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    Health & Fitness

    Emergency Medical Minute

    Our near daily podcasts move quickly to reflect current events, are inspired by real patient care, and speak to the true nature of what it’s like to work in the Emergency Room or Pre-Hospital Setting. Each medical minute is recorded in a real emergency department, by the emergency physician or clinical pharmacist on duty – the ER is our studio and everything is live.

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    Copyright: © Copyright Emergency Medical Minute 2019

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    Latest Episodes:
    Episode 904: Cardiovascular Risks of Epinephrine May 20, 2024
    Show notes

    Contributor: Aaron Lessen MD

    Educational Pearls:

    Epinephrine is essential in the treatment of anaphylaxis, but is epinephrine dangerous from a cardiovascular perspective?

    A 2024 study in the Journal of the American College of Emergency Physicians Open sought to answer this question.

    Methods:

    • Retrospective observational study at a Tennessee quaternary care academic ED that analyzed ED visits from 2017 to 2021 involving anaphylaxis treated with IM epinephrine.

    • The primary outcome was cardiotoxicity

    Results:

    • Out of 338 patients, 16 (4.7%) experienced cardiotoxicity. Events included ischemic EKG changes (2.4%), elevated troponin (1.8%), atrial arrhythmias (1.5%), ventricular arrhythmia (0.3%), and depressed ejection fraction (0.3%).

    • Affected patients were older, had more comorbidities, and often received multiple epinephrine doses.

    Bottom line:

    • All adults presenting with anaphylaxis should be rapidly treated with epinephrine but monitored closely for cardiotoxicity, especially in patients with a history of hypertension and those who receive multiple doses.

    These results are supported by a 2017 study that found that 9% (4/44) of older patients who received epinephrine for anaphylaxis had cardiovascular complications.

    References

    1. Kawano, T., Scheuermeyer, F. X., Stenstrom, R., Rowe, B. H., Grafstein, E., & Grunau, B. (2017). Epinephrine use in older patients with anaphylaxis: Clinical outcomes and cardiovascular complications. Resuscitation, 112, 53–58. https://doi.org/10.1016/j.resuscitation.2016.12.020

    2. Pauw, E. K., Stubblefield, W. B., Wrenn, J. O., Brown, S. K., Cosse, M. S., Curry, Z. S., Darcy, T. P., James, T. E., Koetter, P. E., Nicholson, C. E., Parisi, F. N., Shepherd, L. G., Soppet, S. L., Stocker, M. D., Walston, B. M., Self, W. H., Han, J. H., & Ward, M. J. (2024). Frequency of cardiotoxicity following intramuscular administration of epinephrine in emergency department patients with anaphylaxis. Journal of the American College of Emergency Physicians open, 5(1), e13095. https://doi.org/10.1002/emp2.13095

    Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit OMS II


    Episode 903: Treating Precipitated Opioid Withdrawal May 13, 2024
    Show notes

    Contributor: Aaron Lessen MD

    Educational Pearls:

    • Opioid overdoses that are reversed with naloxone (Narcan), a mu-opioid antagonist, can precipitate acute withdrawal in some patients

    • Treatment of opioid use disorder with buprenorphine can also precipitate withdrawal

    • Opioid withdrawal symptoms include nausea, vomiting, diarrhea, and agitation

    • Buprenorphine works as a partial agonist at mu-opioid receptors, which may alleviate withdrawal symptoms

      • The preferred dose of buprenorphine is 16 mg

    • Treatment of buprenorphine-induced opioid withdrawal is additional buprenorphine

    • Adjunctive treatments may be used for other opioid withdrawal symptoms

      • Nausea with ondansetron

      • Diarrhea with loperamide

      • Agitation with hydroxyzine

    References

    1. Quattlebaum THN, Kiyokawa M, Murata KA. A case of buprenorphine-precipitated withdrawal managed with high-dose buprenorphine. Fam Pract. 2022;39(2):292-294. doi:10.1093/fampra/cmab073

    2. Spadaro A, Long B, Koyfman A, Perrone J. Buprenorphine precipitated opioid withdrawal: Prevention and management in the ED setting. Am J Emerg Med. 2022;58:22-26. doi:10.1016/j.ajem.2022.05.013

    Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit


    Episode 902: Liver Failure and Cirrhosis May 06, 2024
    Show notes

    Contributor: Travis Barlock MD

    Educational Pearls:

    How do you differentiate between compensated and decompensated cirrhosis?

