February 8, 2021

Background: What if we lived in a world where we didn’t call “STEMI alerts”, but instead paged out “OMI alerts”? In the Reperfusion Era of the late 20th century, many large trials showed the benefits of emergent reperfusion therapy, with even greater benefit in the subgroup of patients with undefined ST elevation. As the best idea available, the STEMI-NSTEMI paradigm replaced the Q-wave vs. non-Q-wave MI paradigm in 2000. STEMI-NSTEMI has been a primary determinant of cath lab activations, hospital metrics, and many other patient factors and outcomes. However, the STEMI criteria fail us frequently, missing upwards of 30% of acute coronary occlusion. Additionally, the STEMI/NSTEMI paradigm is dependent on ST segment elevation defined by millimeter criteria, however many occlusion myocardial infarctions (OMI), have no ST segment elevation at all.  To many of us, this idea is not new; we are often taught about STEMI equivalents and “subtle STEMI” that also deserve aggressive management. Over the last 15 years, there has been increased interest in identifying which patients would benefit most from emergent reperfusion therapy. Occlusion myocardial infarction (OMI) vs non-occlusion myocardial infarction (NOMI) is a new paradigm that emerged a few years ago (courtesy of Dr. Stephen Smith, Dr. Pendell Myers, and Dr. Scott Weingart) that might change the way we think about acute myocardial infarction. Their OMI Manifesto is an incredible document (which I highly recommend you read) outlining the historical, clinical, and academic perspectives of why the STEMI-NSTEMI paradigm should be replaced by the OMI-NOMI paradigm. OMI is defined as acute coronary occlusion or near occlusion with insufficient collateral circulation where without emergent catheterization and reperfusion myocardium will undergo necrosis. Patients with OMI are the only ones who benefit from emergent reperfusion therapy, and these patients can present with or without ST elevation on ECG.

November 26, 2020

Background: We have covered tranexamic acid (TXA) on this blog in several posts. Its use has been studied for everything that bleeds from abnormal uterine bleeding to GI hemorrhage and from multisystem trauma to intracranial hemorrhage. While over the past few years it has been touted as the wonderdrug for bleeding, newer research is beginning to challenge that thought (CRASH-3 trial, HALT-IT trial, etc.). The CRASH-2 trial showed that early administration of TXA (within 3 hours) to trauma patients improved all-cause mortality. However, obtaining rapid IV access in low resource, rural, or combat settings can be challenging. Only recently has research been conducted about intramuscular administration of TXA. Actually…we should really say that there has been a resurgence of interest in IM TXA. There were a couple studies published about its pharmacokinetics and pharmacodynamics in the 1970s and 80s, followed by radio silence on the subject.1,2 Curiosity about the drug has picked back up over the past decade as its cost dropped and access to TXA increased exponentially. In fact, finding alternative routes of TXA administration in postpartum hemorrhage is a WHO priority.3 Today, we will review a recent article that explored the pharmacokinetics of intramuscular TXA in bleeding trauma patients.

October 26, 2020

Orbital compartment syndrome (OCS) is a rare, vision-threatening diagnosis that requires rapid identification and immediate treatment for preservation of vision.1-4 As with other compartment syndromes, rapidly increasing and sustained high intraocular pressures (IOP) can result in devastating consequences. OCS causes retinal and optic nerve ischemia due to increased pressure on those structures. Due to the time-sensitive nature of this condition, the emergency physician (EP) plays a critical role in the diagnosis and management of OCS.5 The definitive therapy for this condition is lateral canthotomy and inferior cantholysis (LCIC).
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