Emergency Medical Minute

Contributor: Aaron Lessen MD Educational Pearls: A recent study assessed EMS treatment of high blood pressure in the field 2404 patients randomized to prehospital treatment (1205)  vs. usual care (1199) Included patients with prehospital BP greater than 150 mm Hg The treatment arm’s BP goal was 130-140 mm Hg The primary efficacy outcome was functional status 90 days out Stroke was confirmed by imaging upon hospital arrival On arrival, the mean SBP of the treatment arm was 159 mm Hg compared with 170 mm Hg in the usual care group No significant difference in functional outcomes between the treatment group and the usual care group (Common Odds Ratio of 1.00, 95% CI = 0.87-1.15) Post-imaging analysis revealed 46.5% of the undifferentiated patients had a hemorrhagic stroke Prehospital reduction in BP did reduce the odds of poor functional outcome in hemorrhagic stroke patients alone (Common Odds Ratio 0.75, 95% CI 0.60-0.92) Those with ischemic stroke had increased odds of poor functional outcome (Common Odds Ratio 1.30, 95% CI 1.06-1.60) Bottom line: it is challenging to identify the stroke type in the prehospital setting and therefore not necessarily helpful to treat the blood pressure References 1. Ren X, Zhang C, Xu P, et al. Intensive Ambulance-Delivered Blood- Pressure Reduction in Hyperacute Stroke. New England Journal of Medicine. 2024;390(20):1862-1872. doi:10.1056/NEJMoa2314741 Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit  

Contributor: Taylor Lynch MD Educational Pearls: Overview: Sympathomimetic drugs mimic the fight or flight response, affecting monoamines such as dopamine, norepinephrine, and epinephrine Limited therapeutic use, often abused. Types: Amphetamines: Methamphetamine, Adderall, Ritalin, Vyvanse MDMA (Ecstasy) Cocaine (Both hydrochloride salt & free based crack cocaine) Theophylline (Asthma treatment) Ephedrine (For low blood pressure) BZP, Oxymetazoline (Afrin), Pseudoephedrine (Sudafed) MAO Inhibitors (treatment-resistant depression) Mechanisms: Act on adrenergic and dopaminergic receptors. Cocaine blocks dopamine and serotonin reuptake. Methamphetamines increase stimulatory neurotransmitter release MAO Inhibitors prevent neurotransmitter breakdown. Symptoms: Agitation, tachycardia, hypertension, hyperactive bowel sounds, diuresis, hyperthermia. Severe cases: Angina, seizures, cardiovascular collapse. Diagnosis: Clinical examination and history. Differentiate from anticholinergic toxidrome by diaphoresis and hyperactive bowel sounds. Tests: EKG, cardiac biomarkers, chest X-ray, blood gas, BMP, CK, coagulation studies, U-tox screen. Treatment: Stabilize ABCs, IV hydration, temperature monitoring, benzodiazepines. Avoid beta-blockers due to unopposed alpha agonism. Whole bowel irrigation for body packers; surgical removal if packets rupture. IV hydration for high CK levels. Observation period often necessary. Recap: Mimic sympathetic nervous system. Key symptoms: Diaphoresis, hyperactive bowel sounds. Treatment: Supportive care, benzodiazepines. Use poison control as a resource. References: Costa VM, Grazziotin Rossato Grando L, Milandri E, Nardi J, Teixeira P, Mladěnka P, Remião F. Natural Sympathomimetic Drugs: From Pharmacology to Toxicology. Biomolecules. 2022;12(12):1793. doi:10.3390/biom12121793 Kolecki P. Sympathomimetic Toxicity From Emergency Medicine. Medscape. Updated March 11, 2024. https://emedicine.medscape.com/article/818583-overview Williams RH, Erickson T, Broussard LA. Evaluating Sympathomimetic Intoxication in an Emergency Setting. Lab Med. 2000;31(9):497-508. https://doi.org/10.1309/WVX1-6FPV-E2LC-B6YG Summarized by Steven Fujaros | Edited by Jorge Chalit, OMSIII  

