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Emergency Medical Minute

Emergency Medical Minute

Emergency Medical Minute
Salute, Scienza e Medicina

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.

1048 - Episode 900: Ketamine Dosing
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  • 1048 - Episode 900: Ketamine Dosing

    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

      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

      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

      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

    Mon, 22 Apr 2024 - 02min
  • 1047 - Episode 899: Thrombolytic Contraindications

    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 < 100,000

    BGL < 50

    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

    Mon, 15 Apr 2024 - 03min
  • 1046 - Episode 898: Takotsubo Cardiomyopathy

    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

      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

      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

      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

      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

    Wed, 10 Apr 2024 - 03min
  • 1045 - Episode 897: Adrenal Crisis

    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

     

    Mon, 01 Apr 2024 - 04min
  • 1044 - Podcast 896: Cancer-Related Emergencies

    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

      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

      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

      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

      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

      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

     

    Mon, 25 Mar 2024 - 02min
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