Faculty Bibliography

Introduction: Carbon monoxide exposure is a relatively unknown risk of smoking hookah. Dozens of cases of hookah-associated carbon monoxide toxicity have been described over the past decades, but smoking hookah is generally perceived as safe. Only recently have larger series of hookah-associated carbon monoxide toxicity been published. This study evaluates the incidence of hookah-associated carbon monoxide toxicity over 4 years, and compares the exposures from hookah against other carbon monoxide sources.Methods: This is a retrospective cohort study of all patients with carbon monoxide toxicity referred for hyperbaric oxygen therapy at an urban hyperbaric oxygen referral center from January 2015 through December 2018. Cases of hookah-associated carbon monoxide toxicity were compared to patients exposed to other carbon monoxide sources, with an analysis of patient comorbidities, symptomatology, and laboratory evaluation.Results: Over a 48-month period, 376 patients underwent hyperbaric oxygen therapy for carbon monoxide exposure. After exclusions, 265 patients with carbon monoxide toxicity from various sources were analyzed. There were 58 patients with hookah-associated carbon monoxide toxicity (22%). The proportion of hookah-associated carbon monoxide cases increased markedly in the latter years: 2015: 9.5%, 2016: 8.6%, 2017: 24.1%, 2018 41.6%. In the final 2 years analyzed, hookah smoking was the most frequent source of carbon monoxide toxicity referred for therapy. Hookah-associated carbon monoxide patients were younger(28.1 vs. 45.0 years, mean difference 16.8 years, 95% confidence interval: 11.5, 22.1 years, p < 0.001) and more likely to be female (60% vs. 46.6%, p = 0.06) than patients exposed to other carbon monoxide sources. The mean difference in carboxyhemoglobin concentration between hookah associated and those exposed to other carbon monoxide sources was 4.6% (mean 20.1% vs. 24.6%, 95%CI: 1.7, 7.5, p = 0.002).Conclusion: A substantial portion of patients with severe carbon monoxide toxicity was exposed through smoking hookah. The incidence of hookah-related carbon monoxide toxicity appears to be increasing.

INTRODUCTION/BACKGROUND:Hypoglycemia is a common adverse effect when intravenous (IV) insulin is administered for hyperkalemia. A prolonged infusion of dextrose 10% (D10) may mitigate hypoglycemia compared to dextrose 50% (D50) bolus. Our objective was to evaluate whether D10 infusion is a safe and effective alternative to D50 bolus for hypoglycemia prevention in hyperkalemic patients receiving IV insulin. METHODS: > 5.5) and received IV insulin and D10 infusion or D50 bolus within 3 h. The primary endpoint was incidence of hypoglycemia, defined as blood glucose (BG) ≤ 70 mg/dL, in the 24 h following IV insulin administration for hyperkalemia. RESULTS:A total of 134 patients were included; 72 in the D50 group and 62 in the D10 group. There was no difference in incidence of hypoglycemia between the D50 and D10 groups (16 [22%] vs. 16 [26%], p = 0.77). Symptomatic hypoglycemia, severe hypoglycemia, and hyperglycemia rates in the D50 and D10 groups were [5 (7%) vs. 2 (3%), p = 0.45], [5 (7%) vs. 1 (2%), p = 0.22], and [34 (47%) vs. 23 (37%), p = 0.31] respectively. Low initial BG was a predictor for developing hypoglycemia. CONCLUSIONS:In our study, D10 infusions appeared to be at least as effective as D50 bolus in preventing hypoglycemia in hyperkalemic patients receiving IV insulin. In context of ongoing D50 injection shortages, D10 infusions should be a therapeutic strategy in this patient population.

