Jennie A. Buchanan
University of Colorado Denver
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Featured researches published by Jennie A. Buchanan.
JAMA | 2011
Jennie A. Buchanan; Kennon Heard; Cynthia Burbach; Michael L. Wilson; Richard C. Dart
1988, Filly, in an editorial, called ultrasound the stethoscope of the future but was concerned about its use in untrained hands. In 2002, Dodd encouraged teaching the technique of ultrasound usage to medical students beginning in the gross anatomy laboratory and ending in ward rounds and senior electives. In 2003, Greenbaum projected that in the near future “medical students will also be buying a ‘sonoscope’” in addition to a stethoscope. He envisioned the sonoscope as enhancing the physical examination of all patients. With the advent of smaller, better-quality, and lessexpensive machines, and medical schools beginning to provide technical training for their students, the use of pointof-care ultrasound is increasing, with applications in physical diagnosis, screening, and guiding procedures. Small, portable, handheld ultrasound units are now inexpensive enough for this to be a reasonable addition to a clinician’s everyday armamentarium. Little, however, has been written about use of this technology in obese patients or about the upper limits of its usefulness. Because ultrasound penetrates fluid and solid organs well, it may be useful in the physical examination of the obese patient.
Journal of Medical Toxicology | 2011
Jennie A. Buchanan; Jody A. Vogel; Aaron Eberhardt
Based on the best available data, approximately 2.1 million Americans use illicit cocaine each month; for the last several months, 30% of that cocaine has been “cut” with a veterinary pharmaceutical, levamisole. Levamisole can cause agranulocytosis, leaving patients susceptible to fulminate and opportunistic infections and also can cause a debilitating cutaneous necrotizing vasculitis. In this manuscript, we describe a case and provide an image of levamisole-induced necrotizing vasculitis of the ears.
Current Opinion in Hematology | 2012
Jennie A. Buchanan; Eric J. Lavonas
Purpose of reviewMost of the illicit cocaine consumed in the United States and elsewhere is contaminated with levamisole, a veterinary medication. Agranulocytosis caused by levamisole exposure through cocaine abuse was first described in 2009. Since then, levamisole has also been shown and is known to cause vascular and neurologic complications. In this review, we provide an overview of the medical consequences of exposure to levamisole from adulterated cocaine. Recent findingsWithin the past year, several new case series have deepened our understanding of the levamisole–agranulocytosis vasculopathy syndrome. The common nature of this exposure has been delineated, cocaine contaminated with levamisole. Significant controversy surrounds the role of granulocyte colony stimulating factor (GCSF) in levamisole-associated agranulocytosis. SummaryMore than three fourths of cocaine users in the United States are exposed to levamisole; a significant minority of these individuals will develop autoimmune-mediated neutropenia, cutaneous vascular complications, and/or leukoencephalopathy. Levamisole exposure should be considered in the differential diagnosis of patients who present with these conditions in the setting of cocaine abuse. Neutropenia appears to resolve rapidly with cessation of exposure, so that GCSF therapy and a work-up for other causes may not be needed in all patients.
International Journal of Cardiology | 2011
Bonnie Kaplan; Jennie A. Buchanan; Mori J. Krantz
Dextromethorphan, d-3-methoxy-N-methylmorphine, (DXM) is an antitussive drug. It was approved by the Food and Drug Administration for over-the-counter sale in 1958. DXM, is an active ingredient found in many over the counter cough and cold medications. There are over 140 products which contain DXM along with other agents including: acetaminophen, antihistamines, decongestants, topical anesthetics, guaifenesin, promethazine and ethanol [1]. It is often abused recreationally, especially by teens [2]. When taken in excess it acts as a dissociative hallucinogen. Patients also may present with nausea, vomiting, dizziness, diaphoresis, clumsiness, ataxia, nystagmus, mydriasis, auditory and visual hallucinations, tachycardia, hypertension, seizure, stupor and coma [1]. Withdrawal can also occur from DXM, manifesting as nausea, vomiting, diaphoresis, myalgias, diarrhea, and restlessness beginning approximately 3 days after discontinuation of DXM [3]. DXM is the dextrorotary enantiomer of the methyl ether of levorphanol (a synthetic opioid analgesic). Its pharmocodynamics include: uncompetitive NMDA receptor antagonism, nicotinic and acetylcholine receptor antagonism, serotonin transporter blocker, and NAPDH oxidase inhibition [1]. Time to achieve peak serum concentrations vary from 2 to 3 h and serum elimination half-lives are approximately 3 h in liquid, tablet, or extended-release formulations [1]. Various side effects have been noted in overdose for DXM; however, prolonged QT interval is not one of them.
