Emergency Medical Minute
Emergency Medical Minute is medicine's most prolific podcast. Geared towards physicians, nurses and paramedics! Tune in weekly for real, raw and relevant medical education.
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Episode 927: Functional Gallbladder Syndrome
10/22/2024
Episode 927: Functional Gallbladder Syndrome
Contributor: Jorge Chalit-Hernandez, OMS3 Typically presents with biliary colic Right upper quadrant abdominal pain lasting more than 30 minutes and subsiding over several hours Often associated with fatty meals but not always Must rule out other causes of pain Peptic ulcer disease - typically presents with epigastric pain Pancreatitis - pain that radiates to the back or family history of pancreatitis Laboratory workup LFTs including ALT, AST, and alkaline phosphatase are within the reference range Lipase and amylase within the reference range Imaging workup RUQ ultrasound is unremarkable Upper endoscopy with ultrasound can help rule out peptic ulcer disease and small stones HIDA scan may show a reduced gallbladder ejection fraction below 30-35% or it may be normal Opiates may give false-positive results Opiates can sometimes make biliary colic worse due to their contractile effect on the sphincter of Oddi Some patients may benefit from surgical intervention i.e. cholecystectomy Classic biliary-type pain (best predictor of response to cholecystectomy) Pain for > 3 months duration Positive HIDA scan References Alhayo S, Eslick GD, Cox MR. Cholescintigraphy may have a role in selecting patients with biliary dyskinesia for cholecystectomy: a systematic review. ANZ J Surg. 2020;90(9):1647-1652. doi:10.1111/ans.16003 Arshi J, Layfield LJ, Esebua M. Mast cell infiltration and activation in the gallbladder wall: Implications for the pathogenesis of functional gallbladder disorder in adult patients. Ann Diagn Pathol. 2021;54:151798. doi:10.1016/j.anndiagpath.2021.151798 Carr JA, Walls J, Bryan LJ, Snider DL. The treatment of gallbladder dyskinesia based upon symptoms: results of a 2-year, prospective, nonrandomized, concurrent cohort study. Surg Laparosc Endosc Percutan Tech. 2009;19(3):222-226. doi:10.1097/SLE.0b013e3181a74690 Joehl RJ, Koch KL, Nahrwold DL. Opioid drugs cause bile duct obstruction during hepatobiliary scans. Am J Surg. 1984;147(1):134-138. doi:10.1016/0002-9610(84)90047-3 Mahid SS, Jafri NS, Brangers BC, Minor KS, Hornung CA, Galandiuk S. Meta-analysis of cholecystectomy in symptomatic patients with positive hepatobiliary iminodiacetic acid scan results without gallstones. Arch Surg. 2009;144(2):180-187. doi:10.1001/archsurg.2008.543 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 926: Supraventricular Tachycardia
10/21/2024
Episode 926: Supraventricular Tachycardia
Contributor: Taylor Lynch MD Supraventricular tachycardias (SVTs) arise above the bundle of His The term SVT includes AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia, atrial fibrillation, atrial flutter, and multifocal atrial tachycardia AVNRT is the most common form of SVT Paroxysmal Spontaneous or provoked by exertion, coffee, alcohol, or thyroid disease More common in women (3:1 women:men ratio) HR 160-240 Narrow complex with a normal QRS Unstable patients receive synchronized cardioversion at 0.5-1 J/kg Valsalva maneuver is attempted before pharmaceutical interventions Increases vagal tone at the AV node to slow conduction and prolongs its refractory period to normalize the conduction Traditionally, patients are asked to bear down, but this only works in 17% of patients REVERT trial assessed a modified valsalva that worked in 43% of patients Adenosine Slows conduction at the AV node by activating potassium channels and inhibiting calcium influx Extremely uncomfortable for most patients Not commonly used anymore Nondihydropyridine calcium-channel blockers are preferred A 2009 RCT investigated low-infusion CCBs compared with adenosine bolus The study found a conversion rate of 98% in the CCB group vs. adenosine group at 86.5% The main adverse effect of CCB is hypotension, which a slow infusion rate can mitigate Diltiazem dose is 0.25 mg/kg/2min and repeat at 0.35 mg/kg/15 minutes or slow infusion at 2.5 mg/min up to a conversion or 50 mg total References 1. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): A randomised controlled trial. Lancet. 2015;386(10005):1747-1753. doi:10.1016/S0140-6736(15)61485-4 Belz MK, Stambler BS, Wood MA, Pherson C, Ellenbogen KA. Effects of enhanced parasympathetic tone on atrioventricular nodal conduction during atrioventricular nodal reentrant tachycardia. Am J Cardiol. 1997;80(7):878-882. doi:10.1016/s0002-9149(97)00539-0 Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80(5):523-528. doi:10.1016/j.resuscitation.2009.01.017 Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2016 Sep 13;134(11):e234-5. doi: 10.1161/CIR.0000000000000448]. Circulation. 2016;133(14):e506-e574. doi:10.1161/CIR.0000000000000311 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 925: Table Sugar for Tongue Entrapment
10/14/2024
Episode 925: Table Sugar for Tongue Entrapment
Contributor: Aaron Lessen, MD Educational Pearls: Pediatric case study where the child’s tongue was stuck in the opening of a hard plastic drink lid Entrapment restricts circulation which causes fluid to build and the tongue becomes more edematous with time There is a risk of ischemia with prolonged entrapment Initially tried 2% viscous lidocaine for analgesia and lubricant The ER recognized that this mucosal, edematous tongue could benefit from the trick for ostomies and rectal prolapses → table sugar! Sugar granules absorb water which decreases tissue edema This option avoids sedation and aggressive treatment References A Young Girl with Tongue Swelling Jarjour, Jane et al. Annals of Emergency Medicine, Volume 84, Issue 3, 317 - 318 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 924: Pregnancy Cold Remedies