OBJECTIVE. The purpose of this study is to assess the perceptions of radiologists and emergency medicine (EM) providers regarding the quality, value, and challenges associated with using outside imaging (i.e., images obtained at facilities other than their own institution). MATERIALS AND METHODS. We surveyed radiologists and EM providers at a large academic medical center regarding their perceptions of the availability and utility of outside imaging. RESULTS. Thirty-four of 101 radiologists (33.6%) and 38 of 197 EM providers (19.3%) responded. A total of 32.4% of radiologists and 55.3% of EM providers had confidence in the quality of images from outside community facilities; 20.6% and 44.7%, respectively, had confidence in the interpretations of radiologists from these outside facilities. Only 23.5% of radiologists and 5.3% of EM physicians were confident in their ability to efficiently access reports (for outside images, 47.1% and 5.3%). Very few radiologists and EM providers had accessed imaging reports from outside facilities through an available stand-alone portal. A total of 40.6% of radiologists thought that outside reports always or frequently reduced additional imaging recommendations (62.5% for outside images); 15.6% thought that reports changed interpretations of new examinations (37.5% for outside images); and 43.8% thought that reports increased confidence in interpretations of new examinations (75.0% for outside images). A total of 29.4% of EM providers thought that access to reports from outside facilities reduced repeat imaging (64.7% for outside images), 41.2% thought that they changed diagnostic or management plans (50.0% for outside images), and 50.0% thought they increased clinical confidence (67.6% for outside images). CONCLUSION. Radiologists and EM providers perceive high value in sharing images from outside facilities, despite quality concerns. Substantial challenges exist in accessing these images and reports from outside facilities, and providers are unlikely to do so using separate systems. However, even if information technology solutions for seamless image integration are adopted, providers' lack of confidence in outside studies may remain an important barrier.

Objective: Ranolazine is an antianginal drug, used for chronic angina refractory to first line agents. In oral therapeutic doses, the time to peak plasma concentration is 2-5 hours, with a halflife of 7 hours. High oral doses can produce dizziness, nausea, and vomiting. Ranolazine affects cardiac conduction in multiple ways. It inhibits the late phase of the inward sodium current in myocardial cells. This current exchanges Ca2+ via a Na+/Ca2+ antiporter, which causes calcium-induced calcium release from the sarcoplasmic reticulum. Thus, ranolazine indirectly acts as a calcium channel blocker. Ranolazine also inhibits the delayed rectifier potassium current (hERG) causing QT prolongation. In cellular models, ranolazine blocks neuronal sodium channels. This may underlie the occurrence of seizures reported in overdose. Few reports of ranolazine overdoses exist, limiting definitive management recommendations. We present a case report of a fatal ranolazine overdose. Case report: A 67-year-old man with a past medical history of hypertension, coronary artery disease, chronic angina, and schizophrenia presented to the emergency department with a complaint of emesis. He reported ingesting approximately 30 g of extended-release ranolazine several hours prior in a suicide attempt. Physical examination demonstrated an alert male in no acute distress. Vitals signs were: blood pressure 160/87 mmHg; heart rate 72 beats/min; respiratory rate 18 breaths/minute; and pulse oximetry 99% (room air). An electrocardiogram (ECG) showed normal sinus rhythm (73 beats/minute), QTC 434ms and QRS 96 ms. Laboratory analysis showed normal electrolytes, renal and hepatic function. Acetaminophen, ethanol, and salicylate concentrations were undetectable. Seven hours after presentation, he developed acute altered mental status with confusion. The ECG showed a first-degree atrioventricular block at 66 beats/minute; PR, 220 ms; QRS 108 ms; and QTC, 450 ms. Nine hours after presentation, three convulsive episodes occurred, each lasting several minutes, before spontaneously resolving. Shortly thereafter, he developed pulseless electrical activity for 20 minutes, followed by ventricular tachycardia, and ultimately asystole. He received defibrillation, continuous cardiopulmonary resuscitation, and advanced cardiac life support, but resuscitation was unsuccessful. An ante-mortem serum ranolazine concentration was 12 mg/L (therapeutic 0.4-6.1mg/L). Ranolazine is primarily metabolized by CYP3A and CYP2D6. The contributions of his home medications atorvastatin, clonazepam, and clopidogrel (CYP3A substrates) to his clinical picture are unknown.
Conclusion(s): Based on limited literature reports and this case, ranolazine overdose can cause severe morbidity and delayed mortality, despite initial apparent clinical stability. Patients with ranolazine overdose should be closely monitored for rapid cardiac and neurologic decompensation along with potential consideration for extracorporeal life support (ECLS)