Journal of Emergency Medicine | 2013
Jennie A. Buchanan; Aaron Eberhardt; Zachary D. Tebb; Kennon Heard; Richard F. Wendlandt; Michael J. Kosnett
BACKGROUND Because the toxicity of arsenic is well known, arsenic-containing compounds have frequently been ingested for suicidal purposes. We report a case of attempted suicide by massive ingestion of arsenic trisulfide, an arsenic mineral of low solubility, which resulted in minimal symptoms. CASE REPORT An asymptomatic 57-year-old man presented to an Emergency Department 13h after his reported ingestion of approximately 84g of arsenic contained in a mineral specimen of orpiment (arsenic trisulfide) that had been crushed and mixed with an alcoholic beverage and food. His only symptom before presentation was nausea. Physical examination was unremarkable, and diagnostic tests included a normal electrolyte panel, a normal serum lactate, and a normal electrocardiogram. An abdominal radiograph revealed hyper-dense material scattered throughout the large intestine. As per the recommendations of the regional poison center, the patient was managed with whole bowel irrigation with a polyethylene glycol solution, maintenance intravenous hydration, and observation on a telemetry unit. Chelation was not performed. A spot urine specimen collected 12h after admission contained 1490μg of total arsenic per liter (background range<50μg per liter). The patient remained asymptomatic throughout his hospital course. Follow-up studies revealed a diminution in both intra-abdominal radiopacities and urine arsenic concentration. X-ray diffraction analysis of the specimen confirmed its identity as arsenic trisulfide. CONCLUSIONS Our experience demonstrates that massive ingestion of a poorly soluble inorganic arsenic compound can be successfully managed with gastrointestinal decontamination alone without chelation, provided that the patient remains asymptomatic during close clinical monitoring.
International Journal of Cardiology | 2012
George Sam Wang; Eric Tham; Jody Maes; Jennie A. Buchanan
Flecainide is a Vaughn–Williams class 1c antidysrhythmic. It is typically an oral medication administered for the treatment of atrial fibrillation or supraventricular tachycardia (SVT) [1,2]. It is sparingly used in the pediatric population, but can be used in the treatment of SVT [1,2]. We describe a 9 month old male who received an accidental overdose of his medication due to differences in pharmacy compounding. A 9 month old male with a history of Wolff–Parkinson White (WPW) and SVT was seen at a local childrens hospital the day prior to admission due to breakthrough SVT. At that time, he was initially refractory to adenosine, and his SVT resolved with propranolol. His maintenance medication was flecainide 15 mg (3 ml) twice daily. He was discharged home on an increased dose of flecainide to 21 mg (4 ml) by mouth twice daily. Later that morning, patient received 4 ml of his home flecainide when his mother noted him to be pale and fussy. EMS was called and brought him to a local emergency department. En route, he was noted to be in ventricular tachycardia (VT). Upon arrival to the emergency department (ED), his vitals were 37 ° C, RR of 24, and a HR of 180. He was alert, crying and fighting IV attempts. He was noted to be tachycardic on cardiovascular exam withoutmurmurs, rubs or gallops, no hepatosplenomegaly, and normal perfusion. ECG revealed sinus tachycardia with a PR interval of 160 ms and QRS interval of 180 ms. The patient had intermittent episodes of VT in the ED with normal pulses and without change in his clinical status (Fig. 1). It was eventually noted that his original concentration was changed to 20 mg/1 ml rather than the originally prescribed 5 mg/1 ml. Toxicology and cardiology were consulted at that time. IV access was obtained after 1 h in the ED, at that time, no episodes of VT were noted, and the QRS interval was 160 ms. Electrolytes including sodium, potassium, bicarbonate, magnesium, phosphorus, and calcium were all within normal range. Patient was admitted and placed on telemetry upon in the intensive care unit (ICU). Approximately 8 h into his hospital stay, QRS interval widened from 140 ms to 160 ms, his clinical status remained stable. Per toxicology recommendations, 2 mEq/kg of NaHCO3 IV was given and QRS interval was reduced to 120 ms. He subsequently remained hemodynamically stable during his ICU stay without further episodes of ventricular tachycardia, and his QRS