    Use the acronym VIBE to look for signs of being decompensated.

    • V-Volume

      • Cirrhosis can cause volume overload through a variety of mechanisms such as by increasing pressure in the portal vein system and the decreased production of albumin.

      • Look for pulmonary edema (dyspnea, orthopnea, wheezing/crackles, coughing up frothy pink sputum, etc.) or a tense abdomen.

    • I-Infection

      • The ascitic fluid can become infected with bacteria, a complication called Spontaneous Bacterial Peritonitis (SBP).

      • Look for abdominal pain, fever, hypotension, and tachycardia. Diagnosis is made with ascitic fluid cell analyses (polymorphonuclear neutrophils >250/mm3)

    • B-Bleeding

      • Another consequence of increased portal pressure is that blood backs up into smaller blood vessels, including those in the esophagus.

      • Over time, this increased pressure can result in the development of dilated, fragile veins called esophageal varices, which are prone to bleeding.

      • Look for hematemesis, melena, lightheadedness, and pale skin.

    • E-Encephalopathy

      • A failing liver also does not clear toxins which can affect the brain.

      • Look for asterixis (flapping motion of the hands when you tell the patient to hold their hands up like they are going to stop a bus)

    Other complications to look out for.

    • Hepatorenal syndrome

    • Hepatopulmonary syndrome

    References

    1. Engelmann, C., Clària, J., Szabo, G., Bosch, J., & Bernardi, M. (2021). Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction. Journal of hepatology, 75 Suppl 1(Suppl 1), S49–S66. https://doi.org/10.1016/j.jhep.2021.01.002

    2. Enomoto, H., Inoue, S., Matsuhisa, A., & Nishiguchi, S. (2014). Diagnosis of spontaneous bacterial peritonitis and an in situ hybridization approach to detect an "unidentified" pathogen. International journal of hepatology, 2014, 634617. https://doi.org/10.1155/2014/634617

    3. Mansour, D., & McPherson, S. (2018). Management of decompensated cirrhosis. Clinical medicine (London, England), 18(Suppl 2), s60–s65. https://doi.org/10.7861/clinmedicine.18-2-s60

    Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMS II


    Episode 901: Underdosing in Status Epilepticus Apr 29, 2024
    Show notes

    Contributor: Aaron Lessen MD

    Educational Pearls:

    • Lorazepam (Ativan) is dosed at 0.1 mg/kg up to a maximum of 4 mg in status epilepticus

      • Some ED protocols only give 2 mg initially

    • The maximum recommended dose of levetiracetam (Keppra) is 60 mg/kg or 4.5 g

    • In one retrospective study, only 50% of patients received the correct dose of lorazepam

      • For levetiracetam, it was only 35% of patients

    • Underdosing leads to complications

      • Higher rates of intubations

      • More likely to progress to refractory status epilepticus

    References

    1. Cetnarowski A, Cunningham B, Mullen C, Fowler M. Evaluation of intravenous lorazepam dosing strategies and the incidence of refractory status epilepticus. Epilepsy Res. 2023;190(November 2022):107067. doi:10.1016/j.eplepsyres.2022.107067

    2. Sathe AG, Tillman H, Coles LD, et al. Underdosing of Benzodiazepines in Patients With Status Epilepticus Enrolled in Established Status Epilepticus Treatment Trial. Acad Emerg Med. 2019;26(8):940-943. doi:10.1111/acem.13811

    Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit


    Episode 900: Ketamine Dosing Apr 22, 2024
    Show notes

    Contributor: Travis Barlock MD

    Educational Pearls:

    Ketamine is an NMDA receptor antagonist with a wide variety of uses in the emergency department. To dose ketamine remember the numbers 0.3, 1, and 3.

    Pain dose

    • For acute pain relief administer 0.3 mg/kg of ketamine IV over 10-20 minutes (max of 30 mg).

    • Note: There is evidence that a lower dose of 0.1-0.15 mg/kg can be just as effective.

