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Objectives: To determine if emergency physicians' (EP) use droperidol has changed since the United States Food and Drug Administration (FDA) warning of December 2001 concerning QT interval prolongation, torsade de pointes, and sudden death; and to query EP opinions regarding droperidol before and after the FDA warning and regarding potential alternative drugs. Methods: An internet-based survey was designed with questions regarding droperidol use in the emergency department (ED). Data collected included EP demographics, use of droperidol before and after the FDA warning, use of alternative drugs, and incidence of arrhythmias. A representative sample of EPs were contacted by e-mail and asked to complete the survey. Results: A total of 2,000 e-mails resulted in 506 (25%) completed surveys. There was no second mailing. Responders' average years practicing was 12.6 +_ 9.2. EP responders worked in private/community (n=278, 55%), academic/county (n=187, 37%), and HMO (n=41,8%) hospitals. The majority (n=455, 90%) used droperidol and were aware of the FDA warning (n=460, 91%). Droperidol was no longer available at 122 (24%) of the respondents' EDs as a result of the FDA warning. Prior to the FDA warning, EPs who had used droperidol used it as an antiemetic (n=408, 90%), for control of agitation (n=330, 73%), for treatment of headache (n=247, 54%), and for treatment of vertigo (n=106, 23%). After the FDA warning, 387 (85%) of EPs reported their use of droperidol had decreased or ceased altogether, and 68 (15%) always obtained an electrocardiogram prior to administration. Of those who used droperidol for agitation, 137 (42%) felt there were no other drugs with greater efficacy. Haloperidol was the most cited alternative agent (n=160, 79%) followed by benzodiazepines (n=223, 68%). Of those who used droperidol for antiemesis, 116 (28%) felt there were no other drugs with greater efficacy than droperidol; promethazine was the most cited alternative agent (n=26O, 64%). Two (0.4%) EPs reported arrhythmias in patients who received droperidol. Only 37 (8%) EPs reported they were unconcerned with potential loss of droperidol from the market. Conclusion: Based on this survey, EP use of droperidol has decreased dramatically as a result of the FDA warning. However, EPs believe that there are few or no alternative antiemetic drugs that have an improved adverse effect profile.

The purpose of this study was to describe the clinical findings in patients with splenic injury and to determine if isolated left lower chest injury may be the single clinical indicator of splenic injury. The medical records of all adult blunt trauma patients with splenic injury over a 14 month period were reviewed. Significant left lower chest injury was considered present if the patient had left sided pleuritic chest pain with tenderness to ribs 7-12 or if these ribs were visualized as fractured on any imaging study. Patients were considered to have clinical findings suggestive of splenic injury if they had pre-hospital or emergency department hypotension, abdominal pain or tenderness, a Glasgow coma scale < 15, or gross hematuria. Ninety patients had splenic injury. Thirty-nine (43%. 95% CI 33, 54%) patients had significant left lower chest injury. In five (6%. 95% CI 2, 12%) patients, injury to this portion of the chest was the single indicator of splenic injury. Nearly half the patients with splenic injury will have significant injury to the left lower chest and this finding may be the only indicator of splenic injury.

Background and aimsThe Psychoactive Surveillance Consortium and Analysis Network (PSCAN) is a national network of academic emergency departments (ED), analytical toxicologists and pharmacologists that collects clinical data paired with biological samples to identify and improve treatments of medical conditions arising from use of new psychoactive substances (NPS). The aim of this study was to gather clinical data with paired drug identification from NPS users who presented to EDs within PSCAN during its first year (2016-17).DesignObservational study involving patient records and biological samples.SettingSeven academic emergency medical centers across the United States.ParticipantsED patients (n = 127) > 8 years of age with possible NPS use who were identified and enrolled in PSCAN by clinical providers or research personnel.MeasurementsClinical signs, symptoms and treatments were abstracted from the patients' health records. Biological samples were collected from leftover urine, serum and whole blood. Biological and drug samples, when available, were tested for drugs and drug metabolites via liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF/MS).FindingsPatients in whom synthetic opioids were detected (n = 9) showed higher rates of intubation (four of nine), impaired mental status (four of nine) and respiratory acidosis (five of nine) compared with the rest of the cohort (nine of 118, P-value

BackgroundIn the last decade there has been a worldwide surge in the recreational abuse of novel psychoactive substances, particularly amphetamine derivatives and synthetic cannabinoids. Synthetic opioids such as AH-7921, MT-45, and U-47700, with structures distinct from those ever used therapeutically or described recreationally, have also recently emerged.Case detailsWe report a patient who suffered respiratory failure and depressed level of consciousness after recreationally using a novel synthetic opioid labeled U-47700. A single dose of naloxone administered by paramedics completely reversed his opioid poisoning. Comprehensive laboratory analysis confirmed the presence of a novel synthetic opioid and excluded other drugs. The drug used appeared to have caused a false positive benzodiazepine result on the initial urine drugs of abuse panel.ConclusionThe case we describe of toxicity from the synthetic opioid labeled U-47700 highlights the emerging trend of novel synthetic opioid abuse.

Tranexamic acid is a commonly used hemostatic agent with broad clinical uses across multiple specialties. Systemic toxicity is due to gamma-aminobutyric acid type A and glycine receptor competitive antagonism and has been reported by multiple routes, but toxicity after pulmonary administration via nebulization and BAL has not yet been described. A 44-year-old man with a history of congenital pulmonary arteriovenous malformations underwent routine bronchoscopy for hemoptysis. He received preprocedure nebulized tranexamic acid 500 mg three times daily for 48 h. An additional 1,000 mg was given via BAL for intraprocedural hemostasis. One hour after the procedure, he developed altered mental status, myoclonus, and hyperthermia, which was ultimately controlled with propofol and vecuronium. As the use of pulmonary tranexamic acid increases, toxicity from this agent should be considered. Dose reductions and alternate treatment modalities should be considered in patients with advanced age, arteriovenous malformations, and renal insufficiency. [ABSTRACT FROM AUTHOR]

Vascular neck restraint (VNR), an effective technique practiced within police and military combatives and in mixed martial arts and grappling sports, is of both interest and controversy. In any context the goal of VNR (referred to as a choke within combat sports) is to restrict brain blood flow enough to threaten or result in unconsciousness. The physiologic basis for the resultant unconsciousness has been depicted as being solely because of restriction of carotid blood flow due to direct external compression. This view is likely simpler than what is actually going on, but it's an area not well explored in the medical literature. Brain blood flow is maintained through mechanisms that allow for a relatively wide acceptable cerebral perfusion pressure (CPP). If CPP drops below the threshold of this auto-regulation, blood flow and brain oxygen delivery begin to decline. CPP is the difference of the mean arterial pressure (MAP) coming into the brain and the intracranial pressure (ICP). Lowering the MAP and/or raising the ICP reduce the CPP. The best literature-established physiologic component of VNR is carotid compression and resultant reduction in functional carotid MAP, thus lowering the CPP. Most studies have looked at this essentially to the exclusion of two other contributing entities: jugular compression resulting in increased ICP from reduction of outflow, and reduction of actual whole body MAP due to reduced cardiac output from vagal stimulation coming from a pressure affected carotid body. This article fleshes out some of these physiologic variables and discusses the related available literature. [ABSTRACT FROM AUTHOR]