10/07/2024
Episode 924: Pregnancy Cold Remedies
Contributor: Megan Hurley, MD Educational Pearls: Fevers Tylenol Up until 20 weeks NSAIDs are ok but after 20 weeks they are contraindicated Can limit the amount of amniotic fluid produced Can lead to growth restriction Can cause premature closure of the ductus arteriosus Cough Cough drops Humidifier Guafenesine and dextromethorphan (Mucinex) is not well studied but is probably ok with caution in certain circumstances such as post-tussive emesis causing poor PO intake and weight loss Congestion Flonase (Fluticasone nasal spray) Nasal rinses Humidifier 1st generation anti-histamines (Diphenhydramine, Doxylamine, etc.) However, these tend to have more side effects such as fatigue, drowsiness, and dizziness Concider switching to a 2nd generation (Cetirizine, Loratidine, etc.) during the day Disease specific treatments Flu (A and B) gets tamiflu (Oseltamivir) Covid gets paxlovid (Nirmatrelvir/ritonavir) Antibiotics for suspected pneumonia Additional recommendations Elevating the head of bed Nasal strips Stay well hydrated Tea Ice chips Echinacea Zinc Rest Avoid NSAIDs Pseudophedrine Afrin (Oxymetazoline) Combined meds in general References Antonucci, R., Zaffanello, M., Puxeddu, E., Porcella, A., Cuzzolin, L., Pilloni, M. D., & Fanos, V. (2012). Use of non-steroidal anti-inflammatory drugs in pregnancy: impact on the fetus and newborn. Current drug metabolism, 13(4), 474–490. https://doi.org/10.2174/138920012800166607 Black, E., Khor, K. E., Kennedy, D., Chutatape, A., Sharma, S., Vancaillie, T., & Demirkol, A. (2019). Medication Use and Pain Management in Pregnancy: A Critical Review. Pain practice : the official journal of World Institute of Pain, 19(8), 875–899. D'Ambrosio, V., Vena, F., Scopelliti, A., D'Aniello, D., Savastano, G., Brunelli, R., & Giancotti, A. (2023). Use of non-steroidal anti-inflammatory drugs in pregnancy and oligohydramnios: a review. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 36(2), 2253956. https://doi.org/10.1080/14767058.2023.2253956 Summarized by Jeffrey Olson MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3
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Episode 923: Blunt Cerebrovascular Injury
09/30/2024
Episode 923: Blunt Cerebrovascular Injury
Contributor: Travis Barlock MD Educational Pearls: Assessment of head and neck vascular injury due to blunt trauma Symptomatic patients require screening head and neck CT angiography EAST guidelines include the following criteria for a screening CT angiography in blunt head trauma: Unexplained neurological deficits Arterial nosebleed GCS < 6 Petrous bone fracture Cervical spine fracture Any size fracture through the transverse foramen LeFort fractures type II or type III EAST guidelines include a grading scale for vascular injury: Grade I: Luminal irregularity or dissection with <25% luminal narrowing Grade II: Dissection or intramural hematoma with >25% luminal narrowing, intraluminal thrombus, or raised intimal flap Grade III: Pseudoaneurysm Grade IV: Occlusion Grade V: Transection with free extravasation References Bensch FV, Varjonen EA, Pyhältö TT, Koskinen SK. Augmenting Denver criteria yields increased BCVI detection, with screening showing markedly increased risk for subsequent ischemic stroke. Emerg Radiol. 2019;26(4):365-372. doi:10.1007/s10140-019-01677-0 Biffl WL, Moore EE, Offner PJ, et al. Optimizing screening for blunt cerebrovascular injuries. Am J Surg. 1999;178(6):517-522. doi:10.1016/s0002-9610(99)00245-7 Kim DY, Biffl W, Bokhari F, et al. Evaluation and management of blunt cerebrovascular injury: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2020;88(6):875-887. doi:10.1097/TA.0000000000002668 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 922: Chest Tube Irrigation
09/23/2024
Episode 922: Chest Tube Irrigation
Contributor: Aaron Lessen, MD Educational Pearls: Hemothorax: blood in the pleural cavity, most commonly due to chest trauma Treatment: thoracostomy tube for blood drainage helps to avoid clotting, scarring, and infection A recent study looked at patients with hemothorax who either received or did not receive thoracic irrigation with saline Evaluated incidence of secondary intervention, such as video-assisted thoracoscopic surgery (VATS), for persistent hemothorax Patients who received irrigation had a slight decrease in secondary intervention frequency Multi-center study - all patients who had the irrigation procedure were at two centers Study limitation: variability in approaches at each location could be a confounder Technique that could potentially prevent future complications References Carver TW, Berndtson AE, McNickle AG, et al. Thoracic irrigation for prevention of secondary intervention after thoracostomy tube drainage for hemothorax: A Western Trauma Association multi-center study. J Trauma Acute Care Surg. Published online May 20, 2024. doi:10.1097/TA.0000000000004364 Yi JH, Liu HB, Zhang M, et al. Management of traumatic hemothorax by closed thoracic drainage using a central venous catheter. J Zhejiang Univ Sci B. 2012;13(1):43-48. doi:10.1631/jzus.B1100161 Summarized by Meg Joyce, MS | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 921: Pediatric Hypoglycemia
09/22/2024
Episode 921: Pediatric Hypoglycemia
