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Emergency Medical Minute
Hosted by Emergency Medical Minute · EN
Our near daily podcasts move quickly to reflect current events, are inspired by real patient care, and speak to the true nature of what it's like to work in the Emergency Room or Pre-Hospital Setting. Each medical minute is recorded in a real emergency department, by the emergency physician or clinical pharmacist on duty – the ER is our studio and everything is live.
45episodes
Episodes
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Episode 990: Tramadol, or rather, Trama-don't
Jan 1200:05:15Tap to summarizeContributor: Taylor Lynch, MD Educational Pearls: What is tramadol and how does it work? Tramadol is a Schedule IV opioid analgesic used for moderate pain and is often perceived as safer than other opioids due to lower abuse potential. It is a prodrug with weak direct μ-opioid receptor activity. The parent compound also inhibits serotonin and norepinephrine reuptake, giving it SSRI/SNRI-like properties. Tramadol is metabolized by CYP2D6 into O-desmethyltramadol (ODT), which has significantly stronger μ-opioid receptor agonism than the parent drug. What are the concerns with tramadol? Ultrarapid CYP2D6 metabolizers (more common in Middle Eastern and North African populations) rapidly convert tramadol to ODT, increasing the risk of opioid toxicity. Poor CYP2D6 metabolizers generate little ODT and may experience primarily serotonergic effects, increasing the risk of serotonin syndrome, especially when combined with SSRIs or SNRIs. CYP2D6 inhibitors (e.g., bupropion, paroxetine, terbinafine, celecoxib) can block tramadol's conversion to ODT, potentially precipitating opioid withdrawal or increasing serotonergic toxicity. Tramadol is also associated with an increased risk of first-time seizures, even at therapeutic doses. Key takeaways Tramadol's effects are highly unpredictable, varying from minimal analgesia to exaggerated opioid effects depending on metabolism. Drug–drug interactions can lead to serotonin syndrome or opioid withdrawal. Despite its Schedule IV classification and reputation for safety, alternative analgesics may be preferable in many patients. References DailyMed - TRAMADOL HYDROCHLORIDE tablet, coated. Accessed January 10, 2026. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=61fb5ba7-6896-4ee4-83de-caee69b06a8e#ID57 Dean L, Kane M. Tramadol Therapy and CYP2D6 Genotype. In: Pratt VM, Scott SA, Pirmohamed M, Esquivel B, Kattman BL, Malheiro AJ, eds. Medical Genetics Summaries. National Center for Biotechnology Information (US); 2012. Accessed January 10, 2026. http://www.ncbi.nlm.nih.gov/books/NBK315950/ Aly SM, Tartar O, Sabaouni N, Hennart B, Gaulier JM, Allorge D. Tramadol-Related Deaths: Genetic Analysis in Relation to Metabolic Ratios. J Anal Toxicol. 2022;46(7):791-796. doi:10.1093/jat/bkab096 Summarized and edited by Dan Orbidan OMS2 Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf
Transcribe →Episode 989: Young Strokes
Jan 500:03:32Tap to summarizeContributor: Aaron Lessen, MD Educational Pearls: The Case 24F brought in for anxiety. Patient is tearful, not talking, and potentially hyperventilating. History from boyfriend is that she suddenly stopped talking and started crying and it was hard to understand what she was saying. On exam, patient appears anxious and has a gaze preference for the right side and is still having difficulty speaking. Decision is made to stroke alert patient. CT shows early MCA stroke and M2 occlusion. Patient is treated by IR with mechanical thrombectomy. What are the risk factors for strokes in young people ( Traditional risk factors still matter Hypertension Most important modifiable risk factor, present in 30-50% of young stroke patients Diabetes Especially insulin dependent type 1 HLD Smoking Substance use Cocaine Meth Alcohol, especially binge drinking IV drug use Structural heart disease PFO Valvular heart disease like rheumatic disease Hypercoagulable states Factor V Leiden Protein C or S deficiency Antithrombin III deficiency Vertebral dissections Recent trauma References Aigner A, Grittner U, Rolfs A, Norrving B, Siegerink B, Busch MA. Contribution of Established Stroke Risk Factors to the Burden of Stroke in Young Adults. Stroke. 