Contributor: Travis Barlock MD Educational Pearls: Wide-complex tachycardia is defined as a heart rate > 100 BPM with a QRS width > 120 milliseconds Wide-complex tachycardia of supraventricular origin is known as SVT with aberrancy Aberrancy is due to bundle branch blocks Mostly benign Treated with adenosine or diltiazem Wide-complex tachycardia of ventricular origin is also known as VTach Originates from ventricular myocytes, which are poor inherent pacemakers Dangerous rhythm that can lead to death Treated with amiodarone or lidocaine 80% of wide-complex tachycardias are VTach 90% likelihood for patients with a history of coronary artery disease In assessing a wide-complex tachycardia, it is best to treat it as a presumed ventricular tachycardia Treating SVT with amiodarone or lidocaine does no harm  However, treating VTach with adenosine or diltiazem may worsen the condition References 1. Littmann L, Olson EG, Gibbs MA. Initial evaluation and management of wide-complex tachycardia: A simplified and practical approach. Am J Emerg Med. 2019;37(7):1340-1345. doi:https://doi.org/10.1016/j.ajem.2019.04.027 2. Viskin S, Chorin E, Viskin D, Hochstadt A, Schwartz AL, Rosso R. Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy. Circulation. 2021;144(10):823-839. doi:10.1161/CIRCULATIONAHA.121.055783 3. Williams SE, O’Neill M, Kotadia ID. Supraventricular tachycardia: An overview of diagnosis and management. Clin Med J R Coll Physicians London. 2020;20(1):43-47. doi:10.7861/clinmed.cme.20.1.3 Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit

Contributor: Aaron Lessen MD Educational Pearls: The case: A gentleman came in from a nursing home with symptoms concerning for sepsis. He was hypotensive, hypoxic, febrile, and mentally altered. His past medical history included previous strokes which had left him with deficits for which he required a feeding tube. Initial workup included some point of care labs which revealed a sodium of 165 mEq/L (normal range 135-145) Hypernatremia What causes it? Dehydration, from insufficient fluid intake. This might happen in individuals who cannot drink water independently, such as infants, elderly, or disabled people, as was the case for this patient. Other causes of dehydration/hypernatremia include excessive sweating; diabetes insipidus; diuretic use; kidney dysfunction; and severe burns which can lead to fluid loss through the damaged skin. How do you correct it? Need to correct slowly, not more than 10 to 12 meq/L in 24 hours Can do normal saline (0.9%) or half saline (0.45%) and D5, at 150-200 mL per hour. Check the sodium frequently (every 2-3 hours) Will likely need ICU-level monitoring What happens if you correct it too quickly? Cerebral edema Seizures Bonus fact: Correction of hyponatremia too quickly causes osmotic demyelination syndrome (ODS). References Chauhan, K., Pattharanitima, P., Patel, N., Duffy, A., Saha, A., Chaudhary, K., Debnath, N., Van Vleck, T., Chan, L., Nadkarni, G. N., & Coca, S. G. (2019). Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clinical journal of the American Society of Nephrology : CJASN, 14(5), 656–663. https://doi.org/10.2215/CJN.10640918 Lindner, G., & Funk, G. C. (2013). Hypernatremia in critically ill patients. Journal of critical care, 28(2), 216.e11–216.e2.16E20. https://doi.org/10.1016/j.jcrc.2012.05.001 Muhsin, S. A., & Mount, D. B. (2016). Diagnosis and treatment of hypernatremia. Best practice & research. Clinical endocrinology & metabolism, 30(2), 189–203. https://doi.org/10.1016/j.beem.2016.02.014 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII

Contributor: Aaron Lessem MD Educational Pearls:  Oseltamivir (Tamiflu) is an antiviral medication used commonly to treat influenza Trials show that the medication reduces the duration of illness by less than 1 day (~16 hours in one systematic review) Benefit only occurs if taken within 48 hours of symptom onset Must be taken for 5 days A 2024 meta-analysis reviewed 15 randomized-controlled trials for the risk of hospitalization No reduction in hospitalizations with oseltamivir in patients over the age of 12 No difference in high-risk patients over the age of 65 or those with comorbidities The authors note that the confidence interval in these populations is wide, indicating a need for subsequent studies in high-risk populations Oseltamivir is associated with adverse effects including nausea, vomiting, and neurologic symptoms The risk of adverse effects may outweigh the benefits of a small reduction in the duration of illness References 1. Hanula R, Bortolussi-Courval É, Mendel A, Ward BJ, Lee TC, McDonald EG. Evaluation of Oseltamivir Used to Prevent Hospitalization in Outpatients with Influenza: A Systematic Review and Meta-Analysis. JAMA Intern Med. 2024;184(1):18-27. doi:10.1001/jamainternmed.2023.0699 2. Jefferson T, Jones M, Doshi P, Spencer EA, Onakpoya I, Heneghan CJ. Oseltamivir for influenza in adults and children: Systematic review of clinical study reports and summary of regulatory comments. BMJ. 2014;348(April):1-18. doi:10.1136/bmj.g2545 Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit  