    Dissociative dose

    • To use ketamine as an induction agent for intubation or for procedural sedation administer 1 mg/kg IV over 1-2 minutes.

    IM for acute agitation

    • If a patient is out of control and a danger to themselves or others, administer 3 mg/kg intramuscularly (max 500 mg).

    • If you are giving IM ketamine it has to be in the concentrated 100 mg/ml vial.

    Additional pearls

    • Pushing ketamine too quickly can cause laryngospasm.

    • Between .3 and 1 mg/kg is known as the recreational dose. You want to avoid this range because this is where ketamine starts to pick up its dissociative effects and can cause unpleasant and intense hallucinations. This is colloquially known as being in the "k-hole".

    References

    1. Gao, M., Rejaei, D., & Liu, H. (2016). Ketamine use in current clinical practice. Acta pharmacologica Sinica, 37(7), 865–872. https://doi.org/10.1038/aps.2016.5

    2. Lin, J., Figuerado, Y., Montgomery, A., Lee, J., Cannis, M., Norton, V. C., Calvo, R., & Sikand, H. (2021). Efficacy of ketamine for initial control of acute agitation in the emergency department: A randomized study. The American journal of emergency medicine, 44, 306–311. https://doi.org/10.1016/j.ajem.2020.04.013

    3. Stirling, J., & McCoy, L. (2010). Quantifying the psychological effects of ketamine: from euphoria to the k-Hole. Substance use & misuse, 45(14), 2428–2443. https://doi.org/10.3109/10826081003793912

    Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMS II


    Episode 899: Thrombolytic Contraindications Apr 15, 2024
    Show notes

    Contributor: Travis Barlock MD

    Educational Pearls:

    • Thrombolytic therapy (tPA or TNK) is often used in the ED for strokes

    • Use of anticoagulants with INR > 1.7 or PT >15

      • Warfarin will reliably increase the INR

    • Current use of Direct thrombin inhibitor or Factor Xa inhibitor

      • aPTT/PT/INR are insufficient to assess the degree of anticoagulant effect of Factor Xa inhibitors like apixaban (Eliquis) and rivaroxaban (Xarelto)

    • Intracranial or intraspinal surgery in the last 3 months

      • Intracranial neoplasms or arteriovenous malformations also increase the risk of bleeding

    • Current intracranial or subarachnoid hemorrhage

      • History of intracranial hemorrhage from thrombolytic therapy also contraindicates tPA/TNK

    • Recent (within 21 days) or active gastrointestinal bleed

    • Hypertension

      • BP >185 systolic or >110 diastolic

      • Administer labetalol before thrombolytics to lower blood pressure

    • Timing of symptoms

      • Onset > 4.5 hours contraindicates tPA

    • Platelet count

    • BGL

      • Potential alternative explanation for stroke-like symptoms obviating need for thrombolytics

    References

    1. Fugate JE, Rabinstein AA. Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke. The Neurohospitalist. 2015;5(3):110-121. doi:10.1177/1941874415578532

    2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke a Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Vol 50.; 2019. doi:10.1161/STR.0000000000000211

    Summarized by Jorge Chalit, OMSII | Edited by Jorge Chalit


    Episode 898: Takotsubo Cardiomyopathy Apr 10, 2024
    Show notes

    Contributor: Ricky Dhaliwal, MD

    Educational Pearls:

    • Takotsubo cardiomyopathy, also known as "broken heart syndrome," is a temporary heart condition that can mimic the symptoms of a heart attack, including troponin elevations and mimic STEMI on ECG.

    • The exact cause is not fully understood, but it is often triggered by severe emotional or physical stress. The stress can lead to a surge of catecholamines which affects the heart (multivessel spasm/paralysed myocardium).

    • The name "Takotsubo" comes from the Japanese term for a type of octopus trap, as the left ventricle takes on a distinctive shape resembling this trap during systole. The LV is dilated and part of the wall becomes akenetic. These changes can be seen on ultrasound.

    • The population most at risk for Takotsubo are post-menopausal women.

    • Coronary angiography is one of the only ways to differentiate Takotsubo from other acute coronary syndromes.

    • Most people with Takotsubo cardiomyopathy recover fully.

