Volume 10 Issue 4

West

Volume X, Number 4, November 2009

Western Journal of Emergency Medicine

International Issue PAID

Permit #646 Orange, CA

PRSTD STD US POSTAGE

A Peer-Reviewed Professional Journal

Open Access at www.westjem.org

ISSN 1936-900X

EMERGENCY MEDICAL SERVICES 208 Factors Associated With False-Positive Emergency Medical Services

Triage for Percutaneous Coronary Intervention (Original Research)

PY Swan, B Nighswonger, GL Boswell, SJ Stratton 213

International Disaster Medical Sciences Fellowship: Model Curriculum and Key Considerations for Establishment of an Innovative International Educational Program (Original Contribution) KL Koenig, T Bey, CH Schultz

JOURNAL PERSPECTIVES 220 CAL/ACEP Joins CAL/AAEM and UC Irvine in Sponsoring the Western

Journal of Emergency Medicine

WK Mallon, SP Swadron 222

Boarder Patrol: A Reform Policy for America’s Paralyzed Emergency Departments PJ Bloomfied, AB Landman, RC Rosenbloom

INTERNATIONAL CONTRIBUTIONS 225 The Role of WestJEM in Promoting International Emergency Medicine

MI Langdorf, F Della Corte, R Petrino 227

Introducing a Clinical Practice Guideline Using Early CT in the Diagnosis of Scaphoid and Other Fractures (Original Research) S Pincus, M Weber, A Meakin, R Breadmore, D Mitchell, L Spencer, N Anderson, P Catterson, S Farish, J Cruickshank

233

Crowding and Delivery of Healthcare in Emergency Departments: The European Perspective (Review Article)

240

Paramedics’ Ability to Perform Drug Calculations (Review Article) KJ Eastwood, MJ Boyle, B Williams

244

Lead Toxicity Resulting from Chronic Ingestion of Opium (Case Report) M Jalili, R Azizkhani

247

Thyroid Gland Hematoma after Blunt Neck Trauma (Case Report) B Saylam, B Çomçali, MV Ozer, F Coskun

250

Chilaiditi’s Syndrome (Images In Emergency Medicine) RF McNamara, P Hallihan, S Cusack

N Jayaprakash, R O’Sullivan, T Bey, SS Ahmed, S Lotfipour

Western Journal of Emergency Medicine Table of Contents, continued

Volume X, Number 4 : November 2009 www.westjem.org

TRAUMA/CRITICAL CARE 251 Wound Botulism in Injection Drug Users: Time to Antitoxin Correlates with Intensive Care Unit

Length of Stay (Original Research)

SR Offerman, M Schaefer, JG Thundiyil, MD Cook, JF Holmes 257

Terrain Park Injuries (Original Research) C Moffat, S McIntosh, J Bringhurst, K Danenhauer, N Gilmore, CL Hopkins

263

The Utility of Bedside Ultrasound in the Detection of a Ruptured Globe in a Porcine Model (Original Research) A Chandra, T Mastrovitch, H Ladner, V Ting, MS Radeos, S Samudre

267

Cervical Spine Fracture in Ankylosing Spondylitis (Images In Emergency Medicine) J Carnell, J Fahimi, CP Wills

NEURO-PSYCHIATRIC 268 Emergency Department Patients with Psychiatric Complaints Return at Higher Rates than

Controls (Original Research)

TE Madsen, A Bennett, S Groke, A Zink, C McCowan, A Hernandez, S Knapp, D Byreddy, S Mattsson,

N Quick 273

The Clinical Differentiation of Cerebellar Infarction from Common Vertigo Syndromes (Review Article) JA Nelson, E Viirre

GENITOURINARY 278 The Back Alley Revisited: Sepsis after Attempted Self-Induced Abortion (Case Report)

TA Saultes, D Devita, JD Heiner 281

Non Traumatic Urologic Emergencies in Men (Review Article) CS Kessler, J Bauml

Online Manuscripts (Full text manuscripts available open access at http://escholarship.org/uc/uciem_westjem) CLINICAL PRACTICE 288 Bilateral Psoas Abscess in the Emergency Department (Case Report)

EB Tomich, D Della-Giustina 292

Lidocaine Toxicity Misinterpreted as a Stroke (Case Report) B Bursell, RM Ratzan, AJ Smally

Author instructions, policies for peer review, conflicts of interest, and human and animal subjects protections can be found online at www.westjem.org.

Western Journal of Emergency Medicine

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Volume X, no. 4 : November 2009

Western Journal of Emergency Medicine Table of Contents, continued

295

Molar Pregnancy in the Emergency Department (Case Report) L Masterson, SB Chan, B Bluhm

297

Scrotal Swelling after Penetrating Chest Trauma (Images In Emergency Medicine) JD Heiner, EC Skeins, D DeVita, JS Litner

298

Supraglottic Laryngeal Mass (Images In Emergency Medicine) L Andrews, SO Henderson

300

Non-Communicating Hydrocephalus (Images In Emergency Medicine) KJ Yablonicky, SP Swadron

302

Rhabdomyolysis-Induced Severe Hyperkalemia (Images In Emergency Medicine) C Rosenberry, F Stone, K Kalbfleisch

303

Ultrasound Confirmed Frontal Bone Fracture (Images In Emergency Medicine) J Johnson, DF McBride, S Crandall, C Kang

304

Non-traumatic Shoulder Dislocation (Images In Emergency Medicine) J Manteuffel

305

All That Wheezes Is Not Asthma (Images In Emergency Medicine) AC Miller, RM Rashid, EM Elamin

WestJEM Seeking Section Editors and Reviewers WestJEM is seeking Section Editors in the fields of: • Emergency Cardiac Care • Emergency Department Administration • Public Health • Neurosciences • Behavioral Emergencies WestJEM also seeks reviewers in all topics of emergency medicine.

Please send CV and letter of interest to Editor-in-Chief, Dr. Mark Langdorf at WestJEM@gmail.com.

Volume X, no. 4 : November 2009

iii

Western Journal of Emergency Medicine

Western Journal of Emergency Medicine Mark I. Langdorf, MD, MHPE, Editor-in-Chief University of California, Irvine School of Medicine Shahram Lotfipour, MD, MPH, Managing Associate Editor University of California, Irvine School of Medicine

Sean O. Henderson, MD, Senior Associate Editor Keck School of Medicine, University of Southern California

Section Editors Behavioral Emergencies Leslie Zun, MD Chicago Medical School

ED Administration Jeffrey Druck, MD University of Colorado

Clincal Practice Eric Snoey, MD Alameda County Medical Center Rick McPheeters, DO Kern Medical Center

Emergency Cardiac Care Matthew Strehlow, MD Stanford University

Critical Care H. Bryant Nguyen, MD, MS Loma Linda University Jeffrey Sankoff, MD University of Colorado

Scott Rudkin, MD, MBA University of California, Irvine Injury Prevention Bharath Chakravarthy, MD, MPH Loma Linda University Shahram Lotfipour, MD, MPH University of California, Irvine

Emergency Medical Services Christopher Kahn, MD, MPH University of California, Irvine David E. Slattery, MD University of Nevada

Public Health Policy Michael Menchine, MD, MPH University of California, Irvine

International Medicine Tareg Bey, MD Resident/Student/Fellow Forum University of California, Irvine Laleh Gharahbaghian, MD Chris Mills, MD, MPH Santa Clara Valley Medical Center Stanford University Beau Briese, MD, MA Stanford University Legal Medicine Greg P. Moore, MD, JD Toxicology Madigan Army Medical Center Jeffrey R. Suchard, MD University of California, Irvine Methodology and Biostatistics Brandon Wills, DO, MS Craig Anderson, MPH, PhD Virginia Commonwealth University University of California, Irvine Christian McClung, MD Ultrasound University of Southern California Seric Cusick, MD, RDMS University of California, Davis Neurosciences J. Christian Fox, MD, RDMS Kurt Denninghoff, MD University of California, Irvine University of Arizona

Geriatrics Teresita M. Hogan, MD Resurrection Medical Center, Chicago

Disaster Medicine Christopher Kang, MD Madigan Army Medical Center Infectious Disease Colleen Buono, MD University of California, San Diego Robert Derlet, MD University of California, Davis Sukhjit S Takhar, MD Education University of California, San Michael Epter, DO Francisco, Fresno University of Nevada H. Gene Hern, MD, MS Information Technology Alameda County Medical Center James Killeen, MD University of California, San Diego

Pediatric Emergency Medicine Judith Klein, MD University of California, San Francisco Paul Walsh, MD, MSc Kern Medical Center

Editorial Board

Editorial Staff

Barry E. Brenner, MD, MPH Case Western University

Susan Promes, MD Univ. of California, San Francisco

Suleman S. Ahmed, BS, BA Editorial Director

Daniel Joseph, BA Editorial Assistant

Robert W. Derlet, MD University of California, Davis

Robert M. Rodriguez, MD Univ. of California, San Francisco

June Casey, BA Copy Editor

Pamela Swan, BA Editorial Assistant

Edward Michelson, MD Case Western University

Scott Rudkin, MD, MBA University of California, Irvine

Christina Cheng, BS Design Editor

Warren Wiechmann, MD, MBA Webmaster

Jonathan Olshaker, MD Boston University

Thomas Terndrup, MD Pennsylvania State University

Kate Filipiak AAEM Liaison

Sonia Johnson, MD Graphic Design Consultant

Edward Panacek, MD, MPH University of California, Davis

Leslie Zun, MD Chicago Medical School

Publisher

Department of Emergency Medicine, University of California, Irvine

Official Journal of the California Chapter of the American Academy of Emergency Medicine and the California Chapter of the American College of Emergency Physicians Articles now available on Pub Med, Pub Med Central, Journal Watch EM, Google Scholar, eScholarship, Melvyl (The Catalog of the University of California Libraries), Directory of Open Access Journals, Medscape and MDLinx Emergency Med. WestJEM, 101 The City Drive, Rt. 128-01, Orange, CA 92868-3201: Office (714) 456-6389; Email: WestJEM@gmail.com Volume X, no. 4 : November 2009

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Western Journal of Emergency Medicine

Thank you to our sponsors Society Sponsors California Chapter of the American Academy of Emergency Medicine

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Department of Emergency Medicine Sponsors University of California, Irvine Medical Center Orange, CA Denver Health Medical Center Denver, CO

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This open access publication would not be possible without the generous support of our society sponsors, the Department of Emergency Medicine at the University of California Irvine, advertisers and department sponsors.

To become a departmental sponsor of the journal, receive print, as well as electronic copies, and free advertisement space please visit www.calaaem.org/westjem or contact: Kate Filipiak Cal/AAEM: WestJEM 555 East Wells Street Milwaukee, WI 53202 Phone: (800) 884-2236 KFilipiak@aaem.org Western Journal of Emergency Medicine

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Shahram Lotfipour, MD, MPH Managing Associate Editor Phone: (714) 456-2326 Shahram.Lotfipour@uci.edu

Volume X, no. 4 : November 2009

Original Research

Factors Associated With False-Positive Emergency Medical Services Triage for Percutaneous Coronary Intervention Pamela Yamamoto Swan, BA* Beverly Nighswonger, RN† Gregory L. Boswell, RN† Samuel J. Stratton, MD, MPH*

* University of California, Irvine School of Medicine, Department of Emergency Medicine, Orange, CA † Emergency Medical Services, Orange County California Health Care Agency, Santa Ana, CA

Supervising Section Editor: Christopher Kahn, MD, MPH Submission history: Submitted April 15, 2009; Revision Received May 28, 2009; Accepted June 1, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Background: In 2005, Orange County California Emergency Medical Services (EMS) initiated a field 12lead program to minimize time to emergency percutaneous coronary intervention (PCI) for field-identified acute myocardial infarction (MI). As the program matured, “false-positive” (defined as no PCI or coronary artery occlusion upon PCI) field MI activations have been identified as a problem for the program.

Objectives: To identify potentially correctable factors associated with false-positive EMS triage to PCI centers.

Methods: This was a retrospective, outcome study of EMS 12-lead cases from February 2006 to June 2007. The study system exclusively used cardiac monitor internal interpretation algorithms indicating an acute myocardial infarction as the basis for triage. Indicators and variables were defined prior to the study. Data, including outcome, was from the Orange County EMS database, which included copies of 12-lead ECGs used for field triage. Negative odds ratios (OR) of less than 1.0 for positive PCI were the statistical measure of interest.

Results: Five hundred forty-eight patients were triaged from the field for PCI. We excluded 19 cases from the study because of death prior to PCI, refusal of PCI, and co-morbid illness (sepsis, altered consciousness) that precluded PCI. Three hundred ninety-three (74.3%) patients had PCI with significant coronary lesions found. False-positive field triages were associated with underlying cardiac rhythm of sinus tachycardia [OR = 0.38 (95% CI 0.23, 0.62)]; atrial fibrillation [OR = 0.43 (95% CI = 0.20, 0.94)]; an ECG lead not recorded [OR = 0.39 (95% CI = 0.20, 0.76)]; poor ECG baseline [OR = 0.59 (95% CI = 0.25, 1.37)]; One of three brands of monitors used in the field [OR = 0.35 (95% CI = 0.21, 0.59)]; and female gender [OR = 0.50 (95% CI = 0.34, 0.75)]. Age was not associated with falsepositive triage as determined by ordinal regression (p=1.00).

Conclusion: For the urban-suburban EMS field 12-lead program studied, age was not associated with false-positive triage. It was unexpected that female gender was associated with false-positive triage. False-positive triage from the field was associated with poor ECG acquisition, underlying rhythms of atrial fibrillation and sinus tachycardia, and one brand of 12-lead monitor.

[West J Emerg Med. 2009;10(4):208-212]

INTRODUCTION Studies have shown that percutaneous coronary intervention (PCI) may be preferred over intravenous thrombolytics in achieving reperfusion and reducing mortality for those presenting to an emergency department Volume X, no. 4 : November 2009

(ED) with acute myocardial infarction and associated electrocardiographic ST segment elevation (STEMI).1-4 It has also been shown that myocardial reperfusion after onset of a STEMI has greater effectiveness the sooner it is achieved.5 A time period of less than 90 minutes from the time a STEMI 208

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Swan et al.

False-Positive EMS STEMI Triage victim enters an ED to having PCI with balloon inflation and reperfusion of a blocked coronary artery has become a standard goal in many developed countries.4 In the U.S. it has been found that a majority of adults (75%) live closest to a hospital that does not provide PCI.6 While patients with STEMI can initially be stabilized at a non-PCI provider hospital and transferred by critical care ambulance to a PCI capable facility, studies show that the time for initiation of PCI can be significantly reduced when emergency medical services (EMS) personnel identify STEMI victims in the field and transport them directly to a PCI capable hospital.7-10 To facilitate field triage of potential STEMI patients to PCI centers, many EMS systems have developed prehospital 12-lead electrocardiography (12-lead) protocols that allow EMS personnel at the scene to obtain data and triage a potential STEMI patient directly to a PCI capable facility.11-14 Reducing time in the field before arrival to a PCI center further decreases overall time for reperfusion of occluded coronary arteries.9,10 Three common models are used for EMS field 12-lead identification of potential STEMI.14 The least expensive model is use of an algorithm interpretation preprogrammed within the cardiac monitor that rapidly generates the field 12-lead. This method for field interpretation requires no wireless or electrical transmission system and allows for 12lead acquisition and STEMI determination without intensive education of EMS field providers. A second method, using paramedic interpretation, requires training of EMS personnel in the interpretation of the various 12-lead signs of STEMI. While training and maintaining the skill of EMS personnel interpretation may be costly, it has been shown to be effective with paramedic-identified STEMI sensitivity ranging from 71% to 97% and specificity ranging from 91% to 100%.14 A final method is wireless and electronically transmits a fieldacquired 12-lead to a physician for interpretation. This method is costly and may add to time a STEMI patient is in the field while 12-lead transmission is accomplished. In addition, some systems may require significant effort or cost to have a physician or other personnel trained in ECG interpretation available at all times to read the transmitted ECG. While the monitor algorithm STEMI determination method described above is rapid and inexpensive, falsepositive field triage to a PCI center is a concern.14 One result of false-positive triage is the unnecessary rapid transport of assumed critical patients beyond a nearby hospital to a more distant PCI facility, placing emergency response crews and the community at increased risk for motor vehicle accidents.15 It can also result in unnecessary redirection of personnel and equipment at the receiving hospital. In addition, when emergency response personnel are assigned to a false-positive incident, fewer available units remain in the area. A decrease in false-positive field STEMI triages could result in better utilization of resources and allow for safer EMS operations.

Western Journal of Emergency Medicine

Another adverse effect of excessive false-positive triages could be the decreased willingness of the emergency physician to allow direct transportation to a PCI center without having first personally interpreted the ECG. Considering the above discussion, minimization of EMS false-positive STEMI transports when using a monitor algorithm exclusive triage system would benefit a healthcare system. To address the issue, this study was designed to identify the rate and variables associated with false-positive triage within an EMS monitor algorithm interpretation triage system.

METHODS This was a retrospective, sequential, case-control outcome study of EMS responses triaged in the field to designated PCIcapable hospitals. Study variables of interest were those that may have been associated with false-positive field triage for PCI. Potential variables to test for a potential false-positive association were identified in a pre-study (Table 1). Cases considered for the study included all those triaged from the field to a PCI center by exclusive use of a 12-lead monitor algorithm that included the terms “Acute MI Suspected” or “Acute MI.” Indications for obtaining a 12-lead ECG reading were chest pain, shortness of breath, dizziness or syncope.

Excluded from the study were cases appropriate for triage to a PCI but for whom cardiac arrest and death prior to PCI occurred or who had co-morbid conditions that precluded PCI. These co-morbid conditions included sepsis, decreased mental capacity that did not allow for PCI consent, diabetic ketoacidosis, acute cerebral vascular accident, concurrent trauma with hemorrhage, and refusal of a competent person to consent for PCI. Table 1. Variables tested for association with false-positive field triage to a facility providing percutaneous coronary intervention.

209

•

Age

•

Gender

•

Responding EMS Provider

•

Base hospital

•

Receiving hospital

•

Indication signs for initiation of 12-lead ECG reading

•

ECG rhythm

•

ECG rate

•

ECG baseline

•

QRS morphology

•

Lead placement o Which, if any, leads missing

•

60-cycle interference presence

•

ECG monitor brand

EMS, emergency medical services; ECG, electrocardiogram.

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False-Positive EMS STEMI Triage

A code book defining study variables was developed before conducting the study. We validated the code book by first collecting data for 20 patients who met criteria for inclusion. We clarified inconsistent terms and variables to ensure that study definitions were standardized. Data was collected on a collection form that used field and receiving hospital records with a copy of the original field 12-lead attached. We developed a database using Microsoft Excel 2003 (Microsoft Corp, Redmond, WA, USA), and used a double data entry method to enter data. We corrected errors when conflicting data were entered. If a conflict in interpretation still existed, the senior investigator’s entry took precedence for consistency. Prior to the study we determined that for interpretation of odds ratios (OR), a confidence interval precision of 10% or less was necessary for the findings to be clinically significant. Using this assumption, the number of cases needed for adequate sample size was determined to be at least 500, based on a desired power of 80%. We conducted this power calculation using Statistics with Confidence v2.0 software (CIA Software, Bristol, UK).

For this study, false-positive triage was the outcome of interest. Because there is potential for variability in the definition for false-positive, we used a conservative definition indicating no acute coronary artery occlusion (disease).

False-positive was defined as a patient who had no significant coronary artery occlusion by PCI or was determined after evaluation by receiving PCI-center physicians to lack need for PCI (Figure 1). We used SPSS v13.0 software (SPSS Inc, Chicago, Il, USA) to calculate OR for association of each study variable and positive PCI outcome. Therefore, a reported OR of less than 1.0 was associated with false-positive triage.

Confidence intervals (95%) were calculated for each OR to determine precision of the statistical estimate. For age as a variable, we used ordinal regression for statistical analysis, with a p-value of less than 0.05 considered significant.

The study setting was Orange County, California with a population of 3.02 million persons living in an urban-suburban environment. EMS units were 911 computer-aided-dispatched with a two-tiered basic life support (BLS)-advanced life support (ALS) response. Thirteen fire departments with 880 paramedics provided ALS resources and transported to 25 receiving hospitals of which 12 were designated PCI centers.

Field medical control was provided by blended off-line protocols and on-line base hospital radio contact.

This study received Institutional Review Board approval by a committee recognized by Federal-wide Assurance submitted to the U.S. Department of Health and Human Services.

RESULTS Paramedics triaged 548 sequential patients from the field for PCI during the study period. Nineteen cases were excluded because of cardiac arrest prior to PCI or co-morbid conditions that precluded PCI. During the study, three types of field Volume X, no. 4 : November 2009

Definition of false positive

Positive Field ECG Triaged to CRC N=529

No MI, No PCI (False Positive) N = 121

To PCI

No CAD (False Positive) N = 15

CAD present (True Positive) N = 393

Figure. Study definition for false-positive emergency medical services triage from the field for percutaneous coronary intervention (PCI). ECG, electrocardiogram; CRC, Cardiac (PCI) Receiving Center; MI, myocardial infarction; CAD, coronary artery disease.

12-lead cardiac monitors were used: the Zoll M Series (Zoll Medical Corp., Chelmsford, MA, USA); LifePAK 12 (PhysioControl, Inc., Redmond, WA, USA); and the Philips HeartStart Rx (Philips Electronics, Amsterdam, Netherlands). The average age for those entered into the study was 64.7 years with 60.0% male. Of the 529 cases included, 393 (74.3%) patients had PCI with coronary lesions treated by balloon angioplasty or coronary artery bypass graft. The remaining 136 (25.7%) were considered false-positives, defined as a patient who was determined after evaluation by receiving PCIcenter physicians to lack need for PCI (121; 22.9%) or had no coronary artery occlusion by PCI (15; 2.8%) (Figure 1). Falsepositive cases were associated with the following variables: a specific brand of one of three monitors used in the system (OR = 0.35, 95% CI = 0.21, 0.59); sinus tachycardia (OR = 0.38, 95% CI = 0.23, 0.62); missing lead recording on 12-lead printout (0.39, 95% CI = 0.20, 0.76); atrial fibrillation (OR = 0.43, 95% CI = 0.20, 0.94); female gender (OR = 0.50, 95% CI = 0.34, 0.75); and poor ECG baseline (OR = 0.59, 95% CI = 0.25, 1.37) (Table 2). Age was not associated with falsepositive triage for PCI as determined by Ordinal Regression (p = 1.00).

DISCUSSION This study showed a substantial number (25.7%) of falsepositive triages to specialty centers for PCI based on field 12-lead monitor algorithms. We found multiple variables associated with false-positive triage within the EMS system studied.

Poor ECG baseline and failure to record all 12 leads for machine algorithm interpretation are false-positive associated variables that can be addressed by improved quality in field acquisition of 12-leads. Variables more difficult to address are sinus tachycardia and atrial fibrillation, which had a tendency to be wrongly interpreted by machine algorithm as acute MI. EMS system adjustments to disregard readings of acute MI in the setting of sinus tachycardia and atrial fibrillation could result in missing true MI patients and would require

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False-Positive EMS STEMI Triage Table 2. Odds Ratio (OR) with 95% Confidence Interval for association with false-positive triage to a facility providing percutaneous coronary intervention (PCI). Note that an OR of less than 1.0 is associated with false-positive triage and OR of greater than 1.0 is associated with triage and positive PCI. Odds Ratio

95% Confidence Interval

Monitor Type

0.35

0.21, 0.59

Sinus tachycardia

0.38

0.23, 0.62

Missing lead

0.39

0.20, 0.76

Atrial fibrillation

0.43

0.20, 0.94

Female gender

0.50

0.34, 0.75

Poor baseline

0.59

0.25, 1.37

further study to insure the rate of missed true positives is not unacceptable. An unexpected finding was the association of one type of 12-lead machine with false-positive triage. Once this was re-validated by repeat data analysis, we advised the device manufacturer of the findings. Adjustments and changes to the algorithm for the device have been made and follow-up study is in progress. The type of monitor associated with false-positive 12-leads is not identified in this paper because the oversight Institutional Review Committee for the study requires that a written release from the manufacturer be obtained and such a release was declined.

Another interesting finding was an association of false-positive triage with female gender. We collected demographic data with the intent to show that the study population was homogenous with no difference in gender outcomes. The association of female gender with falsepositive triage was unexpected and deserves further study for confirmation and explanation.

Field EMS determination of STEMI has been shown to be beneficial in rapid identification, transport, treatment, and decreased mortality.7,11,16 To maximize this benefit and decrease the problems earlier described for false-positive triage, this study suggests that in addition to the mechanics of attaining a field ECG, additional paramedic education may be required to help recognize ST elevation MI in field ECG recordings.

In a 2008 article Ting et al.14 noted that current knowledge of false-positive and false-negative rates for EMS triage of STEMI patients to PCI centers is poorly characterized, supporting the findings of this paper.

Their study describes poor field ECG acquisition as a factor associated with false-positive triage, and finds that movement artifact, lead misplacement, and poor skin contact can cause the poor-quality tracings that can be misinterpreted

by ECG monitor software or EMS personnel.

Decreasing false-positive system activation could inadvertently increase false-negatives. To mitigate this adverse effect, it has been suggested that electronic transmission of Western Journal of Emergency Medicine

12-lead ECG to a receiving hospital for over-read may be effective.17 LIMITATIONS One limitation of this study is the retrospective method used for data acquisition. The retrospective method increases risk for loss of original data, erroneous recording of data elements on original records, selection bias, and confounding due to lack of control of study variables. A more subtle limitation is that our definition of false-positive triage does not take into account patients who were determined by the receiving physicians to lack evidence for an acute STEMI MI, when in fact such an MI was present and PCI could have been a benefit. Studies show there is a background risk that approximately 3% of MI patients requiring PCI will be misdiagnosed and discharged by cardiologists without appropriate coronary intervention, and approximately 6-10% by emergency physicians.18,19 While left bundle branch block was analyzed within the study population 12-leads, there was not an association of this finding with false-positive triage; on the other hand the study was limited in that we did not test for false-positive association with left ventricular hypertrophy, pericarditis, left ventricular aneurysm, and early repolarization.

Another limitation is the focus on false-positive triage and lack of data for false-negative cases. This study does not consider patients who were false-negatives. Knowing the false-negatives would have allowed for better system description and calculation of field 12-lead sensitivity and specificity.

And because we conducted this study in an urbansuburban setting with multiple hospital options within a few minutes transport time, the findings may lack external validity. Additionally, selection bias by paramedics could have occurred in that some cases eligible for 12-lead application may not have had an ECG. Finally, outcomes were obtained from hospital billing and discharge databases and not independently confirmed.

CONCLUSION For the EMS field 12-lead program studied, there was a false-positive triage rate of 25.7%. False-positive field triage was associated with one brand of 12-lead ECG monitor, poor ECG acquisition, and underlying rhythms of sinus tachycardia and atrial fibrillation. Unexpectedly, female gender was also associated with false-positive triage. Age was not associated with false-positive field triage for PCI. Aknowledgements This paper is dedicated to Beverly Nighswonger, RN, who passed away October 29, 2008. She was a dedicated professional of highest ethics. In her shortened lifetime, she accomplished more than most and was generous to all.