Objective: We present a patient who developed prolonged coma following treatment of ethanol withdrawal with large doses of diazepam and demonstrated prolonged elimination toxicokinetics. Case report: A 68-year-old man who drank 5-6 alcoholic beverages/day was admitted for an elective transcatheter aortic valve replacement. Two days post-procedure, he developed agitation and was presumptively treated for ethanol withdrawal with diazepam (470 mg IV over 24 hours). He remained comatose for four days prompting a toxicology consult. On day 7 of persistent coma from presumed benzodiazepine excess, flumazenil (0.5 mg) was administered; he opened his eyes for the first time, began speaking, and answering simple questions, but 30 minutes later was comatose again. Flumazenil infusion 0.25mg/h was trialed with unclear effect. His hospitalization was complicated by gastrointestinal bleeding and mild ischemic stroke deemed noncontributory to his clinical status. The flumazenil infusion was discontinued 1 week later. His evaluation was extensive (brain magnetic resonance imaging and computerised tomography, lumbar puncture, and blood cultures) and unremarkable. On hospital week 4, he became only gradually more awake, and was eventually discharged to a rehabilitation facility on hospital week 6, awake, conversive but still confused. Six weeks later, he was discharged home fully recovered. He remains amnestic to his hospitalization. Serum diazepam and nordiazepam concentrations were determined via liquid-chromatography mass-spectrometry. Concentrations obtained four days after the last dose were: diazepam 963 mug/L (therapeutic: 200-1000 mug/L) and nordiazepam 240 mug/L (therapeutic: 100-1500 mug/L). Elimination kinetics were calculated with apparent half-lives of 294 hours and 797 hours for diazepam and nordiazepam, respectively. Genotyping of CYP3A4 and CYP2C19, the two primary metabolizers of diazepam, demonstrated no abnormalities.
Conclusion(s): Diazepam demonstrated extremely atypical elimination kinetics despite normal renal and hepatic function. Acute tolerance which is expected after prolonged benzodiazepine exposure was not clearly demonstrated. The relationship between his serum concentration and clinical status is unclear at this time

PURPOSE/OBJECTIVE:The aim of this study was to determine rates of and possible reasons for guideline-discordant ordering of CT pulmonary angiography for the evaluation of suspected pulmonary embolism (PE) in the emergency department. METHODS:A retrospective review was performed of 212 consecutive encounters (January 6, 2016, to February 25, 2016) with 208 unique patients in the emergency department that resulted in CT pulmonary angiography orders. For each encounter, the revised Geneva score and two versions of the Wells criteria were calculated. Each encounter was then classified using a two-tiered risk stratification method (PE unlikely versus PE likely). Finally, the rate of and possible explanations for guideline-discordant ordering were assessed via in-depth chart review. RESULTS:The frequency of guideline-discordant studies ranged from 53 (25%) to 79 (37%), depending on the scoring system used; 46 (22%) of which were guideline discordant under all three scoring systems. Of these, 18 (39%) had at least one patient-specific factor associated with increased risk for PE but not included in the risk stratification scores (eg, travel, thrombophilia). CONCLUSIONS:Many of the guideline-discordant orders were placed for patients who presented with evidence-based risk factors for PE that are not included in the risk stratification scores. Therefore, guideline-discordant ordering may indicate that in the presence of these factors, the assessment of risk made by current scoring systems may not align with clinical suspicion.