Emergency Medical Minute

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/

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. https://doi.org/10.1097/00005053-199403000-00007 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  

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  

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 https://nida.nih.gov/research-topics/trends-statistics/overdose-death-rates#:~:text=Drug%20overdose%20deaths%20involving%20prescription,of%20deaths%20declined%20to%2014%2C716. 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. https://doi.org/10.1080/20009666.2020.1854417 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. https://doi.org/10.1097/ALN.0000000000004622 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. https://doi.org/10.22114/ajem.v0i0.279 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII

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. 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  

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

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