study, high rates of coffee consumption were found to have a reduced risk of stroke, even in those who smoked. 

Finally, a recent review published in the New England Journal of Medicine summarizes some of the consistent findings of coffee consumption and its effects on the human body (Van Dam et al., 2020). In the CNS, caffeine:

  1. Reduces fatigue, increases alertness, and improves vigilance (Note: caffeine does not compensate for chronic sleep deprivation!).
  2. Improves pain tolerance.
  3. Increases anxiety when >200 mg is consumed in one sitting or >400 mg is consumed in a day.

Caffeine withdrawal presents with headache, fatigue, and depressed mood 1-2 days after cessation of coffee consumption. Withdrawal effects last between 2-9 days. In addition, coffee toxicity (1.2g or higher) can lead to altered thought and speech, anxiety, insomnia, dysphoria, and cardiovascular toxicity—more on cardiovascular toxicity in peripheral effects. I briefly mention it here, as it is part of the toxicity presentation. 

Peripherally, coffee intake increases epinephrine release by stimulating the adrenal glands and subsequently increases blood pressure transiently, as tolerance develops over time. Coffee intake (non-toxic levels) can reduce the risk of cardiovascular disease (see coffee paradox above). Coffee may potentially improve metabolism and reduce appetite, thus causing minimal effects on weight loss. Coffee may also decrease insulin sensitivity with short-term use (long-term use counteracts these effects). Furthermore, breakdown products of coffee may act as an antioxidant and protect against reactive oxidative species (ROS). Finally, coffee has been reported to reduce the risk of mortality from any cause. 

Conclusion

Coffee is a staple among many households, including our patients. Though used as a stimulant, coffee can have many physiological effects, many being beneficial. However, there can be too much of a good thing. Too much coffee can increase the risk of agitation, anxiety, insomnia, and arrhythmias. Coffee is a tool, but it is our job to use it wisely and educate patients that may be at risk of too much caffeine consumption.

References and Further Reading

  1. de Melo Pereira, G. V., de Carvalho Neto, D. P., Júnior, A. I. M., do Prado, F. G., Pagnoncelli, M. G. B., Karp, S. G., & Soccol, C. R. (2020). Chemical composition and health properties of coffee and coffee by-products. In Advances in food and nutrition research (Vol. 91, pp. 65-96). Academic Press.
  2. International Coffee Organization. The Current State of the Global Coffee Trade. Coffee Trade Stats. (2016). Retrieved from: http://www.ico.org/monthly_coffee_trade_stats.asp.
  3. Kummer, C. (2003). The joy of coffee: the essential guide to buying, brewing, and enjoying. Houghton Mifflin Harcourt.
  4. Liebeskind, D. S., Sanossian, N., Fu, K. A., Wang, H. J., & Arab, L. (2016). The coffee paradox in stroke: Increased consumption linked with fewer strokes. Nutritional neuroscience, 19(9), 406-413.
  5. McLellan, T. M., Caldwell, J. A., & Lieberman, H. R. (2016). A review of caffeine’s effects on cognitive, physical, and occupational performance. Neuroscience & Biobehavioral Reviews, 71, 294-312.
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Question Of The Day #53

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause for this patient’s condition?

  • A) Increased systemic vascular resistance (SVR)
  • B) Occult hemorrhage
  • C) Damage to the sympathetic nervous system
  • D) Tension pneumothorax

This patient endured a high-speed motor vehicle accident, arrives with hypotension and bradycardia, and has a C6 vertebral body fracture on imaging.  These details support a diagnosis of neurogenic shock, a type of distributive shock.

Shock is an emergency medical state characterized by cardiovascular or circulatory failure.  Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure.  Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic.  The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap.  The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam.  Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management.  The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

Neurogenic shock is caused by spinal cord damage above the T6 level.  Unlike other types of shock, neurogenic shock is characterized by hypotension and bradycardia (not tachycardia).  These vital sign abnormalities are caused by damage to sympathetic nervous system (Choice C).  Neurogenic shock has decreased systemic vascular resistance (warm extremities), not increased systemic vascular resistance (cool extremities) (Choice A).  Occult hemorrhage (Choice B) is always a concern in a trauma patient.  However, this would present with findings of hypovolemic/hemorrhagic shock (tachycardia, hypotension, cool extremities).  Tension pneumothorax (Choice D) is also unlikely as the patient has clear bilateral lung sounds on exam.  The best answer is Choice C.