Contributor: Taylor Lynch, MD Educational Pearls: When it comes to hypoglycemia, the age dictates possible causes Neonate: Hormonal deficiency Congenital Adrenal Hyperplasia (21-hydroxylase deficiency, 11β-hydroxylase deficiency) Primary or Secondary Adrenal Insufficiency leading to cortisol deficiency Hypopituitarism Inborn errors of metabolism Systemic infection (Under 30 days old should trigger a full infectious workup) Toddler Accidental ingestions Sulfonylureas such as glipizide or glyburide Older children Addison’s Disease (Hypocortisolism) Accidential or intentional ingestions Exogenous insulin How is it diagnosed? Child or infant Glucose <60 Newborn Glucose <45 and symptomatic or glucose <35 and asymptomatic Treatment Awake: oral glucose Altered: IV glucose Rule of 50’s. The dose you give times the concentration should equal 50 Neonate to 2 months get 5 mg/kg of D10W (5*10=50) 2 months to 8 years old get 2 mg/kg of D25W (2*25=50) Over 8 gets 1 mg/kg of D50W (1*50=50) Bonus fact: Rough estimate of weight for a child is 2*patients age plus 8 Recheck sugar every 15 minutes If they stay hypoglycemic give another bolus and consider starting a drip at 1.5 maintenance dose of D10NS. If you don’t have an IV you can consider glucagon at 0.03 mg/kg IM, although you might be better off trying glucose gel buccally. If standard therapy still fails you can give hydrocortisone 25 mg IV for neonates and infants 50 mg IV for toddlers and smaller school aged children 100 mg for anyone older than that How do you test for exogenous insulin? Check a c-peptide which would be low if a patient is taking exogenous insulin References Lang, T. F., & Hussain, K. (2014). Pediatric hypoglycemia. Advances in clinical chemistry, 63, 211–245. Lee, S. C., Baranowski, E. S., Sakremath, R., Saraff, V., & Mohamed, Z. (2023). Hypoglycaemia in adrenal insufficiency. Frontiers in endocrinology, 14, 1198519. https://doi.org/10.3389/fendo.2023.1198519 Thompson-Branch, A., & Havranek, T. (2017). Neonatal Hypoglycemia. Pediatrics in review, 38(4), 147–157. Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Laboring Under Pressure Episode 3: Hypertensive Disorders of Pregnancy with Dr. Kiersten Williams
09/12/2024
Laboring Under Pressure Episode 3: Hypertensive Disorders of Pregnancy with Dr. Kiersten Williams
Contributor: Kiersten Williams MD, Travis Barlock MD, Jeffrey Olson MS3 Show Pearls Hypertensive disorders of pregnancy are one of the leading causes of maternal mortality worldwide. Hypertension (HTN) complicates 2-8% of pregnancies The definition of HTN in pregnancy is a systolic >140 or diastolic >90, measured 4 hours apart There is a range of HTN disorders Chronic HTN which could have superimposed preeclampsia (preE) on top Gestational HTN in which there are no lab abnormalities PreE w/o severe features Protein in urine Urine protein >300 mg in 24 hours Urine Protein to Creatinine ratio of .3 +2 Protein on urine dipstick PreE w/ severe features Systolics above 160 mmHg Diastolics above 110 mmHg Headache, especially not going away with meds, or different than previous headaches Visual changes, anything that lasts more than a few minutes RUQ pain, which could present as heartburn Pulmonary edema Low platelets, if <150 perk up ears, <100 definitely look into Renal insufficiency, creatinine 1.1 or higher or doubling of baseline Impaired liver function Note: Hemoconcentration and LDH >600 are not diagnostic but worth paying attention to Treatment Labetalol, IV Avoid in bradycardia, asthma, or myocardial disease Quick up titrate, with dosing regimens such as 20-20-40 or 20-40-80 (mg) Hydralazine, IV 5 mg starting, then another 5 mg then 10 mg if not working Nifedipine, Oral Can cause a headache Goal is not to normalize BP but bring it down slowly How to give magnesium Start with 6 g or 4 g over 20 minutes if the patient is small or has bad kidney function Follow with 2 g per hour or 1 g per hour Don’t give in myasthenia gravis What should you do if the patient progresses to eclampsia (seizures) Magnesium is the best drug Can use phenytoin or benzos IV as an alternate Diazepam is available PR which is a good option if you don’t have IV access IM magnesium is doable but painful, mix with lidocaine and split dose between the butt cheeks Facts about post-partum PreE 20% of women will have HTN post-partum Most resolve by 6 weeks If it lingers past 6 months this is chronic HTN If the patient has severe features (see above) they desevere 24 hours on magnesium while being monitored on the L&D floor Post-partum is the most common time for strokes Providers can be much more aggressive with HTN treatment because the fetus is no longer being exposed Enalapril is safe in breast feeding Some patients might need to give up breast feeding to be on even more aggressive HTN therapy Are NSAIDs safe while breastfeeding? Motrin is pretty safe Pulm edema is a risk, be careful with fluids Last pearl: Put pregnant patients in left or right lateral decubitus while in ER or put a folded towel under their hip to help with venous return which can also help with nausea References Metoki, H., Iwama, N., Hamada, H., Satoh, M., Murakami, T., Ishikuro, M., & Obara, T. (2022). Hypertensive disorders of pregnancy: definition, management, and out-of-office blood pressure measurement. Hypertension research : official journal of the Japanese Society of Hypertension, 45(8), 1298–1309. https://doi.org/10.1038/s41440-022-00965-6 Rana, S., Lemoine, E., Granger, J. P., & Karumanchi, S. A. (2019). Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circulation research, 124(7), 1094–1112. https://doi.org/10.1161/CIRCRESAHA.118.313276 Reed, B. (2020, May 2). ‘They didn’t listen to me’: Amber Rose Isaac tweeted about her death before dying in childbirth. The Guardian. https://www.theguardian.com/us-news/2020/may/02/amber-rose-isaac-new-york-childbirth-death Reisner, S. H., Eisenberg, N. H., Stahl, B., & Hauser, G. J. (1983). Maternal medications and breast-feeding. Developmental pharmacology and therapeutics, 6(5), 285–304. https://doi.org/10.1159/000457330 Wilkerson, R. G., & Ogunbodede, A. C. (2019). Hypertensive Disorders of Pregnancy. Emergency medicine clinics of North America, 37(2), 301–316. https://doi.org/10.1016/j.emc.2019.01.008 Wu, P., Green, M., & Myers, J. E. (2023). Hypertensive disorders of pregnancy. BMJ (Clinical research ed.), 381, e071653. https://doi.org/10.1136/bmj-2022-071653 Produced by Jeffrey Olson, MS3 | Edited by Jeffrey Olson and Jorge Chalit, OMSIII
