Episodes
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Contributor: Taylor Lynch, MD
Educational Pearls:The KLM Flight Disaster, also known as the Tenerife Airport Disaster, occurred on 27 March 1977. It involved the collision of two Boeing 747 passenger jets from KLM and Pan Am Airlines, resulting in 583 fatalities.
What fell through the cracks to cause this incident?
The captain of the KLM flight believed he had received clearance from air traffic control to take off, when in fact he had not. This captain was one of the most senior pilots in the organization, and the culture often saw senior pilots as infallible and not to be questioned. The co-pilot, who noticed improper communication resulting from power dynamics, did not assertively speak up.What lessons can be taken from the tragedy and applied to healthcare?
Aviation and healthcare are both high-stakes industries that require extensive communication for the safety of passengers and patients. Within medicine, an inherent hierarchy exists, and it is crucial not to let this hierarchy and perceived power imbalance prevent people from speaking up. In healthcare, providers such as nurses, paramedics, and technicians may spend more time with patients and thus may notice warning signs earlier. It is imperative to foster a culture where they can speak up freely and without hesitation if something concerning is caught in a patient.When might mistakes happen most often?
Hanna et al. found that radiological interpretation errors were more likely to occur later in shifts, peaking around the 10-to-12-hour mark. Leviatan et al. found that medication prescription errors were more likely to occur by physicians working on 2nd and 3rd consecutive shifts. Hendey et al. found medication ordering errors were higher on overnight and post-call shifts. Gatz et al. found that surgical procedural complication rates are higher during the last 4 hours of a 12-hour shift.In Short, Ends of shifts are when mistakes are most likely to occur.
Overall takeaway?
In a healthcare team, it is critical to look after each other regardless of years of experience or post-nominal letters, and speak up for patient safety. Making a special note that we may need to do so more towards the end of shifts, where we might not be at our sharpest.
References
Gatz JD, Gingold DB, Lemkin DL, Wilkerson RG. Association of Resident Shift Length with Procedural Complications. Journal of Emergency Medicine. 2021 Aug 1;61(2):189–97. Hanna TN, Lamoureux C, Krupinski EA, Weber S, Johnson JO. Effect of Shift, Schedule, and Volume on Interpretive Accuracy: A Retrospective Analysis of 2.9 Million Radiologic Examinations. Radiology. 2018 Apr;287(1):205–12. Hendey GW, Barth BE, Soliz T. Overnight and postcall errors in medication orders. Acad Emerg Med. 2005 Jul;12(7):629–34. Leviatan I, Oberman B, Zimlichman E, Stein GY. Associations of physicians’ prescribing experience, work hours, and workload with prescription errors. J Am Med Inform Assoc. 2021 Jun 12;28(6):1074–80.Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan & Jorge Chalit, OMS4
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Contributor: Aaron Lessen, MD
Educational Pearls:How do we take care of kids in severe pain?
There are many non-pharmacologic options for pain (i.e. ice, elevation) as well as more conventional medication options (i.e. acetaminophen, NSAIDS) but in severe pain stronger medications might be indicated. These stronger medications include options such as IV morphine, a subdissociative dose of ketamine, as well as intranasal fentanyl. Intranasal fentanyl has many advantages: Studies have shown it might be more effective early on in controlling pain, as in the first 15-20 minutes after administration, and then becomes equivalent to other pain control options Total adverse effects were also lower with IN fentanyl, including low rates of nausea and vomiting To administer, use the IV formulation with an atomizer and spray into the nose; therefore, you do not need an IV line Dose is 1-2 micrograms per kilogram, can be redosed once at 10 minutes. Don’t forget about gabapentinoids for neuropathic pain, muscle relaxants for muscle spasms, and nerve blocks when appropriate. (Disclaimer: muscle relaxers have not been well studied in children)References
Alsabri M, Hafez AH, Singer E, Elhady MM, Waqar M, Gill P. Efficacy and Safety of Intranasal Fentanyl in Pediatric Emergencies: A Systematic Review and Meta-analysis. Pediatr Emerg Care. 2024 Oct 1;40(10):748-752. doi: 10.1097/PEC.0000000000003187. Epub 2024 Apr 11. PMID: 38713846. Bailey B, Trottier ED. Managing Pediatric Pain in the Emergency Department. Paediatr Drugs. 2016 Aug;18(4):287-301. doi: 10.1007/s40272-016-0181-5. PMID: 27260499. Hadland SE, Agarwal R, Raman SR, Smith MJ, Bryl A, Michel J, Kelley-Quon LI, Raval MV, Renny MH, Larson-Steckler B, Wexelblatt S, Wilder RT, Flinn SK. Opioid Prescribing for Acute Pain Management in Children and Adolescents in Outpatient Settings: Clinical Practice Guideline. Pediatrics. 2024 Sep 30:e2024068752. doi: 10.1542/peds.2024-068752. Epub ahead of print. PMID: 39344439.Summarized by Jeffrey Olson, MS4 | Edited by Jorge Chalit, OMS4
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Missing episodes?