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False-Positive EMS STEMI Triage

Address for Correspondence: Samuel J. Stratton, MD, MPH Health Disaster Management/Emergency Medical Services, Orange County Health Care Agency, 405 W. Fifth Street, Suite 301A, Santa Ana, CA 92701. Email sstratton@att.net

9.

Brown JP, Mahmud E, Dunford JV, et al. Effect of prehospital 12lead electrocardiogram on activation of the cardiac catheterization laboratory and door-to-balloon time in ST-segment elevation acute myocardial infarction. Am J Cardiol. 2008; 101:158-161.

10. Le May MR, So DY, Dionne R, et al. A citywide protocol for primary

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2008; 358:231-40.

11. Le May MR, Davies RF, Dionne R, et al. Comparison of early mortality of paramedic-diagnosed ST-segment elevation myocardial infarction with immediate transport to a designated primary

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Nallamothu BK, Bates ER, Wang Y, et al. Driving times and distances

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to hospitals with percutaneous coronary intervention in the United

J Emerg Med. 2005; 23:443-448.

States: implications for prehospital triage of patients with ST-elevation

17. Davis DP, Graydon C, Stein R, et al. The positive predictive value of

myocardial infarction. Circulation. 2006; 113:1189-95.

7.

benefit of prehospital diagnosis, triage, and therapy by paramedics

8.

paramedic versus emergency physician interpretation of the prehospital

van’t Hof AW, Rasoul S, van de Wetering H, et al. Feasibility and

12-lead electrocardiogram. Prehosp Emerg Care. 2007; 11:399-402.

18. Turnipseed SD, Bair AE, Kirk JD, et al. Electrocardiogram

only in patients who are candidates for primary angioplasty for acute

differentiation of benign early repolarization versus acute myocardial

myocardial infarction. Am Heart J. 2006; 151:1255.e1-5.

infarction by emergency physicians and cardiologists. Acad Emerg

Afolabi BA, Novaro GM, Pinski SL, et al. Use of the prehospital ECG improves door-to-balloon times in ST segment elevation myocardial

Med. 2006; 13:961-966.

19. Brady WJ, Perron A, Ullman E. Errors in emergency physician

infarction irrespective of time of day or day of week. Emerg Med J.

interpretation of ST-segment elevation in emergency department

2007; 24:588-91.

chest pain patients. Acad Emerg Med. 2000; 7:1256-60.

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Original Contribution

International Disaster Medical Sciences Fellowship: Model Curriculum and Key Considerations for Establishment of an Innovative International Educational Program Kristi L. Koenig, MD Tareg Bey, MD Carl H. Schultz, MD

University of California Irvine School of Medicine, Department of Emergency Medicine, Orange, CA

Supervising Section Editor: Shahram Lotfipour, MD, MPH Submission history: Submitted October 19, 2009; Revision Received October 31, 2009; Accepted October 31, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

As recent events highlight, a global requirement exists for evidence-based training in the emerging field of Disaster Medicine. The following is an example of an International Disaster Medical Sciences Fellowship created to fill this need. We provide here a program description, including educational goals and objectives and a model core curriculum based on current evidence-based literature. In addition, we describe the administrative process to establish the fellowship. Information about this innovative educational program is valuable to international Disaster Medicine scholars, as well as U.S. institutions seeking to establish formal training in Disaster Medical Sciences.

[West J Emerg Med. 2009;10(4):213-219]

INTRODUCTION There is a need for international training in Disaster Medical Sciences. Scholars and health policy makers from some regions of the world may have limited access to cuttingedge training in the emerging field of Disaster Medicine. It is critical to use the best science and evidence-based approaches available when training future leaders in this field. To this end, a diverse core faculty of Disaster Medical Sciences academicians (Table 1) has developed a formal program for international applicants seeking training in Disaster Medicine.1 Requirements include the following: the sponsoring country must confirm the need for qualified practitioners, and the applicant must describe how the skills and knowledge gained during the fellowship could be applied to improve future disaster management in the home country. To assist potential international Disaster Medical Sciences scholars and U.S.-based educational institutions that wish to engage in similar training programs, this paper provides a detailed description of the program, key considerations for its establishment, and a model core curriculum. The same Disaster Medical Sciences Fellowship is established and available for U.S. applicants; however, U.S. candidates are not subject to sponsorship and visa requirements.

Disaster Medicine is a global issue. In managing disasters of all types and sizes, it is desirable to use a broad-based allhazard, comprehensive emergency management approach that includes assessments of worldwide challenges and variable Western Journal of Emergency Medicine

Table 1. Disaster Medical Sciences Core Faculty – Typical Titles and Functions Director of Public Health Preparedness Director of International Emergency Medicine Director of Disaster Medical Services Medical Directors of Emergency Medical Services (county government and fire authority) Nursing Director of Emergency and Trauma Services

approaches to their solutions. In order to establish Disaster Medicine as a distinct academic discipline, a unique body of knowledge must be demonstrated. Textbooks and definitive references2,3,4,5 have emerged and are one of the criteria.

Fellowships are an additional element needed to form the basis of a unique academic discipline. While several Disaster Medicine Fellowships exist,6 few have focused on international applicants or disaster medicine specifically.7 FELLOWSHIP OVERVIEW Introduction The emergency department (ED) offers a one- to two-year post-graduate fellowship in Disaster Medical Sciences to U.S. and international physicians. The Fellowship Year 1 covers the core curriculum. The optional Fellowship Year 2 is for applicants

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who wish to pursue a Masters of Public Health and more in-depth research and training in Disaster Medical Sciences. Participants in the two-year fellowship program may choose to begin Masters work during their first year of training. It is anticipated that most applicants will complete the two-year program.

•

Demand for Training For international applicants, the sponsoring country must confirm in writing the need for qualified practitioners in Disaster Medicine. The applicant must describe how the skills and knowledge gained during the fellowship will be applied to improve future disaster management in the home country.

•

Institutional Resources Full access to the resources of the university is provided to the successful applicant. This includes library and internet resources, access to training and simulation materials, office space, statistical support for research, and access to administrative and educational meetings and multidisciplinary faculty including nurse disaster experts. In addition, the applicant will have access to the county Emergency Medical Services Agency and the county Fire Authority as off-site resources. The university hospital is a Level I trauma center, burn center, cardiac center and stroke receiving center with a well-established emergency medicine residency and traditional (domestic) disaster medicine fellowship program.

Research • Understand the fundamentals of disaster research including the unique characteristics that separate it from traditional research approaches • Compare and contrast the pros and cons of disaster research methodologies • Critically analyze existing disaster literature • Develop proposals for important research questions for the future of Disaster Medical Sciences

DETAILS OF THE TRAINING PROGRAM Educational Goals and Objectives The educational goals and objectives of the Fellowship are to acquire the knowledge and skills related to Disaster Medical Sciences and to implement those skills with the aim of improving the home country’s level of preparedness (both national and hospital-based) for critical incidents and disasters. To achieve this overriding objective, the following are specific goals:

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•

Administrative • Acquire skills in regional emergency response plans and concept of operations • Learn prehospital and hospital-based management of mass casualty incidents from both conventional and chemical-biological-radiological-nuclear causes • Gain skills in developing and participating in a minimum of two large-scale disaster preparedness exercises, each focusing specifically on prehospital and hospital responses • Develop the skills to understand and apply the National Incident Management System

Funding The sponsoring country of the applicant is responsible for all salary, tuition, and expenses, including insurance and benefits, related to the fellowship. An official letter is required of the applicant to confirm this coverage for the duration of the fellowship period.

Clinical • Gain expertise in treating trauma patients with penetrating injuries and blast injuries • Learn and master how to evaluate and manage hazardous materials casualties • Improve knowledge of procedures and clinical skills by close observation in the ED, e.g., trauma patients with penetrating injuries (gunshot wounds), blast injuries, hazardous materials casualties • Obtain expertise in mass casualty triage

•

Acquire skills in the evaluation of trauma patients with penetrating and blast injuries Learn to diagnose and manage hazardous materials casualties Master mass causality and large-scale event management Gain skills in post mass casualty management, planning, reevaluation of resources, preparing for a second surge and utilizing the data and the experiences gained to improve future responses and research

Prehospital • Learn how triage systems work • Understand casualty flow management and tracking and the use of novel devices • Gain familiarity with communications systems and casualty-dispatch management in mass casualty incidents • Develop knowledge of unique hazards and scene safety during disasters Hospital • Learn how the Hospital Incident Command System functions • Describe hospital decontamination protocols for chemical, biological and radiological hazards • Understand the principles of maximizing hospital surge capacity • Develop skills in the allocation of scarce resources after a disaster

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International Disaster Medical Sciences Fellowship Table 2. ABEM/ECFMG–Approved - International Disaster Medical Sciences Fellowship Core Curriculum Disaster Medicine Core Content Categories

2.11

2.12

2.13

2.14

2.15

2.16

2.17

1.0 Conceptual Framework and Strategic Overview of Disasters

1.1 Disaster Nomenclature

1.2 Disaster Research and Epidemiology

1.3 Disaster Education and Training: Linking Individual and

Organizational Learning and Performance

1.4 Surge Capacity

1.4.1 Critical Thinking in a Resource Poor Environment

1.4.2 Alternate Care Sites

1.5 International Perspectives on Disaster Management

1.6 Ethical Issues in Disaster Medicine

1.7 Emerging Infectious Diseases: Concepts in Preparing for

and Responding to the Next Microbial Threat

1.8 Disaster Mental and Behavioral Health

1.9 Special Populations

Emergency Medical Services Scene Management 2.11.1 Recognition, Notification, Initiation 2.11.2 Scene Safety 2.11.3 Search and Rescue 2.11.4 Transportation Health Care Facility Disaster Management 2.12.1 Hospital Incident Command System 2.12.2 Allocation of Scare Resources 2.12.3 Evacuation Mortuary Affairs Crisis and Emergency Risk Communication Telemedicine and Telehealth Role in Public Health Emergencies Complex Public Health Emergencies Patient Identification and Tracking

3.0 Clinical Management

3.1 Chemical-Biological-Radiological-Nuclear and

Hazardous Materials

3.1.1 Traumatic and Explosive Events

3.1.1.1 Management of Crush Injury

3.1.1.2 Management of Compartment

Syndrome

3.1.1.3 Management of Crush Syndrome

3.1.2 Burn Patient Management

3.1.3 Clinical Aspects of Large-Scale Chemical Events

3.1.4 Biological Events

3.1.5 Nuclear and Radiological Events

3.1.5.1 Dirty Bomb

3.1.5.2 Nuclear Detonation

3.1.6 Hazmat, Toxic, and Industrial Events

3.2 Environmental Events

3.2.1 Floods

3.2.2 Hurricanes

3.2.3 Tornadoes

3.2.4 Earthquakes

3.2.5 Tsunamis

3.2.6 Winter Storms

3.2.7 Heat Waves

3.2.8 Volcanoes

2.0 Operational Issues

2.1 Public Health and Emergency Management Systems

2.1.1 National Incident Management System

2.1.2 Incident Command System

2.1.3 Communications

2.1.4 Media

2.1.5 Phases of Emergency Management (Mitigation,

Preparedness, Response, Recovery)

2.1.6 All-Hazard Approach

2.1.7 Resource Management

2.1.8 Volunteer Management

2.1.9 National Disaster Medical System

2.1.10 Personal Preparedness

2.2 Legislative Authorities and Regulatory Issues

2.3 Syndromic Surveillance

2.4 Disaster Triage

2.5 Personal Protective Equipment

2.6 Decontamination

2.7 Quarantine

2.8 Mass Dispensing of Antibiotics and Vaccines

2.9 Management of Mass Gatherings

2.10 Transportation Disasters

ABEM, American Board of Emergency Medicine; ECFMG, Educational Commission on Foreign Medical Graduates.

CORE CURRICULUM The Disaster Medical Sciences Core Curriculum is based on the experience of the developers (including academic and government), review of existing professional organizations’ committee products, and definitive disaster medicine references.

As outlined in Table 2, the core content categories are divided into a Conceptual Framework and Strategic Overview of Disasters (including terminology), Operational Issues, and Clinical Management. This Core Curriculum was submitted to the American Board of Emergency Medicine (ABEM) and the Accreditation Council for Graduate Medical Education (ACGME) as part of the approval process for the Fellowship (see below).

DESCRIPTION OF REQUIRED ROTATIONS Sample educational and learning opportunities and activities are listed in Table 3. Specific rotations include: University Medical Center and Campus Clinical Participate in patient care and management discussions Western Journal of Emergency Medicine

on rounds, at morbidity and mortality conferences, and at journal clubs as related to Disaster Medical Sciences. Engage in interactive discussions and training sessions with experienced Professors of Emergency Medicine. At the end of this rotation, the candidate will have gained an understanding of triage and clinical management of disaster casualties including those from chemical, biological, radiological/nuclear, and blast/high explosive causes.

Research Study the fundamentals of disaster research and the unique characteristics of disaster research methodologies. Critically analyze existing disaster literature and present critiques at conferences and journal clubs. Develop proposals for important cutting-edge disaster research questions. At the end of this rotation, the candidate will have gained an understanding of the unique issues surrounding disaster research, limitations of current published data, and critical areas for future exploration.

Teaching Develop and deliver didactic, interactive, and hands-on

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sessions for medical students, residents, and nurses involved with disaster management. Participate in training for disaster drills and disaster preparedness including the Hospital Incident Command System, personal protective equipment, and decontamination procedures. At the end of this rotation, the candidate will have gained experience with teaching multidisciplinary groups of disaster healthcare providers using various teaching methodologies.

Table 3. Sample Educational and Learning Opportunities and Activities

Administrative Coordinate input to hospital and university committees and task forces for disaster planning based on a regional hazard vulnerability analysis. Participate in protocol development using evidence-based methodologies. Work with the University-wide Program in Public Health, including campus-associated research centers such as the Urban Water Research Center, and the Nursing Administration to address critical disaster management issues. At the end of this rotation, the candidate will have gained critical thinking skills and practical experience in addressing cutting-edge disaster challenges for healthcare systems.

Meetings, Workshops and Conferences Hospital disaster planning committee meetings Meetings for the county EMS network Hospital emergency preparedness coordinator meetings Regional paramedic supervisory committee meetings Emergency Medical Services base hospital director meetings Workgroup conference calls County Public Health Department training, meetings, and conferences Disaster Medical Assistance Team meetings Medical Reserve Core meetings Regional fire authority meetings and ride-alongs Meetings with regional fire authority medical director Emergency department personal protective equipment and decontamination training Annual statewide disaster exercise Visits to federal authorities in Washington DC

Off-site Emergency Medical Services and Fire Authority Attend meetings, participate in drills and evaluate protocols.

One-on-one experience with the county Fire Authority Medical Director, visits to the Emergency Operations Center, and paramedic ride-alongs. At the end of this rotation, the candidate will have gained experience in managing prehospital disaster scenarios.

Annual local and regional emergency medicine conferences National Disaster Life Support conferences and trainings American College of Emergency Physicians Scientific Assembly Medical library workshops, e.g., Refworks, Pubmed University meetings on public health topics such as urban water supplies Teaching Opportunities

Public Health Participate in planning activities, evaluate strategies for public health preparedness, and recognize cutting-edge public health threats. One-on-one experience with the Medical Director, Emergency Medical Services, County Health Care Agency and evaluation of incident management systems for public health. At the end of this rotation, the candidate will have an understanding of the role public health plays in disasters and have gained enhanced knowledge of public health emergency systems and management.

Teaching medical students • Triage • Mass Casualty Management • Pandemic Preparedness • Bioterrorism European Master in Disaster Medicine curriculum development Paramedic teaching Continuing Education Weekly emergency medicine grand rounds Monthly journal clubs

Disaster Management Systems Evaluate local, regional, state and national systems for disaster management, inter and intra-agency communications, and cross-cutting issues. One-on-one experience with the Director of Emergency and Trauma Services, Disaster Medical Assistance Team, stockpiling and antidote strategies and planning, and surge capacity approaches. At the end of this rotation, the candidate will have gained knowledge of approaches to organizing disaster response at all levels and experience in allocation of scarce resources during a disaster.

Grand rounds for other services • Internal Medicine • Neurology • Trauma

State Activities Participate in statewide advisory group planning meetings

University on-line basic disaster training and extension courses

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Self Learning Centers for Disease Control and Prevention conference calls and webcasts Federal Emergency Management Agency, Emergency Management Institute Independent Study Program Professional Development Series

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International Disaster Medical Sciences Fellowship and related action items. One-on-one experience with the state senior health advisor for disaster management and analysis of disaster planning approaches. At the end of this rotation, the candidate will have gained experience in statewide approaches to disaster management including barriers and opportunities.

Disaster Congresses Attend symposia, meetings, and congresses related to disaster medicine. Participate in the National American College of Emergency Physicians Scientific Assembly Disaster Committee and Disaster Section Meetings and attend short courses related to disaster medicine. Meetings with national leaders in disaster medicine will be facilitated by the fellowship director. At the end of this rotation, the candidate will have gained national level perspectives and understand variable strategies and operational approaches to disaster management.

Federal Government (second year of program) Evaluate federal systems for disaster management and participate in one-on-one meetings with key government officials in Washington, DC including at the Office of the Assistant Secretary for Public Health Preparedness and Response, Health and Human Services; Office of Health Affairs and Federal Emergency Management Agency, Department of Homeland Security; the Institute for Global and Regional Readiness,8 and the Institute of Medicine. At the end of this rotation, the candidate would be able to demonstrate an understanding of federal disaster management systems and explain critical gaps in the federal management of catastrophic disasters.

International (second year of program) Participate in health policy advisory groups (such as the German Institute for Emergency Medicine),9 research centers (such as the Israeli Ben Gurion Center for Research of Preparedness and Response to Emergencies and Disasters),10 and teaching via the European Master in Disaster Medicine.11 At the end of this rotation, the candidate will have gained knowledge regarding various international approaches to disaster management, established relationships with internationally renowned disaster researchers, and acquired an understanding of distance learning approaches to international teaching.

Masters of Public Health (completed in the second year of the program) Complete rigorous course work and a publishable thesis for the university’s public health program. At the end of this rotation, the candidate will have gained the ability to solve public health problems in disasters by applying professional multi-disciplinary approaches and methods in a specialized environment such as local, state or national public health agencies and health care organizations.

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SKILLS DEVELOPMENT A variety of methods are used to develop the applicant’s skills. These include: • Didactic sessions (e.g., attend weekly emergency medicine grand rounds, participate in medical student disaster training sessions) • Hands-on training sessions (disaster simulations and drills) • Distance learning over the internet • Exposure to clinical management of disaster casualties • Master current disaster literature – attend monthly journal clubs • Assigned readings and discussion of chapters in Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices published

by Cambridge University Press, Sponsored by the American College of Emergency Physicians, Foreward

by Dr. Richard Carmona, 17th Surgeon General of the United States.2,12 • Attend and participate in disaster health policy meetings and forums at hospital, county, statewide and national levels • Perform “action item” assignments from disaster task forces that address current threats OPTION FOR TWO-YEAR TRAINING In order to extend the training to two years, satisfactory progress and a progression of activities must be demonstrated.

Requirements include: • Successful completion of the first year of Fellowship training • Masters of Public Health course work • Disaster Medical Sciences publishable research project • Additional Rotations o Federal Government (Department of Homeland Security, Federal Emergency Management Agency, Department of Health and Human Services, Office of the Assistant Secretary for Public Health Preparedness and Response, Agency for Healthcare Research and Quality) o World Association of Disaster and Emergency Medicine o European Master in Disaster Medicine o International Disaster Conferences – presentation of research and participation in health policy committees and task forces EVALUATION METHODS A rigorous method of evaluation includes the following: • Daily communications with Fellowship director • Weekly meetings with core faculty to evaluate progress

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Successful completion of research project on disaster medicine topic Twice yearly formal evaluations and feedback from Fellowship Director

Table 4. Administrative Requirements for International Disaster Medical Sciences Fellowship Applicants The applicant needs at least 9 months for processing of the paperwork.

PROCESS TO ESTABLISH AN INTERNATIONAL DISASTER MEDICAL SCIENCES FELLOWSHIP AT A U.S. ACADEMIC INSTITUTION While an alternate body (the American Board of Physician Specialists) provides board certification for Disaster Medicine,13 ABEM, a mainstream accrediting body and one of the 24 medical certification boards recognized by the American Board of Medical Specialties, does not currently recognize Disaster Medicine as a subspecialty. The International Disaster Medical Sciences Fellowship is therefore classified as a nonstandard training program per the Accreditation Council for Graduate Medical Education (ACGME), subject to a number of requirements.14 The American Board of Emergency Medicine (ABEM) updated their policy in April 2009 to allow for approval of non-standard fellowships.15 A J-1 visa is necessary for entrance into the United States for such nonstandard educational experiences. Because the fellowship is non-standard, the process to issue a J-1 student exchange visa through the Educational Commission for Foreign Medical Graduates (ECFMG) is different than the much simpler procedure followed for an accredited fellowship, such as toxicology or sports medicine.

The prospective foreign medical applicant must complete an application that includes specific documentation requirements to be eligible for sponsorship for a visa from the ECFMG. The ECFMG is the only entity permitted to provide a J-1 visa. Once the applicant successfully completes the application process, the ECFMG issues a one-year visa. This must be renewed if the candidate remains for an additional year.

The renewal process should be started about 6 months prior to the end of the first year.

In addition to paperwork from the applicant, the sponsoring U.S. institution must submit a variety of items to an academic entity, in this case the ABEM, which in turn must give approval of the fellowship’s academic content to the ECFMG. The ECFMG requests a document, signed by the fellowship director, that contains the fellowship core curriculum and confirms that the sponsoring institution has an accredited residency program.

There are two types of applicants: 1) Someone already training in the U.S. who needs a “continuation” visa and 2) someone residing outside the U.S. who needs an “initial” visa.16 The paperwork is more complex for an applicant who needs a “continuation visa” from an accredited training program (such as a U.S. emergency medicine residency) since the visa type must be modified rather than simply extended. In either case, at least 9 months is needed to progress through the application process. Table 4 provides a detailed outline of steps and timelines for international applicants.

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1)

ABEM LETTER OF SUPPORT FOR THE FELLOWSHIP (obtained for this International Disaster Medicine Sciences Fellowship in May 2009 after new ABEM policy enacted in April 2009). Needs 8 weeks.

2)

GRADUATE MEDICAL EDUCATION COMMITTEE (GMEC) ENDORSEMENT AND PROGRAM VERIFICATION FORM. Last page on the application that requires signatures of the dean, program directors, department chairs, and others at the host university.

3)

FELLOWSHIP PROGRAM DESCRIPTION. The same one should be sent to both ABEM and the ECFMG to avoid the delays.

4)

CONTRACT OR LETTER OF OFFER from host institution to embassy of sponsoring country.

5)

APPLICATION FORM FOR INITIAL SPONSORSHIP. Pages number 4 and 5 of the applications must be completed by the applicant and the remainder by the Training Program Liaison (TPL) of the host university.

6)

STATEMENT OF NEED. Ministry of Health or other sponsor (e.g., University, Military, or Private Sector/ Industry) in applicant’s home country - needs 8-12 weeks to complete the application process.

7)

CURRENT CURRICULUM VITAE

8)

COPY OF PASSPORT NAME PAGE(S)

9)

STATEMENT OF EDUCATIONAL OBJECTIVES. Personal letter.

10)

ADMINISTRATIVE FEE. Payable on line prior to processing.

11)

SEVIS I-901 FEE AND THE US EMBASSY FEE when applying for a visa at the US Embassy in the applicant’s home country. Note: these fees are not part of the ECFMG application, but must be submitted in order to get the visa.

12)

ADDITIONAL DOCUMENTATION Copies of Form(s) IAP-66/DS-2019 if the applicant has previously held a J-1 visa status (not applicable for an initial application).

FUTURE DIRECTIONS In the future, when Disaster Medicine becomes an ABEM recognized subspecialty, the fellowship would no longer be considered “non-standard,” and therefore this entire process would be markedly streamlined for a foreign applicant who has completed a U.S. emergency medicine residency. On the other hand, it might become impossible for a U.S. institution to sponsor someone from outside the country. This must be closely monitored, as the importance of global training in Disaster Medical Sciences will remain for the foreseeable future and perhaps even increase as new issues such as global warming emerge.17

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International Disaster Medical Sciences Fellowship Since Disaster Medicine is, by its nature, a multidisciplinary field of science, diverse groups have addressed its development.

In the future, a comprehensive multidisciplinary national or even international core curriculum should be developed and endorsed by major academic societies involved in disaster management.

A consortium for international disaster medicine fellowships would be desirable. These fellowships should contribute to an international database of Disaster Medical Sciences literature (including non-English language papers) and research projects should be completed as part of each fellowship to further improve the science. International research databases would improve access to seminal and cutting-edge work and foster collaboration on future initiatives.

Long term follow-up of health effects on the host country should be tracked and used to inform changes in national and international health policy. Flexibility should be built in to fellowship training to accommodate teaching country-specific skills (based on needs and resources). The issues of different cultures and languages should be addressed. Researchers should be trained to share knowledge without the artificial boundaries produced by lack of English language skills. A standardized disaster nomenclature that integrates across all languages and cultures is urgently needed.

and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

REFERENCES 1.

emergencymed.uci.edu/emsdms_faculty.htm. Accessed October 19, 2009.

2.

Koenig KL, Schultz CH. Koenig and Schultz’s Disaster Medicine, Comprehensive Principles and Practices. Cambridge, UK: Cambridge University Press; 2010.

3.

Hogan DE, Burstein JL. Disaster Medicine. Philadelphia, PA: Lippincott Williams and Wilkins; 2007.

4.

Ciottone GR. Disaster Medicine. Philadelphia, PA: Mosby; 2006.

5.

Noji EK. The Public Health Consequences of Disasters. New York, NY: Oxford University Press; 1997.

6.

Society of Academic Medicine. Disaster Medicine. September 23, 2009. Available at: http://www.saem.org/saemdnn/Home/Communities/ Fellows/Fellowship/DisasterMedicine/tabid/851/Default.aspx. Accessed October 19, 2009.

7.

Bledsoe GH, Dey CC, Kabrhel C, et al. Current status of International Emergency Medicine fellowships in the United States. Prehosp Disaster Med. 2005; 20:32-5.

8.

Barbisch D. The Institute for Global and Regional Readiness.

Available at http://www.cnp.pitt.edu/members/IGRR/home.htm.

CONCLUSION The process to establish a one to two-year International Disaster Medical Sciences Fellowship including a model evidence-based core curriculum is described. This information will prove useful to both prospective international fellowship candidates and U.S.-based institutions that seek to establish comprehensive International Disaster Medical Sciences programs. Educating people in disaster medicine globally influences education and research and furthers collaboration beyond the fellowship. This extends into areas of research and health policy. In addition, these informal networks of trained personnel will facilitate management of real-time disasters.

Intangible future rewards will result by connecting the spheres of influence of thought leaders in disaster medicine.

Accessed October 19, 2009.

9.

German Institute for Emergency Medicine. Available at: http://www.ifnhamburg.de/internationale_Berater.html. Accessed October 19, 2009.

10. Aharonson-Daniel L. PReparED Center -The University Center for Research on Preparedness and Response to Emergencies and Disasters. Ben-Gurion University of the Negev. Available at: http:// cmsprod.bgu.ac.il/Eng/Centers/emergency. Accessed October 19, 2009.