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Episode 920: Pediatric Growth Estimates
09/09/2024
Episode 920: Pediatric Growth Estimates
Contributor: Sean Fox, MD Educational Pearls: Newborns may lose up to 10% of their birth weight in the first week of life Weight loss is greatest in exclusively breastfed infants Should regain birth weight by age 2 weeks Newborns should gain an average of 30g (1 oz) per day in the first 3 months of life Some will gain more and some will gain less Infants double their birth weight by 6 months of life and triple their weight by 12 months A 1-year-old should weigh on average 10 kg (22 lbs) A 3-year-old should weigh on average 15 kg (33 lbs) 2-year-olds are between 10-15 kg on average Weight assessment can help determine causes of forceful vomiting Not all “projectile” vomiting is due to pyloric stenosis Some infants may experience vigorous vomiting from overfeeding Weight estimates can also provide information for quick decisions on medical management for children coming via EMS Helps to prepare medications and dosages based on predicted average weight References Crossland DS, Richmond S, Hudson M, Smith K, Abu-Harb M. Weight change in the term baby in the first 2 weeks of life. Acta Paediatr. 2008;97(4):425-429. doi:10.1111/j.1651-2227.2008.00685.x Grummer-Strawn LM, Reinold C, Krebs NF; Centers for Disease Control and Prevention (CDC). Use of World Health Organization and CDC growth charts for children aged 0-59 months in the United States [published correction appears in MMWR Recomm Rep. 2010 Sep 17;59(36):1184]. MMWR Recomm Rep. 2010;59(RR-9):1-15. Macdonald PD, Ross SR, Grant L, Young D. Neonatal weight loss in breast and formula fed infants. Arch Dis Child Fetal Neonatal Ed. 2003;88(6):F472-F476. doi:10.1136/fn.88.6.f472 Paul IM, Schaefer EW, Miller JR, et al. Weight Change Nomograms for the First Month After Birth. Pediatrics. 2016;138(6):e20162625. doi:10.1542/peds.2016-2625 Summarized & Edited by Jorge Chalit, OMS3 Special thanks to the Carolinas Medical Center for their contribution to this episode Donate: https://emergencymedicalminute.org/donate/
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Episode 919: EKG Criteria for Adenosine
09/04/2024
Episode 919: EKG Criteria for Adenosine
Contributor: Travis Barlock, MD Educational Pearls: SVT: supraventricular tachycardia Pharmacotherapy for SVT includes drugs that block the AV node, such as adenosine EKG criteria before adenosine administration in SVT Regular rhythm Monomorphic: all QRS complexes are identical If the EKG is polymorphic, with QRS complexes displaying changing morphologies, it is unsafe to administer adenosine Adenosine can worsen polymorphic VTach and lead to VFib References Ganz, Leonard I., and Peter L. Friedman. “Supraventricular Tachycardia.” New England Journal of Medicine, vol. 332, no. 3, 19 Jan. 1995, pp. 162–173, . Smith JR, Goldberger JJ, Kadish AH. Adenosine induced polymorphic ventricular tachycardia in adults without structural heart disease. Pacing Clin Electrophysiol. 1997;20(3 Pt 1):743-745. doi:10.1111/j.1540-8159.1997.tb03897.x Viskin, Sami, et al. “Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy.” Circulation, vol. 144, no. 10, 7 Sept. 2021, pp. 823–839, https://doi.org/10.1161/circulationaha.121.055783. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 918: Automated Blood Pressure Cuffs
08/26/2024
Episode 918: Automated Blood Pressure Cuffs
Contributor: Aaron Lessen, MD Educational Pearls: How does an automated blood pressure cuff work? Automated blood pressure cuffs work differently than taking a manual blood pressure. While taking a manual blood pressure, one typically listens for Korotkoff sounds (turbulent flow) while slowly deflating the cuff. An automatic blood pressure cuff only senses the pressure in the cuff itself and specifically pays attention to oscillations in the pressure caused by when the pressure of the cuff is between the systolic (heart squeezing) and diastolic (heart relaxed) pressures. These oscillations are at a maximum when the pressure in the cuff matches the mean arterial pressure (MAP) and therefore the machines are most accurate at reporting the MAP. The machines then use the MAP and other information about the oscillations to estimate the systolic and diastolic pressures, which are less accurate. What should you do if you need more accurate systolic and diastolic blood pressures? Take a manual blood pressure. Get an arterial-line (a-line), which provides continuous data for the blood pressure at the end of a catheter. What happens if the cuff is too big or too small for the patient? If the cuff is too small it will overestimate the pressure. If the cuff is too large it will underestimate the pressure. What should you do if the cuff cycles a bunch of times before reporting a blood pressure? It probably isn’t very accurate so consider another method. Bonus fact! The MAP is not directly in the middle of the systolic and diastolic pressures but is weighted towards the diastolic pressure. The MAP can be calculated by adding two-thirds of the diastolic pressure to one third of the systolic pressure. For example if the BP is 120/90 the MAP is 100 mmHg. References Benmira, A., Perez-Martin, A., Schuster, I., Aichoun, I., Coudray, S., Bereksi-Reguig, F., & Dauzat, M. (2016). From Korotkoff and Marey to automatic non-invasive oscillometric blood pressure measurement: does easiness come with reliability?. Expert review of medical devices, 13(2), 179–189. https://doi.org/10.1586/17434440.2016.1128821 Liu, J., Li, Y., Li, J., Zheng, D., & Liu, C. (2022). Sources of automatic office blood pressure measurement error: a systematic review. Physiological measurement, 43(9), 10.1088/1361-6579/ac890e. Vilaplana J. M. (2006). Blood pressure measurement. Journal of renal care, 32(4), 210–213. https://doi.org/10.1111/j.1755-6686.2006.tb00025.x Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 917: Heat-Related Illnesses