2017 Jul;48(7):1744-1751. doi: 10.1161/STROKEAHA.117.016599. Epub 2017 Jun 15. PMID: 28619986. Ekker MS, Boot EM, Singhal AB, Tan KS, Debette S, Tuladhar AM, de Leeuw FE. Epidemiology, aetiology, and management of ischaemic stroke in young adults. Lancet Neurol. 2018 Sep;17(9):790-801. doi: 10.1016/S1474-4422(18)30233-3. PMID: 30129475. Khan M, Wasay M, O'Donnell MJ, Iqbal R, Langhorne P, Rosengren A, Damasceno A, Oguz A, Lanas F, Pogosova N, Alhussain F, Oveisgharan S, Czlonkowska A, Ryglewicz D, Yusuf S. Risk Factors for Stroke in the Young (18-45 Years): A Case-Control Analysis of INTERSTROKE Data from 32 Countries. Neuroepidemiology. 2023;57(5):275-283. doi: 10.1159/000530675. Epub 2023 May 17. PMID: 37231971. Summarized and edited by Jeffrey Olson MS4 Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf
Transcribe →Episode 988: Infant Botulism
Dec 2900:02:30Tap to summarizeContributor: Aaron Lessen, MD Educational Pearls: A 2025 multistate outbreak of infant botulism has been linked to ByHeart infant formula As of December 10-17th, there have been at least 51 infants with suspected or confirmed botulism who were exposed to this formula across 19 states All reported cases resulted in hospitalization but no deaths reported to date Infant botulism Occurs when C. botulinum spores germinate in the infant's intestine, producing toxin Spores are classically found in honey but can also be in dirt or contaminated in infant formula Infants are particularly susceptible because their body can't neutralize the spores Symptoms may include initial constipation, poor feeding, weak cry, floppy movements, loss of head control, difficulty swallowing, generalized weakness, and respiratory compromise if progressive Can be treated with antitoxin Maintain a high index of suspicion for infant botulism in infants fed the recalled formula presenting with neuromuscular symptoms. References Human Foods Program. Outbreak Investigation of Infant Botulism: Infant Formula. U.S. Food and Drug Administration. Published 2025. https://www.fda.gov/food/outbreaks-foodborne-illness/outbreak-investigation-infant-botulism-infant-formula-november-2025 Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jeffrey Olson, MS4 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Emergency Medicine Cases with Dr. Barlock
Sep 9Tap to summarizeContributors: Travis Barlock MD, Jeffrey Olson MS4 Feel free to use the cases below for your own practice. All of the scenarios are completely made up and designed to hit several teaching points. Case 1 25 M, presents to the ED with chest pain. Stabbing, started a few hours ago, substernal. Thinks it is GERD. After 2-3 minutes, pain worsens and radiates to the back. VS: BP 125/50 (Right arm 190/110). HR 120. RR of 18. Sat 98% on RA. Additional VS: Temp of 37.2, height of 6'5", BMI of 18. PMH: None, doesn't see a doctor. Meds: None FH: Weird heart thing (Mitral Valve Prolapse), weird lung thing (spontaneous pneumothorax), tall family members with long fingers and toes Physical Exam: Cards: Diastolic decrescendo at the RUSB, diminished S2. UE pulses are asymmetric, LE pulses are asymmetric, carotid pulses are asymmetric, BP is asymmetric MSK: Knees, elbows, and wrists are hypermobile. Imaging: CXR #1 normal, #2 widened mediastinum (no read yet but shows widened mediastinum), POCUS shows small effusion CTA/MRA doesn't come back until after the case. ECG: Sinus