11. European Master in Disaster Medicine - EMDM. About the EMDM. 2009. Available at: http://www.dismedmaster.com/public/. Accessed October 19, 2009.

12. Cambridge University Press. Koenig and Schultz’s Disaster Medicine.

2009. Available at: http://www.cambridge.org/us/catalogue/catalogue. asp?isbn=0521873673. Accessed October 19, 2009.

Acknowledgements The authors gratefully acknowledge the support of Amal Khalil, emergency department administrator and Darlene Bradley, RN, MSN, MAOM, CCRN, CEN, Director of Emergency and Trauma Services, University of California, Irvine (UCI) Medical Center. In addition, appreciation is expressed to the first pioneers of the UCI International Disaster Medical Sciences Fellowship: Drs. Hoon Chin Lim (Singapore) and Anwar AL-Awadhi (Kuwait).

13. American Board of Physician Specialties. Eligibility Requirements.

September 2008. Available at: http://www.abpsus.org/certification/ disaster_medicine/eligibility.html. Accessed October 19, 2009 14. Educational Commission for Foreign Medical Graduates. Summary of Discussions on J-1 Sponsorship Issues. Available at: http://www.ecfmg. org/evsp/summary1002.pdf. Accessed October 19, 2009 15. American Board of Emergency Medicine. Policy on J-1 Visa Recognition. April 2009. Available at: Policy on J-1 Visa Recognition.

Accessed October 19, 2009.

16. Educational Commission for Foreign Medical Graduates. Non-Standard

Address for Correspondence: Kristi L. Koenig MD, Department of Emergency Medicine, University of California, Irvine. Email: KKoenig@uci.edu

Training: Application Materials. June 30, 2009. Available at: http://www. ecfmg.org/evsp/nonstand.html#emerg. Accessed October 19, 2009.

17. Bey T, von Weizsäcker EU, Koenig KL. Global warming: polar bears

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources,

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EMS and Disaster Medicine Faculty. Available at: http://www.

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and people--implications for public health preparedness and disaster medicine: a call to action. Prehosp Disaster Med. 2008; 23:101-2.

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Perspectives

CAL/ACEP Joins CAL/AAEM and UC Irvine in Sponsoring the Western Journal of Emergency Medicine William K. Mallon, MD* Stuart P. Swadron, MD†

* Immediate Past-President, California Chapter of the American College of Emergency Physicians † Immediate Past-President, California Chapter of the American Academy of Emergency Medicine

Supervising Section Editor: Mark I. Langdorf, MD, MHPE Submission history: Submitted October 1, 2009; Accepted October 14, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[WestJEM. 2009;10(4):220-221.]

When you look at the Western Journal of Emergency Medicine’s (WestJEM) cover and masthead this month you will see something new: two logos side by side, the California Chapter of AAEM (CAL/AAEM) and the California Chapter of ACEP (CAL/ACEP). Based on an agreement forged this year, CAL/ACEP has joined CAL/AAEM and the Department of Emergency Medicine at the University of California, Irvine (UCI) in the sponsorship of the journal. All members of CAL/ ACEP will now receive the journal electronically through the CAL/ACEP Sacramento office.

WestJEM and its predecessor, the California Journal of Emergency Medicine (CalJEM), have been a part of the peer-reviewed literature in emergency medicine for almost a decade. Over the past few years, the editorial staff has devoted itself to the task of transforming WestJEM from a regional journal to one of national (and indeed international) significance. The journal provides a venue for authors to present high quality research and educational content of interest to a worldwide community of emergency physicians, both academic and clinical. As the number and variety of submissions have increased briskly, a growing and conscientious editorial team has improved standards for reporting, disclosure and methodology. An important measure of the journal’s success is its recent inclusion in Pub Med Central (www.pubmedcentral.nih.gov), the electronic archive service of the U.S. National Institutes of Health. This is a critical milestone for any independent journal, and it indicates a broad acceptance into the academic community.

WestJEM has always been an open access journal – that means that it is free to access from any web portal in the world at www.westjem.org. In today’s global outreach to help advance medical care in developing countries, as well as the U.S., free timely access to medical knowledge is vital. WestJEM is also doing its part to provide information to increase the spread of the specialty of emergency medicine throughout the world.

WestJEM is an open access journal with high transparency Volume X, no. 4 : November 2009

and academic fidelity, adhering to a Creative Commons non-commercial attribution license, which allows authors to retain copyright and promotes others to build on the presented findings through referencing the original work.

So, while many have asked the question “do we really need another journal for emergency medicine?,” we feel that the very nature and success of WestJEM make the answer selfevident. We obviously need this type of journal in our field.

It has not been easy. Early this year, the founding sponsors, CAL/AAEM and UC Irvine, were struggling with the financial burden of maintaining WestJEM’s viability.

As the size and scope of the journal expanded over the past couple of years, the financial burden was increasing and WestJEM was reaching out for additional sponsorship that would guarantee the journal’s future. In an unusual move, the founders of WestJEM reached across what many perceive as a “divide” to approach CAL/ACEP as a potential partner in sponsoring the journal.

While at the national level AAEM and ACEP have had their share of rows, in California a spirit of cooperation and collaboration has existed between the two state chapters for many years. In California we can agree to disagree on some issues, and genuinely agree on many more. Through it all the discourse remains civil and productive to both societies. Dr. Tom Sugarman took the lead negotiating position on behalf of the CAL/ACEP board, and we are both grateful for his efforts.

We would also like to recognize the efforts of Drs. Steve Gabaeff and Ingrid Lim on behalf of CAL/AAEM and Drs. Shahram Loftipour and Mark Langdorf at the journal to help us reach an agreement that enables the three organizations to come together to ensure a bright future for a burgeoning journal.

Finalizing this deal was the last important piece of business in both of our respective presidencies, and it is gratifying to see this once-distant dream become a reality. Although important issues needed to be addressed initially to safeguard the interests

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CAL/ACEP Joins CAL/AAEM and UC Irvine of both societies, it soon became apparent that the vast majority on both Boards of Directors wanted this agreement to proceed.

After months of meetings, drafts, redrafts, votes, conference calls and a lot of patience, we were eventually able to find a way to address the concerns of all parties.

This collaboration means a lot to both of us. We believe that the California emergency medicine community as a whole benefits when we work together. Hopefully this will also help push along other collaborations between our two societies in other states and throughout the whole nation. While CAL/ AAEM and CAL/ACEP still have differences in philosophy and approach, we feel that our efforts on many issues can be synergistic and constructive. We recommend that our residents become members of both CAL/ACEP and CAL/AAEM, and we recognize that they both have a role in protecting their future and that of their chosen specialty.

Western Journal of Emergency Medicine

One more important point: both CAL/ACEP and CAL/ AAEM have agreed that the journal is a place for scholarship, not politics. The editorial board remains appropriately independent of all sponsoring societies and its singular goal is to generate the best possible journal each quarter.

So, please continue to enjoy WestJEM. Encourage your colleagues to read it, participate in its content and consider receiving a print copy for all emergency physicians in a practice at a very low yearly departmental subscription rate.

Now, more than ever, we can truly say, “This is our journal!�

Address for Correspondence: Stuart Swadron, MD, Department of Emergency Medicine, LAC+USC Medical Center, Unit #1, Room 1011, 1200 N. State Street, Los Angeles, CA 90033. Email: swadron@usc.edu

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Perspectives

Boarder Patrol: A Reform Policy for America’s Paralyzed Emergency Departments Peter J. Bloomfied, MD, MPH* Adam B. Landman, MD, MS, MIS† Robert C. Rosenbloom, MD*

* Olive View-UCLA Medical Center, Department of Emergency Medicine, Sylmar, CA; Brotman Medical Center, Department of Emergency Medicine, Culver City, CA † Robert Wood Johnson Foundation Clinical Scholars Program, Yale University School of Medicine, Department of Emergency Medicine, New Haven, CT; US Department of Veterans Affairs, West Haven, CT

Supervising Section Editor: Mark I. Langdorf, MD, MHPE Submission history: Submitted August 8, 2008; Revision Received August 12, 2009; Accepted August 22, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[WestJEM. 2009;10(4):222-224.]

The story is not new. America’s emergency departments (EDs) are frequently overcrowded, their ability to provide high quality emergency care compromised by lack of space and required attention to admitted patients boarding in the ED, awaiting a hospital bed upstairs.

We first experienced ED boarding as residents where signouts were along the lines of: “Sixty-year-old male, sign-out of a sign-out, admitted, boarding for the past 48 hours, chest pain patient, I think.” To an ED resident, the problem was clear. Later, at a California Chapter of the American College of Emergency Physicians (Cal/ACEP) meeting, we were surprised when a visiting state representative, asked about her approach to ED boarding, replied, “What’s boarding?” We realized that many of our elected representatives, patients, and hospital leaders are not aware of the true cause of ED crowding. With the support of Cal/ACEP, we developed a short video to explain to the layperson what boarding is, its causes, consequences, and possible solutions (availble under “Supporting Material” of the article at http://escholarship.org/ uc/uciem_westjem).

The Problem and Consequences What we saw in our training program is actually a national problem. According to the National Hospital Ambulatory Medical Care Survey, 87% of large, high volume EDs board patients, and 83% of EDs overall board patients.1 A growing body of evidence shows that ED crowding negatively impacts patients’ health. According to a recent Government Accounting Office (GAO) report, the average wait time for a critical patient that should be seen IMMEDIATELY was 28 minutes.2 Crowding has been shown to increase the rate of medical errors,3 and studies suggest an increased mortality of 30%4,5 and a doubling of the rate of serious complications from acute coronary syndrome.6 Recent studies have also shown an association between ED crowding and delay or failure to receive antibiotics or Volume X, no. 4 : November 2009

pain medications.7-9 Even more concerning, a 2007 study of ICU boarders found that they had 30% higher mortality than non-boarders, after adjustment for severity of illness.10 This suggests that boarding critically ill patients, in terms of mortality, may be equivalent to withholding aspirin from patients having heart attacks.

The Causes The causes of crowding are complex; however, studies have repeatedly shown that the major driver of ED crowding is lack of inpatients beds for admitted ED patients.11,12 These “boarders” spend hours to days in the ED, taking up space where new patients should be seen.

Some common misconceptions about ED crowding are worth clarifying. Uninsured patients are not the driver of ED crowding; growth in ED visits is actually due to insured individuals.13 Moreover, the problem is not one of inadequate ED beds. Although 45 hospitals and 44 EDs closed in California between 1996 and 2007, existing EDs have expanded beds by 26%,14 at a rate outpacing population growth. The ratio of ED beds to patient visits has actually improved.

Finally, the issue is not one of EDs being crowded by non-emergent patients. In fact, the true cause of crowding and boarding is that the EDs are crowded by sicker patients. In 2002 in California, 48% of total ED visits were urgent or nonurgent. In 2007, the proportion of these lower acuity patients fell to 33%, leaving more moderate, severe, or critical acuity patients.14 With sicker patients presenting to the ED, it makes sense that the admission rate climbed as well, contributing to more patients boarding in the ED.14

Possible Solutions With costs to build new hospital inpatient and ED beds approximately $1 million per bed, new construction is an untenable short-term solution.15 The key to alleviating

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Boarder Patrol crowding is improving patient flow, from ED entry to in-patient bed and ultimately to appropriate discharge, requiring the commitment and cooperation of leadership and staff throughout the hospital. One effective strategy at State University of New York-Stony Brook relocates admitted patients during times of ED and hospital crowding to inpatient wards regardless of bed availability. This strategy has reduced ED crowding and is preferred by patients.16,17 Even a bed in a hallway upstairs on an inpatient unit is preferable to the chaos and noise of the ED. At Los Angeles County+USC Medical Center, a hospital-wide surge plan is routinely activated as their hospital or ED reaches threshold crowding levels. Hospital resources are successively mobilized, including inpatient hallways, to maximize ability to delivery patient care.18 Other creative approaches include inpatient discharge lounges, streamlining nurse sign-outs, reducing specialty consultant response times, encouraging timely patient discharge, and improving admission and discharge processes.14,19

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias.

Disclosures: Dr. Rosenbloom is President of the California Chapter of the American College of Emergency Physicians (Cal/ACEP).

Funding: This project was generously funded by the California Chapter of the American College of Emergency Physicians (Cal/ACEP). Dr. Landman is currently in the Robert Wood Johnson Foundation Clinical Scholars Program and is funded by the US Department of Veterans Affairs and the Robert Wood Johnson-- Foundation.

REFERENCES 1.

Nawar EW, Niska RW, Xu J. National Hospital Ambulatory Medical Care Survey: 2005 emergency department summary. Adv Data.

2007; 386:1-32.

2.

US Government Accounting Office. Hospital emergency departments: crowding continues to occur, and some patients wait longer than recommended time frames. GAO-09-347. April 2009. Available at:

CONCLUSION The “Boarder Patrol” video complements recent popular press and review articles and represents our effort to inform non-emergency caregivers on how ED boarding plays a significant role in ED crowding and increases patient morbidity and mortality.20,21 Emergency physicians can be leaders, guiding efforts to reduce ED crowding using evidence-based practices.

We highly encourage policy makers to enact legislation, such as California’s AB-911,22 enabling and encouraging hospital administrations to bring about critical and necessary structural and cultural changes to help admitted patients depart the ED so patients in waiting rooms and in ambulances can be seen promptly. California’s overcrowding bill was unfortunately vetoed because the Governor apparently misunderstood that emergency physicians and hospitals were aligned in the goal to decrease boarding admitted patients in the ED when in fact hospitals may have a perverse financial incentive to divert inpatient beds for patients undergoing elective procedures.23 Increased public pressure on hospitals, The Joint Commission, governors and legislators demonstrates that boarding is an unacceptable practice.

http://www.gao.gov/new.items/d09347.pdf. Accessed August 6, 2009.

3.

Weissman JS, Rothschild JM, Bendavid E, et al. Hospital workload and adverse events. Med Care. 2007; 45:448-55.

4.

Richardson DB. Increase in patient mortality at 10 days associated with emergency department overcrowding. Med J Aust. 2006; 184:213-6.

5.

Sprivulis PC, Da Silva JA, Jacobs IG, et al. The association between hospital overcrowding and mortality among patients admitted via Western Australian emergency departments. Med J Aust. 2006; 184:208-12.

6.

Pines JM, Pollack CV Jr, Diercks DB, et al. The association between emergency department crowding and adverse cardiovascular outcomes in patients with chest pain. Acad Emerg Med. 2009; 16:617-25.

7.

Fee C, Weber EJ, Maak CA, et al. Effect of emergency department crowding on time to antibiotics in patients admitted with communityacquired pneumonia. Ann Emerg Med. 2007; 50:501-9,509e.1.

8.

Pines JM, Hollander JE. Emergency department crowding is associated with poor care for patients with severe pain. Ann Emerg Med. 2008; 51:1-5.

9.

Pines JM, Localio AR, Hollander JE, et al. The impact of emergency department crowding measures on time to antibiotics for patients with community-acquired pneumonia. Ann Emerg Med. 2007; 50:510-16.

10. Chalfin DB, Trzeciak S, Likourezos A, et al. Impact of delayed

Acknowledgements The Boarder Patrol video would not have been possible without the contributions and commitment of all the patients, actors, and content experts as well as the leadership and staff of Cal/ACEP. A special thank you to Arna Vodenos and Robert Davidian, who provided much of their high quality, professional film making services in kind for this project.

transfer of critically ill patients from the emergency department to the intensive care unit. Crit Care Med. 2007; 35:1477-83.

11. Hoot NR, Aronsky D. Systematic review of emergency department crowding: causes, effects, and solutions. Ann Emerg Med. 2008; 52:126-136.

12. Khare RK, Powell ES, Reinhardt G, et al. Adding more beds to the emergency department or reducing admitted patient boarding times:

Address for Correspondence: Adam Landman, Robert Wood Johnson Clinical Scholars Program, Yale University, 333 Cedar Street, IE-61 SHM, PO Box 208088, New Haven, CT 06510-8088.

Email: adam.landman@yale.edu

which has a more significant influence on emergency department congestion? Ann Emerg Med. 2009; 53:575-85.

13. Newton MF, Keirns CC, Cunningham R, et al. Uninsured adults presenting to US emergency departments: assumptions vs data.

JAMA. 2008; 300:1914-24.

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14. California HealthCare Foundation. Is California’s Hospital-Based

Boarder Patrol 19. ACEP Task Force on Boarding. Emergency department crowding:

ED System Eroding? July 2009. Available at: http://www.chcf.org/

high-impact solutions�. April 2008. Available at: http://www.acep.org/

documents/hospitals/EDSystemCapacityDemand.pdf. Accessed

workarea/downloadasset.aspx?id=37960. Accessed August 6, 2009.

August 6, 2009.

20. Meisel Z and Pines JM. Weaiting doom: how hospitals are killing ER

15. Gregor A. Hospitals merge design and building to cut costs. New York Times. April 15, 2009:B7.

patients. Slate. 2008.

21. DeLia D and Cantor J. Emergency department utilization and capacity.

16. Garson C, Hollander JE, Rhodes KV, et al. Emergency department

July 2009. Available at: http://www.rwjf.org/files/research/072109policy

patient preferences for boarding locations when hospitals are at full capacity. Ann Emerg Med. 2008; 51:9-12,12 e.11-13.

synthesis17.emergencyutilization.pdf. Accessed August 6, 2009.

22. Lieu, California Legislature. Assembly Bill No. 911. February 26, 2009.

17. Walsh P, Cortez V, Bhakta H. Patients would prefer ward to

Available at: http://leginfo.ca.gov/cgi-bin/postquery?bill_number=ab_91

emergency department boarding while awaiting an inpatient bed. J Emerg Med. 2008; 34:221-6.

1&sess=CUR&house=B&author=lieu. Accessed August 6, 2009.

23. Schwarzenegger A. Bill nubmer: AB 911, vetoed. Letter to the

18. Celentano C. LAC+USC Medical Center surge plan. July 10, 2008.

members of the California State Assembly. October 12, 2009.

Available at: http://www.calacep.org/pdfs/surgeplan_2008.pdf.

Available at: http://www.leginfo.ca.gov/pub/09-10/bill/asm/ab_0901-

Accessed August 6, 2009.

0950/ab_911_vt_20091012.html. Accessed November 16, 2009.

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Editorial

Promoting International Emergency Medicine through WestJEM Mark I. Langdorf, MD, MHPE* Francesco Della Corte, MD† Roberta Petrino, MD‡

* University of California, Irvine School of Medicine, Department of Emergency Medicine, Orange, CA † University of Eastern Piedmont School of Medicine, Department of Anesthesia, Critical Care and Critical Emergency Medicine, Novara, Italy ‡ St. Andrea Hospital, Department of Emergency Medicine, Vercelli, Italy

Submission history: Submitted October 1, 2009; Accepted October 14, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[WestJEM. 2009;10(4):225-226.]

Western Journal of Emergency Medicine

50 45

N=45

40

Countries

This issue of the Western Journal of Emergency Medicine (WestJEM) is devoted to the dissemination of international research and education in emergency medicine (EM). As the specialty gains recognition across the globe, the sharing of ideas from East to West, North to South becomes not only more feasible, but more important. One of the reasons for the name, “Western Journal of Emergency Medicine” was to provide an English language outlet to the Western hemisphere for Eastern hemisphere research. Over the past three years, we have increasingly received submissions from international authors. To recognize this expanded scope, we have chosen to cluster our international papers into a single issue.

Figure 1 shows the number of nations where EM has become a recognized medical specialty from 1970 to 2008. Similarly, in Europe EM is growing rapidly. The European Society of EM (EuSEM) held its 10th annual meeting and currently includes 25 European national societies of EM, representing more than 20,000 emergency physicians. Figure 2 shows the status of specialty recognition for the European continent.

The objectives of EuSEM are to ensure the highest quality emergency care for patients, delivered by physicians trained in EM. Furthermore, EM should be developed as a primary medical specialty in all European countries and foster the organization of comparable training programs across Europe.1 On the educational front, the Task Force for European Training Curriculum in EM was established in 2007 to include delegates from 17 national societies, and was chaired by Dr. Roberta Petrino, director of the ED in Vercelli, Italy.2 The curriculum was approved by the UEMS in October 2009, and now forms the basis for EM education across Europe.

The European Masters in Disaster Medicine is another substantial marker of EM’s reach across the world. Figure 3 shows where students for this two-year master degree have come from within Europe, and Figure 4 shows their distribution across the globe.

Among the potential leadership roles identified for

35 30 25 20 15 10 5 0 1970

1980

1990

2000

2010

Year of EM Specialty Recognition Figure 1. Number of nations where EM has become a recognized medical specialty (provided by courtesy of Dr. Philip Anderson).

Specialty in EM -

Basic specialty Superspecialty No formal specialty

ICEM – San Francisco – April 3 -6, 2008

Figure 2. Status of recognition of the specialty of EM across the European continent.

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Finland

Canada

Sweden The Netherlands

Germany Belgium Austria Switzerland

Croatia

Portugal Spain

USA

Italy Malta

Mexico

Nicaragua Ecuador Colombia Peru Brasil

Romania

Turkey China Israel Saudi Arabia Japan Algeria Quatar EgyptBahrainUAE India Oman Malaysia Sudan

South Africa

Serbia

Albania

Australia New Zealand

Greece Cyprus ICEM – San Francisco – April 3 -6, 2008

ICEM – San Francisco – April 3 -6, 2008

Figure 4. Distribution of European Master in Disaster Medicine students across the globe.

Figure 3. Distribution of European Master in Disaster Medicine students across Europe.

international EM organizations, Arnold and Della Corte included the following initiatives:3 1. Identification and promotion of clinical policies and practices that benefit emergency patients.

2. Fulfillment of moral imperative to advocate for and promote global equity in emergency care systems, particularly those serving world’s most vulnerable populations, including its poorest countries and communities.

3. Development of international ethical and clinical norms and standards in EM. 4. Organization of conferences, symposia, teaching programs.

5. Use of open website.

6. Encouraging submission of publication in peer-reviewed journals.

WestJEM contributes to several of these, through dissemination of curricula for international EM (see Koenig, Bey, Schultz in this issue), practice guidelines, the journal’s open-access electronic format, which is freely available to the world’s poorest areas, and, of course, through the publication of worldwide research.

The five biannual Mediterranean EM Congresses are another marker of the specialty’s growth around the world. Figure 5 shows the number of delegates and the countries represented, while Figure 6 (availble under “Supporting Material” of the article at http://escholarship.org/uc/uciem_westjem) shows similar growth in abstracts presented.

Truly EM has become a global specialty, but much work remains. We at WestJEM seek to foster free dissemination of ideas, research, educational advances and intellectual discourse. Thank you for your support of this vital initiative.

1800

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45 2001 2003 Stresa Barcelona

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Figure 5. Growth in participation for the Mediterranean Emergency Medicine Congress.

REFERENCES 1.

European Society for Emergency Medicine. Policy Statement on Emergency Medicine in Europe. September 2007. Available at: http://www.eusem.org/Pages/About_EuSEM/Policy_Statements/ Policy_Statements.html. Accessed November 1, 2009.

2.

UEMS Multidisciplinary Joint Committee on Emergency Medicine, European Society for Emergency Medicine. European Curriculum for Emergency Medicine. April 25, 2009; Brussels, Belgium.

Available at: http://www.eusem.org/assets/PDFs/Curriculums/ European_Curriculum_for_EM-Aug09-DJW.pdf. Accessed

Address for Correspondence: Mark I. Langdorf, MD, MHPE, Department of Emergency Medicine, 101 The City Drive, Rte 12801 Orange, CA 92868. Email: milangdo@uci.edu

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November 1, 2009.

3.

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Arnold J, Della Corte F. International Emergency Medicine: Recent Trends and Future Challenges. Eur J Emerg Med. 2003; 10:180-8.

Western Journal of Emergency Medicine

Original Research

Introducing a Clinical Practice Guideline Using Early CT in the Diagnosis of Scaphoid and Other Fractures Steven Pincus, MBBS, BSc* Ұ * Emergency Department, Ballarat Health Services, Ballarat, Victoria, Australia † Merle Weber, MBBS* Radiology Department, Ballarat Health Services, Ballarat, Victoria, Australia ‡ Alex Meakin, MBBS† Orthopaedic Unit, Ballarat Health Services, Ballarat, Victoria, Australia Ross Breadmore, MBBS, M Med† Ұ Rural Clinical School Ballarat, University of Melbourne, Ballarat, Victoria, Australia ₣ David Mitchell, MBBS‡ School of Medicine, University of Melbourne, Parkville, Victoria, Australia Luke Spencer, MBBS‡ Nathan Anderson* Ұ Phil Catterson, BN, MBA* Steve Farish, BSc, Med₣ Jaycen Cruickshank, MBBS, MCR* Ұ Supervising Section Editor: Paul Walsh, MD, MSc Submission history: Submitted April 24, 2009; Revision Received September 24, 2009; Accepted September 29, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Objective: We developed and implemented clinical practice guideline (CPG) using computerized tomography (CT) as the initial imaging method in the emergency department management of scaphoid fractures. We hypothesized that this CPG would decrease unnecessary immobilization and lead to earlier return to work.

Methods: This observational study evaluated implementation of our CPG, which incorporated early wrist CT in patients with “clinical scaphoid fracture”: a mechanism of injury consistent with scaphoid fracture, anatomical snuff box tenderness, and normal initial plain x-rays. Outcome measures were the final diagnosis as determined by orthopaedic review of the clinical and imaging data. Patient outcomes included time to return to work and patient satisfaction as determined by telephone interview at ten days.

Results: Eighty patients completed the study protocol in a regional emergency department.

In this patient population CT detected 28 fractures in 25 patients, including six scaphoid fractures, five triquetral fractures, four radius fractures, and 13 other related fractures. Fifty-three patients had normal CT. Eight of these patients had significant ongoing pain at follow up and had an MRI, with only two bone bruises identified. The patients with normal CTs avoided prolonged immobilization (mean time in plaster 2.7 days) and had no or minimal time off work (mean 1.6 days). Patient satisfaction was an average 4.2/5.

Conclusion: This CPG resulted in rapid and accurate management of patients with suspected occult scaphoid injury, minimized unnecessary immobilization and was acceptable to patients.

[WestJEM. 2009;10(4):227-232.]

INTRODUCTION The traditional approach to diagnosis of scaphoid fracture is based upon a combination of historical clinical signs that are sensitive but not specific.1,2 When combined with dedicated scaphoid radiographs in acute wrist injury, this process fails to diagnose a scaphoid fracture in 7-36% of cases.3-10 Clinical scaphoid fracture is defined as patients with suspected Western Journal of Emergency Medicine

fracture not seen on initial radiographs, a mechanism of injury consistent with scaphoid fracture, and anatomical snuff box tenderness. Historically these were immobilized for 10-14 days, before re-examination and repeat radiographs. Early definitive diagnosis has the potential to avoid unnecessary immobilization. Our center has previously demonstrated the potential benefit of computerized tomography (CT) scanning

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in the early diagnosis of scaphoid fractures.11 This follow-up study examined the implementation of a Clinical Practice Guideline (CPG) incorporating early CT in patients with clinical scaphoid fracture. We did not review patients with wrist and scaphoid fractures seen on x-rays. Previous research in our center made it difficult to compare the CPG outcomes to a historical control.