08/19/2024
Episode 917: Heat-Related Illnesses
Contributor: Megan Hurley, MD Educational Pearls: Heat cramps Occur due to electrolyte disturbances Most common electrolyte abnormalities are hyponatremia and hypokalemia Heat edema Caused by vasodilation with pooling of interstitial fluid in the extremities Heat rash (miliaria) Common in newborns and elderly Due to accumulation of sweat beneath eccrine ducts Heat syncope Lightheadedness, hypotension, and/or syncope in patients with peripheral vasodilation due to heat exposure Treatment is removal from the heat source and rehydration (IV fluids or Gatorade) Heat exhaustion Patients have elevated body temperature (greater than 38º C but less than 40º C) Symptoms include nausea, tachycardia, headache, sweating, and others Normal mental status or mild confusion that improves with cooling Treatment is removal from the heat source and hydration Classic heat stroke From prolonged exposure to heat Defined as a core body temperature > 40.5º C, though not required for diagnosis or treatment Presentation is similar to heat exhaustion with the addition of neurological deficits including ataxia Patients present “dry” Exertional heat stroke Prolonged exposure to heat during exercise Similar to classic heat stroke but the patients present “wet” due to antecedent treatment in ice baths or other field treatments Management of heat-related illnesses includes: Cooling Rehydration Evaluation of electrolytes Antipyretics are not helpful because heat-induced illnesses are not due to hypothalamic dysregulation References Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev 2007; 35:141. Ebi KL, Capon A, Berry P, et al. Hot weather and heat extremes: health risks. Lancet 2021; 398:698. Epstein Y, Yanovich R. Heatstroke. N Engl J Med 2019; 380:2449. Gardner JW, JA K. Clinical diagnosis, management, and surveillance of exertional heat illness. In: Textbook of Military Medicine, Zajitchuk R (Ed), Army Medical Center Borden Institute, Washington, DC 2001. Khosla R, Guntupalli KK. Heat-related illnesses. Crit Care Clin 1999; 15:251. Lipman GS, Gaudio FG, Eifling KP, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. Wilderness Environ Med 2019; 30:S33. Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce, MS1 Donate: https://emergencymedicalminute.org/donate/
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Episode 916: Central Cord Syndrome
08/12/2024
Episode 916: Central Cord Syndrome
Contributor: Taylor Lynch, MD Educational Pearls: What is Central Cord Syndrome (CCS)? Incomplete spinal cord injury caused by trauma that compresses the center of the cord More common in hyperextension injuries like falling and hitting the chin Usually happens only in individuals with preexisting neck and spinal cord conditions like cervical spondylosis (age-related wear and tear of the cervical spine) Anatomy of spinal cord Motor tracts The signals the brain sends for the muscles to move travel in the corticospinal tracts of the spinal cord The tracts that control the upper limbs are more central than the ones that control the lower limbs The tracts that control the hands are more central than the ones that control the upper arm/shoulder Fine touch, vibration, and proprioception (body position) tracts These sensations travel in separate tracts in the spinal cord than the sensation of pain and temperature Their pathway is called the dorsal column-medial lemniscus (DCML) pathway This information travels in the most posterior aspect of the spinal cord Pain, crude touch, pressure, and temperature tracts These sensations travel in the spinothalamic tract, which is more centrally located These signals also cross one side of the body to the other within the spinal cord near the level that they enter How does this anatomy affect the presentation of CCS? Patients typically experience more pronounced weakness or paralysis in their upper extremities as compared to their lower extremities with their hands being weaker than more proximal muscle groups Sensation of pain, crude touch, pressure, and temperature are much morelikely to be diminished while the sensation of fine touch, vibration, and proprioception are spared What happens with reflexes? Deep tendon reflexes become exaggerated in CCS This is because the disruption in the corticospinal tract removes inhibitory control over reflex arcs What happens to bladder control? The neural signals that coordinate bladder emptying are disrupted, therefore patients can present with urinary retention and/or urge incontinence What is a Babinski’s Sign? When the sole of the foot is stimulated a normal response in adults is for the toes to flex downward (plantar flexion) If there is an upper motor neuron injury like in CCS, the toes will flex upwards (dorsiflexion) How is CCS diagnosed? CCS is mostly a clinical diagnosis These patient also need an MRI to see the extent of the damage which will show increased signal intensity within the central part of the spinal cord on T2-weighted images How is CCS treated? Strict c-spine precautions Neurogenic shock precautions. Maintain a mean arterial pressure (MAP) of 85-90 to ensure profusion of the spinal cord Levophed (norepinephrine bitartrate) and/or phenylephrine can be used to support their blood pressure to support spinal perfusion Consider intubation for injuries above C5 (C3, 4, and 5 keep the diaphragm alive) Consult neurosurgery for possible decompression surgery Physical Therapy References Avila, M. J., & Hurlbert, R. J. (2021). Central Cord Syndrome Redefined. Neurosurgery clinics of North America, 32(3), 353–363. Brooks N. P. (2017). Central Cord Syndrome. Neurosurgery clinics of North America, 28(1), 41–47. Engel-Haber, E., Snider, B., & Kirshblum, S. (2023). Central cord syndrome definitions, variations and limitations. Spinal cord, 61(11), 579–586. Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 915: Severe Burn Injuries
