Emergency Medical Minute

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**Emergency Medical Minute**

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.

Latest Episodes:

Podcast 914: Neuroleptic Malignant Syndrome (NMS) Jul 29, 2024

Show notes

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

Episode 913: Vasopressors after ROSC Jul 23, 2024

Show notes

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

Podcast 912: Narcan (Naloxone) Jul 15, 2024

Show notes

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

Episode 911: Anticholinergic Toxicity Jul 08, 2024

Show notes

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
- 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

Episode 910: Cellulitis Recovery Timeline Jul 02, 2024

Show notes

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

Episode 909: Prehospital Blood Pressure Management in Suspected Stroke Jun 24, 2024

Show notes

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

Episode 908: Sympathomimetic Drugs Jun 17, 2024

Show notes

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

Episode 907: Wide-Complex Tachycardia Jun 12, 2024

Show notes

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

Episode 906: Case Study of Hypernatremia Jun 03, 2024

Show notes

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

Episode 905: Oseltamivir (Tamiflu) for Influenza May 27, 2024

Show notes

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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