Contributor: 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

1. 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

2. 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.

3. PAXLOVID™. Drug interactions. PAXLOVIDHCP. Accessed March 16, 2025. https://www.paxlovidhcp.com/drug-interactions

Summarized & Edited by Jorge Chalit, OMS3

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Educational 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

1. 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.

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

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Contributor: 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

1. 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

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Contributor: 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

1. 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

2. 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

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Contributor: Aaron Lessen, MD

Educational Pearls:

• Colchicine is most commonly used for the prevention and treatment of gout

• There is research investigating the anti-inflammatory and cardioprotective effects of colchicine 

• This drug has a narrow therapeutic index: a small margin between effective dose and toxic dose

• Colchicine overdoses can be unintentional or intentional and are associated with poor outcomes

• Phase 1: 10 - 24 hours after ingestion

• Patient looks well but may have mild symptoms mimicking gastroenteritis

• Phase 2: 24 hours - 7 days after ingestion

• Multiple organ dysfunction syndrome (MODS)

• Phase 3: recovery is usually within a few weeks of ingestion

• Treatment for colchicine overdose

• Treat early and aggressively

• Gastrointestinal decontamination with activated charcoal and orogastric lavage 

• Dialysis and ECMO for MODS treatment

References

1. Finkelstein Y, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y. Colchicine poisoning: the dark side of an ancient drug. Clin Toxicol (Phila). 2010 Jun;48(5):407-14. doi: 10.3109/15563650.2010.495348. PMID: 20586571.

2. Gasparyan AY, Ayvazyan L, Yessirkepov M, Kitas GD. Colchicine as an anti-inflammatory and cardioprotective agent. Expert Opin Drug Metab Toxicol. 2015;11(11):1781-94. doi: 10.1517/17425255.2015.1076391. Epub 2015 Aug 4. PMID: 26239119.

Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3

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Contributor: Travis Barlock, MD

Educational Pearls:

What is Portal Vein Thrombosis?

• The formation of a blood clot within the portal vein, which carries blood from the gastrointestinal tract, pancreas, and spleen to the liver

• Not only can this cause problems downstream in the liver, but the backup of venous blood can cause ischemia in the bowels

How does it present?

• Similar to acute mesenteric ischemia: Sudden onset of abdominal pain, nausea, vomiting, and fever

How is it diagnosed?

• Abdominal CT or MRI with contrast

What causes it?

• Cirrhosis

• Coagulopathy (Factor V Leiden mutation, Prothrombin gene mutation, Antiphospholipid syndrome, Protein C, protein S, antithrombin III deficiency, etc.)

• Oral Contraceptive Pills (OCPs)

• Cancer such as hepatocellular carcinoma

How is it treated?

• Aggressive fluid resuscitation

• Antibiotics. Be sure to cover enteric gram-negative bacteria and anaerobes

• Heparin, same dosing as a bolus for a DVT

• Endovascular treatment, such as a thrombectomy with IR

• Surgical evaluation if there has been tissue death in the mesentery

References

• Hilscher, M. B., Wysokinski, W. E., Andrews, J. C., Simonetto, D. A., Law, R. J., & Kamath, P. S. (2024). Portal Vein Thrombosis in the Setting of Cirrhosis: Evaluation and Management Strategies. Gastroenterology, 167(4), 664–672. https://doi.org/10.1053/j.gastro.2024.05.017

• Intagliata, N. M., Caldwell, S. H., & Tripodi, A. (2019). Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis. Gastroenterology, 156(6), 1582–1599.e1. https://doi.org/10.1053/j.gastro.2019.01.265

• Ju, C., Li, X., Gadani, S., Kapoor, B., & Partovi, S. (2022). Portal Vein Thrombosis: Diagnosis and Endovascular Management. Pfortaderthrombose: Diagnose und endovaskuläres Management. RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin, 194(2), 169–180. https://doi.org/10.1055/a-1642-0990

Summarized by Jeffrey Olson MS3 | Edited by Jorge Chalit, OMS3

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Contributor: Jorge Chalit-Hernandez, OMS3

Educational Pearls:

• Acute mountain sickness (AMS) is the term given to what is otherwise colloquially known as altitude sickness

• High altitude cerebral edema (HACE) is a severe form of AMS marked by encephalopathic changes

