Synthetic Cannabinoids, a NEW Problem

Image Credit: Image from
Lance Cpl. Damany S. Coleman

This post was peer reviewed.
Click to learn more.

   Author: Nishma Sachedina, MD
   Emergency Medicine Resident
   University of Chicago
   AAEM/RSA Publications Committee Member

In the 1980s, scientists developed synthetic cannabinoids as a means to study the endocannabinoid system.[1,2] While some earnest chemists characterized cannabinoid receptors, more entrepreneurial chemists created a novel market of NEW drugs—nontraditional emerging web-based drugs.[3] Synthetic cannabinoids (SCs) are one varietal of these NEW drugs, and their use has been growing exponentially since they were first recognized as drugs of abuse in Europe in 2000.[4]

When SCs came to the USA in 2008, they flourished because of a lack of legislation against them and because they evaded standard medical toxicology screening tests.[1] Sold over the internet, in head shops, and in even in gas stations and convenient stores, SCs are often marketed as “legal highs.”[1] They can be consumed in a number of ways, from adding the compound to plant materials to dissolving the compounds in liquid for use in e-cigarettes or beverages.

Ocular Emergency: Chemical Burns, A Non-Ophthalmologist Approach to Initial Treatment and Referral

Image from Maxxl2 - Wikimedia Commons

This post was peer reviewed.
Click to learn more.

Author: 
Fernando Pellerano, MS-V Universidad Iberoamericana (UNIBE) School of Medicine

Chemical burns represent potentially blinding ocular injuries and constitute a true ocular emergency requiring immediate assessment and initiation of treatment. The sequelae of an ocular burn can be severe and particularly challenging to manage. An appropriate initial emergency management may be the most important factor in determining visual outcome.[1]

Chemical eye injuries can occur from any exogenous material contacting the eye. This includes alkalis (e.g., lye, cements, plasters, airbag powder, bleach, and ammonia), acids (e.g., battery acid, pool cleaner, and vinegar), solvents, detergents, and irritants (e.g., mace).[2] Severity of the eye injury depends on the pH, concentration, and the nature of the chemical.

TXA Literature Review

Author: Alexandra Murray, DO PGY1
Mercy St. Vincent Medical Center Emergency Medicine

Originally Published: Modern Resident - December-January 2016

What is tranexamic acid (TXA)?
When the body experiences vascular injury, the hemostatic system tries to maintain circulation by balancing the formation and degradation of blood clots. In response to severe blood loss, this balance is challenged and hyper-fibrinolysis can occur. The conversion of plasminogen to plasmin plays a large role in fibrin binding and degradation. Tranexamic acid is a synthetic derivative of lysine that reversibly blocks binding sites on plasminogen and inhibits fibrinolysis.[1] TXA has been approved by the FDA since 1986 as an antifibrinolytic and has been marketed for menorrhagia (Lysteda) and dental hemorrhage in hemophiliacs (Cyklokapron).[2,3] More recently, TXA has been investigated as a treatment for posttraumatic hemorrhage, postpartum hemorrhage and prevention of surgical blood loss.

Diphenhydramine Overdose in the ED

Image Credit: Flickr Andrew Ranta

Author: Kaylinn Dokken, OMSIV
Western University of Health Sciences

You are just at the beginning of your shift when paramedics call in and notify you that they are bringing in a 35 year old female who reports that she took 3,000 mg of diphenhydramine in a suicide attempt. Her BP is 145/80, her pulse is 160 beats per minute (bpm) with sinus tachycardia on the monitor, and her respiratory rate is 24 breaths per minute. Upon presentation, the patient is disoriented, continuously writhing, and having intermittent myoclonic jerks. An initial EKG is obtained and is shown below.

Expanding the Differential: What Else Can an Elevated Troponin Signify?

Author: Shyam Sivasankar, MD
Stanford-Kaiser Emergency Medicine

Originally Published: Modern Resident, December-January 2015

We often underestimate the utility of modern laboratory technology—we become shortsighted and we forget that a lab value can tell us more than what we are naturally used to it representing. One such lab value is cardiac troponin.

Instinctively, we assume that an elevated troponin is a sign of a myocardial infarction (MI), but that is not always the case. Troponin is released by cardiac muscle fibers in the setting of irreversible cell injury.

Occasionally, we can be fooled into thinking that all chest pain with an elevated troponin is a definitive diagnosis of MI, but other life-threatening causes of chest pain such as pulmonary embolism (PE) or aortic dissection can also present with an elevated troponin. The ‘troponin leak’ from PE results from right-sided heart strain and from direct myocardial injury in dissection. Elevated troponin can also be seen in pericarditis (which can also present with ST segment changes), myocarditis, blunt chest trauma and arrhythmias. Patients who have suffered from cardiac arrest and undergone CPR can also have elevated troponin levels.