08/05/2024
Episode 915: Severe Burn Injuries
Contributor: Megan Hurley, MD Educational Pearls: Initial assessment of patients with severe burn injuries begins with ABCs Airway: consider inhalation injury Breathing: circumferential burns of the trunk region can reduce respiratory muscle movement Circulation: circumferential burns compromise circulation Exposure: Important to assess the affected surface area Escharotomy: emergency procedure to release the tourniquet-ing effects of the eschar Differs from a fasciotomy in that it does not breach the deep fascial layer PEEP = positive end-expiratory pressure The positive pressure remaining in the airway after exhalation Keeps airway pressure higher than atmospheric pressure Common formulas for initial fluid rate in burn shock resuscitation Parkland formula: 4 mL/kg body weight/% TBSA burns (lactated Ringer's solution) Modified Brooke formula: 2 mL/kg/% (also lactated Ringer's solution) Less fluid = lower risk of intra-abdominal compartment syndrome Lactated Ringer’s solution is preferred over normal saline in burn injuries Normal saline is avoided in large quantities due to the possibility of it leading to hyperchloremic acidosis References Acosta P, Santisbon E, Varon J. “The Use of Positive End-Expiratory Pressure in Mechanical Ventilation.” Critical Care Clinics. 2007;23(2):251-261. doi:10.1016/j.ccc.2006.12.012 Orgill DP, Piccolo N. Escharotomy and decompressive therapies in burns. J Burn Care Res. 2009;30(5):759-768. doi:10.1097/BCR.0b013e3181b47cd3 Snell JA, Loh NH, Mahambrey T, Shokrollahi K. Clinical review: the critical care management of the burn patient. Crit Care. 2013;17(5):241. Published 2013 Oct 7. doi:10.1186/cc12706 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit Donate: https://emergencymedicalminute.org/donate/
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Podcast 914: Neuroleptic Malignant Syndrome (NMS)
07/29/2024
Podcast 914: Neuroleptic Malignant Syndrome (NMS)
Contributor: Taylor Lynch, MD Educational Pearls: What is NMS? Neuroleptic Malignant Syndrome Caused by anti-dopamine medication or rapid withdrawal of pro-dopamenergic medications Mechanism is poorly understood Life threatening What medications can cause it? Typical antipsychotics Haloperidol, chlorpromazine, prochlorperazine, fluphenazine, trifluoperazine Atypical antipsychotics Less risk Risperidone, clozapine, quetiapine, olanzapine, aripiprazole, ziprasidone Anti-emetic agents with anti dopamine activity Metoclopramide, promethazine, haloperidol Not ondansetron Abrupt withdrawal of levodopa How does it present? Slowly over 1-3 days (unlike serotonin syndrome which has a more acute onset) Altered mental status, 82% of patients, typically agitated delirium with confusion Peripheral muscle rigidity and decreased reflexes. AKA lead pipe rigidity. (As opposed to clonus and hyperreflexia in serotonin syndrome) Hyperthermia (>38C seen in 87% of patients) Can also have tachycardia, labile blood pressures, tachypnea, and tremor How is it diagnosed? Clinical diagnosis, focus on the timing of symptoms No confirmatory lab test but can see possible elevated CK levels and WBC of 10-40k with a left shift What else might be on the differential? Sepsis CNS infections Heat stroke Agitated delirium Status eptilepticus Drug induced extrapyramidal symptoms Serotonin syndrome Malignant hyperthermia What is the treatment? Start with ABC’s Stop all anti-dopaminergic meds and restart pro-dopamine meds if recently stopped Maintain urine output with IV fluids if needed to avoid rhabdomyolysis Active or passive cooling if needed Benzodiazapines, such as lorazepam 1-2 mg IV q 4hrs What are active medical therapies? Controversial treatments Bromocriptine, dopamine agonist Dantrolene, classically used for malignant hyperthermia Amantadine, increases dopamine release Use as a last resort Dispo? Mortality is around 10% if not recognized and treated Most patients recover in 2-14 days Must wait 2 weeks before restarting any medications References Oruch, R., Pryme, I. F., Engelsen, B. A., & Lund, A. (2017). Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatric disease and treatment, 13, 161–175. https://doi.org/10.2147/NDT.S118438 Tormoehlen, L. M., & Rusyniak, D. E. (2018). Neuroleptic malignant syndrome and serotonin syndrome. Handbook of clinical neurology, 157, 663–675. https://doi.org/10.1016/B978-0-444-64074-1.00039-2 Velamoor, V. R., Norman, R. M., Caroff, S. N., Mann, S. C., Sullivan, K. A., & Antelo, R. E. (1994). Progression of symptoms in neuroleptic malignant syndrome. The Journal of nervous and mental disease, 182(3), 168–173. Ware, M. R., Feller, D. B., & Hall, K. L. (2018). Neuroleptic Malignant Syndrome: Diagnosis and Management. The primary care companion for CNS disorders, 20(1), 17r02185. https://doi.org/10.4088/PCC.17r02185 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Episode 913: Vasopressors after ROSC
07/23/2024
Episode 913: Vasopressors after ROSC