Our primary hypothesis was that early CT with this CPG would avoid unnecessary immobilization. We also hypothesized that this would result in early return to normal duties and satisfied patients.

METHODS This was a prospective observational study of the care of a group of patients with a clinical diagnosis of scaphoid fracture presenting to a regional emergency department (ED) of a 230-bed hospital. The ED has an annual census of ~40,000 patients. The clinical practice guideline was approved via the institutional clinical governance process. These resources are freely available at www.scaphoidfracture.com. au. The study was approved by the local Human Research Ethics Committee. The procedures followed conform to the provisions of the Declaration of Helsinki in 1995 (as revised in Edinburgh in 2000) and Australian ethical requirements.

Informed written consent was obtained by in all participants.

Patients < 18 years old also required written consent from parent or legal guardian. The study was registered on the Australian Clinical Trials Registry and conforms to International Conference on Harmonisation/Good Clinical Practice guidelines.

We designed our implementation strategy using the features described by Grimshaw et al.12 as having a high probability of being effective. First, a local development strategy to develop a CPG for scaphoid fracture was led by a multidisciplinary team with members from the orthopaedic, radiology, and emergency departments. This CPG is described below and available at www.scaphoidfracture.com.au.

Second, our dissemination strategy for this CPG involved specific educational interventions. Web-based online tutorials were available 24/7 on our intranet and at www.meditute. org. Education sessions for medical and nursing staff were conducted and repeated to allow for staff rotations. Third, our implementation strategy included patient-specific reminders at the time of consultation: promotional flyers in every treatment room; stickers with checkboxes for improved documentation of clinical signs, including snuff box tenderness, tenderness on anterior-posterior compression of scaphoid, and tenderness on axial compression of the thumb. Scaphoid x-ray and CT were ordered on specially designed radiology request forms with checkboxes.

This study involved minimal additional cost and human resources. Clinical leaders facilitated and promoted the CPG. Our staff developed the materials, study database, and Volume X, no. 4 : November 2009

education program as a part of work duties. Our institution had already developed the web-based tutorials and maintains them on our intranet.

Patients who presented to the ED were identified by triage nursing and medical staff who gave patients a study information sheet. Trained ED faculty or residents obtained informed consent.

Inclusion criteria were as follow: age of at least 14; a mechanism of injury consistent with scaphoid trauma and tenderness in the anatomical snuff box; and normal x-rays of wrist and scaphoid. ED faculty or residents determined the x-ray diagnosis, which was later confirmed on formal report by a specialist radiologist and included in the results.

Exclusion criteria were as follow: less than 14 years of age; pregnancy; unable to consent or refused consent. These criteria were consistent with published literature and reflect the scope of practice of our CPG. CT was performed on a Siemens Somatom Sensation 64 slice CT scan (Siemens, Munich, Germany), using 1mm slices, and reported in an unblinded fashion by a radiologist.

Radiation dose of extremity CT is 0.5 mSv.13 Patients with a diagnosis fracture of the scaphoid or any other fracture were immobilized in a plaster of Paris cast and referred to the orthopaedic fracture clinic for further treatment. The patient and CT images were reviewed by orthopaedic consultant or registrar to confirm diagnosis, and duration of plaster and further treatment were recorded.

Patients with normal CT and without significant pain (rated <5/10) were allowed to commence mobilizing the wrist immediately. Supportive plaster was offered to patients if they had significant pain. They were subsequently surveyed at day 10 with a telephone interview and asked about loss of function and to rate ongoing pain on a scale of 1-10. Patients with pain >4/10 were reviewed and MRI arranged. Our final diagnosis of “no fracture” was based on resolution of symptoms at day 10, or normal MRI. We asked patients at this stage if they had days off work and how many, and if they had returned to normal duties. We recorded occupation and asked participants if they would have been able to perform normal duties if they had plaster immobilization for 10 days. A research assistant recorded demographic details, reviewed each medical record to ensure that the patient met the criteria for the study, recorded the initial x-ray and subsequent CT reports, and any additional medical imaging performed.

The patient information sheet advised that the CPG involved early CT instead of the historical immobilization for 10 days and repeat imaging and review. Patient satisfaction with their treatment was rated on a scale of 1-5, poorexcellent, under the headings: “overall impression of new protocol,” “explanation of management protocol,” “waiting times,” “attention to detail,” “quality of service,” “patient centeredness,” and “met or exceeded expectations.”

We performed a power calculation using MedCalc for

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CPG Using Early CT in Diagnosis of Scaphoid Clinical Scaphoid Fracture n= 87 Enrolled participants Excluded patients n=4 Did not return for CT Advised us symptoms had resolved

No fracture on CT n = 56

No wrist fracture on CT n=2 1 = scapholunate dissociation 1= wrist normal, radial head fracture

Normal CT n=3 Lost to follow up

Fracture on CT n = 28 (25 patients) CT/clinical review in fracture clinic Patient satisfaction

Scaphoid = 6 Triquetral = 5 Lunate = 4 Radius = 4 Day ten review Significant pain > 4/10

Metacarpal = 3 Trapezium = 2 Trapezoid = 2 Capitate and Hamate = 1 each

Days in plaster Days off work Patient satisfaction Return to normal duties

No n = 45 Follow up as needed No fractures diagnosed.

Yes n=8 Review and MRI arranged

Bone bruise n=2 1 = scaphoid 1 = radius

No fracture n=6

Figure 1. STARD diagram: STAndards for the Reporting of Diagnostic accuracy studies

Windows, version 9.3.0.0 (MedCalc Software, Mariakerke, Belgium). A sample of 81 would give 90% power to detect a result of 98% for sensitivity, or negative predictive value (a= 0.05, b = 0.9). Graphpad quickcalcs (GraphPad Software San Diego, California) was used to calculate confidence intervals for percentages and means.

RESULTS We enrolled 87 patients between April 2006 and March 2008, 80 of whom completed the study protocol (Figure 1).

We extended the original recruitment period from one to two years to obtain a larger sample size. The four patients who withdrew without returning for CT cited resolution of symptoms, with one patient being advised by their general practitioner that CT was not necessary.

Forty-one patients were male, median age was 25 (interquartile range, 18-43). Clinical examination findings from medical staff included anatomical snuff box tenderness present in all patients (inclusion criteria). Tenderness on axial compression of thumb present in 6/6 scaphoid fractures, 21/25 patients with fractures overall, and 43/53 patients without fracture. Tenderness on anterior-posterior compression of scaphoid present in 6/6 scaphoid fractures, 22/25 patients with fractures overall, and 44/53 of patients without fracture. CT was performed on average 1.3 days post injury (range 1-10).

There were 28 fractures in 25 patients. These fractures Western Journal of Emergency Medicine

included scaphoid (6 *one with lunate), triquetral (5 *one with lunate), radius (4), lunate (4), metacarpal (3), trapezoid (2), trapezium (2), capitate and hamate (1 each in same patient). Retrospective review of the original x-ray report by specialist radiologist revealed that one scaphoid and one triquetral fractures were reported (but not identified prior to CT), one scaphoid and one triquetral were reported as “possible fracture” (with further imaging recommended). One radiologist report of fracture radius (ED faculty report normal) was not confirmed when the CT was reported. Two patients had no fracture on wrist CT, but other injuries occurred: one patient had scapho-lunate dissociation, and the other had normal wrist but a co-existent fracture of the radial head. They were not analysed in the group with “normal CT.” Of the 56 patients with a normal CT scan, three were lost to follow up (unable to be contacted via phone or mail). Fiftythree with no fracture on CT were further analyzed. These patients reported a mean pain score of 1.6/10 (range 0-10) on review, with 29/53 reporting ongoing pain and 20/53 patients ongoing reduced function. For the 8/53 with significant symptoms at day 10, MRI did not reveal any missed cortical fractures, but two patients had bone bruises (one scaphoid, one radius). The two with bone bruising skewed the results for duration of plaster; the scaphoid bone bruise had duration of plaster lasting 56 days (Figure 2).

Sensitivity of CT (compared to final diagnosis) was 100%

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CPG Using Early CT in Diagnosis of Scaphoid Days off work and time in plaster if CT normal 100

Number of people : Days off work or in plaster

35

days off work days in plaster Cumulative % out of plaster Percent off work

30

25

90 80 70 60 50

20

40

15

Percentage

40

30 10 20 5

10

0

0 1

2

3

4

5

6

7

8

9

10

11

12

13

14

More

Days

Figure 2. Days off work and time in plaster with a normal CT.

(95% CI 93.5-100) and negative predictive-value was 100% (95% CI 93.5 – 100%). Participants spent a mean 2.85 days (range 0-56) in plaster, and while only 25/53 required time off work, the mean time off was 1.6 days (range 0-14). Most participants had three or less days off work (45/53), with 51/53 back at work by day seven. While 39/53 participants had already returned to normal duties before day 10, only 10/53(19%) felt they could have returned to normal duties if they had plaster immobilization.

Table 1. Patient satisfaction in patients surveyed at day ten post injury.* Mean Median

Range

95% CI

Overall impression with the new protocol

4.4

4

2-5

4.25 to 4.60

Explanation of management protocol

4.5

5

1-5

4.23 to 4.69

Waiting times

3.5

4

1-5

3.17 to 3.87

Attention to detail

4.4

4

2-5

4.26 to 4.63

Quality of service

4.4

4

3-5

4.25 to 4.60

Patient centeredness

4.5

5

3-5

4.36 to 4.68

Service met or exceeded expectations

4.2

4

2-5

3.99 to 4.39

*1= poor, 2= fair, 3= average, 4= very good, 5= excellent

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The average patient satisfaction score for waiting times was lower compared to other questions (Table 1). This was supported by the qualitative feedback provided, with a number of comments relating to waiting “too long” to be told the CT report was normal. There were no significant differences between other scores, with average scores of 4.2-4.5, reflecting relatively good patient satisfaction with their management using the protocol.

DISCUSSION The aim of this study was to evaluate implementation of our CPG for patients presenting with clinical scaphoid fracture, incorporating early CT. It has previously been suggested that well designed CPGs guide practice and improve quality and efficiency, as well as saving costs.14-16 To be effective, a CPG must have adequate administrative support and be designed to support medical staff in their practice, without being seen as disempowering.15 Our previous research demonstrated 96.7% negative predictive value for fracture in this population, with no missed scaphoid fractures.11 This study involved collaboration between the orthopaedic, radiology and emergency departments, with agreement that there was enough evidence to support the use of early CT in our CPG.We developed a guideline with a clear purpose, scope, and inclusion and exclusion criteria. In implementing the evidence, our CPG ensured the targeted use of radiological investigations in a consistent manner by ED medical staff.

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CPG Using Early CT in Diagnosis of Scaphoid diagnosis have been described. Bone scan at day 4 post injury17,18 has excellent sensitivity and negative predictive values (95-100%), although the poor specificity (60-95%) and positive predictive value (65%) represent a limitation to its use.17,19,20 Ultrasound, while a potentially useful diagnostic tool, has not been shown to diagnose fractures of adjacent bones masquerading as or associated with scaphoid injuries, as is the case with other advanced imaging techniques.21 MRI has been demonstrated to be accurate in the diagnosis of scaphoid fractures, with a reported 100% negative predictive value, sensitivity and specificity.5,6,22-26 It is now regarded by many as the gold standard for the imaging of suspected scaphoid fractures when initial radiographs are normal.3,27 CT has been shown to be useful in the diagnosis of scaphoid fractures (sensitivity 72-100% and specificity of 80100%),7,11,28-35 and is superior to other modalities in the detection of clinically significant displacement, which is fundamental to potentially poor clinical outcomes.28,36 In Australian practice, CT is roughly half the cost of MRI and has a significantly higher availability.37,38 Additionally, CT scans may be ordered by any medical practitioner, unlike MRI which generates a Medicare rebate only when ordered by registered specialists, thus generally restricting its use. In our population, patients with scaphoid tenderness and normal plain x-ray and a normal early CT scan were only immobilized to treat symptoms. For the 15% with significant symptoms at day 10, the use of MRI did not demonstrate any missed fractures, but two patients had bone bruises and required longer immobilization. This confirms both the excellent negative predictive value of CT and the need for further medical review if symptoms persist.

Eighty-five percent of patients with normal CT scans had less than three days in plaster, and less time in plaster may mean earlier return to normal duties. Using a traditional approach to scaphoid fracture, all of these patients would have had 10 days of plaster immobilization, with 43/53 of our patients reporting they would have been unable to return to normal duties. Overall our patients were highly satisfied with their management (score 4.2/5). To our knowledge this is the first study to publish results of patient satisfaction for management of this clinical condition.

Several studies have highlighted the difficulties of implementing and using clinical guidelines to direct practice in the diagnosis of clinical scaphoid fracture. In the absence of established practice guidelines there tends to be marked variation in the approach to this condition.39 Where guidelines have been developed, the use and knowledge of them is often poor. This may be especially relevant in clinical settings such as EDs with high staff turnover.37 We have demonstrated the successful implementation of a CPG for diagnosis of occult scaphoid and carpal fractures.

Generalized use of such a guideline requires a balance between expert consensus and local resources. While the British guideline for the diagnosis of scaphoid fracture is currently Western Journal of Emergency Medicine

being updated, most American guidelines rank MRI over CT in situations where plain radiography is normal.39 As yet there is no national Australian guideline.

To improve the probability of success at a local level we found Grimshaw’s13 principles to be useful. Our study provides evidence to support both early CT and a CPG in current practice, especially given the recommendations that use of guidelines could be improved. Our research has the potential to change current practice. It is possible that national bodies, institutions, or clinicians at a local level may decide to place a different emphasis on different medical imaging technologies.

Issues such as access, availability and cost may be subject to local variation, and follow up may vary between EDs, general practitioners and Fracture Clinics.

LIMITATIONS Rather than comparing CT to a reference standard such as MRI, we have assessed the performance of early CT in a clinical practice guideline for suspected scaphoid fracture. We had a safety net with all patients who had persisting symptoms despite a normal CT receiving an MRI, yet missed fractures are still possible. Our reported figure of sensitivity and negative predictive value should be interpreted with some caution.

All patients with CT diagnosis of scaphoid fracture were reviewed in our fracture clinic at 10 days by an orthopedic surgeon or specialist registrar (resident), who agreed with the original CT report after review of both the patient and the CT images. It is possible that some patients may have had a false positive diagnosis on CT, and hence specificity and positive predictive value are not reported.

Patient satisfaction answers may have been biased by the word “new” in front of protocol, and by the interview process.

Time off work and return to normal duties will depend on the patient population, and not necessarily be applicable to other populations.

CONCLUSION Successful implementation of a CPG in our institution resulted in early diagnosis using CT, including scaphoid and other fractures. Patients with a normal CT avoided unnecessary periods of plaster immobilization, returned to work and normal duties earlier, and were satisfied with this approach.

Address for Correspondence: Address for Correspondence: Dr Jaycen Cruickshank, MBBS, FACEM, MCR, Department of Emergency Medicine, Ballarat Health Services, Ballarat, 3350, Victoria, Australia Email jaycenc@bhs.org.au Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. This study was funded by Ballarat Health Services, supported by an “implementing the evidence” research grant from the National Institute of Clinical Studies.

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26. Kumar S, O’Connor A, Despois M, et al. Use of early magnetic resonance

Roolker W, Tiel-van Buul MM, Ritt MJ, et al. Experimental evaluation of scaphoid X-series, carpal box radiographs, planar tomography, computed

imaging in the diagnosis of occult scaphoid fractures: the CAST Study

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(Canberra Area Scaphoid Trial). N Z Med J. 2005; 118:U1296.

27. Johnson KJ, Haigh SF, Symonds KE. MRI in the management of scaphoid

scaphoid fracture. J Trauma. 1997; 42:247-53.

8.

fractures in skeletally immature patients. Pediatr Radiol. 2000; 30:685-8.

Tiel-van Buul MM, van Beek EJ, Dijkstra PF, Bakker AD, Griffioen FM,

28. Lozano-Calderon S, Blazar P, Zurakowski D, et al. Diagnosis of scaphoid

Broekhuizen TH. Radiography of the carpal scaphoid. Experimental

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evaluation of “the carpal box” and first clinical results. Inves Radiol. 1992;

fracture displacement with radiography and computed tomography. J Bone

27:954-9.

Joint Surg Am. 2006; 88:2695-703.

29. Adey L, Souer JS, Lozano-Calderon S, et al. Computed tomography of

Brondum V, Larsen CF, Skov O. Fracture of the carpal scaphoid:

suspected scaphoid fractures. J Hand Surg Am. 2007; 32:61-6.

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30. Kusano N. Diagnosis of Occult Scaphoid Fracture: A Comparison of Magnetic

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Resonance Imaging and Computed Tomography Techniques. Tech Hand Up

10. Pillai A, Jain M. Management of clinical fractures of the scaphoid: results

Extrem Surg. 2002; 6:119-23.

of an audit and literature review. Eur J Emerg Med. 2005; 12:47-51.

31. Tiel-van Buul MM, van Beek EJ, Borm JJ, et al. The value of radiographs

11. Cruickshank J, Meakin A, Breadmore R, et al. Early computerized

and bone scintigraphy in suspected scaphoid fracture. A statistical analysis. J

tomography accurately determines the presence or absence of scaphoid

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32. Breederveld RS, Tuinebreijer WE. Investigation of computed tomographic

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scan concurrent criterion validity in doubtful scaphoid fracture of the wrist. J

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Trauma. 2004; 57:851-4.

13. Cross TM, Smart RC, Thomson JE. Exposure to diagnostic ionizing

33. Memarsadeghi M, Breitenseher MJ, Schaefer-Prokop C, et al. Occult

radiation in sports medicine: assessing and monitoring the risk. Clin J

scaphoid fractures: comparison of multidetector CT and MR imaging--initial

Sport Med. 2003; 13:164-70.

experience. Radiology. 2006; 240:169-76.

14. Little AB, Whipple TW. Clinical pathway implementation in the acute care

34. Sanders WE. Evaluation of the humpback scaphoid by computed

hospital setting. J Nurs Care Qual. 1996; 11:54-61.

tomography in the longitudinal axial plane of the scaphoid. J Hand Surg Am.

15. Abbott J, Hronek C, Mirecki JK. The leap to automating clinical pathways.

1988; 13:182-7.

J Healthc Resour Manag. 1995; 13:8-16.

16. Jousimaa J, Kunnamo I, Makela M. An implementation study of the PDRD

35. Haisman JM, Rohde RS, Weiland AJ; American Academy of Orthopaedic S. Acute fractures of the scaphoid. J Bone Joint Surg Am. 2006; 88:2750-8.

primary care computerized guidelines. Scand J Prim Health Care. 1998; 16:149-53.

36. Ring D, Jupiter JB, Herndon JH. Acute fractures of the scaphoid. J Am Acad Orthop Surg. 2000; 8:225-31.

17. Beeres FJ, Hogervorst M, Den Hollander P, et al. Diagnostic strategy for suspected scaphoid fractures in the presence of other fractures in the

37. Tai CC, Ramachandran M, McDermott ID, Ridgeway S, Mirza Z. Management of suspected scaphoid fractures in accident and emergency

carpal region. J Hand Surg Br. 2006; 31:416-8.

departments--time for new guidelines. Ann R Coll Surg Engl 2005;87-5:353-7.

18. Akdemir UO, Atasever T, Sipahiolu S, Turkolmez S, Kazimolu C, Sener E. Value of bone scintigraphy in patients with carpal trauma. Ann Nucl Med.

38. N’Dow J, N’Dow K, Maffulli N, Page G. The suspected scaphoid fracture. How useful is a unit policy? Bulletin of the Hospital for Joint Diseases 1998;57-2:93-5.

2004; 18:495-9.

19. Tiel-van Buul MM, Broekhuizen TH, van Beek EJ, et al. Choosing a

39. Groves AM, Kayani I, Syed R, et al. An international survey of hospital practice

strategy for the diagnostic management of suspected scaphoid fracture: a

in the imaging of acute scaphoid trauma. AJR Am J Roentgenol. 2006;

cost-effectiveness analysis. [see comment]. J Nucl Med. 1995; 36:45-8.

187:1453-6.

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Review Article

Crowding and Delivery of Healthcare in Emergency Departments: The European Perspective Namita Jayaprakash, MB BCh, BAO* Ronan O’Sullivan, MB BCh† Tareg Bey, MD‡ Suleman S. Ahmed, BS, BA‡ Shahram Lotfipour, MD, MPH‡

* St. Vincent’s University Hospital, Department of Emergency Medicine, Dublin, Ireland † Our Lady’s Children’s Hospital Crumlin, Department of Emergency Medicine, Dublin, Ireland ‡ University of California, Irvine School of Medicine, Department of Emergency Medicine, Orange, CA

Supervising Section Editor: Chris Mills, MD, MPH Submission history: Submitted October 5, 2008; Revision Received August 14, 2009; Accepted September 30, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Emergency department (ED) crowding is a multifactorial problem, resulting in increased ED waiting times, decreased patient satisfaction and deleterious domino effects on the entire hospital. Although difficult to define and once limited to anecdotal evidence, crowding is receiving more attention as attempts are made to quantify the problem objectively. It is a worldwide phenomenon with regional influences, as exemplified when analyzing the problem in Europe compared to that of the United States. In both regions, an aging population, limited hospital resources, staff shortages and delayed ancillary services are key contributors; however, because the structure of healthcare differs from country to country, varying influences affect the issue of crowding. The approach to healthcare delivery as a right of all people, as opposed to a free market commodity, depends on governmental organization and appropriation of funds. Thus, public funding directly influences potential crowding factors, such as number of hospital beds, community care facilities, and staffing. Ultimately ED crowding is a universal problem with distinctly regional root causes; thus, any approach to address the problem must be tailored to regional influences. [West J Emerg Med. 2009; 10:233-239].

INTRODUCTION Emergency department (ED) crowding is a global problem that has drawn increasing international attention.1 The nature of emergency medicine (EM) has changed significantly in recent years with the advent of new treatment options and the availability of more medical technology, such as specialized intravenous thrombolysis in stroke, stent placement in acute myocardial infarction, and the use of ultrasound. Many of these are time-critical procedures, leading to greater emphasis on the resuscitation, stabilization, investigation and initial management in the ED. Conditions for which patients were previously admitted and observed are now managed in the ED, allowing for direct discharge without the added cost of inpatient hospitalization. In the United States (U.S.), EDs are required to provide appropriately resourced 24-hour emergency care, 365 days a year. There is a direct correlation between an aging population and increased utilization of emergency services.2 The precise definition of crowding is unclear. Some define Western Journal of Emergency Medicine

it as an inability of ED staff to deliver optimal care because of work overload. Others believe it to be accurately assessed through quality indicators, such as waiting times, treatment times and actual patient census, while trying to provide the best care, service and safety.3 The American College of Emergency Physicians (ACEP) Crowding Resources Task Force has adopted this definition of ED crowding: “…a situation in which the defined need for emergency services outstrips available resources in the ED…occurs in hospital EDs where there are more patients than staffed ED treatment beds and wait times exceed a reasonable period.”4 The concept of crowding has been difficult to define scientifically. Documentation was once limited to photographs of congested EDs and anecdotes over empirical data. In recent times more efforts have been made to document the problem.

Derlet et al.5 surveyed ED directors nationwide to describe the definition, extent and factors associated with the problem as perceived by them. They identified an array of issues as

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Table 1. Factors affecting crowding Factors within the hospital

Outside factors affecting the hospital

Increased hospital occupancy

Inadequate access of the general population to primary care and specialists as an outpatient

Increasing patient acuity

Ambulance and EMS design

Inappropriate patient referral

Expectations of the general public of health care delivery and the role of health care providers and institutions (outpatient and hospital)

Inadequate out-of-hours service

Demographics with an aging population

Inappropriate triage

Percentage of illegal immigrants with no access to structured outpatient health care

Inexperienced medical staff

Social reasons (no transportation, prevalence of homelessness, prison population, nursing homes)

Staff shortages

Insurance practices like Health Maintenance Organization (HMO) practices of public insurers

Delayed ancillary services (resulting Influence of media and internet on patients behavior in accessing emergency care and sense of in increased administrative burden individual entitlement to medical staff)

reasons for crowding: increased patient acuity, hospital bed shortage, increasing ED volume, radiology delays, insufficient ED space, laboratory delays, consultation delays, nursing shortage, physician shortage and managed care issues. A qualitative Irish study6 described the problem from the point of view of patients and/or relatives/significant others who had spent 12 hours or more in the ED awaiting admission.

Descriptions by the participants of this study portrayed an ED that was overcrowded, dirty, lacking in resources and resembling a disaster zone or hospital scene from a Third World country.

Weiss et al.7 attempted to quantify crowding through the National ED OverCrowding Study (NEDOCS). The NEDOCS score was calculated using institutional constants: number of ED beds and number of hospital beds. This was combined with model variables: total patients in the ED, total admits in the ED, number of respirators in the ED, longest admit time (in hours), and waiting room time of last patient put in bed (in hours). They determined that the NEDOCS score (0-20 = not busy, 20-60 = busy, 60-100 = extremely busy but not overcrowded, 100-140 = overcrowded, 140-180 = severely overcrowded, 180-200 = dangerously overcrowded) was a useful indicator of the degree of crowding and could be used reliably to determine the status of an ED at any given time. In 1999, 91% of ED directors in the U.S. reported crowding as a problem, defining it by the presence of patients in hallways, occupied ED beds, full waiting rooms > 6 hours/day, and acutely ill patients waiting > 60 minutes to see a physician.5 A recent study by McCarthy et al.8 showed that ED occupancy rate (total number of patients in the ED divided by total number of licensed beds) can serve as a valid measure of crowding.

International studies have shown that where a patient is waiting in the ED beyond the time the decision is made to admit, clinical outcomes are adversely affected.9-11 This correlates to the reality that EDs cannot adequately fulfil their primary function of stabilization and disposition while also Volume X, no. 4 : November 2009

functioning as an inpatient ward. As a result, both functions are performed suboptimally with consequent predictable adverse effects on patient outcome.

FACTORS THAT INFLUENCE CROWDING ACROSS EUROPE EM across Europe is still in a developing state with many European countries having yet to form their own EM societies or have dedicated EM journals. The Casualty Surgeons Association was formed in the United Kingdom (UK) in 1967.

The name was changed in 1990 to the British Association of Accident and Emergency Medicine and then again in 2004 to the British Association for Emergency Medicine (BAEM).

A collaboration of BAEM and the Faculty of Accident and Emergency Medicine (formed in 1992) developed the College of Emergency Medicine in 2005.12 In the UK and Ireland, the ED is sometimes referred to as “casualty” or the “accident and emergency department.”

The majority of studies looking at quantifying ED crowding have emerged from the U.S. and Australasia. In Europe, as in the U.S., the problem is multifactorial (Table 1), and the issue is becoming one of major societal concern.13 Increased Hospital Occupancy One of the most significant reported causes of ED crowding is hospital bed shortage, especially ICU and telemetry beds.3,5,14,15 The ability to move admitted patients from the ED to hospital beds depends upon the availability of hospital beds, nursing staff, nursing ratios, ancillary service availability, local structure and likely many other factors.

Hospitals in the UK and Ireland are faced with the situation in which elective and emergency admissions compete for bed occupancy. In these countries the typical picture is one in which elective surgical patients are often brought in over the weekend for procedures scheduled to occur later in the week.

