Contributor: Aaron Lessen, MD

Educational Pearls:

• Many trauma patients are placed on oxygen via non-rebreather
• A large, multicenter, controlled trial evaluated the outcomes of oxygen administration in trauma patients
• Patients were randomized to two groups
  • 1. 8-hour restrictive oxygen strategy: only receiving oxygen when the patient’s saturation dropped below 94%
    2. 8-hour liberal oxygen strategy: 12-15 liters of oxygen per minute or fraction of inspired oxygen of 0.6-1.0
• The study evaluated rates of death or major respiratory complications at 30 days
• There was no statistical difference between the two groups
  • Therefore, there is no clear benefit to administering liberal amounts of oxygen to trauma patients, but there is also no clear harm
• Ultimately, trauma patients do not need to be on oxygen via non-rebreather unless they are hypoxic or short of breath

References

1. Arleth T, Baekgaard J, Siersma V, et al. Early Restrictive vs Liberal Oxygen for Trauma Patients: The TRAUMOX2 Randomized Clinical Trial. JAMA. 2025;333(6):479-489. doi:10.1001/jama.2024.25786

Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4

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Contributor: Aaron Lessen, MD

Educational Pearls:

• Prehospital seizures are typically managed with intramuscular midazolam (Versed)
• Seizures theoretically involve the NMDA pathway, and ketamine is a potent NMDA antagonist
• A recent retrospective cohort study analyzed a Florida EMS protocol that uses ketamine in seizures refractory to midazolam
  • One group received two doses of midazolam for seizure control
  • The other group received a dose of midazolam followed by a dose of ketamine
• After matching, 82% of the midazolam-only group patients had resolution of convulsions prior to ED arrival
  • 94.4% of patients in the midazolam + ketamine group experienced resolution
  • Absolute difference between groups was 12.4% (95% CI 3.1% to 21.7%)
• Limitations to the study include its prehospital setting and limited long-term follow-up

References

1. Zitek T, Scheppke KA, Antevy P, et al. Midazolam and Ketamine for Convulsive Status Epilepticus in the Out-of-Hospital Setting. Ann Emerg Med. 2025;85(4):305-312. doi:10.1016/j.annemergmed.2024.11.002

Summarized & Edited by Jorge Chalit, OMS4

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Contributor: Alec Coston, MD

Educational Pearls:

For patients presenting to the emergency room with hypertension, clinicians should determine if it is isolated and uncomplicated, or involves comorbidities with more complex underlying pathophysiology.

For uncomplicated and isolated hypertension, first-line treatment is thiazide diuretics.

How do thiazide diuretics work to treat hypertension?

• Thiazide diuretics work by blocking sodium and chloride resorption in the kidneys.
  “Where sodium goes, water follows,” thus promoting diuresis and lowering blood pressure.

Examples of thiazide diuretics and their benefits?

• Hydrochlorothiazide (HCTZ): First-line medication in uncomplicated and chronic hypertensive states. Cheaper and fewer significant adverse effects compared to chlorthalidone.
• HCTZ can be associated with decreased risk of stroke and myocardial infarction.
• However, for more complicated hypertension, especially in the setting of heart failure, Angiotensin Converting Enzyme (ACE) Inhibitors should be considered.

How do ACE Inhibitors manage blood pressure?

• The body’s kidneys drive the Renin-Angiotensin-Aldosterone-System (RAAS) to regulate blood pressure.
• It is easiest to understand RAAS as being pro-hypertensive as a response to decreased renal perfusion. As renal perfusion decreases, renin is released and activates angiotensin I, which is converted by ACE to Angiotensin II, which causes release of aldosterone.
• ACE Inhibitors prevent the conversion of Angiotensin I to Angiotensin II, thus decreasing the kidneys' production of Angiotensin II and Aldosterone levels.

Why, in the context of heart failure, are ACE Inhibitors preferred?

• In heart failure, especially left-sided or left-ventricular heart failure, a vicious cycle can develop wherein the left ventricle fails to perfuse the kidneys due to over-dilation.
• The kidneys are hypoperfused and activate RAAS to try to retain volume and increase peripheral vasoconstriction, promoting renal perfusion.
• The increase in blood pressure puts further strain on the heart, thereby further decreasing cardiac output. The cycle develops, and extremely elevated blood pressures can develop.
• ACE Inhibitors can directly block this cycle, hence their preference in heart failure.

Big takeaway?

• In uncomplicated hypertensive patients, consider thiazide diuretics. When comorbidities, especially heart failure, are introduced, then consider ACE Inhibitors.

References

1. Carey RM, Moran AE, Whelton PK. Treatment of Hypertension: A Review. JAMA. 2022;328(18):1849-1861. doi:10.1001/jama.2022.19590
2. Fan M, Zhang J, Lee CL, Zhang J, Feng L. Structure and thiazide inhibition mechanism of the human Na-Cl cotransporter. Nature. 2023;614(7949):788-793. doi:10.1038/s41586-023-05718-0
3. Hripcsak G, Suchard MA, Shea S, et al. Comparison of Cardiovascular and Safety Outcomes of Chlorthalidone vs Hydrochlorothiazide to Treat Hypertension. JAMA Internal Medicine. 2020;180(4):542-551. doi:10.1001/jamainternmed.2019.7454
4. Yu D, Li JX, Cheng Y, et al. Comparative efficacy of different antihypertensive drug classes for stroke prevention: A network meta-analysis of randomized controlled trials. PLoS One. 2025;20(2):e0313309. doi:10.1371/journal.pone.0313309

Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan & Jorge Chalit, OMS4

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