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Contributor: Travis Barlock, MD
Wheezing is classically heard in asthma and COPD, but it can be the result of a wide range of processes that cause airflow limitation Narrowed bronchioles lead to turbulent airflow → creates the wheezing Crackles (rales) suggest pulmonary edema which is often due to heart failure Approximately 35% of heart failure patients have bronchial edema, which can also produce wheezing COPD and heart failure can coexist in a patient, and both of these diseases can cause wheezing It’s vital to differentiate whether the wheezing is due to the patient’s COPD or their heart failure because the treatment differs Diagnosing wheezing due to heart failure (cardiac asthma): Symptoms: orthopnea, paroxysmal nocturnal dyspnea Diagnostic tools: bedside ultrasound Treatment: diuresis and BiPAP for respiratory support Not all wheezing is asthma Consider heart failure in the differential and tailor treatment accordingly
Educational Pearls:References
1. Buckner K. Cardiac asthma. Immunol Allergy Clin North Am. 2013 Feb;33(1):35-44. doi: 10.1016/j.iac.2012.10.012. Epub 2012 Dec 23. PMID: 23337063.2. Hollingsworth HM. Wheezing and stridor. Clin Chest Med. 1987 Jun;8(2):231-40. PMID: 3304813.
Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3
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Contributor: Jorge Chalit-Hernandez, OMS3
Psychedelics are being studied for their therapeutic effects in mental illnesses, including major depressive disorder, post-traumatic stress disorder, anxiety, and many others Classic psychedelics include compounds like psilocybin, LSD, and ayahuasca MDMA and ketamine are often included in psychedelic research, but have a different mechanism of action than the others Their mechanism of action involves agonism of the 5HT2A receptor, among others Given their resurgence, there is an increase in recreational use of these substances A recent study assessed the risks of recreational users developing subsequent psychotic disorders Individuals who visited the ED for hallucinogen use had a greater risk of being diagnosed with a schizophrenia spectrum disorder in the following 3 years Hazard ratio (HR) of 21.32 After adjustment for comorbid substance use and other mental illness, the hazard ratio was 3.53 - still a significant increase compared with the general population They also found an elevated risk for psychedelics when compared to alcohol (HR 4.66) and cannabis (HR 1.47) The study did not assess whether patients received antipsychotics or other treatments in the ED
Educational Pearls:References
Lieberman JA. Back to the Future - The Therapeutic Potential of Psychedelic Drugs. N Engl J Med. 2021;384(15):1460-1461. doi:10.1056/NEJMe2102835 Livne O, Shmulewitz D, Walsh C, Hasin DS. Adolescent and adult time trends in US hallucinogen use, 2002-19: any use, and use of ecstasy, LSD and PCP. Addiction. 2022;117(12):3099-3109. doi:10.1111/add.15987 Myran DT, Pugliese M, Xiao J, et al. Emergency Department Visits Involving Hallucinogen Use and Risk of Schizophrenia Spectrum Disorder. JAMA Psychiatry. 2025;82(2):142-150. doi:10.1001/jamapsychiatry.2024.3532Summarized & Edited by Jorge Chalit, OMS3
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Contributor: Ricky Dhaliwal, MD
Educational Pearls:What factors are considered in a COVID-19 infection?
The viral load: Understood as the impact of SARS-CoV-2 viral particles infecting host cell tissue itself (utilizing ACE-2 receptors). Pro-Inflammatory Response: Post-infection, the body's downstream systemic cytokine release (can be both normal or hyperactive, aka “cytokine storm”).What cardiac impacts have been observed with COVID-19?