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References

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Can I Eat This? – A Helpful Guide To Plant Toxicology

~ Mohammad Anzal Rehman, UAE ~ Leave a comment

Not only is identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, it is a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

This is the third part in a series of blog posts dedicated to providing you with original mnemonics and visual aids that serve to highlight a few classes of common toxic plants prominent for both their inclusion in academic assessment as well as their prevalence in the community. These memory tools will attempt to highlight key features in the identification of well-known toxic plant species and are designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 67-year-old man, known to have dementia secondary to Alzheimer’s disease, was brought to the Emergency Department with complaints of abdominal pain and 3 episodes of vomiting after being found by his grandson consuming some roots and leaves from a ‘berry-looking plant’ he had found in a local garden. Following the vomiting, the patient was lethargic, diaphoretic and had an ataxic gait, which prompted the family to bring him to the ED.

Upon arrival to the ED, patient looks tired and restless. Vital signs reveal the following:

BP 78/43                   HR 50                           RR 12                           Temp 37.7 C

You start IV fluids, obtain a Point-of-Care venous blood gas and order an ECG and laboratory investigations for the patient. The BP improves slightly up to 80/50, and the venous blood gas shows no significant acid/base disturbance, Sodium of 137 mEq/L, Potassium of 3.7 mEq/L, Hgb of 12.6 g/dL and Lactate 1.4. All other parameters seem to also fall within normal limits. The ECG, however, revealed a widened QRS. As you bring the rhythm strip to your Attending Physician, you hear the patient’s cardiac monitor beep and notice similar, but wider QRS intervals at a faster rate on the screen. You recognize the rhythm as Ventricular Tachycardia.

Recognizing the patient to be in shock with a persistently low blood pressure and a cardiac rhythm of ventricular tachycardia, you decide to perform synchronized electrical cardioversion. After delivery of shock, the patient’s rhythm converts to sinus rhythm. Your Attending Physician arrives with some additional family members who brought with them the berries the patient had reportedly ingested (Figure 1).

Figure 1- Photograph of the berry-like fruit ingested by the patient, identified later as a species of yew

Overview of Taxus Yew Toxicity

The poisonous nature of the Yew (Taxus spp.) has been attributed to taxine alkaloids present in all parts of the plant except the scarlet ‘berry’. The mechanism of toxicity from taxine alkaloids centers on their ability to antagonize sodium as well as calcium channels, primarily acting on cardiac myocytes. [1,2]

While most ingestions are accidental, with non-significant complaints reported, serious fatal outcomes can often be encountered when large amounts of the plant are consumed, usually with suicidal intent. [3]

Typical symptoms post-ingestion range from gastrointestinal complaints such as nausea and abdominal pain, but can easily progress to neurologic complaints of paresthesias and ataxias, along with the dreaded cardiovascular manifestations of bradycardia, conduction delays, wide-complex ventricular dysrhythmias that can cause rapid and fatal instability.

Unfortunately, no specific antidote exists to counter the effect of taxine alkaloids. Ventricular dysrhythmias causing instability are preferably controlled through cardioversion as per ACLS guidelines, though this admittedly treats the effect rather than the cause. [4] Anti-arrhythmic agents have not been shown to have a significant impact on management. Some limited reports show no benefit from hemodialysis,[5] but some promise of Extracorporeal life support with Membrane Oxygenation (ECMO)[6,7] in treating Yew berry poisoning, making management largely reactionary rather than targeted.

Identifying Plants with Sodium Channel Actions

Yew berry (Taxine alkaloid) poisonings can be grouped with other toxic plant species solely due to their common mechanism of action on the sodium channel. Three major plant types that are often encountered in literature are highlighted below:[8]

  1. Aconitum spp., commonly referred to by names such as monkshood, wolfsbane and helmet flower: Contain aconitine and other similar alkaloids that prevent inactivation of voltage-gated sodium channels in cardiac and CNS cells, producing both neurological (paresthesias, weakness, seizures) and cardiovascular (hypotension, bradycardia) effects.
  2. Taxine spp., commonly referred to as Yew plants: Contain taxine alkaloids as highlighted above, with actions of sodium and calcium channel blockade, producing effects primarily on the cardiovascular system, with chances of severe ventricular dysrhythmias and cardiac arrest.
  3. Rhododendron spp., commonly referred to as death camas, azalea and mountain laurel: Contain grayanotoxins that can be concentrated in honey (‘mad honey’), with actions propagated by binding to sodium channels, resulting in sustained depolarization and an increased vagal tone. This results in cardiovascular effects as with the other plants above (bradydysrhythmias, hypotension) as well as symptoms of diaphoresis, hypersalivation and dizziness/syncope.