Tach Labs: NT-proBNP 500 pg/mL D-Dimer: 7000 ng/L CBC: Hemoglobin: 13.5 g/dL, WBC: 20,000/µL, Platelets: 250,000/µL Chem 7: Na 138, K, 5.7, Cl 102, Bicarb 17, BUN 45, Creatinine: 3.5 mg/dL, Glucose: 180 LFTs: Albumin 2.4, Total protein 5.5, ALP: 140, AST: 3500, ALT: 2800, TBili: 3.2, DirectBili: 2.4, Ca: 7.8 LDH: 2200 PT: 20.5, INR: 2.2, Fibrinogen: 170 5th gen High-Sensitivity Troponin: <3 Lactate: 7 mmol/L VBG: pH 7.22, paCO2 28, bicarb 15 Notes: Can have patient crash somewhere in middle and show 2nd xray Case 2: A 67-year-old female is brought to the ED by her daughter due to progressive weakness, confusion, and fatigue that have worsened over the past week. Unable to get out of bed and has become increasingly lethargic. Also having some nausea, constipation. The daughter denies any preceding illness, recent trauma, or travel. Does not know her meds but will head home to get them after talking with you. VS: BP 88/55 mmHg, HR 110, RR 20, O2 Sat 98% on room air. Additional VS: Temp 36.8°C. PMH: Hypertension, osteoarthritis, and depression. Physical exam: General: Thin, somnolent but arousable. HENT: Dry mucous membranes Neuro: Confused, A&Ox1 (self), hyporeflexia Labs (Includes many that would not return in the ED in case you want to take this case forward to the floor) CBC: WBC 9,500, Hb 16.5, Hct: 50%, Platelets 220,000 Chem7: Na 129, K 2.1, Cl 95, HCO3 34, Creatinine 1.6, BUN 40, Glucose 115 LFTs: normal Magnesium: 1.1 Calcium: 10.8 mg/dL (corrects to 12.8) iCal: 3.2 Phosphate: 2.3 mg/dL Albumin: 2 BUN:Cr ratio: 25 VBG: pH: 7.49, PaCO2 45, HCO3: 34 Lactate: 2.8 Serum Osmolality: 276 mOsm/kg (Osmolal gap of 2) Urine Osmolality: 550 mOsm/kg Urine Sodium (UNa): 10 mEq/L (low). Urine Potassium (UK): 25 mEq/L (elevated). Urine Chloride (UCl): 12 mEq/L (low). Urine Magnesium (UMg): 20 (Elevated). Urine Calcium (UCa): 50 in 24 hrs (Low) 100 cc of urine with foley FeNa Plasma renin activity: 15 mg/mL/hr (elevated), Aldosterone: 25 ng/dL (Elevated), ADH: Elevated, Diuretic screen: Positive for thiazides PTH: 8 (low), HsTrop: 32, Cortisol and ACTH: Normal. EKG: Hypokalemia features CXR: Normal Renal US: shows stones Improves with fluids Note: Can have daughter return with med list at some point including HCTZ, ibuprofen, and sertraline Case 3: Patient Presentation EMS Report: A 27-year-old male involved in a high-speed motorcycle collision is brought to the emergency department by EMS. The patient was found unconscious at the scene with evidence of severe thoracic and extremity trauma. He was intubated en route for airway protection due to altered mental status (GCS 7). VS: HR 130, BP 90/60, RR: bagging at 12 bpm, satting 88% on 100% FiO2 Primary Survey Airway: Endotracheal tube in place. Breathing: Decreased breath sounds on the left side with visible chest asymmetry and paradoxical chest wall movement. Circulation: Mottled extremities noted, with significant deformity of the right thigh. Pulses are diminished in the right leg Disability: GCS remains 7 (E1 V2 M4). Pupils equal and reactive. Exposure: Full-body examination reveals an open fracture of the right femur, multiple abrasions, and bruising over the chest wall. Vent alarms Peak Inspiratory Pressure (PIP) 40 cm H₂O (elevated) Plateau Pressure (Pplat) 35 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 55 mmHg High-Pressure Alarm Triggering frequently Glucose 120 CBC: Hgb 8.9, Hct 27, WBC 14.2, platelets 220,000 VBG: pH 7.28, pCO2 33, bicarb 18, lactate 4.5 CXR with tension pneumothorax Patient improves after chest tube, pigtail catheter, or needle decompression. Ready to be transferred upstairs and O2 starts tanking again Vent alarms- second episode Peak Inspiratory Pressure (PIP) 35 cm H₂O (elevated) Plateau Pressure (Pplat) 30 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 20 mmHg HR: 140, satting 84%, temp 38.5, ABG: pH 7.32, pCO₂ 30 mmHg, pO₂ 60 mmHg on 100% FiO₂, HCO₃⁻ 18 mmol/L (hypoxemia and metabolic acidosis). D-dimer: Elevated Thrombocytopenia: Platelets 90,000/µL. US shows blown right ventricle ECG shows new RBBB CT PE: Ground glass opacities, consolidation, centrilobular nodules, septal thickening, and fat-attenuating lesions. Note: Management is largely supportive care so once the diagnosis is made, end the case. References Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1;67(9):1959-66. PMID: 12751658. Coelho SG, Almeida AG. Marfan syndrome revisited: From genetics to the clinic. Rev Port Cardiol (Engl Ed). 2020 Apr;39(4):215-226. English, Portuguese. doi: 10.1016/j.repc.2019.09.008. Epub 2020 May 18. PMID: 32439107. Palmer BF. Metabolic complications associated with use of diuretics. Semin Nephrol. 2011 Nov;31(6):542-52. doi: 10.1016/j.semnephrol.2011.09.009. PMID: 22099511. Reed MJ. Diagnosis and management of acute aortic dissection in the emergency department. Br J Hosp Med (Lond). 2024 Apr 30;85(4):1-9. doi: 10.12968/hmed.2023.0366. PMID: 38708978. Roberts DJ, Leigh-Smith S, Faris PD, Blackmore C, Ball CG, Robertson HL, Dixon E, James MT, Kirkpatrick AW, Kortbeek JB, Stelfox HT. Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review. Ann Surg. 2015 Jun;261(6):1068-78. doi: 10.1097/SLA.0000000000001073. PMID: 25563887. Rothberg DL, Makarewich CA. Fat Embolism and Fat Embolism Syndrome. J Am Acad Orthop Surg. 2019 Apr 15;27(8):e346-e355. doi: 10.5435/JAAOS-D-17-00571. PMID: 30958807. Produced by Jeffrey Olson, MS4 Special thanks to Evan Fisch MD Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 950: Ultrasound Pulse Check During Cardiac Arrest
Mar 31, 202500:02:37Tap to summarizeContributor: Aaron Lessen, MD Educational Pearls: Point-of-care ultrasound (POCUS) is used to assess cardiac activity during cardiac arrest and can identify potential reversible causes such as pericardial tamponade Ultrasound could be beneficial in another way during cardiac arrest as well: pulse checks Manual palpation for detecting pulses is imperfect, with false positives and negatives Doppler ultrasound can be used as an adjunct or replacement to manual palpation for improved accuracy Options for Doppler ultrasound of carotid or femoral pulses during cardiac arrest: Visualize arterial pulsation Use color doppler Numerically quantify the flow and correlate this to a BP reading - slightly more complex Doppler ultrasound is much faster than manual palpation for pulse check Can provide information almost instantaneously without waiting the full 10 seconds for a manual pulse check The main priority during cardiac arrest resuscitation is to maintain quality compressions If pulses are unable to be obtained through Doppler within the 10-second window, resume compressions and try again during the next pulse check References Cohen AL, Li T, Becker LB, Owens C, Singh N, Gold A, Nelson MJ, Jafari D, Haddad G, Nello AV, Rolston DM; Northwell Health Biostatistics Unit. Femoral artery Doppler ultrasound is more accurate than manual palpation for pulse detection in cardiac arrest. Resuscitation. 2022 Apr;173:156-165. doi: 10.1016/j.resuscitation.2022.01.030. Epub 2022 Feb 4. PMID: 35131404. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 949: Hoover's Sign