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 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 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

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  

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 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 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 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  

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  

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

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

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

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  

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  

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  

Contributor: Ricky Dhaliwal, MD Educational Pearls: What are DKA and HHS? DKA (Diabetic Ketoacidosis) and HHS (Hyperosmolar Hyperglycemic State) are both acute hyperglycemic states. DKA More common in type 1 diabetes. Triggered by decreased circulating insulin. The body needs energy but cannot use glucose because it can’t get it into the cells. This leads to increased metabolism of free fatty acids and the increased production of ketones. The buildup of ketones causes acidosis. The kidneys attempt to compensate for the acidosis by increasing diuresis. These patients present as dry and altered, with sweet-smelling breath and Kussmaul (fast and deep) respirations. HSS More common in type 2 diabetes. In this condition there is still enough circulating insulin to avoid the breakdown of fats for energy but not enough insulin to prevent hyperglycemia. Serum glucose levels are very high – around 600 to 1200 mg/dl. Also presents similarly to DKA with the patient being dry and altered. Important labs to monitor Serum glucose Potassium Phosphorus Magnesium Anion gap (Na - Cl - HCO3) Renal function (Creatinine and BUN) ABG/VBG for pH Urinalysis and urine ketones by dipstick Treatment Identify the cause, i.e. Has the patient stopped taking their insulin? Aggressive hydration with isotonic fluids. Normal Saline (NS) vs Lactated Ringers (LR)? LR might resolve the DKA/HHS faster with less risk of hypernatremia. Should you bolus with insulin? No, just start a drip. 0.1-0.14 units per kg of insulin. Make sure you have your potassium back before starting insulin as the insulin can shift the potassium into the cells and lead to dangerous hypokalemia. Should you treat hyponatremia? Make sure to correct for hyperglycemia before treating. This artificially depresses the sodium. Should you give bicarb? Replace if the pH < 6.9. Otherwise, it won’t do anything to help. Don’t intubate, if the patient is breathing fast it is because they are compensating for their acidosis. References Andrade-Castellanos, C. A., Colunga-Lozano, L. E., Delgado-Figueroa, N., & Gonzalez-Padilla, D. A. (2016). Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. The Cochrane database of systematic reviews, 2016(1), CD011281. https://doi.org/10.1002/14651858.CD011281.pub2 Chaithongdi, N., Subauste, J. S., Koch, C. A., & Geraci, S. A. (2011). Diagnosis and management of hyperglycemic emergencies. Hormones (Athens, Greece), 10(4), 250–260. https://doi.org/10.14310/horm.2002.1316 Dhatariya, K. K., Glaser, N. S., Codner, E., & Umpierrez, G. E. (2020). Diabetic ketoacidosis. Nature reviews. Disease primers, 6(1), 40. https://doi.org/10.1038/s41572-020-0165-1 Duhon, B., Attridge, R. L., Franco-Martinez, A. C., Maxwell, P. R., & Hughes, D. W. (2013). Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. The Annals of pharmacotherapy, 47(7-8), 970–975. https://doi.org/10.1345/aph.1S014 Modi, A., Agrawal, A., & Morgan, F. (2017). Euglycemic Diabetic Ketoacidosis: A Review. Current diabetes reviews, 13(3), 315–321. https://doi.org/10.2174/1573399812666160421121307 Self, W. H., Evans, C. S., Jenkins, C. A., Brown, R. M., Casey, J. D., Collins, S. P., Coston, T. D., Felbinger, M., Flemmons, L. N., Hellervik, S. M., Lindsell, C. J., Liu, D., McCoin, N. S., Niswender, K. D., Slovis, C. M., Stollings, J. L., Wang, L., Rice, T. W., Semler, M. W., & Pragmatic Critical Care Research Group (2020). Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. JAMA network open, 3(11), e2024596. https://doi.org/10.1001/jamanetworkopen.2020.24596 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII

Contributor: Aaron Lessen MD Educational Pearls: Button batteries cause alkaline corrosion and erosion of the esophagus when swallowed Children swallow button batteries, which create a medical emergency as they can perforate the esophagus A recent study compared various home remedies as first-aid therapy for button battery ingestion Honey, jam, normal saline, Coca-Cola, orange juice, milk, and yogurt The study used a porcine esophageal model to assess resistance to alkalinization with the different home remedies Honey and jam demonstrated a significantly lower esophageal tissue pH compared with normal saline Histologic changes in the tissue samples appeared 60 minutes later with honey and jam compared with normal saline These treatments do not preclude medical intervention and battery removal References 1. Chiew AL, Lin CS, Nguyen DT, Sinclair FAW, Chan BS, Solinas A. Home Therapies to Neutralize Button Battery Injury in a Porcine Esophageal Model. Ann Emerg Med. 2023:1-9. doi:10.1016/j.annemergmed.2023.08.018 Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit  

Contributor: Ricky Dhaliwal, MD Educational Pearls: What can you do to control bleeding in a penetrating wound? Apply direct pinpoint pressure on the wound as well as proximal to the wound. Build a compression dressing. How do you build a compression dressing? Think about building an upside-down pyramid with the gauze. Consider coagulation agents such as an absorbent gelatin sponge material, microporous polysaccharide hemispheres, oxidized cellulose, fibrin sealants, topical thrombin, or tranexamic acid. What are the indications to use a tourniquet? The Stop The Bleed campaign recommends looking for the following features of “life-threatening” bleeding. Pulsatile bleeding. Blood is pooling on the ground. The overlying clothes are soaked. Bandages are ineffective. Partial or full amputation. And if the patient is in shock. How do you put on a tourniquet? If using a Combat Application Tourniquet (C-A-T) tourniquet, apply it proximal to the wound, then rotate the plastic rod until the bleeding stops. Then secure the plastic rod with a clip and make sure the Velcro is in place. Mark the time - generally, there is a spot on the tourniquet to write. Have a plan for the next steps. Does the patient need emergent surgery? Do they need to be transfered? How long can you leave a tourniquet on? Less than 90 minutes. What are the risks? Nerve injury. Ischemia. References Latina R, Iacorossi L, Fauci AJ, Biffi A, Castellini G, Coclite D, D'Angelo D, Gianola S, Mari V, Napoletano A, Porcu G, Ruggeri M, Iannone P, Chiara O, On Behalf Of Inih-Major Trauma. Effectiveness of Pre-Hospital Tourniquet in Emergency Patients with Major Trauma and Uncontrolled Haemorrhage: A Systematic Review and Meta-Analysis. Int J Environ Res Public Health. 2021 Dec 6;18(23):12861. doi: 10.3390/ijerph182312861. PMID: 34886586; PMCID: PMC8657739. Martinson J, Park H, Butler FK Jr, Hammesfahr R, DuBose JJ, Scalea TM. Tourniquets USA: A Review of the Current Literature for Commercially Available Alternative Tourniquets for Use in the Prehospital Civilian Environment. J Spec Oper Med. 2020 Summer;20(2):116-122. doi: 10.55460/CT9D-TMZE. PMID: 32573747. Resources poster booklet. (n.d.). Stop the Bleed. https://www.stopthebleed.org/resources-poster-booklet/ Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII  