    References

    1. Amin, H. Z., Amin, L. Z., & Pradipta, A. (2020). Takotsubo Cardiomyopathy: A Brief Review. Journal of medicine and life, 13(1), 3–7. https://doi.org/10.25122/jml-2018-0067

    2. Bossone, E., Savarese, G., Ferrara, F., Citro, R., Mosca, S., Musella, F., Limongelli, G., Manfredini, R., Cittadini, A., & Perrone Filardi, P. (2013). Takotsubo cardiomyopathy: overview. Heart failure clinics, 9(2), 249–x. https://doi.org/10.1016/j.hfc.2012.12.015

    3. Dawson D. K. (2018). Acute stress-induced (takotsubo) cardiomyopathy. Heart (British Cardiac Society), 104(2), 96–102. https://doi.org/10.1136/heartjnl-2017-311579

    4. Kida, K., Akashi, Y. J., Fazio, G., & Novo, S. (2010). Takotsubo cardiomyopathy. Current pharmaceutical design, 16(26), 2910–2917. https://doi.org/10.2174/138161210793176509

    Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMSII


    Episode 897: Adrenal Crisis Apr 01, 2024
    Show notes

    Contributor: Ricky Dhaliwal MD

    Educational Pearls:

    • Primary adrenal insufficiency (most common risk factor for adrenal crises)

      • An autoimmune condition commonly known as Addison's Disease

      • Defects in the cells of the adrenal glomerulosa and fasciculata result in deficient glucocorticoids and mineralocorticoids

      • Mineralocorticoid deficiency leads to hyponatremia and hypovolemia

        • Lack of aldosterone downregulates Endothelial Sodium Channels (ENaCs) at the renal tubules

        • Water follows sodium and generates a hypovolemic state

      • Glucocorticoid deficiency contributes further to hypotension and hyponatremia

        • Decreased vascular responsiveness to angiotensin II

        • Increased secretion of vasopressin (ADH) from the posterior pituitary

    • An adrenal crisis is defined as a sudden worsening of adrenal insufficiency

      • Presents with non-specific symptoms including nausea, vomiting, fatigue, confusion, and fevers

      • Fevers may be the result of underlying infection

    • Work-up in the ED includes labs looking for infection and adding cortisol + ACTH levels

    • Emergent treatment is required

      • 100 mg hydrocortisone bolus followed by 50 mg every 6 hours

      • Immediate IV fluid repletion with 1L normal saline

    • The most common cause of an adrenal crisis is an acute infection in patients with baseline adrenal insufficiency

      • Often due to a gastrointestinal infection

    References

    1. Bancos I, Hahner S, Tomlinson J, Arlt W. Diagnosis and management of adrenal insufficiency. Lancet Diabetes Endocrinol. 2015;3(3):216-226. doi:10.1016/S2213-8587(14)70142-1

    2. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(2):364-389. doi:10.1210/jc.2015-1710

    3. Cronin CC, Callaghan N, Kearney PJ, Murnaghan DJ, Shanahan F. Addison disease in patients treated with glucocorticoid therapy. Arch Intern Med. 1997;157(4):456-458.

    4. Feldman RD, Gros R. Vascular effects of aldosterone: sorting out the receptors and the ligands. Clin Exp Pharmacol Physiol. 2013;40(12):916-921. doi:10.1111/1440-1681.12157

    5. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597-602. doi:10.1530/EJE-09-0884

    Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit


    Podcast 896: Cancer-Related Emergencies Mar 25, 2024
    Show notes

    Contributor: Travis Barlock, MD

    Educational Pearls:

    Cancer-related emergencies can be sorted into a few buckets:

    • Infection

      • Cancer itself and the treatments (chemotherapy/radiation) can be immunosuppressive. Look out for conditions such as sepsis and neutropenic fever.

    • Obstruction

      • Cancer causes a hypercoagulable state. Look out for blood clots which can cause emergencies such as a pulmonary embolism, stroke, superior vena cava (SVC) syndrome, and cardiac tamponade.

    • Metabolic

      • Cancer can affect the metabolic system in a variety of ways. For example, certain cancers like bone cancers can stimulate the bones to release large amounts of calcium leading to hypercalcemia. Tumor lysis syndrome is another consideration in which either spontaneously or due to treatment, tumor cells will release large amounts of electrolytes into the bloodstream causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.