Arrhythmias: The mechanism of COVID-19 infection and arrhythmias is believed to be multifactorial. However, evidence suggests T-cell-mediated toxicity and cytokine storm may contribute to cardiac myocyte damage, precipitating proarrhythmias instead of direct viral entry. Bradycardia: Increased prevalence in patients with severe COVID-19 infection, but not associated with increased adverse outcomes. Atrial Fibrillation: Most common cardiac complication and risk factor for worsened outcomes in patients with COVID-19. Biggest associated risk is strokes, and may require heightened monitoring and anticoagulation therapy to mitigate stroke risk. Fibrosis of Cardiac Tissue: Similar to arrhythmias, believed to be inflammation-mediated in COVID-19. Fibrosis of cardiac tissue increases the risk that any arrhythmias that develop during infection may persist after the infection has resolved. Ventricular damage: Also inflammation mediated by an active infection and contributes to myocarditis. No evidence suggests that COVID-19 vaccination contributes to myocarditis. Sinus node dysfunction induced by inflammation that may lead to or be similar to Postural Orthostatic Tachycardia Syndrome (POTS).Big takeaway?
Patients who have had or currently have COVID-19 are at an increased risk of developing arrhythmias and sustaining them post-infection. However, a majority of patients will recover. Due to atrial fibrillation being the most prevalent arrhythmia associated with COVID-19 infection, increased monitoring and potential anticoagulation therapy are required.References
Gopinathannair R, Olshansky B, Chung MK, Gordon S, Joglar JA, Marcus GM, et al. Cardiac Arrhythmias and Autonomic Dysfunction Associated With COVID-19: A Scientific Statement From the American Heart Association. Circulation. 2024 Nov 19;150(21):e449–65. Khan Z, Pabani UK, Gul A, Muhammad SA, Yousif Y, Abumedian M, et al. COVID-19 Vaccine-Induced Myocarditis: A Systemic Review and Literature Search. Cureus. 14(7):e27408.Summarized by Dan Orbidan, OMS1 | Edited by Dan Orbidan & Jorge Chalit, OMS3
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Contributor: Aaron Lessen, MD
Educational Pearls:
What is a Rescue Inhaler?
A rescue inhaler is a medication for people with asthma to quickly reverse the symptoms of an asthma attack.
Historically albuterol (Short Acting Beta Agonist (SABA)) monotherapy has been the mainstay rescue inhaler. This is because albuterol works fast and is relatively cheap. \n\n
What are Combination Rescue Inhalers?
Combination rescue inhalers contain a fast-acting bronchodilator as well as an inhaled corticosteroid (ICS)
The steroid helps to reduce some of the chronic airway inflammation that is worsening the asthma attack and can help to prevent future attacks
Examples include budesonide-formoterol and albuterol-budesonide
Global Initiative for Asthma (GINA), states that combination therapy is now the preferred reliever for adults and adolescents with mild asthma
What are the drawbacks of Combination Rescue Inhalers?
These inhalers are generally more expensive than just using a SABA inhaler which can be a barrier for some people \n\n
Improper use can also lead to conditions like thrush due to the addition of the steroid
References
Krings JG, Beasley R. The Role of ICS-Containing Rescue Therapy Versus SABA Alone in Asthma Management Today. J Allergy Clin Immunol Pract. 2024 Apr;12(4):870-879. doi: 10.1016/j.jaip.2024.01.011. Epub 2024 Jan 17. PMID: 38237858; PMCID: PMC10999356.
Papi A, Chipps BE, Beasley R, Panettieri RA Jr, Israel E, Cooper M, Dunsire L, Jeynes-Ellis A, Johnsson E, Rees R, Cappelletti C, Albers FC. Albuterol-Budesonide Fixed-Dose Combination Rescue Inhaler for Asthma. N Engl J Med. 2022 Jun 2;386(22):2071-2083. doi: 10.1056/NEJMoa2203163. Epub 2022 May 15. PMID: 35569035.
Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 \n\n
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Contributor: Geoff Hogan MD
Educational Pearls:
Penicillin allergies are relatively uncommon despite their frequent reports
10% of the population reports a penicillin allergy but only 5% of these cases are clinically significant
90-95% of patients may tolerate a rechallenge after appropriate allergy evaluation
Penicillin Allergy Decision Rule (PEN-FAST) on MD Calc
Useful tool to assess patients for penicillin allergies
Five years or less since reaction = 2 points (even if unknown)
Anaphylaxis or angioedema OR Severe cutaneous reaction = 2 points
Treatment required for reaction (e.g. epinephrine) = 1 point (even if unknown)
A score of 0 on PEN-FAST indicates a less than 1% risk of a positive penicillin allergy test
A score of 1 or 2 indicates a 5% risk of a positive penicillin allergy test
A low score on PEN-FAST should prompt clinicians to proceed with the best empiric antibiotic for the patient’s infection
References
Broyles AD, Banerji A, Barmettler S, et al. Practical Guidance for the Evaluation and Management of Drug Hypersensitivity: Specific Drugs [published correction appears in J Allergy Clin Immunol Pract. 2021 Jan;9(1):603. doi: 10.1016/j.jaip.2020.10.025.] [published correction appears in J Allergy Clin Immunol Pract. 2021 Jan;9(1):605. doi: 10.1016/j.jaip.2020.11.036.]. J Allergy Clin Immunol Pract. 2020;8(9S):S16-S116. doi:10.1016/j.jaip.2020.08.006
Piotin A, Godet J, Trubiano JA, et al. Predictive factors of amoxicillin immediate hypersensitivity and validation of PEN-FAST clinical decision rule [published correction appears in Ann Allergy Asthma Immunol. 2022 Jun;128(6):740. doi: 10.1016/j.anai.2022.04.005.]. Ann Allergy Asthma Immunol. 2022;128(1):27-32. doi:10.1016/j.anai.2021.07.005
Shenoy ES, Macy E, Rowe T, Blumenthal KG. Evaluation and Management of Penicillin Allergy: A Review. JAMA. 2019;321(2):188-199. doi:10.1001/jama.2018.19283
Trubiano JA, Vogrin S, Chua KYL, et al. Development and Validation of a Penicillin Allergy Clinical Decision Rule. JAMA Intern Med. 2020;180(5):745-752. doi:10.1001/jamainternmed.2020.0403
Summarized & edited by Jorge Chalit, OMS3
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Contributor: Travis Barlock, MD
Educational Pearls:
Key clinical considerations when managing heart transplant patients due to their unique pathophysiology
1. Arrhythmias
A transplanted heart is denervated, meaning it lacks autonomic nervous system innervation
The lack of vagal tone results in an increased resting heart rate
Adenosine can be used since it primarily slows conduction through the AV node
Atropine is ineffective in treating transplant bradyarrhythmia because its mechanism is to inhibit the vagus nerve - but the heart lacks vagal tone
Allograft rejection can also cause tachycardia
Consult transplant surgery - treatment is usually 500 mg methylprednisolone
2. Rejection
Transplant patients are administered immunosuppressants
Clinical presentation of acute rejection looks similar to heart failure with increased BNP, increased troponin, and pulmonary edema
Cardiac allograft vasculopathy is a form of chronic rejection
Patients will not report chest pain due to denervated heart
Symptoms are usually weakness and fatigue
3. High risk of infection due to immunosuppression
Increased risk of infections which includes CMV, legionella, tuberculosis, etc
Immunosuppressants have side effects such as acute kidney injury or pancytopenia
4. Radiographic Cardiomegaly
A study found that radiographic cardiomegaly does not connote heart failure
They hypothesized it is instead the result of a mismatch between the size of the transplanted heart and the space in the thoracic cavity
References
Murphy JD, Mergo PJ, Taylor HM, Fields R, Mills RM Jr. Significance of radiographic cardiomegaly in orthotopic heart transplant recipients. AJR Am J Roentgenol. 1998 Aug;171(2):371-4. doi: 10.2214/ajr.171.2.9694454. PMID: 9694454.
Park MH, Starling RC, Ratliff NB, McCarthy PM, Smedira NS, Pelegrin D, Young JB. Oral steroid pulse without taper for the treatment of asymptomatic moderate cardiac allograft rejection. J Heart Lung Transplant. 1999 Dec;18(12):1224-7. doi: 10.1016/s1053-2498(99)00098-4. PMID: 10612382.