• Symptoms begin at elevations as low as 6500 feet above sea level for people who ascend rapidly

• May develop more severe symptoms at higher altitudes

• The pathophysiology involves cerebral vasodilation

• Occurs in everyone ascending to high altitudes but is more pronounces in those that develop symptoms

• The reduced partial pressure of oxygen induces hypoxic vasodilation in the brain, which results in edema and, ultimately, HACE in some patients

• Symptomatic presentation

• Headache, nausea, and sleeping difficulties occur within 2-24 hours of arrival at altitude

• HACE may occur between 12-72 hours after AMS and presents with ataxia, confusion, irritability, and ultimately results in coma if left untreated

• Clinical presentation may be mistaken for simple exhaustion, so clinicians should maintain a high index of suspicion

• Notably, if symptoms occur more than 2 days after arrival at altitude, clinicians should seek an alternative diagnosis but maintain AMS/HACE on the differential

• Treatment and management

• AMS

• Adjunctive oxygen and descent to lower altitude

• Acetazolamide is used as a preventive measure but is not helpful in acute treatment

• +/- dexamethasone

• HACE

• Patients with HACE should receive dexamethasone to help reduce cerebral edema

• Immediate descent to a lower altitude

References

1. Burtscher M, Wille M, Menz V, Faulhaber M, Gatterer H. Symptom progression in acute mountain sickness during a 12-hour exposure to normobaric hypoxia equivalent to 4500 m. High Alt Med Biol. 2014;15(4):446-451. doi:10.1089/ham.2014.1039

2. Levine BD, Yoshimura K, Kobayashi T, Fukushima M, Shibamoto T, Ueda G. Dexamethasone in the treatment of acute mountain sickness. N Engl J Med. 1989;321(25):1707-1713. doi:10.1056/NEJM198912213212504

3. Luks AM, Beidleman BA, Freer L, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention, Diagnosis, and Treatment of Acute Altitude Illness: 2024 Update. Wilderness Environ Med. 2024;35(1_suppl):2S-19S. doi:10.1016/j.wem.2023.05.013

Summarized & Edited by Jorge Chalit, OMS3

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Contributor: Meghan Hurley, MD

Educational Pearls:

• Gastroenteritis clinical diagnoses:

• Diarrhea with or without vomiting and fever

• Vomiting in the absence of diarrhea has a large list of differential diagnoses, so the combination of diarrhea and vomiting in a patient is helpful to indicate the gastroenteritis diagnosis

• Symptom timeline is usually 1-3 days, but can last up to 14 days – diarrhea persists the longest

• Treatment for mild to moderate dehydration: oral or IV rehydration

• Begin orally to avoid unnecessary IV in a pediatric patient

1. Administer ODT Ondansetron (Zofran) to prevent vomiting

   1. Meta-analysis showed that 2-8 mg orally, based on body weight, decreased vomiting quickly

2. Wait 15-20 minutes for the medication to take effect

3. Use streamlined method for oral rehydration: Fluids such as over-the-counter Pedialyte, Infalyte, Rehydrate, Resol, and Naturalyte may be used

   1. If patient weighs less than 10kg: administer 5mL of fluid per minute for 20 minutes

   2. If patient weighs 10kg or more: administer 10mL of fluid for 20 minutes

4. If the patient can keep the fluid down, double the fluid volume and repeat

5. If the patient once again keeps the fluid down, double the fluid volume and repeat

• If successful with each attempt, the patient may be discharged home

• Can prescribe ODT Zofran for 1-2 days at home

• If the patient vomits more than once during this oral rehydration process, intravenous rehydration must be initiated

References

1. Churgay CA, Aftab Z. Gastroenteritis in children: Part II. Prevention and management. Am Fam Physician. 2012 Jun 1;85(11):1066-70. PMID: 22962878.

Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3

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Contributor: Aaron Lessen, MD

Educational Pearls:

• If a patient sustains a cut, the provider has several options on how to close the wound. If they choose to suture the wound closed, it involves needles both in the form of injecting numbing medication (lidocaine) as well as with the suture itself. Other techniques are “needleless,” like closing the wound with adhesive strips (Steri-Strips) or skin adhesive (Dermabond). But which method is best?