Thus, beds are occupied and made unavailable to admissions from the ED. A similar situation in the U.S. may exist

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Crowding: The European Perspective (although not studied extensively), as it has been shown that each additional elective surgical admission is associated with a prolonged daily mean length of stay for all ED patients.16 In the UK, it has been shown that the total time spent in EDs, even for patients who are discharged, is related to hospital bed occupancy rates and has negative effects on patient satisfaction and the economic bottom line of the hospital.17 According to an Irish government report entitled “Acute Hospital Bed Capacity: A National Review,” the number of acute hospital beds in 2000 (11,832) was approximately 6,000 lower than that in 1980 (17,655).18 The report also documents that the number of acute hospital beds per capita in Ireland – 3.1 beds per 1,000 population compared to 5.1 per 1,000 in 1980 – is one of the lowest among the European Union (EU) and the Organization for Economic Cooperation and Development (OECD) countries. Germany has also reduced the number of hospital beds. Closure of German hospitals resulted in 49,472 fewer hospital beds between 1995 and 2000 alone, bringing the available bed count to 559,651 (6.8 per 1,000) in the year 2000.19 This trend continued in 2006, when Germany cut another 13,000 hospital beds (or 2.5%), decreasing the total to 511,000 nationally (6.2 per 1,000).20 In one study conducted at a large Irish ED with an annual census of 45,000 patients, over half reported that lack of beds contributed to their prolonged ED stay.21 In the same study 85.9% of patients felt that health authorities were not doing enough to address the crowding issue and over 35% reported that the prospect of a prolonged stay affected their willingness to come to the ED or to return. This latter finding may be particularly important, as there are no real alternatives to ED-delivered emergency care in Ireland, thus raising the possibility that a prior adverse experience might lead to a subsequent delay in future emergency care. According to a study conducted in the U.S., as hospital occupancy increased by 10% the median ED length of stay increased by 18 minutes.22 Factors affecting bed occupancy also include those that lie outside the hospital. Inadequate community services for appropriate transfer of care of patients back to the community leads to prolonged stays in the hospital and blocks acute hospital bed access.23 The recently published report by the Irish Health Service Executive (HSE) identified patients who were clinically discharged but unable to leave the hospital due to lack of community services for continuation of care.24 These facilities are dependent on public funding and limitations on the availability of funds prolong hospital stay and decrease the numbers of available hospital beds. This in turn affects the transfer of patients out of the ED. An estimated 12% of hospital beds are unavailable due to delayed discharges. The equivalent of 675 beds could be made available in acute care hospitals if such measures as improving long term care and rehabilitation facilities, were put in place to improve delays in discharge. One of the authors reported that there are two Western Journal of Emergency Medicine

types of patients in Irish hospitals, those awaiting tests and procedures and those waiting for non-acute, long stay and rehabilitation care.

In 2007 the American Hospital Association published figures suggesting there were 3.1 hospital beds per 1000 population.25 This places the U.S. within the same range as Ireland, which has one of the lowest averages among EU countries. The difference between the two countries is the greater U.S. emphasis on delivery of critical care medicine.

From 1985 to 2000, there was a 6% decrease in the ratio of non-critical care medicine (CCM) beds to hospital beds and a 71.5% increase in the CCM beds to hospital-beds ratio.26 This equated to a 6.7% decrease in the number of inpatient days for non-CCM patients and a 75.2% increase in CCM inpatient days, which reflects the increasing shift in U.S. hospitals towards the delivery of CCM. Increasing Patient Acuity As the population ages, the type of patient presenting to the ED has changed. One study conducted in the UK showed that between 1990 and 2004 the median age of the population increased by 10 years.2 It also showed that in 2004 the proportion of patients presenting to EDs who were 70 years or older was 198% higher than in 1990, and the proportion of patients 90 years or older was 671% higher. The elderly were more often admitted to the hospital and once admitted had a greater length of stay compared to younger patients, an effect attributed to acute exacerbations of chronic diseases that require emergent care. Increasing numbers of patients have comorbidities that prolong evaluation and patient waiting time,3 hence resulting in back logs of patients waiting to be seen.

Patient Self-Referral In countries such as Germany, Ireland, Italy, Netherlands, Norway, Portugal, Spain, Switzerland and the UK, the general practitioner (GP) acts as a gatekeeper to health services whose role is primary health carer. In Europe, as in the U.S., 80 to 90 percent of health-related activities, including diagnosis and treatment, are initiated by the patients themselves, without seeking professional advice.27 Increasing numbers of patients across Europe are bypassing the GP and primary healthcare system to present to EDs.28 Overuse of the ED for minor complaints that could be dealt with at the GP level decreases the quality of care and increases ED costs.28 A study conducted by Lee et al.29 found that 57% of ED attendees were primary care cases. Reasons for ED attendance over GP attendance include a lack of confidence in the primary healthcare system, inadequate outof-hours services, and unavailability of care through GPs.28 Inadequate Out-of-Hours Services Where GPs act as gatekeepers to healthcare systems, they are expected to be available as points of contact 24 hours a

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Jayaprakash et al. day. Different GP groups provide various forms of after-hours service, but there is no uniform system and no guarantee of coverage in every area. When access is unavailable a patient’s only option is the ED. Inadequate after-hours GP services are thus adding to the numbers of patients presenting to the ED. A study conducted by van Uden et al.30 concluded that an afterhours service that optimized the role of the GP as gatekeeper and geared itself towards the patients’ symptoms enabled primary care patients to be dealt with by a GP, thus reducing inappropriate referrals to the ED. Certain initiatives have attempted to offer alternatives of care to patients requiring urgent treatment. The UK National Health Service (NHS) has developed physician and/or nurseled minor injury units, urgent care centers and telephone advice systems, such as NHS Direct.31 However, initial evidence from these initiatives would suggest that they have had little impact on ED attendances and waiting times.

Triage in the Emergency Department A system of ED triaging organizes patients into recognizable groups to prioritize the sickest patients. In the U.S., the commonly accepted “prudent layperson law” in essence requires that the emergent nature of a presentation be judged by the patient’s initial presentation rather than the eventual diagnosis. Furthermore, according to this law, whether the presentation warrants immediate attention should be judged by the patient.32 In contrast, in places such as the UK, the triage system is based on clinical assessment at the pre-hospital level, on arrival at an ED and by the first attending physician.33 A study conducted by Gersenz and Studdert34 found a discrepancy between lay and expert judgments about what constitutes emergency care, a situation underscored by the significant number of ED cases in insurance payment disputes.

Studies in the UK have found that the accepted fivecategory triage is not being used in practice; instead they use a three-category triage system that simply assigns patients as “life-threatening”, “major”, and “minor.”35 This nurse-led three-category triage system, which provides little more information than one could ascertain without clinical evaluation, is time consuming and leaves patients most amenable to treatment in a waiting room while those patients judged more critical are seen first.36 In 2002 the NHS Modernisation Agency in the UK proposed a system of “see and treat,” which suggested abandoning triage and adopting a method in which patients are seen and treated by senior clinical physicians as early as possible.37 As soon as patients arrive at the ED they are seen, assessed, treated, admitted or discharged by one physician.

Several studies have shown that the earlier a person is seen in the ED by a senior clinician the shorter the length of stay.31 It is now widely accepted across the NHS that triage is an exercise of prioritization that needs to be executed when there Volume X, no. 4 : November 2009

Crowding: The European Perspective is a delay in seeing the practitioner.

Other NHS initiatives, such as “streaming,” or “triageout,” assess patients at the point of triage and direct them to appropriate services. An experienced member of the nursing staff assesses whether the ED medical staff, an ED nurse or a member of the primary healthcare team best meets the patient’s needs. The nurse can then direct the patient to the appropriate service. Audits have shown that the use of such initiatives have reduced patient complaints and increased job satisfaction amongnurses.31 Inexperienced Medical Staff Across the EU, medical education generally includes 5-7 years of undergraduate medical training with 1-2 years of initial training as a house officer followed by 4-8 years of specialist training.38,39 In Ireland, for example, medical school consists of five years, followed by one year as a house officer, which is similar to that of a first year intern with broad-based introductory training. The first year is followed by a three-year period as a senior house officer with generalist training (although one can emphasize emergency medicine), after which there are five years of higher specialist training (specialist registrar). Finally, the physician passes an exit examination and becomes a consultant, which is equivalent to full American Board of Emergency Medicine certification conferring attending-physician status.40 Junior doctors, such as a senior house officer, play an integral role in seeing and treating patients in the ED; however, they lack the experiences and expertise of more senior staff members (consultants). Experienced doctors spend less time with patients and order fewer studies to arrive at clinical decisions, while inexperienced doctors are slower in decision making.35 In the UK (population 60 million) there are currently 749 consultant posts in EM, while in Ireland (population 4 million) there are currently 59 consultants in EM, working in 35 EDs. In contrast, there are over 22,000 board-certified emergency physicians in the U.S. (population 282 million). Patients treated by experienced medical personnel have reduced time to medical assessment, laboratory examination, radiology and discharge.36 Staff Shortages Reports suggest that nursing shortages worldwide are a cause of ED crowding.5 Across the EU there is an average of 3.4 doctors per 1000 population.38 In the U.S., between 1980 and 2000, the population grew from 227 million to 282 million and this is projected to increase to 420 million by 2050. Medical school enrollments, however, have remained constant from 1980 to 2005 .41 This would result in an increasing shortage of physicians in coming years.

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Crowding: The European Perspective of patients, implementation of treatment, and final decision on the patientâ&#x20AC;&#x2122;s status. Thus, delays in getting imaging result in delayed assessments and prolonged stays within the ED, especially in the case of trauma patients.42 Similarly, delays in lab reports reporting lab findings also mean patients unnecessarily occupying ED beds, prolonging wait time and decreasing patient satisfaction.

STRUCTURE OF HEALTHCARE IN EUROPE Emergency department crowding is a universal problem.

While several factors that contribute to crowding in Europe are comparative to factors in the U.S., differences in the structure of healthcare between these regions of the world have varying influences.

In Europe, unlike in the U.S., healthcare is viewed as a utility with equal access to the whole population, as opposed to a free-market commodity with supply and demand influencing access to care. All European countries have a legal framework of healthcare delivery for the general population.

It is planned and administered centrally by the respective government ministries with a variety of delivery systems.

For example, in France and the UK the system is controlled centrally with management directly responsible to the Ministry of Health. In Germany, Italy and Spain the healthcare delivery system is decentralized and local government bodies have the autonomy to pass their own legislation.19,27 In Ireland, delivery of health services is the responsibility of the HSE, while the Department of Health and Children oversees the development and overall strategic management of the health system in accordance with legislation.43 For the provision of their healthcare, EU member states rely predominantly on public funding sources, such as taxation or health insurance premiums. Direct out-of-pocket expenditure with private health insurance represents a small proportion of the funding.44 While the U.S. spent 15.2% of its Gross Domestic Product (GDP) on healthcare in 2004, the EU average was 9.43% (Figure 1).45,46 Despite this, the share of public spending on health in the U.S. is 45% compared to well over 80% in the UK and parts of Scandinavia. Public insurance covered just 26.2% of the U.S. population in 2005,47 In contrast to many EU countries where healthcare is a public utility with access to all, the U.S. healthcare system is fragmented and market-driven. Multiple purchasers allow healthcare costs to rise above those of other industrialized countries. Further, the increased administrative overhead required to manage the complex financial system utilizes a high fraction of U.S. spending.48 Ultimately this results in a greater out-of-pocket expenditure for the individual and less dependence on public funding.

In Europe, because healthcare is planned and administered by a central body, policies that affect crowding can be implemented universally. In England, for example, the Department of Health launched the National Health Service Western Journal of Emergency Medicine

Figure 1. Adapted from Kerem et al.45 (printed with permission).

Plan, a policy declaring that the total time for a patient in the ED be no more than four hours.49 Implemented in 2003, the plan was to address the perceived shortcomings in the UK ED system and achieve efficiency.50 With this four-hour target came support systems, such as the Modernization Agency and other government resources, to build capacity, support performance and aid in compliance.51-53 Despite the struggle to achieve this target, massive transformations have occurred and the outcome has been largely positive.53 Muran et al.54 found waiting times reduced and Banerjee et al.55 concluded that â&#x20AC;&#x153;long waits in the ED are a thing of the past in the UK.â&#x20AC;? While implementing a similar plan in the U.S. would seem difficult without a central regulatory body and major support systems to increase bed capacity and support staff, the U.S. may be able to adopt some effective aspects of the four-hour target, such as coordination throughout a hospital system, rather than having crowding be the burden of one department.

CONCLUSION The issue of ED crowding has been brought to the forefront of healthcare, and newspaper photos of patients waiting on gurneys have become a political standpoint for election candidates. The problem has been attributed to many factors, some universal and others specific to certain regions of the world. Overcrowded EDs lead to adverse clinical outcomes. Patient dissatisfaction is increased as waiting times are prolonged and resources are stretched.

To begin to address crowding, the root of the problem has to be determined. There is no single cause and effect scenario; instead there are many causes depending on the region of the world and the governing healthcare system. Within the EU increased hospital occupancy, bed shortages, increased patient

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acuity, staff shortages and delayed ancillary services are all contributing factors, as in the U.S. However, differences in healthcare delivery between the two regions result in a common problem with different roots. The European approach to healthcare as a utility with equal access for everyone and not a free market commodity requires centralized management of healthcare and governments that ensure that adequate allocation of funds for acute hospital and community supports.

In the U.S. however, supply and demand influences the availability of health resources, and the proportion of public spending is significantly less.

The problem of crowding in the ED is one that affects both Europe and the U.S. The ED is the gateway to the hospital; problems arising there have the potential to affect the entire hospital. Because ED crowding has different regional causes, any potential solutions must be tailored to regional variations. These differences suggest that while a universal solution is not necessarily practical, we can look at various policies that have had a positive impact on crowding and implement similar solutions across countries, tailored to the needs of individual regions.

Address for Correspondence: Shahram Lotfipour, MD, MPH, Department of Emergency Medicine, University of California Irvine School of Medicine, 101 The City Drive, Rte 128-01 Orange, CA 92868. Email: SHL@uci.edu Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

7.

emergency department crowding in academic medical centers: results of the National ED crowding study (NEDOCS).Acad Emerg Med. 2004; 11:38-50.

8.

crowding. Ann Emerg Med. 2008; 51:15-24.

9.

with emergency department crowding Med J Aust. 2006; 184:213-6.

10. Sprivulis PC, Silva JD, Jacobs IG, et al. The association between hospital crowding and mortality among patients admitted via Western Australian emergency departments. Med J Aust. 2006; 184:208-12.

11. Cameron PA. Hospital crowding: a threat to patient safety? Managing access block involves reducing hospital demand and optimising bed capacity. Med J Aust. 2006; 184:203-4.

12. Bloomfield J. BAEM - emergency medicine landmark. British Association for Emergency Medicine. Available at: www. emergencymed.org.uk. Accessed March, 2008.

13. Donnellan E. Making beds for those in need. Irish Times. November 25, 2008.

14. Krall S, O’Conner RE, Maercks L. Higher inpatient medical surgical bed occupancy extends admitted patients stay. West J Emerg Med. 2009; 10:93-6.

15. O. Miró M. Sánchez G. Espinosa B, et al. Analysis of patient flow in the emergency department and the effect of an extensive reorganisation. Emerg Med J. 2003; 20:143-8.

16. Rathlev N, Chessare J, Olshaker J, et al. Time series analysis of variables associated with daily mean emergency department length of stay. Ann Emerg Med. 2007; 49:265-271.

17. Cooke MW, Wilson S, Halsall J, et al. Total time in English accident Med J. 2004; 21:575-6.

Sinclair D. Emergency department crowding – implications for

18. Department of Health and Children. Acute hospital bed capacity a national review. Dublin, 2002.

12:491-4.

19. Platz E, Bey T, Walter FG. International report: current state and

George G, Jell C, Todd BS. Effect of population ageing on

development of health insurance and emergency medicine in

emergency department speed and efficiency: a historical

germany. the influence of health insurance laws on the practice of

perspective from a district general hospital in the UK. Emerg Med

emergency medicine in a European country. J Emerg Med 2003;

J. 2006; 23:379-83.

3.

25(2):203-210.

Derlet RW, Richards JR. Crowding in the nation’s emergency

20. Höhere Auslastung der Krankenhausbetten. 2006. Available at: http://

departments: Complex Causes and Disturbing Effects. Ann Emerg

www.destatis.de/jetspeed/portal/cms/Sites/destatis/Internet/DE/

Med. 2000; 35:63-7.

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Presse/pm/2007/09/PD07__350__231. Accessed January 29, 2008.

Schneider SM, Gallery ME, Schafermeyer R, et al. Emergency

21. Gilligan P, Gupta V, Singh I, et al. Why are we waiting? A study of the

department crowding: A Point in Time. Ann Emerg Med. 2003;

patient’s perspectives about their protracted stays in an emergency

42:167-72.

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department. Ir Med J. 2007; 100:627-9.

Derlet RW, Richards JR, Kravitz RL. Frequent crowding in US

22. Forster AJ, Stiell I, Wells G, et al. The effect of hospital occupancy on

emergency departments. Acad Emerg Med. 2001; 8:151-5.

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emergency department length of stay and patient disposition. Acad

Coughlan M, Corry M. The experiences of patients and relatives/ significant others of crowding in accident and emergency in Ireland: A qualitative descriptive study. Accid Emerg Nurs. 2007; 15:201-9.

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Richardson D. Increase in patient mortality at 10 days associated

and emergency departments is related to bed occupancy. Emerg

paediatric emergency medicine. Paediatr Child Health. 2007; 2.

McCarthy ML, Aronsky D, Jones I, et al. The emergency department occupancy rate: a simple measure of emergency department

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39. Dick WF. Anglo-American vs. Franco-German emergency medical

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25. American Hospital Association. Fast facts on U.S. hospitals. Health Forum

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United Kingdom. Ann Emerg Med. 1999; 33:702-9.

Statistics-and-Studies/fast-facts.html. Accessed August 12, 2009.

41. Williams TE Jr, Ellison EC. Populaiton analysis predicts a future

26. Halpern NA, Pastores SM, Greenstein RJ. Critical care medicine in

critical shortage of general surgeons. Surgery. 2008; 144:548-54.

the United States 1985-2000: An analysis of bed numbers, use, and

42. Miele V, Andreoli C, Grassi R. The management of emergency

costs. Crit Care Med. 2004; 32:1408-9.

radiology: key facts. Eur J Radiol. 2006; 59:311-314.

27. Jepson GMH. How do Primary Health Care systems compare across

43. Irish College of General Practitioners. What is the structure of Irish

Western Europe? Pharm J. 2001; 267:269-73.

healthcare? Available at: www.icgp.ie. Accessed September 9,

28. Rieffe C, Oosterveld P, Wijkel D, et al. Reasons why patients bypass

2007.

their GP to visit a hospital emergency department. Accid Emerg Nurs.

44. Ryden L, Stokoe G, Breithardt G, et al. Patient access to medical

1999; 7:217-25.

technology across Europe. Eur Heart J. 2004; 25:611-16.

29. Lee A, Lau F, Hazlett CB, et al. Measuring the inappropriate

45. Davis K, Schoen C, Guterman S, et al. Slowing the growth of u.s.

utilization of accident and emergency services? Int J Health Care

health care expenditures: what are the options? 2007 Bipartisan

Qual Assur. 1999; 12:287-92.

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30. van Uden CJT, Winkens RAG, Wesseling GJ, et al. Use of out of

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46. Kerem K, Puss T, Viess M, et al. Health and convergence of

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31. Cooke MW, Fisher J, Dale J, et al. Reducing attendances and

(Teaching) Conference. Ljubljana, Slovenia; 2007. Available at: www.

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32. Hall MA. The Impact and Enforcement of Prudent Layperson Laws.

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organizations. Ann Emerg Med. 2004; 43:155-62.

51. Departmen of Health. Modernization Agency. Richmond, Surrey UK:

35. Gunal MM, Pidd M. Understanding Accident and Emergency

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53. Cronin JG, Wright J. Breach avoidance facilitator - managing the A&E

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Review Article

Paramedics’ Ability to Perform Drug Calculations Kathryn J Eastwood, BNurs, BSc Malcolm J Boyle, PhD Brett Williams

Monash University Department of Community Emergency Health and Paramedic Practice, Victoria, Australia

Supervising Section Editor: Christopher Kahn, MD, MPH Submission history: Submitted July 1, 2009; Revision Received September 20, 2009; Accepted October 7, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Background: The ability to perform drug calculations accurately is imperative to patient safety.

Research into paramedics’ drug calculation abilities was first published in 2000 and for nurses’ abilities the research dates back to the late 1930s. Yet, there have been no studies investigating an undergraduate paramedic student’s ability to perform drug or basic mathematical calculations. The objective of this study was to review the literature and determine the ability of undergraduate and qualified paramedics to perform drug calculations.

Methods: A search of the prehospital-related electronic databases was undertaken using the Ovid and EMBASE systems available through the Monash University Library. Databases searched included the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, CINAHL, JSTOR, EMBASE and Google Scholar, from their beginning until the end of August 2009. We reviewed references from articles retrieved.

Results: The electronic database search located 1,154 articles for review. Six additional articles were identified from reference lists of retrieved articles. Of these, 59 were considered relevant.

After reviewing the 59 articles only three met the inclusion criteria. All articles noted some level of mathematical deficiencies amongst their subjects.

Conclusions: This study identified only three articles. Results from these limited studies indicate a significant lack of mathematical proficiency amongst the paramedics sampled. A need exists to identify if undergraduate paramedic students are capable of performing the required drug calculations in a non-clinical setting. [WestJEM. 2009;10:240-243.]

INTRODUCTION Paramedics, like many other healthcare professionals, are often required to conduct drug calculations in the daily management of their patients. However, unlike other healthcare professionals, they are often subject to unique pressures due to the dynamic and often unpredictable nature of their working environment. Their role requires them to treat a broad variety of patient complaints, from social issues to life-threatening situations. Their working environment can vary from a well lit bedroom to an overturned car in a ditch on a rainy night with limited lighting and difficult access to an unconscious patient still restrained in his car seat. This work environment requires extreme versatility, and these confounding factors often place extra pressure on them.

However, it is still expected that they will care for the patient Volume X, no. 4 : November 2009

appropriately, problem solve, recall vital information and perform drug calculations swiftly and accurately, as incorrect drug calculations undermine patient safety and outcome.

Errors associated with medications account for up to 20% of all hospital-based healthcare errors in Australia and cost approximately $380 million to the public hospital system annually.1 In the U.S. about 7,000 deaths in 1993 were due to medication errors. This number is higher than that of workplace deaths in the U.S., yet little money is spent on preventing this.2 A study by Barker et al.3 found that 17% of the medication errors in 36 healthcare facilities were due to dosage errors. They also found that medication errors occurred in nearly 20% of all medication administrations. It is estimated that medication-related errors cost the U.S. about $2 billion a year for in-patients.2 While we found no evidence regarding 240

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Drug Calculations the cost of drug-dosage miscalculations in the prehospital setting, Vilke et al.4 found that there have been reports of both significant injuries and death as a result of prehospital medication errors. Two studies found that between 9% and 43% of paramedic respondents admitted to medication errors, and in one of these studies 63% of the errors were doserelated.4 Research into paramedicsâ&#x20AC;&#x2122; abilities to perform drug calculation was first published in 2000 by Hubble et al.5 Their findings have been supported by many studies within the field of nursing, dating back to the late 1930s.5-21 A study by Beilock and Carr22 on pressure situations found that individuals who are more academically inclined have a larger negative variance in mathematical ability when under pressure. These findings were supported by studies on stress and high pressure situations, which demonstrated a decline in mathematical performance amongst both nurses and paramedics.14,23,24 There is also a correlation between a decline in mathematical ability and time pressures.24 The drug calculations required of paramedics are the same as those used throughout the hospital and healthcare system.

Paramedics must be able to calculate pediatric patient weights, drug dosages and volumes, weight-based drug doses, infusion rates, and weight and time-based infusion rates.25 Deficiencies have been found amongst the nursing profession for many years, thus serving as a catalyst in determining if these same deficiencies exist amongst the next generation of universityeducated paramedics.6-13,15-21 No studies to date demonstrate the drug and mathematical calculation ability of undergraduate paramedic students in a classroom environment. The objective of this study was to review the literature and determine the ability of undergraduate and qualified paramedics to perform drug calculations.

METHODS We undertook a search of the prehospital-related electronic databases using the Ovid and EMBASE systems available through the Monash University Library. The databases searched included the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, CINAHL, JSTOR, EMBASE and Google Scholar, from their beginning until the end of August 2009.

The Medical Subject Headings (MeSH) and keywords used in the searches included emergency medical services, emergency medical technician, ambulance, air ambulance, military medicine, emergency treatment, emergency medicine, first aid, prehospital, pre-hospital, out-of-hospital, out of hospital, paramedic, drug calculation, medication calculation, maths, mathematics, students, nursing, maths skills, medication safety, drug administration errors, nurse education, numeracy skills, student nurses, dosage calculations, medication administration, pharmacological skills, problem solving, problem-solving, calculation, medication-related Western Journal of Emergency Medicine

errors, medication calculation skills, calculation methods, mathematical skills, drug calculation skills, conceptualizing drug calculations, drug dosages, mathematical anxiety, math anxiety, mathematical comprehension. The MeSH headings and keywords were used individually and in combination during the search process. We then combined all search results to remove duplicates and provide a list of articles for review.

We reviewed the references from articles gathered to identify additional articles not found in the electronic database search. We included articles if they contained information pertaining to paramedics and drug calculation or mathematical abilities. Articles were excluded if they were not written in English or did not involve paramedics.

RESULTS The electronic database search located 1,154 articles for review. We identified six additional articles by reviewing the reference lists of the located articles. Of these 1,154 articles 59 were considered relevant to assist in answering the research question.

After reviewing the 59 potentially relevant articles only three met the inclusion criteria. The remaining 56 did not involve paramedics.

DISCUSSION This study only located three small studies that reviewed the paramedicâ&#x20AC;&#x2122;s ability to perform drug calculations or basic mathematical calculations in a variety of simulated nonclinical situations.

These studies asked fundamental drug calculation questions. The study by LeBlanc et al.14 gave only one example of a drug calculation (volume related) used in their questionnaire. Hubble et al.5 provided more detail about the calculations they used and some sample questions. They included drug-dosage calculations and medication and intravenous infusion rate calculations, some of which included weight- or percentage-based components. The study by Bernius et al.26 asked eight basic drug calculation questions, two on calculating the appropriate endotracheal size for a pediatric patient and for paramedics qualified to perform RSI, and six questions about the RSI medications. All three studies on paramedicsâ&#x20AC;&#x2122; mathematical abilities demonstrated an alarmingly low level of mathematic competence. Participants in both studies were qualified paramedics who had completed all appropriate training to practice. Despite completion of their basic training, the paramedics in the studies still displayed poor mathematical ability.5,14,26 None of the studies identified if any particular calculations caused more problems than others.