Mar 24, 202500:01:58Tap to summarizeContributor: Travis Barlock, MD Educational Pearls: What is Hoover’s sign used to identify? This physical exam maneuver differentiates between organic vs. functional (previously known as psychogenic) leg weakness. Organic causes include disease processes such as stroke, MS, spinal cord compression, guillain-barre, ALS, and sciatica, among others In Functional Neurologic Disorder, the dysfunction is in brain signaling, and treatment relies on more of a psychiatric approach How is Hoover's Sign performed? Place your hand under the heel of the unaffected leg and ask the patient to attempt to lift the paralyzed leg. If the paralysis is due to an organic cause, then you should feel the unaffected leg push down. This is due to the crossed-extensor reflex mechanism, an unconscious motor control function mediated by the corticospinal tract. If you don’t feel the opposite heel push down, that is a positive Hoover’s Sign. How sensitive/specific is it? An unblinded cohort study in patients with suspected stroke found a sensitivity of 63% and a specificity of 100% Fun Fact There’s also a pulmonary Hoover’s sign, named after the same doctor, Charles Franklin Hoover, which refers to paradoxical inward movement of the lower ribs during inspiration due to diaphragmatic flattening in COPD. References McWhirter L, Stone J, Sandercock P, Whiteley W. Hoover's sign for the diagnosis of functional weakness: a prospective unblinded cohort study in patients with suspected stroke. J Psychosom Res. 2011 Dec;71(6):384-6. doi: 10.1016/j.jpsychores.2011.09.003. Epub 2011 Oct 6. PMID: 22118379. Stone J, Aybek S. Functional limb weakness and paralysis. Handb Clin Neurol. 2016;139:213-228. doi: 10.1016/B978-0-12-801772-2.00018-7. PMID: 27719840. Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 948: CYP Inducers and Inhibitors
Mar 17, 202500:03:57Tap to summarizeContributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: CYP enzymes are responsible for the metabolism of many medications, drugs, and other substances CYP3A4 is responsible for the majority Other common ones include CYP2D6 (antidepressants), CYP2E1 (alcohol), and CYP1A2 (cigarettes) CYP inducers lead to reduced concentrations of a particular medication CYP inhibitors effectively increase concentrations of certain medications in the body Examples of CYP inducers Phenobarbital Rifampin Cigarettes St. John’s Wort Examples of CYP inhibitors -azole antifungals like itraconazole and ketoconazole Bactrim (trimethoprim-sulfamethoxazole) Ritonavir (found in Paxlovid) Grapefruit juice Clinical relevance Drug-drug interactions happen frequently and often go unrecognized or underrecognized in patients with significant polypharmacy A study conducted on patients receiving Bactrim and other antibiotics found increased rates of anticoagulation in patients receiving Bactrim Currently, Paxlovid is prescribed to patients with COVID-19, many of whom have multiple comorbidities and are on multiple medications Paxlovid contains ritonavir, a powerful CYP inhibitor that can increase concentrations of many other medications A complete list of clinically relevant CYP inhibitors can be found on the FDA website: https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers References Glasheen JJ, Fugit RV, Prochazka AV. The risk of overanticoagulation with antibiotic use in outpatients on stable warfarin regimens. J Gen Intern Med. 2005;20(7):653-656. doi:10.1111/j.1525-1497.2005.0136.x Lynch T, Price A. The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects. Am Fam Physician. 2007;76(3):391-396. PAXLOVID™. Drug interactions. PAXLOVIDHCP. Accessed March 16, 2025. https://www.paxlovidhcp.com/drug-interactions Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 947: Hypercapnia
Mar 10, 202500:03:57Tap to summarizeEducational Pearls: Physiologic stimulation of ventilation occurs through changes in levels of: Arterial carbon dioxide (PaCO2) Arterial oxygen (PaO2) Hypercapnia is an elevated level of CO2 in the blood - this primarily drives ventilation Hypoxia is a decreased level of O2 in the body’s tissues - the backup drive for ventilation Patients at risk of hypercapnia should maintain an O2 saturation between 88-92% Normal O2 saturation is 95-100% In patients who chronically retain CO2, their main drive for ventilation becomes hypoxia An audit was performed of SpO2 observations of all