Emergency Medical Minute Emergency Medical Minute
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- Health & Fitness
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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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 -
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 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
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 -
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
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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
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Episode 895: Indications for Exogenous Albumin
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