LeBlanc et al.14 tested 30 paramedics in Canada of two varying qualification levels, under high and low stress conditions. The high stress condition was created by conducting a scenario within a simulator ambulance vehicle with an adult mannequin. The participants were given a

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respiratory failure scenario. Whilst the scenario was designed to be challenging it was within their skills and knowledge capabilities. The overall mean score for the more advanced paramedics was 61.1%, and the less qualified paramedics scored 39.8% (95% CI 50.6%-71.6% and 31.2%-48.4%, respectively). The study also found a decrease in mathematical performance when under the pressure of a patient-based scenario rather than a written scenario. Although the study sample was small, with only 30 participants, they comprised some of the ambulance services’ most qualified paramedics.14 The study by Hubble et al.5 tested 109 practicing paramedics from various counties in North Carolina during a regular in-service meeting. The mean score for this 10item test was 51.4% with a standard deviation of 27.40. No time limit was set, and these participants were allowed the use of a calculator. Theoretically, this means that for similar calculations required of them while on the job, excluding any work-related pressures, they will at best get it right only half of the time.

The study by Bernius et al.26 assessed 523 practicing paramedics; 277 undertook pediatric calculation mentally or using paper (unaided), whilst the remaining participants used a pediatric code card (aided) with all the necessary drug calculations. The paramedics, from five Maryland counties, undertook the study during a mandatory continuing education class. Bernius found a statistically significant difference between the unaided group and the aided (code card) group for mean percentage of correct questions with a 29% difference between the two [65% questions answered correctly (unaided) vs. 94% (aided), p <0.001). The study also found a statistically significant difference between the unaided and aided group in percentage of total question errors [33% vs. 6.6%, respectively (p <0.001)]; severe errors [20.9% vs. 4.9%, respectively (p <0.001)]; tenfold errors [6.2% vs. 0.76%, respectively (p <0.001)]; hundredfold errors [0.4% vs. 005%, respectively (p=0.025)]; correct ETT calculation [23% vs. 98%, respectively (p <0.001)] and time taken to complete the questionnaire [11.4 minutes and 7.1 minutes, respectively (p <0.001)].

Many factors have been attributed to this lack of mathematical ability within both the prehospital and nursing fields. One of the major factors is pressure. Within the prehospital setting the varying pressures and extraneous variables present at any given time are potentially unique to this discipline. These include time, environment, management of distressed individuals and other agencies at incident sites, and the management of the critically ill patients. Other factors attributed to poor mathematical performance include skills decay and poor initial mathematical education.14,22-24 Zautcke et al.27 found that skills diminished amongst paramedics with length of time in the job. Cartwright and Hutton found that nurses’ mathematical skills diminished over time due to a lack of opportunity to practice these skills and the availability of medical equipment that provides Volume X, no. 4 : November 2009

automatic calculations.12,28 While skills decay is one reason for mathematic inability, evidence suggests it may not be the main reason for the poor results in the mathematical calculations found in many studies.5,12-14,19,21,29 All of the testing in the studies by Hubble et al.,5 LeBlanc et al.,14 and Bernius et al.26 were conducted under controlled conditions where many of the confounding factors associated with working as a paramedic were excluded.5,14,26 Even in the high stress condition in the LeBlanc study, the patient was a mannequin and the paramedics were in a simulator ambulance. They were not faced with a real patient (or even an actor displaying the features of respiratory distress) or with any of the environmental conditions commonly encountered by paramedics, such as cramped conditions, poor lighting, weather and distressed family members. Despite the lack of “reality” in the testing, the performance level was still poor.14 Conceptual errors, where the operator is unable to formulate a mathematical question from the information given, have been identified as the most common type of error amongst the paramedics investigated, indicating issues other than infrequent use of mathematical skills or inability to perform calculations while under pressure.24 While these elements are acknowledged to affect mathematical ability, other education issues may have arisen throughout the participants’ secondary education.30 There is a need for further studies into the ability of qualified paramedics and undergraduate paramedics to perform basic mathematical calculations and drug calculations normally required in the prehospital setting. Curriculum changes, including a revision of fundamental mathematical principles and scenario-based mathematical practice, may need to be implemented to address any mathematical deficiencies that may be identified with further investigation.

LIMITATIONS This study is potentially limited by the use of Englishonly articles and the paucity of literature on drug calculation ability among paramedics, especially involving undergraduate or Australian paramedics.

CONCLUSION There have been few studies into the mathematical calculation abilities of paramedics. The results of the three studies we looked at indicate a significant lack of mathematical proficiency amongst the paramedics sampled. These findings are supported by a significant amount of literature within the nursing discipline suggesting a widespread problem. The literature highlights a need for studies to be conducted amongst the Australian paramedic discipline, including undergraduate paramedic students, to determine if the mathematical competence of student paramedics is sound at the beginning of the paramedic education, or whether they are entering their careers with deficiencies already present.

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Eastwood et al.

Drug Calculations Address for Correspondence: Malcolm Boyle, Department of Community Emergency Health & Paramedic Practice, Monash University, PO Box 527, Frankston 3199, Victoria, Australia.

Email: mal.boyle@med.monash.edu.au

14. LeBlanc VR, MacDonald RD, McArthur B, et al. Paramedic

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

16. Pozehl BJ. Mathematical calculation ability and mathematical anxiety

performance in calculating drug dosages following stressful scenarios in a human patient simulator. Prehosp Emerg Care. 2005; 9:439-44.

15. Munday L, Hoyt DP. Predicting academic success for nursing students. Nurs Res. 1965; 14:341-4. of baccalaureate nursing students. J Nurs Educ. 1996; 35:37-9.

17. Sander T, Cleary S. Medication mathematics competency for bachelor of nursing students: results and challenges of a first year screening test. Studies in Learning, Evaluation, Innovation and

REFERENCES 1.

Development. 2004; 1:45-52.

Northern Sydney Central Coast Area Health Service. Reducing

18. Santamaria N, Norris H, Clayton L, et al. Drug calculation

Paediatric Medication Errors. 2006. Available at: http://www.archi.net. au/e-library/awards/awards06/safety/reducing_errors. Accessed July

competencies of graduate nurses. Collegian. 1997; 4:18-21.

19. Wright K. An investigation to find strategies to improve student

18, 2008 2.

nurses’ maths skills. Br J Nurs. 2004; 13:1280-4.

Institutes of Medicine. To Err is Human: Building a safer Health

20. Wright K. An exploration into the most effective way to teach drug

System. Washington DC: National Academy Press; 1999.

3.

calculation skills to nursing students. Nurse Educ Today. 2005;

Barker KN, Flynn EA, Pepper GA, et al. Medication errors observed

25:430-6.

in 36 health care facilities. Arch Intern Med. 2002; 162:1897-903.

4.

21. Wright K. Barriers to accurate drug calculations. Nurs Stand. 2006;

Vilke GM, Tornabene SV, Stepanski B, et al. Paramedic self-reported

20:41-5.

medication errors. Prehosp Emerg Care. 2007; 11:80-4.

5.

22. Beilock SL, Carr TH. When high-powered people fail:Working memory

Hubble MW, Paschal KR, Sanders TA. Medication calculation skills of practicing paramedics. Prehosp Emerg Care. 2000; 4:253-60.

6.

Blais K, Bath JB. Drug calculation errors of baccalaureate nursing

anxiety, and performance. J Exp Psychol Gen. 2001; 130:224-37.

students. Nurse Educ. 1992; 17:12-5.

7.

24. Kellogg JS, Hopko DR, Ashcraft MH. The effect of time pressures on

Brown DL. Does 1 + 1 still equal 2? A study of the mathematic

arithmetic performance. J Anxiety Disord. 1999; 13:591-600.

competencies of associate degree nursing students. Nurse Educ.

8.

25. Ambulance Victoria. Clinical Practice Guidelines. 2006. Available

2002; 27:132-5.

at: http://www.rav.vic.gov.au/What-we-do/Clinical-Service/Clinical-

Brown DL. Can you do the math? Mathematic competencies of

Practice-Guidelines/CPG-Index.html. Accessed September 9, 2009.

baccalaureate degree nursing students. Nurse Educ. 2006; 31:98-100.

9.

and “choking under pressure” in math. Psychol Sci. 2005; 16:101-5.

23. Ashcraft MH, Kirk EP. The relationships among working memory, math

26. Bernius M, Thibodeau B, Jones A, et al. Prevention of pediatric drug

Faddis MO. Eliminating Errors in Medication. Am J Nurs. 1939;

calculation errors by prehospital care providers. Prehosp Emerg

39:1217-23.

10. Grandell-Niemi H, Hupli M, Leino-Kilpi H. Medication calculation

Care. 2008; 12:486-94.

27. Zautcke JL, Lee RW, Ethington NA. Paramedic skill decay. J Emerg

skills of graduating nursing students in Finland. Adv Health Sci Educ Theory Pract. 2001; 6:15-24.

Med. 1987; 5:505-12.

28. Cartwright M. Numeracy needs of the beginning registered nurse.

11. Grandell-Niemi H, Hupli M, Puukka P, Leino-Kilpi H. Finnish nurses’ and nursing students’ mathematical skills. Nurse Educ Today. 2006;

Nurse Educ Today. 1996; 16:137-43.

29. Weeks KW, Lyne P, Torrance C. Written drug dosage errors made by

26:151-61.

students: the threat to clinical effectiveness and the need for a new

12. Hutton BM. Do school qualifications predict competence in nursing calculations? Nurse Educ Today. 1998; 18:25-31.

approach. Clin Eff Nurs. 2000; 4:20-9.

30. Kapborg ID. An evaluation of Swedish nurse students’ calculating

13. Hutton BM. Nursing mathematics: The importance of application.

ability in relation to their earlier educational background. Nurse Educ

Nurs Stand. 1998; 13:35-8.

Western Journal of Emergency Medicine

Today. 1995; 15:69-74.

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Case Report

Lead Toxicity Resulting from Chronic Ingestion of Opium Mohammad Jalili, MD Reza Azizkhani, MD

Tehran University of Medical Sciences, Department of Emergency Medicine, Tehran, Iran

Supervising Section Editor: Jeffrey R. Suchard, MD Submission history: Submitted September 10, 2008; Revision Received July 5, 2009; Accepted July 5, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

A 32-year-old man presented to the emergency department (ED) with lower abdominal pain and constipation. He related chronic ingestion of large amounts of opium. Physical examination showed mild abdominal tenderness and gingival discoloration. Diagnostic studies showed a mild hypochromic, microcytic anemia with basophilic stippling of the red blood cells. Abdominal imaging showed no intraabdominal pathology. A diagnosis of lead toxicity was confirmed through serum lead levels. The patient was put on chelation therapy and his signs and symptoms started to resolve. As a comprehensive search for other sources of lead was unsuccessful, opium adulterants were considered as the culprit.

Chemical analysis of the opium confirmed this. Contaminated drugs have been reported as a source of exposure to toxins such as arsenic or lead. While other reports deal with patients from clinics, this report illustrates lead toxicity from ingestion of contaminated opium in the ED. [West J Emerg Med. 2009;10(4):244-246.]

INTRODUCTION Lead poisoning is the most common toxicity of environmental origin in the United States (U.S.).1 One in every 20 children in the U.S. has toxic blood levels,2 while three million or more adult workers are estimated to be at risk for toxic lead exposure.3 Exposure may result from ingestion or inhalation of lead compounds. It may also be due to direct skin contact with organic lead or resorption from a retained bullet in joints. Although the incidence of occupational and adult lead poisoning has declined,4 the problem still exists in various parts of the world. Chronic lead toxicity often presents gradually and is nonspecific.

Characteristic symptoms and signs of acute lead poisoning include abdominal colic, malaise, nausea, vomiting, constipation, fatigue, anemia, peripheral neuropathy, renal impairment, hepatic disorder, and CNS dysfunction.5 Abdominal pain is one of the common manifestations of lead poisoning and sometimes brings the patient to the emergency department (ED). For the emergency physician (EP), however, this is a challenging diagnosis, due to rarity of the disease combined with the complexity of the presentations.

Furthermore, exposure to lead is usually considered only when the patient’s history points to well-known traditional sources of lead, such as paint or printing material. However, unusual and exotic causes of chronic lead poisoning have been described. Examples include adulterated marijuana,6 Volume X, no. 4 : November 2009

Indian herbal medicine,7 and “moonshine” whiskey.

We report a case of chronic lead poisoning, which occurred as a result of chronic ingestion of opium adulterated with lead.

CASE REPORT A 32-year-old man presented to our ED with five weeks of abdominal pain. It was constant and, though diffuse, was worse in the lower abdomen. It did not radiate to the back, arms, or chest and was not associated with food. He reported constipation for two weeks, which did not respond to laxatives. He also had loss of appetite but denied nausea or vomiting. The pain was not accompanied by chills, diarrhea, or other symptoms. No recent weight loss was reported.

He had no significant co-morbidity such as hypertension, diabetes, or ischemic heart disease, and he had not been hospitalized. He was addicted to opium, and stated that he ingested about 20 grams per day. He conceded that he had obtained opium from the black market, from the same source for many years. He denied intravenous injection. He underwent a course of ultra-rapid detoxification about two months previously, but resumed consumption of opium two weeks later. His medications included ranitidine, vitamin B6, and hyoscine (all without prescription). He was unemployed at the time of presentation but had worked as a janitor, and had no known exposure to lead.

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Lead Toxicity Table 1. Laboratory results for the case patient Laboratory Tests (units)

Results

Normal

Alanine aminotransferase (U/L)

72

10-40

Amylase (U/L)

155

25-85

Aspartate aminotransferase (U/L)

95

20-48

Blood Urea Nitrogen (mg/dL)

20

8-23

Hemoglobin (g/dL)

9.8

14-17.5

Mean Corpuscular Volume (fl)

80

82-92

MCHCa (g/dL)

29

32-36

Reticulocyte count (%)

1.0

0.5-2.5

Potassium (mEq/L)

4.0

3.5-5.0

Serum creatinine (mg/dL)

0.9

0.6-1.2

Sodium (mEq/L)

140

136-142

Total serum calcium (mg/dL)

8.9

8.2-10.2

Lactate dehydrogenase (IU/L)

430

340-670

White blood cell count (x10 /µL)

9.5

4.5-11.0

3

a

MCHC: Mean Corpuscular Hemoglobin Concentration

His vital signs were stable: blood pressure, 100/70 mmHg; pulse rate, 80 beats per minute; and respiratory rate, 14 breaths per minute; pulse oximetry, 98% on room air, and temperature, 98.3°F (37°C). His head and neck examination revealed a dark line along the gingival margin. Chest examination was normal.

Abdomen revealed mild tenderness to deep palpation of the lower abdomen, without rebound, guarding, or costovertebral angle tenderness. Neurological examination was normal.

Laboratory results are presented in Table 1.

A peripheral blood smear revealed basophilic stippling of red cells. An abdominal ultrasound, computed tomography scan with intravenous and oral contrast of the abdomen were normal. The presentation, physical findings, lab studies and lack of another explanation led the EP to suspect lead toxicity.

He was admitted to the floor, and a whole blood lead level result was 50 µg/dL (2.42 µmol/L). The diagnosis of lead toxicity was made and the patient was put on chelation therapy with 2,3-dimercaptosuccinic acid (DMSA). His abdominal pain subsided over the next week and he was discharged.

Marked resolution of all signs and symptoms occurred by onemonth follow up. As thorough investigation of the patient’s past history failed to reveal any other source of exposure except opium, lead toxicity was attributed to the adulterants of opium. Analysis of the opium obtained from the patient’ house, performed by atomic absorption measurement using a Shimadzu AA670 atomic absorption spectrometer (Shimadzu, Japan), showed 35.2 mg of lead per 100 g of opium.

DISCUSSION Toxic effects of lead may occur acutely after a single Western Journal of Emergency Medicine

exposure or, more commonly, through chronic low-level exposure. Recognition of lead poisoning depends on a high index of suspicion and a thorough patient history.

The insidious onset, non-specific complaints,8 and lack of diagnostic signs facilitate the missed diagnosis of lead poisoning. Lead poisoning should be considered in the differential diagnosis of abdominal pain.9 The combination of abdominal or neurological dysfunction with a hemolytic anemia should raise the suspicion of lead toxicity. The definitive diagnosis of lead poisoning rests on finding an elevated blood lead level, regardless of symptoms.10 All patients with symptoms consistent with lead toxicity and an elevated blood lead level should be treated. Treatment includes British anti-Lewisite (BAL) or succimer (DMSA) with or without CaNa-EDTA.11 Some traditionally recognized sources of lead exposure include lead smelting, battery, rubber and plastic manufacturing, printing, and soldering of lead products.12 While attempts have been made to contain these sources of exposure to lead, some others such as herbal medicine7 and adulterated drugs6 are emerging and are worthy of noting.

Opium is still one of the most frequently abused drugs.

Informal, and often illegal, laboratories refine opium into a sticky, brown paste, which is pressed into bricks and sun dried. This material can then be ingested or smoked. This process results in introduction of impurities such as lead into the product. On the other hand, lead is sometimes deliberately added to opium by the smugglers to increase its weight during trading. Although the amount of lead in opium is usually small,13 when taken in large amounts opium adulterated with lead can produce clinical toxicity.

Intravenous injection of adulterated drug and inhalation of contaminated heroin have previously been mentioned as a source of lead poisoning in drug addicts.14 Lead toxicity has also been reported in a case series from Germany following smoking of adulterated marijuana.6 Opium has previously been reported as a source of both arsenic and lead poisoning.13-18 In 1973, in the earliest report of this peculiar source of lead, a middle-aged Chinese woman and her father were diagnosed to suffer from lead poisoning due to ingestion of home-made opium.18 More recently, three cases have been reported from a central province in Iran.19 All were middle-aged men who had been admitted for abdominal pain. The case we are reporting is another piece of evidence showing the relationship between opium ingestion and lead poisoning.

Furthermore, to the best of our knowledge, there has been no report of such cases from the ED. It is interesting that this chronic complication lead to an acute presentation, which brought the patient to us. It is therefore very important for the EP to keep this diagnosis in mind when facing a patient with vague abdominal pain.

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CONCLUSION Metabolic processes, including lead poisoning, should be considered in the differential diagnosis of abdominal pain, especially when its cause is unclear. The sources of lead are numerous and, with new products and processes the list must be updated. In cases of consumption of illicit drugs and substances, where the ingredients and the processing method are not known, the suspicion should be investigated more vigorously. Our case emphasizes the need for a thorough history, including details of social habits in patients with cryptic abdominal pain.

6.

Busse F, Omidi L, Timper K, et al. Lead poisoning due to adulterated marijuana. NEJM. 2008; 358:1641-2.

7.

Dundabin DW, Tallis GA, Popplewell PY, et al. Lead poisoning from Indian herbal medicine (Ayurveda). Med J Aust. 1992; 157:835-6.

8.

Hettmansberger TL, Mycyk MB. Lead poisoning presents a difficult diagnosis. Am Fam Physician. 2002; 66:1839-40.

9.

Sood A, Midha V, Sood N. Pain in abdomen - do not forget lead poisoning. Indian J Gastroenterol. 2002; 21:225-6.

10. Centers for disease control and prevention: screening young children for lead poisoning: guidance for state and local public health officials. Atlanta: CDC, 1997.

11. Lifshitz M, Hashkanazi R, Phillip M. The effect of

Address for Correspondence: Mohammad Jalili, MD, Department of Emergency Medicine, Tehran University of Medical Sciences, Keshavarz Blvd., Tehran, Iran. Email mjalili@tums.ac.ir.

2,3-dimercaptosuccinic acid in the treatment of lead poisoning in adults. Ann Med. 1997; 29:83-5.

12. Heneretig F. Lead. In: Goldfrank LR. Goldfrankâ&#x20AC;&#x2122;s toxicologic emergencies. 6th ed. Stamford, CT: Appleton & Lange; 1998:1277-1309.

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

13. Aghaee-Afshar M, Khazaeli P, Behnam B, et al. Presence of Lead in Opium. Arch Iran Med. 2008; 11: 553-4.

14. Algora M, MartĂ­n-Castillo A, Zabala P, et al. Lead poisoning due to drug addiction: a new source of poisoning with clinical interest and important epidemiological consequences. Ann Med Interna. 1989; 6:483-5.

REFERENCES 1.

Landrigan PJ, Todd AC. Lead poisoning. West J Med. 1994; 161:153-9.

2.

Markowitz G, Rosner D. Cater to the children: the role of the lead industry in a public health tragedy, 1900-1955. Am J Public Health.

15. Jayasinghe KS, Misbah SA, Soosainathan S, et al. Contaminated opium as a source of chronic arsenic poisoning in Sri Lanka. Ceylon Med J. 1983; 28:22-7.

16. Datta DV. Arsenic adulteration in opium (Arsenicosis - a real danger to

2000; 90:36-46.

3.

Paloucek FP. Lead poisoning. Am Pharm. 1993; 33:81-8.

4.

Prickle JL, Brody DJ, Gunter EW, et al. The decline of blood lead levels in the United States: The National Health and Nutrition

health in developing countries). J Assoc Physicians India. 1978; 26:223-7.

17. Narang AP, Chawla LS, Khurana SB. Levels of arsenic in Indian opium eaters. Drug Alcohol Depend. 1987; 20:149-53.

18. Chia BL, Leng CK, Hsii FP, et al. Lead Poisoning From

Examination Surveys (NEHANES). JAMA. 1994; 272:284-91.

5.

Contaminated Opium. Br Med J. 1973; 1:354.

Cullen MR, Robins JM, Eskenazi B. Adult inorganic lead intoxication:

19. Masoodi M., Zali MR, Ehsani-Ardakani MJ, et al. Abdominal pain

presentation of 31 new cases and a review of recent advances in the

due to lead-contaminated opium: a new source of inorganic lead

literature. Medicine (Baltimore). 1983; 62:221-47.

poisoning in Iran. Arch Iran Med. 2006; 9:72-5.

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Case Report

Thyroid Gland Hematoma After Blunt Neck Trauma Baris Saylam, MD Bülent Çomçali, MD Mehmet Vasfi Ozer, MD Faruk Coskun, MD

Ankara Numune Teaching and Research Hospital, Department of 3rd Surgery, Ankara, Turkey

Supervising Section Editor: Teresita M. Hogan, MD Submission history: Submitted May 20, 2009; Revision Received October 2, 2009; Accepted October 12, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Hemorrhage of a previously normal thyroid gland as a result of blunt trauma is a very rare condition.

We report a case of blunt trauma that caused acute hemorrhage into the thyroid gland and presented with hoarseness. The diagnosis of thyroid gland hematoma was made with a combination of fiberoptic laryngoscopy, cervical computed tomography, and carotid angiography. The patient was treated conservatively, had a favorable course without further complications, and was discharged four days after admission. [West J Emerg Med. 2009;10(4):247-249.]

INTRODUCTION Trauma to the thyroid gland following blunt neck trauma is rarely reported in the English-language literature.1-15 Blunt direct thyroid injury is quite rare in trauma patients without preexisting goiter.1 Most of the reported cases have emphasized the need to closely monitor patients with thyroid injuries so that possible upper airway obstruction caused by an associated hematoma can be detected promptly.1,2,3,12 In all cases of blunt trauma involving the neck, a high index of suspicion is warranted as symptoms may not be present on initial examination. We report a case of blunt injury to a previously normal thyroid in which invasive airway management was not necessary and successful non-operative treatment was accomplished.

CASE REPORT The patient, a 69-year-old female, fell in the bathroom on a slippery floor and struck her anterior neck. About three hours after the event, she was admitted by ambulance to the emergency department (ED) of our hospital. On admission, she was conscious and did not appear unduly distressed.

There were no signs of emphysema, stridor or dyspnea. Her breath sounds were equal. The patient didn’t suffer any kind of aspiration or cough. Her vital signs were normal, showing a blood pressure of 130/80 mmHg, a heart rate of 66 bpm and a respiratory rate of 20 breaths per minute. Her arterial blood gas was normal, with an O2 saturation of 98% on room air. Although the vital signs were stable and she was not in respiratory distress, her voice was hoarse immediately Western Journal of Emergency Medicine

following the injury. The patient was only able to speak in a whisper. On examination, her neck was swollen and was tender to palpation. No carotid bruits were auscultated. Plain films of the neck revealed a normal cervical spine with mild tracheal deviation toward the right. Because of the suspicion of a muscular hematoma, the patient underwent a sonographic examination of the neck. The neck ultrasound revealed a moderately hypoechoic, diffuse, infiltrative process presumed to be a hematoma surrounding the left thyroid lobe and extending into the anterior cervical muscular strap.

Computed tomography (CT) scan without contrast was performed to better evaluate the extent of the hematoma and the possible compromise of neighboring structures.

However, neck CT scan demonstrated fragmentation and hematoma within the left lobe of the thyroid gland (Figure 1), as well as tracheal deviation to the right without evidence for laryngotracheal trauma. This study revealed a mass, felt to be a hematoma, in the left neck, measuring 4.7 × 5 × 5 cms.

The left lobe of the thyroid was indistinguishable from the hematoma, and luminal narrowing was noted in the lower neck. A thyroid functional profile showed a moderate thyroid hormone disorder: free thyroxine, 1.05 pg/ml (reference range, 0.70–1.48 ng/dL), free triiodothyronine, 3.95 pg/mL (reference range, 1.71–3.71 pg/mL), and thyrotropin, 1.78 uIU/mL (reference range, 0.35–4.94uIU/mL ). Hematologic analysis showed a WBC of 14 K/uL (normal: 4,4 to 11,3), with no other significant abnormalities.

Because the patient was hemodynamically stable with excellent oxygen saturations upon examination in the ED,

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←

Figure. Neck CT demonstrating thyroid hematoma and displaced trachea.

further evaluation by means of cervical angiography and indirect laryngoscopy were planned. No signs of active bleeding or expanding hematoma were noted; however, cervical angiography was performed to rule out vascular injury. No vascular injury was found. Otolaryngology was consulted to perform indirect laryngoscopy for evaluation of possible laryngeal injury. Fiberoptic laryngoscopy performed by the consulting otolaryngologist revealed a patent supralaryngeal airway with ecchymoses and mild bilateral vocal-cord edema with an otherwise normal airway.

The patient was admitted to the surgical intensive care unit for close airway observation, reverse Trendelenberg and monitoring for progression of her neck hematoma. Over the ensuing four days, the size of the patient’s neck hematoma remained stable, no stridor or respiratory distress developed, and the patient’s voice weakness resolved. Follow-up sonography performed two months later showed a normal left thyroid lobe.

DISCUSSION While blunt neck trauma is relatively common, secondary thyroid hemorrhage of a previously normal thyroid gland as a result of trauma is a very rare condition.2-7 Most of the reported cases affected a goitrous gland, with resultant increased size and vascularity increasing risk for hemorrhage.5,8,9,10,11 In our patient there was no history of goiter, thyroid gland adenoma, or hyperthyroidism.

Several circumstances have been associated with hemorrhage of the thyroid gland: trauma, deceleration injury, cervical hyperflexion, and Valsalva maneuvers that increase venous pressure, including straining during defecation or Volume X, no. 4 : November 2009

heavy lifting.5,9,10 Direct impact to the anterior neck as a result of blunt trauma has been associated with vascular, bony, muscular, laryngeal, tracheal, and esophageal injury. Onset of life-threatening symptoms in previous reports ranges from within 60 minutes5 to greater than 24 hours.8,10 Symptoms in cases of blunt thyroid trauma are similar to those in laryngotracheal trauma, with palpable painful, pretracheal or paratracheal neck mass. Other symptoms suggestive of possible thyroid trauma include respiratory compromise,5,10,12 dysphagia,2.13 or hoarseness.1,2,5,14 Because of the rarity of blunt trauma to the thyroid gland, no consensus has emerged as to itsworkup or management.