Plant Identification

As you may notice, all of the above species have two things in common: they all act on the sodium channel and they all can manifest as hypotension and bradydysrhythmia.

Visual identification of these plants can then be made easier by correlating their appearance with the cartoon image below.

References and Further Reading

  1. Wilson, C. R., Sauer, J., & Hooser, S. B. (2001). Taxines: a review of the mechanism and toxicity of yew (Taxus spp.) alkaloids. Toxicon : official journal of the International Society on Toxinology, 39(2-3), 175–185. https://doi.org/10.1016/s0041-0101(00)00146-x
  2. Jones, R., Jones, J., Causer, J., Ewins, D., Goenka, N., & Joseph, F. (2011). Yew tree poisoning: a near-fatal lesson from history. Clinical medicine (London, England), 11(2), 173–175. https://doi.org/10.7861/clinmedicine.11-2-173
  3. Labossiere, A. W., & Thompson, D. F. (2018). Clinical Toxicology of Yew Poisoning. The Annals of pharmacotherapy, 52(6), 591–599. https://doi.org/10.1177/1060028017754225
  4. Nelson LS, Shih RD, Balick MJ. Handbook of Poisonous and Injurious Plants. 2nd ed. New York, NY: Springer/New York Botanical Garden; 2007:288-290
  5. Dahlqvist M, Venzin R, König S, et al. Haemodialysis in Taxus baccata poisoning: a case report. QJM. 2012;105(4):359-361.
  6. Panzeri C, Bacis G, Ferri F, et al. Extracorporeal life support in severe Taxus baccata poisoning. Clin Toxicol. 2010;48(5):463-465.
  7. Soumagne N, Chauvet S, Chatellier D, Robert R, Charrière JM, Menu P. Treatment of yew leaf intoxication with extracorporeal circulation. Am J Emerg Med. 2011;29(3):354.e5-6.
  8. Lim, C.S., Aks, S.E. (2017), ‘Chapter 158 – Plants, Mushrooms and Herbal Medications’, Rosen’s emergency medicine 9th edition, Pg. 1957 – 1973
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Question Of The Day #52

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) IV normal saline
  • B) IV diphenhydramine
  • C) IM epinephrine
  • D) Endotracheal intubation

This patient has anaphylactic shock, which falls under the category of distributive shock.  Anaphylactic shock is an acutely life-threatening type of allergic reaction that if left untreated, can progress to airway edema, asphyxiation, and death.  Exposure to a known or unknown allergen is the trigger for anaphylaxis.  Diagnosis of this condition requires the below criteria to be met:

  1. Acute onset of skin or mucosal changes (i.e., urticaria, tongue or lip swelling) AND hypotension or respiratory compromise (i.e., wheezing).

OR

  1. Dysfunction of two or more body systems after exposure to a presumed allergen:
    1. Skin/mucosa (i.e., urticaria, swelling of tongue or lips)
    2. Pulmonary (i.e., wheezing)
    3. Cardiovascular (i.e., hypotension)
    4. Gastrointestinal (i.e., vomiting or diarrhea)
    5. End-organ dysfunction

Management of anaphylaxis requires proper evaluation of the patient’s airway, respiratory status, and hemodynamics (“ABCs”).  Mainstays of therapy are intramuscular epinephrine (0.3mg in adults) and IV hydration.  Administration of epinephrine is a time sensitive and life-saving intervention.  Antihistamines, nebulized albuterol or salbutamol, and steroids are additional therapies that are commonly given.  Steroids are thought to prevent recurrent anaphylactic reactions, however, there is little data to support this.  Patients are typically monitored for 4-6 hours after administration of epinephrine to observe for changes in clinical status or the need for additional doses of epinephrine.  Patients who remain stable or improve after this observation period are able to be discharged home with a prescription for an epinephrine injector in the event of future anaphylaxis episodes. 

Intravenous normal saline (Choice A) and diphenhydramine (Choice B) are important therapies to administer in this patient, but intramuscular epinephrine (Choice C) is the most time-sensitive initial therapy to administer.  Without treatment, airway edema may progress and require endotracheal intubation (Choice D).  The patient’s clear voice and lack of stridor indicate that the patient does not need immediate intubation. 