patients with a target range of 88–92% at a single hospital over a four-year period This found that excessive oxygen administration was more common than insufficient oxygen and is associated with an increased risk of harm Individuals at risk of hypercapnia include but are not limited to patients with COPD, hypoventilation syndrome, or altered mental status References Homayoun Kazemi, Douglas C. Johnson, Respiration, Editor(s): V.S. Ramachandran, Encyclopedia of the Human Brain, Academic Press, 2002, Pages 209-216, ISBN 9780122272103, https://doi.org/10.1016/B0-12-227210-2/00302-2. O'Driscoll BR, Bakerly ND. Are we giving too much oxygen to patients at risk of hypercapnia? Real world data from a large teaching hospital. Respir Med. 2025 Mar;238:107965. doi: 10.1016/j.rmed.2025.107965. Epub 2025 Jan 30. PMID: 39892771. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 946: Time to Defibrillation
Mar 3, 202500:02:30Tap to summarizeContributor: Aaron Lessen, MD Educational Pearls: Quick background info Cardiac arrest is when the heart stops pumping blood for any reason. This is different from a heart attack in which the heart is still working but the muscle itself is starting to die. One cause of cardiac arrest is when the electrical signals are very disrupted in the heart and start following chaotic patterns such as Ventricular tachycardia (VTach) and Ventricular fibrillation (VFib) One of the only ways to save a person whose heart is in VFib or VTach is to jolt the heart with electricity and terminate the dangerous arrhythmia. A recent study in the Netherlands looked at how important the time delay is from when cardiac arrest is first identified to when a defibrillation shock from an Automated External Defibrillator (AED) is actually given. Their main take-away: each minute defibrillation is delayed drops the survival rate by 6%! These findings reinforce the importance of rapid AED deployment and early defibrillation strategies in prehospital cardiac arrest response. References Stieglis, R., Verkaik, B. J., Tan, H. L., Koster, R. W., van Schuppen, H., & van der Werf, C. (2025). Association Between Delay to First Shock and Successful First-Shock Ventricular Fibrillation Termination in Patients With Witnessed Out-of-Hospital Cardiac Arrest. Circulation, 151(3), 235–244. https://doi.org/10.1161/CIRCULATIONAHA.124.069834 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Transcribe →Episode 945: Ketorolac vs. Ibuprofen
Feb 24, 202500:03:30Tap to summarizeContributor: Ricky Dhaliwal, MD Educational Pearls: Ketorolac and ibuprofen are NSAIDs with equivalent efficacy for pain in the emergency department Oral ibuprofen provides the same relief as intramuscular ketorolac IM ketorolac is associated with the adverse effect of a painful injection IM ketorolac is slightly faster in onset but not significant Studies have assessed the two medications in head-to-head randomized-controlled trials and found no significant difference in pain scores IM ketorolac takes longer to administer and has a higher cost Ketorolac dosing Commonly given in 10 mg, 15 mg, and 30 mg doses However, higher doses are associated with more adverse effects Gastrointestinal upset, nausea, and bleeding risk Studies have demonstrated equal efficacy in pain reduction with lower doses References Motov S, Yasavolian M, Likourezos A, et al. Comparison of Intravenous Ketorolac at Three Single-Dose Regimens for Treating Acute Pain in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2017;70(2):177-184. doi:10.1016/j.annemergmed.2016.10.014 Neighbor ML, Puntillo KA. Intramuscular ketorolac vs oral ibuprofen in emergency department patients with acute pain. Acad Emerg Med. 1998;5(2):118-122. doi:10.1111/j.1553-2712.1998.tb02595.x Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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