The diagnosis of isolated thyroid gland injury due to blunt neck trauma is difficult. Most of the reported patients are operated on urgently, and neck exploration confirms the diagnosis of thyroid gland injury.1,3,5,8,9,10 Emergency investigations, such as CT scan and/or ultrasonography of the neck, can establish the diagnosis of thyroid gland injury preoperatively. CT confirmed the thyroid gland rupture and surrounding hematoma, facilitating the evaluation of the larynx and the upper digestive tract.

Transient hyperthyroidism15 and thyroid storm7 have been reported after a traumatic hemorrhage into a previously normal thyroid gland. Although thyroid hormone levels in our patient were borderline high immediately after the trauma, subsequently they were normal.

Fiberoptic laryngoscopy is also helpful to rule out laryngotracheal injury, as it is not always obvious on CT scans.2 In cases of blunt neck trauma with massive swelling, the most common injury is major vessel rupture. If this is suspected, then arterial angiography should be obtained.12 Initially, most cases of traumatic hemorrhage into the thyroid gland were treated with surgical evacuation and debridement. More recently, several cases of conservative management of thyroid hematomas have been published in the literature.2,3,4,6,14 CONCLUSION We believe that in the acute setting, a stable thyroid hematoma without airway compromise may be safely observed. Potential airway encroachment is the main endication for neck exploration.

Address for Correspondence: Faruk Coskun, Associate Professor of Surgery, Director of 3rd Surgery Department, Ankara Numune Teaching and Research Hospital, Department of 3rd Surgery, Sehit Adem Yavuz Sokak No: 7/11, 06100-Kizilay, Ankara, Turkey.

Email: mdbsaylam@yahoo.com Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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J Trauma. 1994; 36:408-9.

Neck Surg. 2004; 130:791-3.

Watson AP. Traumatic rupture of the thyroid gland. Aust Radiol. 1999;

14. Hamid CH, Holland AJ, Cummins G, et al. Thyroid transection with spinal injury following blunt trauma in a child. Injury. 2004; 35:332-5.

43:363-4.

7.

Grace RH, Shilling JS. Acute haemorrhage into the thyroid gland following trauma and causing respiratory distress. Br J Surg. 1969; 56:635-7.

61:1012-5.

2.

Behrends RL, Low RB. Acute goitre hematoma following blunt neck trauma. Ann Emerg Med. 1986; 16:1300-1.

Heizmann O, Schmid R, Oertli D. Blunt injury to the thyroid gland:

Delikoukos S, Mantzos F. Thyroid storm induced by blunt thyroid

15. Skowsky WR. Toxic hematoma: an unusual and previously undescribed type of thyrotoxicosis. Thyroid. 1995; 5:129-32.

gland trauma. Am Surg. 2007; 73:1247-9.

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Images In Emergency Medicine

Chilaiditi’s Syndrome Rosa F. McNamara, MCEM, MRCSEd(A&E), MRCPI* Stephen Cusack, FCEM, FRCSEd(A&E)* Patrick Hallihan, MRCS†

* Cork University Hospital, Emergency Department, Wilton, Cork, Ireland † Cork University Hospital, Department of Surgery, Wilton, Cork, Ireland

Supervising Section Editor: Sean Henderson, MD Submission history: Submitted September 29, 2009; Accepted October 8, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[WestJEM. 2009;10(4):250.]

the surgical team for management of a suspected perforated duodenal ulcer.

Subsequent CT imaging of thorax and abdomen revealed hepato-diaphragmatic interposition of the transverse colon, as well as extensive colitis. He was managed conservatively and discharged home well after four days.

Chilaiditi’s sign is the appearance of free air under the diaphragm caused by interposition of the transverse colon between the liver and diaphragm. It is usually asymptomatic and is an incidental finding. It is estimated to occur in 0.25% to 0.28% of the general population1 and was first described

by Demetrious Chilaiditi in 1910.2 When the sign is observed in association with symptoms such as abdominal pain or vomiting it is termed Chilaiditi’s syndrome. It is in this scenario that the radiographic findings may be mistaken for pneumoperitoneum, as occurred in this case.

Figure. Chest radiograph suggestive of a pneumoperitoneum, with an elevated right hemidiaphragm and subdiaphragmatic free air.

A 58-year-old man presented to the Emergency Department with a two-day history of vomiting, diarrhea and intermittent central abdominal pain. His background history was significant for peptic ulcer disease. On examination there was diffuse abdominal tenderness, and a fecal occult blood test was positive. A departmental chest radiograph had appearances suggestive of a pneumoperitoneum, with an elevated right hemidiaphragm and subdiaphragmatic free air. The patient was referred to

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Address for Correspondence: Rosa McNamara, MRCPI, MRCSEd(A&E), MCEM. Department of Emergency Medicine,Cork University Hospital, Wilton, Cork,Ireland. Email rosa.mcnamara@hse.ie REFERENCES 1.

Risaliti A, DeAnna D, Terrosu G, et al. Chilaiditis’s syndrome as a surgical and non surgical problem. Surg Gynecol Obstet.

1993;176:55–58.

2.

Chilaiditi D. Zur Frage der Hapatoptose und Ptose in allgemeinen im Auschluss an drei FŠlle von temporŠrer partieller Leberverlagerung.

Fortschritte auf dem Gebiete der Roentgenstrahlen. 1910;11:173-208.

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Orignal Research

Wound Botulism in Injection Drug Users: Time to Antitoxin Correlates with Intensive Care Unit Length of Stay Steven R. Offerman, MD* Melissa Schaefer, MD† Joseph G. Thundiyil, MD, MPH± Matthew D. CookҰ James F. Holmes, MD, MPH†

* Kaiser Permanente South Sacramento Medical Center, Department of Emergency Medicine, Sacramento, CA † University of California Davis Medical Center, Department of Emergency Medicine, Sacramento, CA ± Orlando Regional Medical Center, Department of Emergency Medicine Ұ University of California San Diego Medical Center, Division of Medical Toxicology, Department of Emergency Medicine

Supervising Section Editor: Jeffrey R. Suchard, MD Submission history: Submitted November 18, 2008; Revision Received April 1, 2009; Accepted April 15, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Objectives: We sought to identify factors associated with need for mechanical ventilation (MV), length of intensive care unit (ICU) stay, length of hospital stay, and poor outcome in injection drug users (IDUs) with wound botulism (WB).

Methods: This is a retrospective review of WB patients admitted between 1991-2005. IDUs were included if they had symptoms of WB and diagnostic confirmation. Primary outcome variables were the need for MV, length of ICU stay, length of hospital stay, hospital-related complications, and death.

Results: Twenty-nine patients met inclusion criteria. Twenty-two (76%) admitted to heroin use only and seven (24%) admitted to heroin and methamphetamine use. Chief complaints on initial presentation included visual changes, 13 (45%); weakness, nine (31%); and difficulty swallowing, seven (24%). Skin wounds were documented in 22 (76%). Twenty-one (72%) patients underwent mechanical ventilation (MV). Antitoxin (AT) was administered to 26 (90%) patients but only two received antitoxin in the emergency department (ED). The time from ED presentation to AT administration was associated with increased length of ICU stay (Regression coefficient = 2.5; 95% CI 0.45, 4.5). The time from ED presentation to wound drainage was also associated with increased length of ICU stay (Regression coefficient = 13.7; 95% CI = 2.3, 25.2). There was no relationship between time to antibiotic administration and length of ICU stay.

Conclusion: MV and prolonged ICU stays are common in patients identified with WB. Early AT administration and wound drainage are recommended as these measures may decrease ICU length of stay. [West J Emerg Med. 2009;10(4):251-256.]

INTRODUCTION Background Six reported forms of botulism exist, including food borne, infantile, wound, iatrogenic, adult infectious (in vivo adult intestinal colonization), and inhalational. Infantile botulism is the most frequently reported form, followed by wound botulism. Although wound botulism remains a rare diagnosis, its incidence has been rising. 1,2,3 In California, where the majority of wound botulism cases have occurred, an average of 0.5 cases per year were reported from 1951-1987.

Western Journal of Emergency Medicine

However, from 1987-1998 there was a 20-fold increase to 9.9 cases per year.4 Early wound botulism cases were related to deep tissue infections in avascular body locations, until the mid-1980s when the first cases associated with injection drug use (IDU were reported. Since then, the vast majority of wound botulism cases are related to IDU.1,4 Although the reasons are not well understood, the majority of wound botulism cases originate in California. 1,2 To date, the largest reported series of wound botulism from injection drug use consists of 129 cases reported from United States public

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health records between 1951-1998. Remarkably, 114 (87%) of these cases were diagnosed in California. The extraordinarily high number of wound botulism cases reported in California was attributed to black tar heroin imported illicitly from Mexico, although a definite causal association could not be made.4,5 A previously published series of 20 patients with wound botulism suggested that early anti-toxin administration was associated with lower frequency and shorter duration of mechanical ventilation.6 Additional evidence from a study of 132 patients with food botulism suggests lower fatality and shorter disease course from early anti-toxin administration.1,7 Although wound botulism is a rare disease, it causes severe disability and potential for adverse outcomes. The treatment frequently entails prolonged hospitalization, consumption of scarce medical resources, and high healthcare costs. It is possible that early identification and intervention by emergency physicians (EPs) may influence hospital course of care and outcomes in these cases.

Goals of this Investigation We sought to describe the characteristics of injection drug users (IDUs) with wound botulism and to identify factors associated with need for mechanical ventilation, length of intensive care unit (ICU) stay, length of hospital stay, hospitalrelated complications, and death. We hypothesized that early anti-toxin administration is associated with improved patient outcomes.

METHODS We conducted a retrospective review examining parenteral drug abusers admitted to any of three University of California hospitals (UC Davis Medical Center, Sacramento, CA; UC San Francisco Medical Center, San Francisco, CA; and UC San Diego Medical Center, San Diego, CA) with a diagnosis of wound botulism between 1991-2005. This study was approved with exemption from formal review by each hospital’s respective institutional review board. Patients were identified by a search for hospital discharges with an ICD-9 code for “Botulism” (005.1) and a review of hospital pharmacy records for patients who received botulinum antitoxin during the study period. Patients were included who had a documented history of IDU and a confirmed diagnosis of wound botulism.

Confirmation of wound botulism, required subjects to have: 1) Symptoms consistent with wound botulism (bulbar palsy and/ or peripheral weakness), and 2) A confirmatory test, including serum detection of botulinum toxin by bioassay or polymerase chain reaction (PCR); electromyography (EMG) findings consistent with botulism; and/or isolation of C. botulinum from wound culture. Pediatric patients (<18 years) and those with incomplete medical records were excluded.

Study definitions were determined a priori. Three abstractors recorded data from medical records onto a Volume X, no. 4 : November 2009

standardized data collection instrument. Inter-rater reliability of the abstractors was not measured. At the time of data collection, abstractors were not blinded to outcome variables, however emergency department (ED) records were abstracted prior to review of hospitalization data. Data collected from the ED record included: patient’s chief complaint, initial vital signs, symptoms, history of illicit drug use, physical examination findings, initial laboratory values, initial chest radiograph findings, negative inspiratory force (NIF) measurement, and ED interventions (oxygen administration, mechanical ventilation, antibiotic administration, anti-toxin administration, wound incision and drainage). Historical data was abstracted from narrative sections of the medical record.

The presence and timing of the following variables were documented from the hospital admission records: time from ED presentation to antitoxin administration in hours, length of ICU stay in hours, length of hospital stay in hours, length of mechanical ventilation in hours, length of time to incision and drainage (I&D) in hours, time to antibiotic administration in hours, chest radiograph findings for pneumonia, and hospitalrelated complications. Patients transferred to an outside hospital or nursing facility were excluded from hospital length of stay analyses as it was not feasible to document the length of stay in these patients. Hospital-related complications were defined as: the development of hospital-acquired pneumonia; venous line infections; pneumothorax during mechanical ventilation; development of a decubitus ulcer; development of venous thromboembolic disease, including deep venous thrombosis and pulmonary embolus; C. difficile colitis; and medication allergy. Pneumonia was defined by chest radiograph finding of infiltrate (by radiology report) with a documented diagnosis of “pneumonia” in the clinical notes. Hospital-acquired pneumonia was defined as pneumonia that was discovered after a normal ED chest radiograph.

Primary outcome variables were the need for mechanical ventilation (either endotracheal intubation or noninvasive ventilation), length of ICU stay, length of hospital stay, hospital-related complications, and death.

Data analysis The study population was described using simple descriptive statistics. Continuous variables are presented as the mean ± one standard deviation for normally distributed variables and as the median with inter-quartile ranges (IQR) for variables with non-normal distribution Ninetyfive percent confidence intervals (CI) are presented where appropriate. Differences in outcomes for continuous variables are compared using the Mann-Whitney two-sample test. Relationships between continuous variables and the outcomes of interest were measured using single variable linear regression analysis. Data analysis was performed with Stata statistical software (Release 8.0. College Station, TX: Stata Corporation; 2004).

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Wound Botulism in Injection Drug Users RESULTS Characteristics of Study Subjects Seventy-two patients with an ICD-9 diagnosis of “Botulism” or receiving botulism anti-toxin were identified.

Forty-three cases were excluded because patients were diagnosed with other forms of botulism (15); alternative neuromuscular diseases (5); or medical records were unavailable (23). Twenty-nine (59%) patients met study inclusion criteria. Case distribution was as follows: UC Davis Medical Center, 17 (59%); UC San Francisco Medical Center, 10 (34%); and UC San Diego Medical Center, two (7%).

The cohort consisted of 21 males (72%) and eight females with a mean age of 45.3 ± 7.9 years. A history of IDU was documented in all cases. IDU was reported as heroin by 22 patients (76%) and heroin and methamphetamine by seven (24%). The reported route of injection drug administration was solely subcutaneous (“skin popping”) in 16 (55%); solely intravenous in three (10%); and both intravenous and subcutaneous in 10 (34%). Data regarding other reported routes of drug use was not collected.

Wound botulism diagnosis was confirmed by bioassay in 14 (48%) patients; PCR in one (4%); EMG in 18 (62%); and wound culture in three (10%). Botulinum toxin type was documented in 16 (55%) cases. Toxin type was type A in 14 (88%) patients, type B in one patient, and “type A & B” in one patient. This last type likely refers to a botulinum confirmation test that did not differentiate type A from type B. Main Results The most commonly recorded ED chief complaints were visual changes (13), including double vision (9) and blurry vision (4). Other chief complaints were weakness (9), difficulty swallowing (7), shortness of breath (4), speech changes (4) (including slurred speech [2] and difficulty speaking [2]), and dizziness (3). Sore throat, numbness, ptosis, arm & tongue heaviness, and altered mental status were reported in 1 patient each.

ED symptoms as reported by patients are presented in Table 1. The most common recorded symptoms were visual changes, speech changes, difficulty swallowing, and generalized weakness. All patients complaining of wound or extremity pain were found to have a soft tissue abscess.

Five of the 22 patients with soft tissue wounds documented on physical examination did not have wound/extremity pain documented on presentation. ED physical examination findings are presented in Table 2. One patient did not have any documented ED physical examination. Vitals signs upon presentation were unremarkable, except for three patients with hypoxia by pulse oximetry, one with tachypnea, and one with bradypnea. No patient had a documented fever (>38°C) on presentation. Every patient in our sample received a complete blood count and chemistry panel in the ED. There were no laboratory abnormalities requiring therapeutic intervention.

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Table 1. Symptoms at emergeny department (ED) presentation (n=29)*^ Symptoms

Cases / Total

Percentage

Bulbar symptoms Double vision / diplopia

24 / 25

92%

Blurry vision

18 / 22

82%

Difficulty swallowing

20 / 24

83%

Voice / speech problems

13 / 15

87%

Generalized weakness

21 / 23

91%

Shortness of breath

17 / 28

61%

9 / 20

45%

3 / 26

12%

10 / 19

53%

0 / 13

0%

3 / 26

12%

12 / 20

60%

Neurological symptoms

Focal weakness Constitutional symptoms Vomiting or diarrhea Dizziness Fainting or syncope Wound-related symptoms Fever Extremity / wound pain

* Symptoms as reported by the patient during ED presentation. ^ Cases were not included in the denominator if the data was missing in the medical record.

Table 2. Physical examination findings at presentation (n=29)*^

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Findings

Cases / Total

Percentage

Bulbar palsy

25 / 28

89%

Extraocular muscle palsy

19 / 28

68%

Ptosis

17 / 27

63%

Dysarthria

18 / 22

82%

Other cranial nerve abnormality

14 / 28

50%

Abnormal gag

6 / 27

18%

Abnormal pupillary exam

5 / 28

18%

16 / 27

59%

Focal motor weakness

9 / 28

32%

Hyporeflexia

7 / 25

28%

22 / 29

76%

9 / 27

33%

Symmetric motor weakness

Skin wound / abscess Pneumonia on chest radiograph

* Physical examination findings as recorded by the examining physicians in the emergency department record. ^ Cases were not included in the denominator if the data was missing in the medical record.

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Data regarding blood cultures was not collected. Further data regarding each patient’s clinical course and treatment is provided in Table 3, available at http://escholarship.org/uc/ uciem_westjem under supporting material for the article.

The median length of hospital stay was 628 hours (26.2 days) (IQR 192-1080 hours). Seven patients were discharged to an outside healthcare facility and one had no time of discharge recorded; therefore, complete data on hospital length of stay is not available. These eight patients were excluded from the hospital length of stay analysis only.

The median length of ICU stay was 348 hours (14.5 days) (IQR 51-716 hours). Twenty-one (72%, 95% CI 53-87%) patients were treated with mechanical ventilation. Length of ICU stay in patients who underwent mechanical ventilation was longer [636.6 hours (26.5 days); 95% CI 456.4-816.8 hours] than those without mechanical ventilation [36.4 hours (1.5 days); 95% CI 9.6-63.2 hours]. Noninvasive ventilation was attempted initially in three cases; however, all failed and ultimately underwent endotracheal intubation. Twenty hospital complications were documented in 13 patients. All complications occurred in mechanically ventilated patients (62% of intubated patients had a complication). Complications included: hospital-acquired pneumonia (10); C. difficile colitis (4); antitoxin allergy (2); pneumothorax (1); venous line infection (1; decubitus ulcer (1); venous thromboembolism (1). No patient (0%, 95% CI 0-10%) died.

Six patients (21%, 95% CI 8-40%) reported a previous presentation to a healthcare facility related to this illness.

Those patients with a preceding presentation to a healthcare facility (missed diagnosis) did not have a higher rate of mechanical ventilation (4/6, 67%; 95% CI 22-97% versus 17/23, 74%; 95% CI 52-90%).

Botulinum antitoxin was administered to 26 (90%) patients. Each of these patients received a single vial of antitoxin. The median time to antitoxin administration was 15.3 hours (IQR 8-42 hours). Only two patients received antitoxin in the ED. The median time from hospital presentation to antitoxin administration was 16 hours (IQR 8-47 hours) in the MV group and 12 hours (IQR 7.5-29 hours) in the non-MV group (p=0.54). Linear regression analysis of the time from presentation to antitoxin administration versus length of ICU stay showed a highly significant relationship (Regression coefficient = 2.5; 95% CI 0.45-4.5; p=0.02).

Two of the 26 patients (7.7%; 95% CI 0.9-25.1) receiving antitoxin had a documented allergic reaction. Both patients were intubated prior to antitoxin allergy. One was described as “mild” and the other “severe.” The mean time from presentation to antitoxin administration in the two patients who received antitoxin in the ED was 6.25 hours (95% CI = 3.8-8.7 hours) versus 44.65 hours (95% CI = 13.0-76.3 hours) in those patients not receiving antitoxin in the ED. All 29 patients (100%) were treated with intravenous antibiotic medications during their hospitalization. The median Volume X, no. 4 : November 2009

time to antibiotics was 11 hours (IQR 4-22 hours). Linear regression analysis of time to antibiotics therapy versus ICU length of stay showed no significant relationship (Regression coefficient = -1.4; 95% CI -5.8-3.0; p=0.52) Incision and drainage of a skin abscess was performed in 17 patients (59%). Of these, 15 had the time to wound incision and drainage documented. The median time to incision and drainage was 17 hours (IQR 9.5-34 hours). Linear regression analysis of time to wound incision and drainage versus length of ICU stay demonstrated a highly significant relationship (Regression coefficient = 13.7; 95% CI = 2.3-25.2; p=0.02).

DISCUSSION These results demonstrate clinical characteristics of patients diagnosed with wound botulism related to IDU. All patients reported abusing heroin and the majority reported “skin popping” as the main route of administration. Chief complaints related to and physical findings of bulbar muscle palsy were documented in the majority of cases. In those cases without physical examination findings of bulbar palsy documented, the patient complaints suggested presence of a bulbar palsy in all cases. Nearly three-fourths of our cases had a skin wound identified, which is consistent with past series of wound botulism.4,6 Essentially all cases with documented serum toxin confirmation were found to have type A botulinum toxin, which is also consistent with prior reported series.1,4 Type A botulinum toxin is the most commonly reported serotype in the Western U.S.8 Patients with wound botulism had prolonged hospitalization and ICU stays. As expected, those who were mechanically ventilated had much longer stays than those not requiring mechanical ventilation. Additionally, all hospitalrelated complications occurred in the group of ventilated patients, with hospital-acquired pneumonia being the most common. In this study, we were unable to identify specific risk factors associated with patients requiring ventilation versus those not. This is unfortunate, as any strategy to prevent mechanical ventilation is likely to benefit the patient and significantly decrease resource utilization.

We found that the time interval from presentation to wound drainage correlated with ICU length of stay.

Additionally, the time to wound drainage was shorter in those patients who did not require ventilation versus those requiring ventilation, but due to the limited sample size, these differences did not reach statistical significance. These associations indicate that early wound drainage may be important in decreasing ICU length of stay and resource utilization in patients with wound botulism.

The time from ED presentation to anti-toxin administration also correlated with ICU length of stay.

Additionally, the time to anti-toxin administration was shorter in those patients who did not undergo mechanical ventilation versus those requiring ventilation, but again these differences

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Wound Botulism in Injection Drug Users did not reach statistical significance due to the small sample size. These associations indicate that early administration of anti-toxin may be important in decreasing ICU length of stay in these patients. Previous studies also suggest the importance of early anti-toxin administration in patients with wound botulism.1,6,7 Only two patients in our series received anti-toxin in the ED. While this finding is not surprising it is noteworthy, as the majority of patients in our study were seen at a facility that actually stocks botulinum anti-toxin in the hospital pharmacy, making ED administration more feasible.

The delay in anti-toxin administration highlights the difficulty of diagnosing wound botulism and administering anti-toxin rapidly.

Wound Botulism poisoning is treated with equine-derived antitoxin. Bivalent anti-toxin (containing antibodies to type A and type B botulinum toxins) is the most commonly available formulation in the U.S.8 A trivalent antitoxin (type A, B, and E) is also available in certain locations. The antitoxin dosage is a single 10 mL vial diluted 1:10 in 0.9% saline administered by slow IV infusion. A second vial may be given in 2-4 hours if clinical progression is observed, but this is rarely necessary as the quantity of neutralizing antibodies within a vial of antitoxin usually far exceeds levels of circulating toxin. Antitoxin antibodies do not reverse paralysis but instead prevent further worsening of symptoms.3,8 For this reason, early antitoxin dosing is critical to stop symptom progression before the patient becomes severely affected and a prolonged hospital course is inevitable.

Unfortunately, the expense and difficulty of obtaining botulinum anti-toxin often discourages its early administration. A strategy of early, empiric dosing in selected, high-risk patients seems warranted and is likely to be overall cost-effective. Any IDU presenting to the ED with bulbar palsy should be considered for early treatment with botulinum anti-toxin.9 The finding of a skin wound should further increase suspicion and heighten the speed of anti-toxin administration. It is noteworthy that patients with botulism may initially present with asymmetric findings.10 Immediate testing of blood glucose, electrolytes, cranial CT scan, and lumbar puncture will help to rapidly narrow the differential diagnosis. Although there are many possible causes of symmetric motor neuropathies, both myasthenia gravis and the Miller-Fisher variant of Guillain-BarrĂŠ syndrome may be confused with botulism, increasing the diagnostic difficulty.9,10 Furthermore, false positive edrophonium challenge tests (suggesting myasthenia gravis) have been reported in cases of wound botulism10 and food-borne botulism9,11,12 causing delays in diagnosis and treatment.

When the diagnosis of wound botulism is suspected, the process for anti-toxin acquisition should be immediately initiated. This requires contacting local (or state) health department authorities to facilitate anti-toxin delivery and specimen collection for confirmatory testing. Anti-toxin Western Journal of Emergency Medicine

administration should generally not be delayed for botulism confirmation. Local health departments should contact the Centers for Disease Control (CDC) at (770) 488-7100 for assistance in acquiring anti-toxin. The CDC website (http:// www.cdc.gov) contains detailed information about botulism epidemiology, diagnosis, confirmation, treatment and emergency response.

Although antitoxin administration should not be delayed for performance of electrophysiological testing, these studies may help to provide further diagnostic clarity while awaiting antitoxin acquisition. Characteristic electromyography (EMG) patterns have been described in association with botulinum toxin poisoning. Therefore, EMG testing may help to diagnose botulism or differentiate botulism from myasthenia gravis and Guillain-BarrĂŠ syndrome.1,3,13 Expected findings with botulism are normal conduction velocities, small motoraction potentials, no change with repetitive stimulation, and fibrillation potentials with EMG.9,13 When electrophysiological testing is performed in the setting of suspected botulism, it is highly recommended that detailed descriptions of electrodiagnostic findings in botulism be reviewed prior to testing.3,14 EMG results are most reliable when performed by a person with experience in this procedure.

The criterion standard testing for botulism is the mouse bioassay procedure.1 Testing is usually performed for type A and type B botulinum toxins, as these are the most common toxin types within the U.S. Evaluation for type E toxin may be performed routinely in certain areas of the Pacific Northwest and Alaska or when a fish source of botulism is suspected.9 The mouse bioassay is performed by intra-peritoneal injection of mice with either pure subject serum or an incubated mixture of subject serum and monovalent anti-toxin. Monovalent antitoxins (Type A, B, C, D, E, F) are distributed by the CDC for testing purposes. Injected mice are then observed for four days for signs of botulism poisoning and death. It should be noted that although botulism usually kills mice within 6-24 hours, cases of delayed death are occasionally observed. If toxin is present all mice are expected to die, except those injected with the mixture containing the involved anti-toxin type.8,9 An enzyme-linked immunosorbent assay (ELISA) test has also been developed, but is generally not available.9,15 LIMITATIONS This study is limited by the restrictions inherent to the use of retrospective data, including incomplete documentation, recording bias, and changes in medical practice that may have occurred during the study period. Unfortunately, because wound botulism is a rare disease, prospective research in this area is difficult. Time estimates for ICU stay, antitoxin administration, and hospital stay may not be entirely accurate due to the retrospective nature of this study. Further, due to the social situations of this patient population, length of hospitalization may depend on factors other than medical

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necessity (e.g. placement, housing, rehabilitation, etc.). All study hospitals are academic centers where resident physicians are primarily responsible for initial patient evaluations and medical record documentation.