narrowed to his baseline. Flecainide overdose can lead to seizures and cardiotoxicity including PR and QRS widening, bradycardia, ventricular tachycardia, and ventricular fibrillation due to its mechanism of action, Na channel blockade. Treatment for flecainide toxicity includes NaHCO3 boluses, hypertonic saline boluses, and extracorporeal circulatory support. Our patient presented immediately after a 4 fold overdose in a wide complex tachycardia, consistent with flecainide toxicity. Previous ECGs showed normal QRS complexes and he had never presented with a wide complex tachycardia due to his WPW. There have been four prior reports of pediatric patients and the toxic effects of flecainide, including an accidental double dose leading to toxicity, and reversal of medication syringes [3–6]. After further investigation for our patient, with the help of access to 2 separate electronic medical records (EMR), a difference in pharmacy compounding was discovered. The child had a flecainide prescription originally written for 15 mg using a 5 mg/1 ml concentration. However, his initial prescription was filled at another pharmacy which compounded the formulation to 20 mg/1 ml and no communication to the original prescribing facilitywasmade.When he returned to the ED, his dose was increased to 21 mg, but hospital records showed he was still using a concentration of 5 mg/1 ml. He was instructed to finish his home medication at the new dose prior to filling the new prescription. Consequently the patient took the correct volume, however at a higher concentration, leading to a 4 fold overdose. Since this case, all the pharmacies in the local metro area have agreed to compound the medication in one standard concentration of 20 mg/1 ml. Other common cardiac medications that are available as multiple concentrations for oral suspensions include verapamil, atenolol, carvedilol, labetalol, propranolol, and tacrolimus. Unverified concentrations in many of these medications can lead to serious morbidity and mortality. Flecainide is a Vaughn–Williams class 1c antidysrhythmic rarely used in pediatrics, indications include SVT. Cardiotoxicity stems from Na channel blockade and includes PR and QRS widening, bradycardia, ventricular tachycardia, ventricular fibrillation. Treatment for toxicity includes NaHCO3 boluses, hypertonic saline boluses, and extracorporeal circulatory support [7,8]. Our case is a reminder when dosing of medications are changed, especially in liquid formulations and with cardiovascular medications, both dosing and concentrations of medications must be confirmed, as accidental overdose and potentially poor comes can result. Finally, access to EMRs remotely can help quickly discover and prevent medical errors.
American Journal of Therapeutics | 2014
Shawn M. Varney; Jennie A. Buchanan; Jamie Kokko; Kennon Heard
N-Acetylcysteine (NAC) dosing for acetaminophen (APAP) overdose is weight based (150 mg/kg intravenous or 140-mg/kg oral loading dose) and, in the United States, the dosing protocol recommends using a maximum patient weight of 100 and 110 kg, respectively. Little clinical data describe the use of NAC for APAP poisoning in patients weighing >100 kg. The aim of this study was to describe the demographics, outcomes, and adverse event (AE) rates of patients weighing >100 kg treated with oral or IV NAC for APAP poisoning. Patients were identified from a multicenter retrospective NAC safety study for APAP overdose. We included patients with a recorded weight. Trained chart abstractors used a standardized form. Selected data included age, gender, weight, serum alanine transaminase, and aspartate transaminases, coingestants, NAC administration route, ingestion type, AEs, and outcome [hepatotoxicity (alanine transaminase > 1000 U/L), liver transplant, or death]. Descriptive statistics were used. Of 503 study patients, 37 (7.4%) had recorded weights >100 kg. The median (range) weight was 110 kg (101–160). The median (range) dosing for patients treated with oral NAC was 140 mg/kg (127–143 mg/kg) and 150 (108–168) mg/kg for IV NAC. Hepatotoxicity occurred in 12/36 (33.3%) patients. Death occurred in 4/36 (11.1%) patients. Thirteen NAC-related AEs occurred in 8 patients (1.6 per person). All AEs were related to NAC and were rated nonserious by the reviewer. Clinicians use an actual weight-based NAC dose rather than a maximum weight cutoff dose. Hepatotoxicity was common in our cohort. AEs were relatively common but not serious.