    • Medication side effect

      • Immunomodulators can have strange side effects. A common one to know is Keytruda (pembrolizumab), which can cause inflammation in any organ. So if you have a cancer patient on immunomodulators with any inflammatory changes (cystitis, colitis, pneumonitis, etc), talk to oncology about whether steroids are indicated.

      • Chemotherapy can cause tumor lysis syndrome (see above), and multiple chemotherapeutics are known to cause heart failure (doxorubicin, trastuzumab), kidney failure (cisplatin), and pulmonary toxicity (bleomycin).

    References

    1. Campello, E., Ilich, A., Simioni, P., & Key, N. S. (2019). The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues. British journal of cancer, 121(5), 359–371. https://doi.org/10.1038/s41416-019-0510-x

    2. Gyamfi, J., Kim, J., & Choi, J. (2022). Cancer as a Metabolic Disorder. International journal of molecular sciences, 23(3), 1155. https://doi.org/10.3390/ijms23031155

    3. Kwok, G., Yau, T. C., Chiu, J. W., Tse, E., & Kwong, Y. L. (2016). Pembrolizumab (Keytruda). Human vaccines & immunotherapeutics, 12(11), 2777–2789. https://doi.org/10.1080/21645515.2016.1199310

    4. Wang, S. J., Dougan, S. K., & Dougan, M. (2023). Immune mechanisms of toxicity from checkpoint inhibitors. Trends in cancer, 9(7), 543–553. https://doi.org/10.1016/j.trecan.2023.04.002

    5. Zimmer, A. J., & Freifeld, A. G. (2019). Optimal Management of Neutropenic Fever in Patients With Cancer. Journal of oncology practice, 15(1), 19–24. https://doi.org/10.1200/JOP.18.00269

    Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII


    Episode 895: Indications for Exogenous Albumin Mar 18, 2024
    Show notes

    Contributor: Travis Barlock MD

    Educational Pearls:

    • There are three indications for IV albumin in the ED

    • Spontaneous bacterial peritonitis (SBP)

      • Patients with SBP develop renal failure from volume depletion

      • Albumin repletes volume stores and reduces renal impairment

      • Albumin binds inflammatory cytokines and expands plasma volume

      • Reduced all-cause mortality if IV albumin is given with antibiotics

    • Hepatorenal syndrome

      • Cirrhosis of the liver causes the release of endogenous vasodilators

      • The renin-angiotensin-aldosterone system (RAAS) fails systemically but maintains vasoconstriction at the kidneys, leading to decreased renal perfusion

      • IV albumin expands plasma volume and prevents failure of the RAAS

    • Large volume paracentesis

      • Large-volume removal may lead to circulatory dysfunction

      • IV albumin is associated with a reduced risk of paracentesis-associated circulatory dysfunction

    • There are many other FDA-approved conditions for which to use exogenous albumin but the data are conflicted about the benefits on mortality

    References

    1. Arroyo V, Fernandez J. Pathophysiological basis of albumin use in cirrhosis. Ann Hepatol. 2011;10(SUPPL. 1):S6-S14. doi:10.1016/s1665-2681(19)31600-x

    2. Bai Z, Wang L, Wang R, et al. Use of human albumin infusion in cirrhotic patients: a systematic review and meta-analysis of randomized controlled trials. Hepatol Int. 2022;16(6):1468-1483. doi:10.1007/s12072-022-10374-z

    3. Batool S, Waheed MD, Vuthaluru K, et al. Efficacy of Intravenous Albumin for Spontaneous Bacterial Peritonitis Infection Among Patients With Cirrhosis: A Meta-Analysis of Randomized Control Trials. Cureus. 2022;14(12). doi:10.7759/cureus.33124

    4. Kwok CS, Krupa L, Mahtani A, et al. Albumin reduces paracentesis-induced circulatory dysfunction and reduces death and renal impairment among patients with cirrhosis and infection: A systematic review and meta-analysis. Biomed Res Int. 2013;2013. doi:10.1155/2013/295153

    5. Sort P, Navasa M, Arroyo V, et al. Effect of Intravenous Albumin on Renal Impairment and Mortality in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis. N Engl J Med. 1999;341(6):403-409.

    Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit


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