Pethig K, Heublein B, Wahlers T, Dannenberg O, Oppelt P, Haverich A. Mycophenolate mofetil for secondary prevention of cardiac allograft vasculopathy: influence on inflammation and progression of intimal hyperplasia. J Heart Lung Transplant. 2004 Jan;23(1):61-6. doi: 10.1016/s1053-2498(03)00097-4. PMID: 14734128.
Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3
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Contributor: Taylor Lynch, MD
Educational Pearls:
Pediatric febrile seizures are defined as seizures that occur between the ages of six months to five years in the presence of a fever greater than or equal to 38.0 ºC (100.4 ºF). It is the most common pediatric convulsive disorder, with an incidence between 2-5%
What are the types of seizures?
Simple: Tonic-clonic seizure, duration 15 minutes, requires medication to stop the seizing, multiple occurrences in a 24-hour period, PRESENCE of focal features, PRESENCE of Todd’s paralysis
What are the causes?
Caused by infectious agents leading to fever. Seen with common childhood infections.
It is debated whether the absolute temperature of the fever or the rate of change of temperature incites the seizure, but current evidence points to the rate of change of the temperature being the primary catalyst
What are the treatment considerations?
For simple febrile seizures, work-up is similar to any pediatric patient presenting with a fever between the ages of six months and five years
Thorough physical exam to rule out any potential of meningeal or intracranial infections
Prophylactic antipyretics are not believed to prevent the occurrence of febrile seizures
Disposition?
If the patient has returned to normal baseline behavior following a simple febrile seizure, and the physical exam is reassuring, the patient can be discharged home.
Additional labs, electroencephalogram, or lumbar punctures are not indicated in simple febrile seizures as long as the physical exam is completely normal
Any evidence of a complex seizure requires further workup
Fast Facts:
Patients with a familial history of febrile seizures and developmental delays have a higher risk of developing febrile seizures
If a child has one febrile seizure, there is a 30-40% chance of another febrile seizure by age 5
Only 2-7% of children with febrile seizures go on to develop epilepsy
References:
1. Berg AT, Shinnar S, Hauser WA, Alemany M, Shapiro ED, Salomon ME, et al. A prospective study of recurrent febrile seizures. N Engl J Med. 1992 Oct 15;327(16):1122–7.
2. Schuchmann S, Vanhatalo S, Kaila K. Neurobiological and physiological mechanisms of fever-related epileptiform syndromes. Brain Dev. 2009 May;31(5):378–82.
3. Nilsson G, Westerlund J, Fernell E, Billstedt E, Miniscalco C, Arvidsson T, et al. Neurodevelopmental problems should be considered in children with febrile seizures. Acta Paediatr. 2019 Aug;108(8):1507–14.
4. Subcommittee on Febrile Seizures, American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011 Feb;127(2):389–94.
5. Pavlidou E, Panteliadis C. Prognostic factors for subsequent epilepsy in children with febrile seizures. Epilepsia. 2013 Dec;54(12):2101–7.
6. Huang CC, Wang ST, Chang YC, Huang MC, Chi YC, Tsai JJ. Risk factors for a first febrile convulsion in children: a population study in southern Taiwan. Epilepsia. 1999 Jun;40(6):719–25.
7. Hashimoto R, Suto M, Tsuji M, Sasaki H, Takehara K, Ishiguro A, et al. Use of antipyretics for preventing febrile seizure recurrence in children: a systematic review and meta-analysis. Eur J Pediatr. 2021 Apr;180(4):987–97.
Summarized by Dan Orbidan, OMS1 | Edited by Dan Orbidan & Jorge Chalit, OMS3
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Contributor: 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
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Contributor: 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
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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
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
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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
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
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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
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
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
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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
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.
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
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
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
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
Administer ODT Ondansetron (Zofran) to prevent vomiting
Meta-analysis showed that 2-8 mg orally, based on body weight, decreased vomiting quickly
Wait 15-20 minutes for the medication to take effect
Use streamlined method for oral rehydration: Fluids such as over-the-counter Pedialyte, Infalyte, Rehydrate, Resol, and Naturalyte may be used
If patient weighs less than 10kg: administer 5mL of fluid per minute for 20 minutes
If patient weighs 10kg or more: administer 10mL of fluid for 20 minutes
If the patient can keep the fluid down, double the fluid volume and repeat
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
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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