Contributor: Travis Barlock MD Educational Pearls: Recent study assessed outcomes after ROSC with epinephrine vs. norepinephrine Observational multicenter study from 2011-2018 285 patients received epineprhine and 481 received norepinephrine Epinephrine was associated with an increase in all-cause mortality (primary outcome) Odds ratio 2.6; 95%CI 1.4-4.7; P = 0.002 Higher cardiovascular mortality (secondary outcome) Higher proportion of unfavorable neurological outcome (secondary outcome) Norepinephrine is the vasopressor of choice in post-cardiac arrest care References Bougouin W, Slimani K, Renaudier M, et al. Epinephrine versus norepinephrine in cardiac arrest patients with post-resuscitation shock. Intensive Care Med. 2022;48(3):300-310. doi:10.1007/s00134-021-06608-7 Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit
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Podcast 912: Narcan (Naloxone)
07/15/2024
Podcast 912: Narcan (Naloxone)
Contributor: Taylor Lynch, MD Educational Pearls: Opioid Epidemic- quick facts Drug overdoses, primarily driven by opioids, have become the leading cause of accidental death in the U.S. for individuals aged 18-45. In 2021, opioids were involved in nearly 75% of all drug overdose deaths The rise of synthetic opioids like fentanyl, which is much more potent than heroin or prescription opioids, has played a major role in the increase in overdose deaths What is Narcan AKA Naloxone? Competitive opioid antagonist. It sits on the receptor but doesn’t activate it. When do we give Narcan? Respiratory rate less than 8-10 breaths per minute Should you check the pupils? An opioid overdose classically presents with pinpoint pupils BUT… Hypercapnia from bradypnea can normalize the pupils Taking other drugs at the same time like cocaine or meth can counteract the pupillary effects Basilar stroke could also cause small pupils, so don’t anchor on an opioid overdose How does Narcan affect the body? Relatively safe even if the patient is not experiencing an opioid overdose. So when in doubt, give the Narcan. What if the patient is opioid naive and overdosing? Use a large dose given that this patient is unlikely to withdraw 0.4-2 mg every 3-5 minutes What if the patient is a chronic opioid user Use a smaller dose such as 0.04-0.4 mg to avoid precipitated withdrawal How fast does Narcan work? Given intravenously (IV), onset is 1-2 min Given intranasal (IN), onset is 3-4 min Given intramuscularly (IM), onset is ~6 min Duration of action is 60 mins, with a range of 20-90 minutes How does that compare to the duration of action of common opioids? Heroine lasts 60 min Fentanyl lasts 30-60 min, depending on route Carfentanyl lasts ~5 hrs Methadone lasts 12-24 hrs So we really need to be conscious about redosing How do you monitor someone treated with Narcan? Pay close attention to the end-tidal CO2 to ensure that are ventilating appropriately Be cautious with giving O2 as it might mask hypoventilation Watch the respiratory rate Give Narcan as needed Observe for at least 2-4 hours after the last Narcan dose Larger the dose, longer the observation period Who gets a drip? If they have gotten ~3 doses, time to start the drip Start at 2/3rds last effective wake-up dose Complications Flash pulm edema 0.2-3.6% complication rate Might be from the catecholamine surge from abrupt wake-up Might also be from large inspiratory effort against a partially closed glottis which creates too much negative pressure Treat with BIPAP if awake and intubation if not awake Should you give Narcan in cardiac arrest? Short answer no. During ACLS you take over breathing for the patient and that is pretty much the only way that Narcan can help Just focus on high quality CPR References . Elkattawy, S., Alyacoub, R., Ejikeme, C., Noori, M. A. M., & Remolina, C. (2021). Naloxone induced pulmonary edema. Journal of community hospital internal medicine perspectives, 11(1), 139–142. van Lemmen, M., Florian, J., Li, Z., van Velzen, M., van Dorp, E., Niesters, M., Sarton, E., Olofsen, E., van der Schrier, R., Strauss, D. G., & Dahan, A. (2023). Opioid Overdose: Limitations in Naloxone Reversal of Respiratory Depression and Prevention of Cardiac Arrest. Anesthesiology, 139(3), 342–353. Yousefifard, M., Vazirizadeh-Mahabadi, M. H., Neishaboori, A. M., Alavi, S. N. R., Amiri, M., Baratloo, A., & Saberian, P. (2019). Intranasal versus Intramuscular/Intravenous Naloxone for Pre-hospital Opioid Overdose: A Systematic Review and Meta-analysis. Advanced journal of emergency medicine, 4(2), e27. Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII
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Episode 911: Anticholinergic Toxicity
07/08/2024
Episode 911: Anticholinergic Toxicity
Contributor: Taylor Lynch MD Educational Pearls: Anticholinergics are found in many medications, including over-the-counter remedies Medications include: Diphenhydramine Tricyclic antidepressants like amitriptyline Atropine Antipsychotics like olanzapine Antispasmodics - dicyclomine Jimsonweed Muscaria mushrooms Mechanism of action involves competitive antagonism of the muscarinic receptor Symptomatic presentation is easily remembered via the mnemonic: Dry as a bone - anhidrosis due to cholinergic antagonism at sweat glands Red as a beet - cutaneous vasodilation leads to skin flushing Hot as a hare - anhidrotic hyperthermia Blind as a bat - pupillary dilation and ineffective accommodation Mad as a hatter - anxiety, agitation, dysarthria, hallucinations, and others Clinical management ABCs Benzodiazepines for supportive care, agitation, and seizures Sodium bicarbonate for TCA toxicity due to widened QRS Activated charcoal if patient present < 1 hour after ingestion Temperature monitoring Contact poison control with questions Physostigmine controversy Physostigmine is a reversible cholinesterase inhibitor that can cross the blood-brain barrier so in theory it would be a useful antidote BUT… There is a black box warning for asystole and seizures when physostigmine is used this way Therefore it is contraindicated in TCA overdoses However, it is still indicated in certain anticholinergic overdoses with delirium Disposition Admission criteria include: symptoms >6 hours, CNS findings, QRS prolongation, hyperthermia, and rhabdomyolysis ICU admission criteria include: delirium, dysrhythmias, seizures, coma, or requirement for physostigmine drip References 1. Arens AM, Shah K, Al-Abri S, Olson KR, Kearney T. Safety and effectiveness of physostigmine: a 10-year retrospective review<sup/>. Clin Toxicol (Phila). 