Comparing the Effectiveness of a Virtual Toxicology Escape Room at Two Emergency Medicine Residencies.

Introduction Physical distancing guidelines during the coronavirus disease 2019 (COVID-19) pandemic forced medical residency programs to move a large portion of required didactics to virtual settings. Toxicology, a core component of emergency medicine (EM) education, was forced to adapt to similar constraints. An in-person escape room style puzzle was modified to a virtual format for educational purposes, and shared with and evaluated by two different residency programs. Materials and methods A virtual escape room, "Escape the Toxin: Online!" was created to test knowledge of toxicologic ingestion and antidote utilizing Google Forms and delivered using Zoom teleconference software to two EM residency programs in the Philadelphia region. After small groups completed the gamified activity, their scores were calculated and they completed an anonymous evaluation. Results Residents at the program where a Medical Toxicology fellowship is located found the virtual escape room to be more effective and enjoyable compared to the second program. Despite some differences in perceived effectiveness, the majority of participants were able to correctly solve the puzzle and get to the antidote. Conclusion The majority of learners who participated from both residencies agreed that they would recommend this virtual program to other EM residents.

Double-blind, Randomized, Placebo-controlled Study Evaluating the Use of Platelet-rich Plasma Therapy (PRP) for Acute Ankle Sprains in the Emergency Department.

BACKGROUND: Over 23,000 people per day require treatment for ankle sprains. Platelet-rich plasma (PRP) is an autologous concentration of platelets that is thought to improve healing by promoting inflammation through growth factor and cytokine release. Studies to date have shown mixed results, with few randomized trials. OBJECTIVES: To determine patient function among patients randomized to receive standard therapy plus PRP, compared to patients who receive standard therapy plus sham injection (placebo). METHODS: Prospective, randomized, double-blinded, placebo-controlled trial. Patients with severe ankle sprains were randomized. Severity was graded on degree of swelling, ecchymosis, and ability to bear weight. PRP with lidocaine and bupivacaine was injected at the point of maximum tenderness by a blinded physician under ultrasound guidance. The control group was injected in a similar fashion with sterile 0.9% saline. Both groups had visual analog scale (VAS) pain scores and Lower Extremity Functional Scale (LEFS) on days 0, 3, and 8. LEFS and a numeric pain score were obtained via phone call on day 30. All participants were splinted, given crutches, and instructed to not bear weight for 3 days; at this time patients were reevaluated. RESULTS: There were 1156 patients screened and 37 were enrolled. Four withdrew before PRP injection was complete; 18 were randomized to PRP and 15 to placebo. There was no statistically significant difference in VAS and LEFS scores between groups. CONCLUSION: In this small study, PRP did not provide benefit in either pain control or function over placebo.

Pharmacobezoars described and demystified.

INTRODUCTION: A bezoar is a concretion of foreign material that forms and persists in the gastrointestinal tract. Bezoars are classified by their material origins. Phytobezoars contain plant material, trichobezoars contain hair, lactobezoars contain milk proteins, and pharmacobezoars contain pharmaceutical products. Tablets, suspensions, and even insoluble drug delivery vehicles can, on rare occasions, and sometimes under specific circumstances, form pharmacobezoars. The goal of this review is to catalog and examine all of the available reports in the English language medical literature that convincingly describe the formation and management of pharmacobezoars. METHODS: Articles included in this review were identified by performing searches using the terms "bezoar," "pharmacobezoar," and "concretion" in the following databases: OVID MEDLINE, PubMed, and JSTOR. The complete MEDLINE and JSTOR holdings were included in the search without date ranges. The results were limited to English language publications. Articles that described nonmedication bezoars were not included in the review. Articles describing phytobezoars, food bezoars, fecal impactions, illicit drug packet ingestions, enteral feeding material bezoars, and hygroscopic diet aid bezoars were excluded. The bibliographic references within the articles already accumulated were then examined in order to gather additional pharmacobezoar cases. The cases are grouped by pharmaceutical agent that formed the bezoar, and groupings are arranged in alphabetical order. Discussions and conclusions specific to each pharmaceutical agent are included in that agent's subheading. DISCUSSION: Patterns and themes that emerged in the review of the assembled case reports are reviewed and presented in a more concise format. CONCLUSION: Pharmacobezoars form under a wide variety of circumstances and in a wide variety of patients. They are difficult to diagnose reliably. Rules for suspecting, diagnosing, and properly managing a pharmacobezoar are highly dependent on the pharmaceutical agent or agents involved. Becoming familiar with the sparse data available on pharmacobezoars and maintaining a high index of suspicion in future clinical encounters may be the best way to improve diagnostic sensitivity and accuracy.

Mutism and persistent dysarthria due to tacrolimus-based immunosuppression following allogeneic liver transplantation.

Tacrolimus is a potent immunosuppressant medication with a low therapeutic index. We report a case of mutism with persistent dysarthria in a patient receiving tacrolimus-based immunosuppression following allogeneic liver transplantation. A 59-year-old female patient with end-stage liver disease secondary to primary sclerosing cholangitis underwent successful allogeneic liver transplantation. The patient was started on tacrolimus for prevention of allograft rejection and subsequently developed complete mutism. Following consultation of the medical toxicology service, tacrolimus was discontinued and the patient's mutism gradually improved. However, the patient still has moderate dysarthria more than 2 years after tacrolimus discontinuation. The Naranjo probability scale revealed a probable adverse reaction of mutism and dysarthria associated with tacrolimus therapy. Mutism is an uncommon complication of calcineurin inhibitors. Both cyclosporine and tacrolimus have been associated with mutism, though mutism may be more common in patients treated with tacrolimus. The mechanism of injury has not been delineated, although liver transplant patients and patients with preexisting hepatic encephalopathy or neurologic disease may be at increased risk for this complication. The mainstay of treatment is tacrolimus dose reduction or discontinuation, although benzodiazepine therapy may be beneficial in the treatment of this disorder. Clinicians should be aware of the potential adverse effects associated with calcineurin inhibitor toxicity in transplant patients and should advocate for aggressive and rapid treatment of this serious adverse drug effect.

Survival of acute myeloid leukemia cells requires PI3 kinase activation.

The mechanisms that regulate the growth and survival of acute myeloid leukemia (AML) cells are largely unknown. We hypothesized that constitutive activation of phosphatidyl-inositide 3 kinase (PI3 kinase) could regulate survival in primary cells from patients with AML. Here we demonstrate that Akt, a critical substrate of PI3 kinase, is activated in AML blasts. In a short-term culture system, most AML patient samples showed a dose-dependent decrease in survival after incubation with the PI3 kinase inhibitor LY294002. This decrease in survival was partially due to the induction of apoptosis. Furthermore, we have shown that p70 S6 kinase and 4EBP-1, downstream mediators of Akt signaling, also are phosphorylated in AML blasts. Phosphorylation of these proteins is inhibited by the mTOR inhibitor RAD001. Incubation of AML blasts with RAD001 induces only a small decrease in survival of the cells; however, when combined with Ara-C, RAD001 enhances the toxicity of Ara-C. These results demonstrate that constitutive activation of the PI3 kinase pathway is necessary for the survival of AML blasts and that targeting of this pathway with pharmacologic inhibitors may be of clinical benefit in treatment of AML.