• A recent study looked to compare guardian-perceived cosmetic outcomes of pediatric lacerations repaired with absorbable sutures, Dermabond, and Steri-Strips. It also assessed pain and satisfaction with the procedure from both guardian and provider perspectives.

• Participants: 55 patients were enrolled; 30 completed the 3-month follow-up.

• Cosmetic Ratings (Median and IQR):

• Sutures: 70.5 (59.8–76.8)

• Dermabond: 85 (73–90)

• Steri-Strips: 67 (55–78)

• (P = 0.254, no statistically significant difference)

• Satisfaction and Pain:

• No significant differences in guardian or provider satisfaction

• Pain levels were comparable across all methods

• Even though there was no statistically significant difference in guardian-perceived cosmetic outcomes, the Dermabond did have the highest ratings at the end of the study.

References

• Barton, M. S., Chaumet, M. S. G., Hayes, J., Hennessy, C., Lindsell, C., Wormer, B. A., Kassis, S. A., Ciener, D., & Hanson, H. (2024). A Randomized Controlled Comparison of Guardian-Perceived Cosmetic Outcome of Simple Lacerations Repaired With Either Dermabond, Steri-Strips, or Absorbable Sutures. Pediatric emergency care, 40(10), 700–704. https://doi.org/10.1097/PEC.0000000000003244

Summarized by Jeffrey Olson MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3

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Contributor: Jorge Chalit-Hernandez, OMS3

Educational Pearls:

• Serotonin syndrome occurs most commonly due to the combination of monoamine oxidase inhibition with concomitant serotonergic medications like SSRIs

• Examples of unexpected monoamine oxidase inhibitors

  • Linezolid - a last-line antibiotic reserved for patients with true anaphylaxis to penicillins and cephalosporins

  • Methylene blue - not mentioned in the podcast due to its uncommon usage for methemoglobinemia

• Other medications that can interact with SSRIs to cause serotonin syndrome

  • Dextromethorphan - primarily an anti-tussive at sigma opioid receptors that also has serotonin reuptake inhibition

• Clinical presentation of serotonin syndrome

  • Altered mental status

  • Autonomic dysregulation leading to hypertension (most common), hypotension, and tachycardia

  • Hyperthermia

  • Neuromuscular hyperactivity - tremors, myoclonus, and hyperreflexia

• Hunter Criteria (high sensitivity and specificity for serotonin syndrome):

  • Spontaneous clonus

  • Inducible clonus + agitation or diaphoresis

  • Ocular clonus + agitation or diaphoresis

  • Tremor + hyperreflexia

  • Hypertonia, temperature > 38º C, and ocular or inducible clonus

• Management of serotonin syndrome

  • Primarily supportive - benzodiazepines can help treat hypertension, agitation, and hyperthermia. Patients often require repeated and higher dosing of benzodiazepines

  • Avoid antipyretics to treat hyperthermia since the elevated temperature is due to sustained muscle contraction and not central temperature dysregulation

  • In refractory patients, cyproheptadine (a 5HT2 antagonist) may be used as a second-line treatment

  • Patients with temperatures > 41.1º C or 106º F require medically induced paralysis and intubation to control their temperature

References

1. Boyer EW, Shannon M. The serotonin syndrome [published correction appears in N Engl J Med. 2007 Jun 7;356(23):2437] [published correction appears in N Engl J Med. 2009 Oct 22;361(17):1714]. N Engl J Med. 2005;352(11):1112-1120. doi:10.1056/NEJMra041867

2. Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. 2003;96(9):635-642. doi:10.1093/qjmed/hcg109

3. Ramsay RR, Dunford C, Gillman PK. Methylene blue and serotonin toxicity: inhibition of monoamine oxidase A (MAO A) confirms a theoretical prediction. Br J Pharmacol. 2007;152(6):946-951. doi:10.1038/sj.bjp.0707430

4. Schwartz AR, Pizon AF, Brooks DE. Dextromethorphan-induced serotonin syndrome. Clin Toxicol (Phila). 2008;46(8):771-773. doi:10.1080/15563650701668625

5. Thomas CR, Rosenberg M, Blythe V, Meyer WJ 3rd. Serotonin syndrome and linezolid. J Am Acad Child Adolesc Psychiatry. 2004;43(7):790. doi:10.1097/01.chi.0000128830.13997.aa

Summarized & Edited by Jorge Chalit, OMS3

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