2018;56(2):101-107. doi:10.1080/15563650.2017.1342828 2. Nguyen TT, Armengol C, Wilhoite G, Cumpston KL, Wills BK. Adverse events from physostigmine: An observational study. Am J Emerg Med. 2018;36(1):141-142. doi:10.1016/j.ajem.2017.07.006 3. Scharman E, Erdman A, Wax P, et al. Diphenhydramine and dimenhydrinate poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2006;44(3):205-223. doi:10.1080/15563650600585920 4. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson "loco" weed abuse in adolescents. Pediatrics. 1979;63(4):520-523. 5. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2007;45(3):203-233. doi:10.1080/15563650701226192 Summarized by Jorge Chalit, OMSIII | Edited by Jorge Chalit
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Episode 910: Cellulitis Recovery Timeline
07/02/2024
Episode 910: Cellulitis Recovery Timeline
Contributor: Aaron Lessen, MD Educational Pearls: How fast does cellulitis recover? A recent prospective cohort study took a look at this question. The study included 300 adults with cellulitis (excluding those with peri-orbital cellulitis or abscesses) in two emergency departments in Queensland, Australia. They collected data from initial and follow-up surveys at 3, 7, and 14 days, and compared clinician and patient assessments at day 14. Improvement was fastest between day 0 and day 3, with gradual progress thereafter. At day 14, many still had skin redness and swelling, though warmth had often resolved. Clinicians reported higher cure rates than patients (85.8% vs. 52.8%). Conclusion: Cellulitis symptoms improve quickly at first but continue to linger for many patients. Patients and doctors often have different views on when cellulitis is fully cured. How should we counsel patients? Even on antibiotics, the margins of the cellulitis may continue to spread a small amount. Skin warmth should be the first symptom to go away. It takes time to get better. Only about 50% of patients believed their cellulitis was cured at 2 weeks. References Nightingale, R. S., Etheridge, N., Sweeny, A. L., Smyth, G., Dace, W., Pellatt, R. A. F., Snelling, P. J., Yadav, K., & Keijzers, G. (2024). Cellulitis in the Emergency Department: A prospective cohort study with patient-centred follow-up. Emergency medicine Australasia : EMA, 10.1111/1742-6723.14401. Advance online publication. https://doi.org/10.1111/1742-6723.14401 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Episode 909: Prehospital Blood Pressure Management in Suspected Stroke
06/24/2024
Episode 909: Prehospital Blood Pressure Management in Suspected Stroke
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
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Episode 908: Sympathomimetic Drugs
06/17/2024
Episode 908: Sympathomimetic Drugs
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. 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
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Episode 907: Wide-Complex Tachycardia
06/12/2024
Episode 907: Wide-Complex Tachycardia
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: 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
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Episode 906: Case Study of Hypernatremia
06/03/2024
Episode 906: Case Study of Hypernatremia
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. Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII
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Episode 905: Oseltamivir (Tamiflu) for Influenza
05/27/2024
Episode 905: Oseltamivir (Tamiflu) for Influenza
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
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Episode 904: Cardiovascular Risks of Epinephrine
05/20/2024
Episode 904: Cardiovascular Risks of Epinephrine
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
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Episode 903: Treating Precipitated Opioid Withdrawal
05/13/2024
Episode 903: Treating Precipitated Opioid Withdrawal
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
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Episode 902: Liver Failure and Cirrhosis
05/06/2024
Episode 902: Liver Failure and Cirrhosis
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. 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
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Episode 901: Underdosing in Status Epilepticus
04/29/2024
Episode 901: Underdosing in Status Epilepticus
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
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Episode 900: Ketamine Dosing
04/22/2024
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. 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. Stirling, J., & McCoy, L. (2010). Quantifying the psychological effects of ketamine: from euphoria to the k-Hole. Substance use & misuse, 45(14), 2428–2443. Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMS II
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Episode 899: Thrombolytic Contraindications
04/15/2024
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
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