Correct Answer: C

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References

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Cognitive load theory and its applications in emergency medicine education

~ Nada Radulovic, Canada ~ Leave a comment

Throughout my medical education thus far, I have been very drawn to simulation and cognitive load research related to emergency medicine. This has provided me with an appreciation for the applications of cognitive load theory to diverse areas within the specialty, including medical education.

What is cognitive load?

The cognitive load theory was developed in the late 1980s and explores the ways in which the amount of mental effort affects your working memory, and subsequently, learning (1). Specifically, learning involves processing sensory stimuli through various forms of memory, until the stimuli are encoded into your long-term memory. When the working memory capacity is surpassed, the ability to acquire or learn new information can become limited and may lead to poor performance or errors. Since the development of this theory, research in this area has been expanding to enhance instructional design to optimize learning.

Fig. 1. The basic structure of memory, extending from sensory input to encoding of long-term memory (obtained from Mancinetti et al. (2019)) - (2)

Objective and subjective measures of cognitive load

Global collaborative and independent research initiatives have identified an array of objective physiologic measures (e.g. pupillometry, heart rate, galvanic skin response and EEG parameters), subjective psychometric measures (e.g. Paas, NASA Task Load Index (NASA-TLX)) and secondary task measures that are indicative of an individual’s cognitive load (3). Current research has been investigating the validity of these physiologic metrics beyond a controlled laboratory setting, in order to determine accurate measures that can be applied within dynamic and real-life settings. This can potentially allow us to monitor learners’ cognitive load in real-time and adjust teaching strategies accordingly to optimize learning.

Fig. 2. NASA-TLX cognitive load scale (obtained from Shively, J, NASA-Ames Research Center (2016)) and the Paas rating scale (obtained from Paas et al. (2008)) - (4-5)

Applications of cognitive load theory to emergency medicine education

A paper by Croskerry (2014) highlighted various factors that can influence cognitive load in the emergency department setting and lead to clinical errors, including overcrowding, and fatigue and circadian dyssynchronization secondary to shiftwork (6). Of relevance, a previous post on emDocs explored numerous strategies for emergency providers to mitigate some of this cognitive load (link here: http://www.emdocs.net/cognitiveload/). Furthermore, experienced emergency physicians have developed strategies to better manage their cognitive resources, effectively reducing their cognitive load relative to trainees in similar clinical scenarios. Therefore, there are many ways in which cognitive load theory can be implicated in emergency medicine and used to not only enhance the functional and spatial design of the emergency department, but to also optimize simulation training and other areas of learning for emergency medicine trainees. For example, Johannessen et al. (2019) evaluated the association between physiologic measures and the Paas scale in trauma team leaders using wearable technology during the resuscitation response, in order to better understand cognitive load expression in emergency physicians during traumas (7). Additionally, another study used galvanic skin response, heart rate and a modified Paas scale to assess the “Beat the Stress Fool” protocol in reducing mental effort during clinical simulation (7). Fraser et al. (2018) investigated the link between the cognitive load theory and debriefing simulations. Specifically, they evaluated whether the categorization of mental loads during debriefing can improve learning of this vital and complex skill, and they additionally discussed strategies to alleviate some of the associated cognitive load (8).  

Overall, cognitive load is an exciting and evolving area in research and has many diverse applications in emergency medicine and medical education as a whole. 

References and Further Reading

  1. Sweller, J. (1988). Cognitive Load During Problem Solving: Effects on Learning. Cognitive Science, 12, 257-285.
  2. Mancinetti, M., Guttormsen, S., Berendonk, C. (2019). Cognitive load in internal medicine: What every clinical teacher should know about cognitive load theory. European Journal of Internal Medicine, 60, 4-8. 
  3. Paas, Fred, et al. (2003). Cognitive Load Measurement as a Means to Advance Cognitive Load Theory. Educational Psychologist, 38(1), 63–71.
  4. Shively, J, NASA-Ames Research Center. (2016). Workload Measurement in Human Autonomy Teaming: How and Why? National Aeronautics and Space Administration. Accessed May 2020 at https://ntrs.nasa.gov/archive/nasa/casi.ntrs.nasa.gov/20160008388.pdf
  5. Paas, F., Ayres, P., Pachman, M. (2008). Assessment of cognitive load in multimedia learning therory, methods and applications. Recent Innovations in Educational Technology that Facilitate Student Learning, Chapter 2, pg.11-35. 
  6. Croskerry, P. (2014). ED cognition: any decision by anyone at any time. CJEM, 16(1), 13-9.
  7. Johannessen, E., Szulewski, A., Radulovic, N., Gilic, F., Braund, H., Wu, K., White, M., Rodenburg, D., Howes, D., Davies, C. (2019). Measuring cognitive load in a clinical setting: Medical learning and practice. (M.A.Sc thesis), Queen’s University, Kingston, Canada. 
  8. Fraser, K.L. et al. (2018). Cognitive Load Theory for debriefing simulations: implications for faculty development. Advances in Simulation, 3, 1-8.
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Question Of The Day #51