Contributors: Kali Olson PharmD, Travis Barlock MD, Jeffrey Olson MS2 Summary: In this episode of Pharmacy Phriday, Dr. Kali Olson joins Dr. Travis Barlock and Jeffrey Olson in studio to discuss a variety of interesting topics in the form of a segment show. Dr. Kali Olson earned her Doctorate of Pharmacy from the University of Colorado, Skaggs School of Pharmacy and completed a PGY1 residency at Detroit Receiving Hospital and a PGY2 residency in Emergency Medicine at Denver Health. She now works as an Emergency Medicine Pharmacist at Denver Health.  In segment one of the show, Kali and Travis answer the Get-To-Know-You questionnaire. In segment two, they work together to answer a series of pharmacy-based riddles. In segment three they play a “Balderdash” like game in which they guess the definitions of medical jargon. In segment four they play the Number Needed to Treat game, invented by the AFP podcast. And in segment five they work together to answer a question about a far-out scenario involving medications and time travel!   References ·       American Family Physician Podcast, https://www.aafp.org/pubs/afp/multimedia/podcast.html ·       Gragnolati, A. (2022, May 5). The Yuzpe method of emergency contraception. GoodRx. https://www.goodrx.com/conditions/emergency-contraceptive/yuzpe-method ·       Manikandan S, Vani NI. Holiday reading: Learning medicine through riddles. CMAJ. 2010 Dec 14;182(18):E863-4. doi: 10.1503/cmaj.100466. PMID: 21149530; PMCID: PMC3001539. ·       Riddle Me This: Mixing Medicine, https://peimpact.com/riddle-me-this-mixing-medicine/ ·       https://thennt.com/nnt/corticosteroids-treatment-kawasaki-disease-children/ ·       https://thennt.com/nnt/aspirin-acute-ischemic-stroke/ ·       https://thennt.com/nnt/tranexamic-acid-treatment-epistaxis/ ·       https://thennt.com/nnt/antibiotics-culture%e2%80%90positive-asymptomatic-bacteriuria-pregnant-women/   Produced, Hosted, Edited, and Summarized by Jeffrey Olson MS2 | Additional editing by Jorge Chalit, OMSII  

Contributor: Taylor Lynch MD Educational Pearls Hypothermia is defined as a core body temperature less than 35 degrees Celsius or less than 95 degrees Fahrenheit  Mild Hypothermia: 32-35 degrees Celsius Presentation: alert, shivering, tachycardic, and cold diuresis Management: Passive rewarming i.e. remove wet clothing and cover the patient with blankets or other insulation Moderate Hypothermia: 28-32 degrees Celsius Presentation: Drowsiness, lack of shivering, bradycardia, hypotension Management: Active external rewarming Severe Hypothermia: 24-28 degrees Celsius Presentation: Heart block, cardiogenic shock, no shivering Management: Active external and internal rewarming Less than 24 degrees Celsius Presentation: Pulseless, ventricular arrhythmia Active External Rewarming Warm fluids are insufficient for warming due to a minimal temperature difference (warmed fluids are maintained at 40 degrees vs. a patient at 30 degrees is not a large enough thermodynamic difference) External: Bear hugger, warm blankets Active Internal Rewarming Thoracic lavage (preferably on the patient’s right side) Place 2 chest tubes (anteriorly and posteriorly); infuse warm IVF anteriorly and hook up the posterior tube to a Pleur-evac Warms the patient 3-6 Celsius per hour Bladder lavage Continuous bladder irrigation with 3-way foley or 300 cc warm fluid Less effective than thoracic lavage due to less surface area Pulseless patients ACLS does not work until patients are rewarmed to 30 degrees High-quality CPR until 30 degrees (longest CPR in a hypothermic patient was 6 hours and 30 minutes) Give epinephrine once you reach 35 degrees, spaced out every 6 minutes ECMO is the best way to warm these patients up (10 degrees per hour) Pronouncing death must occur at 32 degrees or must have potassium > 12 References 1. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 1: Introduction. Circulation. 2005;112(24 SUPPL.). doi:10.1161/CIRCULATIONAHA.105.166550 2. Brown DJA, Burgger H, Boyd J, Paal P. Accidental Hypothermia. N Engl J Med. 2012;367:1930-1938. doi:10.1136/bmj.2.5543.51-c 3. Dow J, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society Clinical Practice Guidelines for the Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia: 2019 Update. Wilderness Environ Med. 2019;30(4S):S47-S69. doi:10.1016/j.wem.2019.10.002 4. Kjærgaard B, Bach P. Warming of patients with accidental hypothermia using warm water pleural lavage. Resuscitation. 2006;68(2):203-207. doi:10.1016/j.resuscitation.2005.06.019 5. Lott C, Truhlář A, Alfonzo A, et al. European Resuscitation Council Guidelines 2021: Cardiac arrest in special circumstances. Resuscitation. 2021;161:152-219. doi:10.1016/j.resuscitation.2021.02.011 6. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest - Report of a case and review of the literature. Resuscitation. 2005;66(1):99-104. doi:10.1016/j.resuscitation.2004.12.024 Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit, OMSII