Western Journal of Emergency Medicine | 2013
Margaret Sande; Kerry B. Broderick; Maria E. Moreira; Brooke Bender; Emily Hopkins; Jennie A. Buchanan
Introduction: There is currently no standard forensic medicine training program for emergency medicine residents. In the advent of sexual assault nurse examiner (SANE) programs aimed at improving the quality of care for sexual assault victims, it is also unclear how these programs impact emergency medicine (EM) resident forensic medicine training. The purpose of this study was to gather information on EM residency programs’ training in the care of sexual assault patients and determine what impact SANE programs may have on the experience of EM resident training from the perspective of residency program directors (PDs). Methods: This was a cross-sectional survey. The study cohort was all residency PDs from approved EM residency training programs who completed a closed-response self-administered survey electronically. Results: We sent surveys to 152 PDs, and 71 responded for an overall response rate of 47%. Twenty-two PDs (31%) reported that their residency does not require procedural competency for the sexual assault exam, and 29 (41%) reported their residents are required only to observe sexual assault exam completion to demonstrate competency. Residency PDs were asked how their programs established resident requirements for sexual assault exams. Thirty-seven PDs (52%) did not know how their sexual assault exam requirement was established. Conclusion: More than half of residency PDs did not know how their sexual assault guidelines were established, and few were based upon recommendations from the literature. There is no clear consensus as to how PDs view the effect of SANE programs on resident competency with the sexual assault exam. This study highlights both a need for increased awareness of EM resident sexual assault education nationally and also a possible need for a training curriculum defining guidelines for EM residents performing sexual assault exams.
Pediatric Emergency Care | 2015
David B. Richards; George Sam Wang; Jennie A. Buchanan
Tea tree oil is an essential oil containing a mixture of aromatic hydrocarbons. We describe an 18-month-old male patient who ingested tea tree oil, developed central nervous system depression, respiratory distress, and received early emergency department treatment with surfactant. Early treatment of hydrocarbon pneumonitis with surfactant has not been previously described. Early administration of surfactant should be further evaluated for treatment of hydrocarbon aspiration.
Annals of Emergency Medicine | 2011
Courtenay M. Holscher; Samantha K. Mauck; Leslie Armstrong; Jennie A. Buchanan
A 58-year-old man presented to the emergency department (ED) with a 1-day history of rash and 3 days of nausea, vomiting, and diarrhea. His history was notable for recent hair transplantation and cephalexin use. He had finished his antibiotic course 5 days before presentation. He denied skin tenderness, oral ulcers, and history of skin disorders. On arrival, he had a pulse rate of 110 beats/ min, respiratory rate of 32 breaths/min, blood pressure of 118/82 mm Hg, temperature of 40.9°C (105.6°F), and an oxygen saturation of 98% on 15 L/minute. About 24 hours before presentation, he noticed erythema in his groin, neck, and axillae and temperature to 40°C (104°F). The rash rapidly spread to his entire body, including his face (Figures 1-3). At presentation, systemic symptoms continued and rash persisted as diffuse erythematous reticulated rash with grouped, nonfollicularly centered pustules, with no vesicles or bullae. Figure 1. An erythematous reticulated rash on patient’s trunk. Figure 2. Grouped nonfollicularly centered pustules on the forehead.