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most likely cause for the patient’s condition?
  • A) Hypovolemic shock
  • B) Distributive shock
  • C) Obstructive shock
  • D) Cardiogenic shock

This patient is in a shock state caused by left-sided pyelonephritis.

Shock is an emergency medical state characterized by cardiovascular or circulatory failure.  Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure.  Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic.  The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap.  The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam.  Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management.  The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.   

The patient’s signs, symptoms, physical exam, and urine studies point towards an infectious etiology.  This patient is in septic shock, which is considered a type of distributive shock (Choice B).  Hypovolemic shock (Choice A), obstructive shock (Choice C), and cardiogenic shock (Choice D) are caused by other conditions reflected in the above table. 

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References

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Infectious mononucleosis

Infectious mononucleosis
~ Nadine Schottler, Great Britain ~ Leave a comment

Case Presentation

A 16-year-old boy presents to A&E with a fever, an extremely sore throat, and a recent blotchy rash on his back that has been concerning him. He complains of feeling extremely tired and lethargic for the past two weeks. He denies having recently been in contact with anyone ill and confirms that he is up-to-date with his vaccinations. He mentions a visit with his local GP last week, where his doctor prescribed a dose of amoxicillin for a suspected throat infection. He has no other significant medical history. Upon further examination, his pharynx and tonsils appear inflamed with whitewash exudate and he has swollen neck lymph nodes in both the anterior and posterior triangles of the neck.

What is/are the most appropriate next step(s) in the patient’s management?

  • A) Reassure the patient and discharge
  • B) Perform a throat swab
  • C) Arrange a full blood count and a monospot test
  • D) Arrange a rapid antigen test for group A streptococcus

The answer is c) Arrange a full blood count and a monospot test

What is Glandular Fever?

Infectious mononucleosis, also known as glandular fever, is an infection resulting most commonly (80-90%) from an Epstein-Barr virus (EBV). About 95% of adults in the world have been infected with EBV; however, it is rare for it to progress into glandular fever. Glandular fever is most commonly seen in individuals aged 15-24, but can present in all age groups. The prevalence of glandular fever is estimated to be between 5-48 cases per 1000 persons. Glandular fever is rather rate in those under 10 or older than 30 (1/1000 persons), so it may not need to be in your top differentials in those age groups! In young adults, the likelihood of developing glandular fever from a primary EBV infection is about 50%; in older adults the chances of EBV infection progressing to glandular fever is slim.

For the most part, glandular fever is not contagious. It’s mostly spread through contact with saliva; such as by kissing, sharing food, or children putting things in their mouths. It can also be spread through sexual contact. Luckily, in most occurrences, glandular fever is self-limiting and lasts two to four weeks. The most common lasting effect is fatigue, which can continue from weeks to months.

When Should You Suspect Glandular Fever?

The classic ‘triad’ of symptoms for glandular fever are: 

  • Fever
  • Lymphadenopathy
  • Pharyngitis (‘sore throat’)

Bilateral posterior cervical lymphadenopathy is typical for glandular fever. Tonsils may also be enlarged, and exudate on the tonsils is described as ‘whitewash’. 

Additional signs and symptoms that could include:

  • Prodromal symptoms: 
    • Fatigue, chills, myalgia, headache
  • Palatal petechiae
    • 1-2mm in diameter and lasting 3-4 days
  • Abdominal pains 
  • Nausea and vomiting 
  • Non-specific rash
    • In this case, the patient had a maculopapular rash which is associated with EBV infection. It can be caused by the infection directly but more commonly presents after being treat with amoxicillin; patients should not take penicillin antibiotics when they have infectious mononucleosis. 
  • Splenomegaly 

If you see, or the patient tells you, of any of the following symptoms during their visit to the emergency department, it requires hospitalization! 

  • Difficulty swallowing 
  • Difficulty breathing 
  • Severe stomach/abdominal pain

These may suggest malignancy. Difficulty swallowing and breathing are most often due to inflamed tonsils and may require steroids. Severe stomach/abdominal pain might suggest a ruptured spleen. Refer to your local guidelines for investigation and treatment if these symptoms present. 

Differential Diagnoses

Viral pharyngitis

  • This is the most common alternative diagnoses
  • Viral pharyngitis tends to be more erythematous 
  • Exudate is not common with viral pharyngitis

Bacterial tonsillitis

  • Bacterial tonsillitis is more commonly described as having ‘speckled’ exudate on tonsils, compared to the ‘whitewash’ exudate on tonsils in glandular fever
  • Lymphadenopathy is usually limited to the upper anterior cervical chain, where in glandular fever, lymphadenopathy can be commonly seen in both anterior and posterior triangles

Other differentials could include other causes of lymphadenopathy, such as inflammation/infection, lymphoma, or leukemia. Alternative viral infections should also be considered (e.g. cytomegalovirus, acute toxoplasmosis, acute viral hepatitis, inter alia). 

Investigations If Glandular Fever Is Suspected

In children younger than 12, or a person who is immunocompromised, a blood test for EBV viral serology should be arranged (if the patient has been ill for seven days). 

In individuals older than 12, a full blood count with differential white cell count and a monospot test should be arranged in their second week of illness. Glandular fever is likely if:

  • The monospot test is positive
  • The full blood count has more than 20% atypical lymphocytes 

OR

More than 10% atypical lymphocytes and the lymphocyte count is more than 50% of the total white cell count.

Treatment

The patient only needs to be hospitalized if they have stridor, difficulty swallowing, are dehydrated, or there is a chance of potentially serious complications (such as a splenic rupture). Steroids should only be used if the patient shows to have difficulty breathing, otherwise, management should be conservative. If the patient doesn’t have any of these concerning signs, it is appropriate to advise the patient of their illness and discharge them for follow-up with their GP.

Some Recommendations To Patients

Some things you can advise the patient on for self-management of glandular fever include:

  • Symptoms usually only last 2-4 weeks 
  • Fatigue may be the last symptom to resolve
  • Relieve symptoms of pain and fever with paracetamol or ibuprofen
  • Encouraging normal daily routines and that exclusion from work or school is not necessary
  • Spreading of disease can be limited by avoiding kissing and not sharing eating utensils
  • They should return to the hospital if they suspect any serious complications (such increased difficulty to breath/swallow, or severe abdominal pain)

References and Further Reading

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Question Of The Day #50

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) IV Physostigmine
  • B) IV Potassium iodide
  • C) IV Propranolol
  • D) PO Propylthiouracil (PTU)

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient arrives hyperthermic, tachycardic in atrial fibrillation, diaphoretic, and altered with psychotic behavior.  Thyroid storm, the most severe manifestation of hyperthyroidism, should always be on the differential diagnosis in patients with fever and altered mental status.  Other considerations are sepsis, sympathomimetic overdose, anticholinergic overdose, serotonin syndrome, and pheochromocytoma. 

This patient has thyroid storm, a life-threatening endocrine emergency that requires prompt recognition and treatment.  Symptoms of thyroid storm include altered mental status, psychosis, seizures, coma, tachycardia, atrial fibrillation, high-output heart failure, dyspnea, vomiting, diarrhea, weight loss, and anterior neck enlargement.  Severe hyperthyroidism should have a low-undetectable TSH level with elevated T3/T4 levels, but in acute illness these levels may be unreliable.  For this reason, the diagnosis and treatment of thyroid storm should be based on clinical grounds.

An anticholinergic toxidrome can appear similar to this patient with tachycardia, hypertension, agitation, and altered mental status.  A key differentiating factor is diaphoresis.  Patients with anticholinergic ingestions should have dry skin, not wet skin. The treatment for anticholinergic toxicity is benzodiazepines and IV physostigmine (Choice A) if symptoms are unresponsive to benzodiazepines.  Physostigmine is not the best next step in this scenario. 

Treatment of thyroid storm is algorithmic.  First, beta blockade (Choice C) should be given to control the heart rate and block T4 to T3 conversion, next anti-thyroid medications (Methimazole or Propylthiouracil (Choice D)) should be given to block thyroid hormone synthesis, and lastly corticosteroids and inorganic iodine (Choice B) can be given to block release of stored thyroid hormone.  The best next step in managing this patient with thyroid storm is administration of IV Propranolol (Choice C).  Propranolol helps manage the tachycardia, systemic symptoms, and also inhibits conversion of T4 to T3. 

 Correct Answer: C

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References

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