While it is likely that changes in intensive care practices did occur during the study period (1991-2005), there have been no significant changes in botulism anti-toxin formulation or known indications. Unfortunately, it was not feasible to adjust for changes in clinical practice over the study period when evaluating length of ICU stay and hospital complications. It is possible that in patients who were critically ill, drainage procedures and antitoxin administration may have been deferred in favor of more critical interventions (such as tracheal intubation), which could confound the observed associations between antitoxin, wound I&D, and ICU length of stay.

Due to the small sample, multivariate analysis to determine the independent contribution of multiple variables is not feasible. Wound botulism is a rare disease and therefore difficult to research. However, our study is the largest series of wound botulism cases in which hospital records were reviewed. Almost all botulism cases were type A; therefore, our results may not be generalizable to other botulinum toxin serotypes.

1.

Centers for Disease Control and Prevention: Botulism in the United States, 1899-1996. Handbook for epidemiologists, clinicians, and laboratory workers, Atlanta, GA. Centers for Disease Control and Prevention, 1998.

2.

Centers for Disease Control and Prevention. Emergency Preparedness & Response: Botulism. October 6, 2006. Available at: http://www.bt.cdc.gov/agent/botulism/. Accessed March 30, 2009.

3.

Cherrington M. Botulism: update and review. Semin Neurol. 2004; 24:155-63.

4.

Werner SB, Passaro D, McGee J, et al. Wound botulism in California, 1951-1998: Recent epidemic in heroin injectors. CID. 2000; 31:1018-24.

5.

Passaro DJ, Werner SB, McGee J, et al. Wound botulism associated with black tar heroin among injecting drug users. JAMA. 1998;279:859-63.

6.

Sandrock CE, Murin S. Clinical predictors of respiratory failure and long-term outcome in black tar heroin-associated wound botulism.

Chest. 2001; 120:562-6.

7.

Tacket CO, Shandera WX, Mann JM, et al. Equine antitoxin use and other factors that predict outcome in type A foodborne botulism. Am J Med. 1984; 76:794-8.

8.

CONCLUSION In this series of wound botulism cases, the time from ED presentation to antitoxin administration and wound drainage both correlated with ICU length of stay. Time of presentation to antibiotics was not associated with length of stay. In cases of suspected wound botulism, early antitoxin administration and wound drainage, possibly while the patient is in the ED, may help to decrease ICU length of stay.

Richardson WH, Frei SS, Williams SR. A case of type F botulism in Southern California. Clin Toxicol. 2004; 42:383-7.

9.

Horowitz BZ. Botulinum toxin. Crit Care Clin. 2005; 21:825-839.

10. Horowtiz BZ, Swenson E, Marquardt K. Wound botulism associated with black tar heroin. JAMA. 1998; 280:1479-80.

11. Hughes JM, Blumenthal JR, Merson MH, et al. Clinical features of types A and B food-borne botulism. Ann Intern Med. 1981; 95:442-5.

12. St Louis ME, Peck SH, Bowering D, et al. Botulism from chopped garlic: delayed recognition of a major outbreak. Ann Intern Med. 1988; 108:363-8.

Address for Correspondence: Steven R. Offerman, MD, Department of Emergency Medicine, Kaiser Permanente South Sacramento Medical Center, 6600 Bruceville Road, Sacramento, CA 95823. Email: steve.offerman@gmail.com

13. Merrison AF, Chidley KE, Dunnett J, et al. Lesson of the week: Wound botulism associated BMJ. 2002; 325:1020-1.

14. Cherington M. Electrophysiologic methods as an aid in diagnosis of botulism: a review. Muscle Nerve. 1982; 5:S28-9.

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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REFERENCES

15. Ferreira JL, Eliasberg SJ, Edmonds P, et al. Comparison of

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the mouse bioassay and enzyme-linked immunosorbent assay procedures for the detection of type A botulinal toxin in food. J Food Prot. 2004; 67:203-6.

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Orignal Research

Terrain Park Injuries Craig Moffat Scott McIntosh, MD, MPH Jade Bringhurst, MD Karen Danenhauer, MD Nathan Gilmore, MD Christy L. Hopkins, MD, MPH

University of Utah, Division of Emergency Medicine, Salt Lake City, UT

Supervising Section Editor: Paul Walsh, MD, MSc Submission history: Submitted November 3, 2008; Revision Received January 23, 2009; Accepted February 2, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Background: This study examined demographics, injury pattern, and hospital outcome in patients injured in winter resort terrain parks.

Methods: The study included patients >12 years of age who presented to a regional trauma center with an acute injury sustained at a winter resort. Emergency department (ED) research assistants collected patient injury and helmet use information using a prospectively designed questionnaire. ED and hospital data were obtained from trauma registry and hospital records.

Results: Seventy-two patients were injured in a terrain park, and 263 patients were injured on nonterrain park slopes. Patients injured in terrain parks were more likely to be male [68/72 (94%) vs.

176/263 (67%), p<0.0001], younger in age [23 Âą 7 vs. 36 Âą 17, p<0.0001], live locally [47/72 (65%) vs.

124/263 (47%), p=0.006], use a snowboard [50/72 (69%) vs. 91/263 (35%), p<0.0001], hold a season pass [46/66 (70%) vs. 98/253 (39%), p<0.0001], and sustain an upper extremity injury [29/72 (40%) vs. 52/263 (20%), p<0.001] when compared to patients injured on non-terrain park slopes. There were no differences between the groups in terms of EMS transport to hospital, helmet use, admission rate, hospital length of stay, and patients requiring specialty consultation in the ED. Conclusions: Patients injured in terrain parks represent a unique demographic within winter resort patrons. Injury severity appears to be similar to those patients injured on non-terrain park slopes.

[West J Emerg Med. 2009;10(4):257-262.]

INTRODUCTION Terrain parks are a relatively recent development in winter resorts. They consist of a variety of man-made obstacles, including rails and boxes on which to slide, various forms of jumps, and half-pipes, which provide an additional challenge to skiers and snowboarders. Terrain parks have become increasingly popular since the mid-1990s.Their popularity increased after the inclusion of snowboarding into the 1998 Winter Olympics.1 There is little information regarding specific injury patterns and severity of injuries in patrons using terrain parks.

Recently, the safety of terrain parks has been called into question. In 2007 all man-made snow jumps were eliminated from terrain parks in five winter resorts in the Canadian Western Journal of Emergency Medicine

Rockies (all owned by one private company). Safety concerns were sited as the reason for closure.

A recent case-controlled study, which examined injuries reported to ski patrol personnel at area winter resorts,2 compared ambulance evacuation and injury severity in skiers and snowboarders injured in the terrain parks as compared to those patrons injured on non-terrain park slopes. The study suggested that patrons injured in terrain parks had a higher rate of ambulance evacuation, skiers sustained more severe injuries (particularly head and neck injuries), and snowboarders were more likely to sustain severe extremity injuries.

Little information regarding hospital outcomes in patients injured on terrain parks has been reported. The purpose of

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this study was to examine the demographics, injury pattern, and hospital outcome of terrain- park patrons presenting to a regional adult ACS level 1 trauma center.

patients on a weekly basis. RAs or medical students contacted missed patients by phone to complete survey information.

Eligible patients were asked to complete a short survey regarding their level of experience, helmet use, location of injury (non-terrain park slope vs. terrain park slope), and mechanism of injury. Surveys also included information from emergency medical service (EMS) run sheets (EMS treatment/ run times), when applicable. Missed patients were contacted to complete a study survey over the phone. No mailed surveys were used. The survey has not been previously validated. [A copy is available for review in Appendix A online at http:// repositories.cdlib.org/uciem/westjem/vol10/iss4/art( ).]

The PI, a board-certified emergency physician, retrospectively reviewed ED and trauma registry records for the following data points: ED interventions, ED consultant involvement (i.e. orthopedics, trauma, and spine service), hospital and intensive care unit (ICU) length of stay (LOS), injury severity scores (ISS), and injury descriptions (from ICD-9 codes). All study patients, including those patients who did not meet institutional trauma criteria, had ISS and ICD-9 diagnoses recorded by trained institutional trauma registry personnel.

METHODS Site of Study The study was performed at one of two American College of Surgeons (ACS) accredited adult Level I trauma centers in a major metropolitan area (estimated population: 2,150,000) surrounded by 10 ski resorts. The state has over four million skier days, and the seven resorts closest to the study center comprise 81.9% of the total skier days for the entire state.3 Winter resorts are located an average distance of 22 (range: 15-25) radial air miles (one-way), and 34 (range: 31-39) road miles (one-way) from the study institution.

Type and Period of Study This is a retrospective chart and trauma registry database review of all patients presenting to the study institution with injuries sustained in winter resorts during the 2006-2007 winter season (November through April). We obtained basic demographics and injury characteristics of terrain-park participants and compared them to patients injured on nonterrain park slopes. The Institutional Review Board (human subjects committee) at the study institution approved this study.

Patient Population This study included all patients age 12 or greater presenting to the study institution’s emergency department (ED). For patients 12 to 17, we obtained both patient assent and parental consent to participate in a short survey. The study center is a major referral center that serves a large rural catchment area. Care at outside facilities is highly variable depending on the resources available in particular communities. Rather than attempt to control for this, the study was limited to only those patients who acutely presented to and were primarily treated at the study center. Patients were excluded if they were injured outside the bounds of the resort (backcountry), if they presented more than 24 hours after their original injury, or if they were transferred to the study facility from an outside hospital.

Data Collection Patients were identified by trained undergraduate research assistants (RAs) present in the ED between the hours of 08002400. When RA coverage was absent (major holidays, winter/ spring break), trained medical students enrolled patients between the hours of 1000-1800. All RAs and medical students attended a one-hour orientation session at the start of each semester to review the survey data collection form, patient enrollment protocol, and to undergo an ED orientation.

The primary investigator (PI) reviewed ED logs for missed Volume X, no. 4 : November 2009

Data Analysis The PI entered all study database entries into Microsoft Excel. Initial patient information and hospital data points were entered into the database when available in the electronic medical record. The PI verified hospital data (age, gender, mode of arrival, hospital admission and discharge information, ICU and hospital LOS, pre-hospital and EMS procedures, and ICD-9 diagnoses) using patient and hospital information obtained through the trauma registry at the end of the study period.

An independent statistician performed the statistical analysis for the study. Descriptive (mean, standard deviation, missing entries, percentages), and comparative statistics were analyzed using SAS statistical package, version 9.1 (SAS Institute Inc., Cary, NC, USA). Comparison between independent continuous variables was performed using the student’s t-test and Wilcoxon Mann-Whitney rank sum test.

Chi-squared analysis and Fisher’s Exact test were used to analyze dichotomous variables. Logistic regression was used to control for age, gender, and ISS when examining hospitalization rates. Statistical significance was defined as a 2-sided p-value ≤ 0.05.

RESULTS We identified 417 patients for the 2006-07 winter resort season. Of these, 335 (80%) had completed surveys, which included information on the site of injury (terrain vs. nonterrain). Seventy-two patients were injured on a terrain park slope and 263 were injured on a non-terrain park slope.

Surveys for seven patients in the terrain park group and eight

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Terrain Park Injuries Table 1. Patient demographics Terrain Park (n=72)

Non-Terrain (n=263)

p=

68/72 (94%)

176/263 (67%)

p<0.0001

Average age (years) ± STD

23 ± 7

36 ± 17

p<0.0001

State resident

47/72 (65%)

124/263 (47%)

p=0.006

Snowboarding

50/72 (69%)

91/263 (35%)

p<0.0001

Season pass holder

46/66 (70%)

98/253 (39%)

p<0.0001

Helmet use

32/69 (46%)

96/260 (37%)

p=0.152

Self-rated expert

41/67 (61%)

108/257 (42%)

p=0.048

Reported average years of experience ± STD

10 ± 7

16 ± 15

p=0.064

Reported average days at resort ± STD

22 ± 27

12 ± 23

p<0.0001

Mechanism of injury

n=71

n=263

Fall

8 (11%)

147 (56%)

p<0.0001

Jump/fall from height

59 (83%)

63 (24%)

p<0.0001

Collision with person

1 (1%)

19 (7%)

p=0.09

Collision with object

3 (4%)

33 (13%)

p=0.08

Other

0 (0%)

1 (0.4%)

p=1.00

Gender (male)

STD, standard deviation Table 2. Hospital data Mode of arrival

Terrain Park (n=72)

Non-Terrain (n=263)

p= p=0.545

n=72

n=263

Ground EMS

42 (58%)

167 (64%)

Helicopter EMS

5 (7%)

22 (8%)

Private vehicle

25 (35%)

74 (28%)

Admission rate

23/72 (32%)

105/261 (40%)

p=0.201

Injury severity scores (Average ± STD)

5±3

4±4

p=0.075

Hospital LOS-days (Average ± STD)

1±2

1±2

p=0.201

ICU admission

2/72 (3%)

9/260 (4%)

p=0.990

ED specialty consult

35/72 (49%)

132/263 (50%)

p=0.690

ED Procedures

n=72

n=263

p=0.802

Joint/fracture reduction

10 (14%)

22 (8%)

Chest tube

1 (1%)

2 (1%)

Intubation

1 (1%)

1(0.4%)

n=72

n=261

Home

68 (94%)

245 (94%)

Nursing home

1 (1%)

6 (2%)

Rehabilitation

1 (1%)

5 (2%)

Home health

0

1 (0.4%)

Skilled nursing facility

2 (3%)

4 (2%)

Discharge status

p=0.899

EMS, emergency medical services; STD, standard deviation; LOS, length of stay; ICU, intensive care unit; ED, emergency department.

in the non-terrain park group were incomplete (missing one or more data elements).

Patient demographics of each group are detailed in Table 1. Patients injured on terrain park slopes were more likely to be younger [23±7 vs. 36±17, (p<0.0001)], male [68/72 (94%)

Western Journal of Emergency Medicine

vs. 176/263 (67%), p<0.0001] and reside in local proximity to area resorts [47/72 (65%) vs. 124/263 (47%), p=0.006]. In addition, injured patients were more likely to be snowboarders [50/72 (69%) vs. 91/263 (35%), p<0.0001], season pass holders [46/66 (70%) vs. 98/253 (39%), p<0.0001] and rate

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Table 3. Predictors of hospital admission Parameter

DF

Standard Estimate

Wald Error

Chi-Square

Intercept

1

8.01

1.43

31.54

Odds Ratio

95% CI

Pr>ChiSq

Terrain

1

0.32

0.40

0.64

1.37

0.63-2.98

0.42

Gender (female)

1

-0.24

0.20

1.51

0.62

0.29-1.33

0.22

Age

1

-1.34

0.39

12.16

0.26

0.12-0.56

<0.001

Injury severity score

1

-2.47

0.29

71.14

0.09

0.05-0.15

<0.0001

<0.0001

Table 4. Injury patterns Terrain Park (n=72)

Non-Terrain (n=263)

p=

Upper extremity

29 (40%)

52 (20%)

p<0.0001

Lower extremity

12 (17%)

57 (22%)

p=0.352

Head/facial

24 (33%)

70 (27%)

p=0.261

Spine

6 (8%)

28 (11%)

p=0.565

Thoracoabdominal

7 (10%)

21 (8%)

p=0.637

themselves as experts when compared to patrons injured on main resort slopes [41/67 (61%) vs. 108/257 (42%), p=0.048] Terrain park patrons were more likely to be injured while going off a jump, or falling from a height [59/71 (83%) vs.

63/263 (24%), p<0.0001].

We found no difference between the groups in terms of transport method to the hospital (private vehicle, ground, or air ambulance), hospital admission rates, hospital LOS for admitted patients, ICU admissions, specialty consultations (orthopedics, trauma service, spine service, etc.) in the ED, ISS, or procedures performed while in the ED (Table 2).

There were no deaths in either group. Predictors of hospital admission included age [odds ratio (OR)=0.26 (0.12-0.56)], and ISS [OR=0.09 (0.05-0.15)]. Terrain park use [OR=1.37 (0.63-2.98)] was not an independent predictor of hospital admission (Table 3).

Patients injured in terrain parks were more likely to sustain significant upper extremity injuries. There were no differences between the groups in terms of lower extremity injuries, thoracoabdominal injuries, spine injuries, or head and facial injuries (Table 4). Specific injuries are listed in Table 5. Strains, sprains, and contusions were not included as significant injuries.

DISCUSSION Terrain parks are designed to have various features that allow skiers and snowboarders to jump and/or perform tricks.

Many of the features resemble those found in skateboarding parks. Common features include jibs, jumps and vertical pipes.

Jibs are fixtures (usually made of steel or plastic) that can be ridden with skis or a snowboard, parallel or perpendicular to the ground, or while spinning around or jumping off. These features resemble stair rails, benches, or tables. Jumps, which range from 5-90 meters and vary from resort to resort, are Volume X, no. 4 : November 2009

usually constructed of snow or snow with a dirt base. Various tricks such as grabs, twists, or spins may be performed while airborne after a jump. Vertical pipes resemble a trough with vertical lips to the side, which terrain park users can use to launch themselves into the air. Terrain park areas are separated from the regular resort slopes, and can be subdivided into large, medium, and small features based on the height of jumps and pipes, and complexity of jibs.

As exemplified in this study, terrain parks attract a unique demographic of winter resort patrons. Patients presenting for treatment were predominately younger males injured after a jump or fall from height. Terrain parks are set up with advanced features that encourage jumps, twists, and other aerial movements, thus it is not surprising that the patrons injured are more likely to rate themselves as experts, and injure themselves in jumping/falling type mechanisms.

This is similar to previous studies, which have suggested that intermediate and expert snowboarders tend to injure themselves more with jumping type activities, and are more likely to try aerial-type maneuvers.1,4 The majority of patients injured in our study were snowboarders, which likely contributed to the higher proportion of upper extremity injuries in this group. In the general winter resort population, the injury rate for upper extremity injuries has been reported to be approximately two times greater in snowboarders than in skiers.4,5 This includes wrist injuries4,6-9 and other upper extremity injuries.2,4,5,10-13 Likely mechanisms include the increased frequency of backward (wrist injuries) and forward falls (shoulder injuries) associated with snowboarding. Our study did not assess the use of protective equipment, such as wrist guards; however their use has been shown to decrease the incidence of wrist injuries and may be especially useful in novice snowboarders.8,14-17

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Terrain Park Injuries Table 5. Specific injuries Terrain Park

Non-Terrain

29 [27 (93%)]

52 [27 (52%)]

Joint dislocations

5 (17%)

12 (23%)

Fractures

22 (76%)

37 (71%)

Soft tissue injuries (arterial/nerve injury/muscle tear)

2 (7%)

3 (6%)

12 [3 (25%)]

57 [7 (12%)]

Joint dislocations

0

3 (5%)

Fractures

12 (100%)

53 (93%)

Soft tissue injuries (arterial/nerve injury/muscle tear)

0

1 (2%)

Upper extremity [n (%) snowboarders]

Lower extremity [n (%) snowboarders]

Head injuries [n (%) snowboarders]

24 [15 (63%)]

70 [24 (34%)]

Closed head injury

10 (42%)

25 (36%)

Concussion

11 (46%)

29 (41%)

Intracranial hemorrhage

0

4 (6%)

Skull/facial fractures

3 (12%)

12 (17%)

Spinal injuries [n (%) snowboarders]

6 [3 (50%)]

28 [9 (32%)]

Cervical spine fractures

1 (17%)

5 (18%)

Thoracic spine fractures

3 (50%)

10 (36%)

Lumbar spine fractures

2 (33%)

13 (46%)

Thoracoabdominal injuries [n (%) snowboarders]

7 [6 (86%)]

21 [7 (33%)]

Solid organ injuries (spleen/liver)

2 (29%)

4 (19%)

Rib fractures

3 (43%)

10 (48%)

Pneumothorax/hemothorax/pulmonary contusion

1 (14%)

6 (28%)

Other (mesenteric artery avulsion)

1 (14%)

1 (5%)

Several authors have also reported an increased incidence of spine and head injuries in snowboarders when compared to skiers,7,8,18-20 particularly if jumping is involved.1,2,19,21-26 In one study, 70% of injuries in intermediate and expert snowboarders are caused by jumping, a common activity in terrain parks.1 Although the majority of users in this study were injured while jumping, the rate of head and spinal injuries did not differ from patients injured on non-terrain park slopes. A larger study may be able to better elucidate whether true differences do exist with regard to these specific injury types in terrain park activities.

A recent study examined terrain park injuries reported to ski patrol personnel.2 This study suggested that users had higher ambulance evacuation rates than non-terrain park slope users. In addition, the study found that skiers had a higher proportion of severe head and neck injuries, while snowboarders had a higher risk of severe extremity injuries (as compared to the skiers and boarders injured on non-terrain slopes).

Although injury rates for terrain and non-terrain slopes were not assessed in this study, it appears that those patients who presented to a hospital for care after an injury sustained in a terrain park did not have a higher rate of ambulance transport, or sustain more severe injuries when compared to patients injured on non-terrain park slopes. ISS were slightly Western Journal of Emergency Medicine

higher in patients injured on terrain park slopes; however, this did not reach statistical significance. Both groups had similar rates of hospital admission, ICU admissions, total hospital LOS, and the majority of injured patients were discharged home in both groups.

Our study suggests that although terrain parks attract a certain demographic of winter resort enthusiasts who are performing more advanced maneuvers, the overall severity of injuries sustained in terrain parks does not differ significantly from injuries sustained on non-terrain park slopes.

LIMITATIONS This study has several limitations. No formal criteria or protocols were used at the winter resorts or resort medical clinics to triage patients injured at area resorts. In addition, injury rate comparisons between terrain parks and traditional slopes were not examined in this study. The location of injury (non-terrain park vs. terrain park) was missing for several of the study patients (not obtained in the survey and information not noted in chart), and could have impacted study findings. Self-reporting bias and recall bias are potential issues with information obtained from patient surveys (level of experience, mechanism of injury and self-reported helmet usage). Information regarding other safety equipment (such as wrist guards) was not obtained. This study was conducted at

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a single site (one of two adult ACS level I trauma centers in the study region). The site has its own air ambulance program, thus referral bias (toward increased injury severity) is likely.

Due to the observational nature of this study, we made no adjustment for multiple comparisons in the data analysis.

Results should be interpreted as exploratory findings.

8.

Machold W, Kwasny O, Gassler P, et al. Risk of injury through snowboarding. J Trauma. 2000; 48:1109-14.

9.

Xiang H, Kelleher K, Shields BJ, et al. Skiing- and snowboardingrelated injuries treated in U.S. Emergency departments, 2002. J Trauma. 2005; 58:112-8.

10. Aslam N, Thomas P. Snowdome, skiers and boarders: Accident and emergency experience. Int J Clin Pract. 2004; 58:122-4.

CONCLUSION While terrain park users do represent a unique demographic population within winter resort patrons, it does not appear that patients injured in terrain parks require more frequent EMS evacuation, or sustain more severe injuries than those patients injured on non-terrain slopes.

11. Ferrera PC, Mckenna DP, Gilman EA. Injury patterns with snowboarding. Am J Emerg Med. 1999; 17:575-7.

12. Hagel BE, Goulet C, Platt RW, et al. Injuries among skiers and snowboarders in Quebec. Epidemiology. 2004; 15:279-86.

13. Sakamoto Y, Sakuraba K. Snowboarding and ski boarding injuries in Niigata, Japan. Am J Sports Med. 2008; 36:943-8.

14. Russell K, Hagel B, Francescutti LH. The effect of wrist guards on

Acknowledgements We thank Xiaoming Sheng for his statistical support, and Janet Cortez for Trauma Registry support.

wrist and arm injuries among snowboarders: a systematic review.

Clin J Sport Med. 2007; 17:145-50.

15. Oâ&#x20AC;&#x2122;Neill DF. Wrist injuries in guarded versus unguarded first time snowboarders. Clin Orthop Relat Res. 2003; 409:91-5.

Address for Correspondence: Christy Hopkins, MD, MPH, FACEP, University of Utah Division of Emergency Medicine 30 North 1900 East, Room 1C026 Salt Lake City, Utah 84132. E-mail: Christy.mccowan@hsc.utah.edu

16. Machold W, Kwasny O, Eisenhardt P, et al. Reduction of severe wrist

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

18. Ackery A, Hagel BE, Provvidenza C, et al. An international review of

injuries in snowboarding by an optimized wrist protection device: a prospective randomized trial. J Trauma. 2002; 52:517-20.

17. Hagel B, Pless IB, Goulet C. The effect of wrist guard use on upperextremity injuries in snowboarders. Am J Epidemiol. 2005;162:149-56. head and spinal cord injuries in alpine skiing and snowboarding. Inj Prev. 2007; 13:368-75.

19. Donald S, Chalmers D, Theis JC. Are snowboarders more likely to damage their spines than skiers? Lessons learned from a study of

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20. Koehle MS, Lloyd-Smith R, Taunton JE. Alpine ski injuries and their

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Goulet C, Hagel B, Hamel D, et al. Risk factors associated with serious

21. Chaze B, Mcdonald P. Head injuries in winter sports: Downhill skiing,

ski patrol-reported injuries sustained by skiers and snowboarders in

snowboarding, sledding, snowmobiling, ice skating and ice hockey.

snow-parks and on other slopes. Can J Public Health. 2007; 98:402-6.

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Governorâ&#x20AC;&#x2122;s Office of Planning and Budget, Demographic and

Neurol Clin. 2008; 26:325-32.

22. Tarazi F, Dvorak MF, Wing PC. Spinal injuries in skiers and

Economic Analysis Section. 2006. Utah Ski Database. Available at: http://governor.utah.gov/dea. Accessed January 5, 2009.

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snowboarders. Am J Sports Med. 1999; 27:177-80.

23. Franz T, Hasler RM, Benneker L, et al. Severe spinal injuries in

Idzikowski JR, Janes PC, Abbott PJ. Upper extremity snowboarding

alpine skiing and snowboarding: A 6-year review of a tertiary trauma

injuries. Ten-year results from the Colorado snowboard injury survey.

centre for the Bernese alps ski resorts, Switzerland. Br J Sports Med.

Am J Sports Med. 2000; 28:825-32.

2008; 42:55-8.

Matsumoto K, Miyamoto K, Sumi H, et al. Upper extremity injuries

24. Fukuda O, Hirashima Y, Origasa H, et al. Characteristics of helmet

in snowboarding and skiing: A comparative study. Clin J Sport Med.

or knit cap use in head injury of snowboarders. Neurol Med Chir (Tokyo). 2007; 47:491-4.

2002; 12:354-9.

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Corra S, Conci A, Conforti G, et al. Skiing and snowboarding injuries

25. Fukuda O, Takaba M, Saito T, et al. Head injuries in snowboarders

and their impact on the emergency care system in south Tyrol: A

compared with head injuries in skiers. A prospective analysis of 1076

restrospective analysis for the winter season 2001--2002. Inj Control

patients from 1994 to 1999 in Niigata, Japan. Am J Sports Med.

Saf Promot. 2004; 11:281-5.

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Hohlrieder M, Eschertzhuber S, Schubert H, et al. Severity and

26. Geddes R, Irish K. Boarder belly: Splenic injuries resulting from

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17:157-62.

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Orignal Research

The Utility of Bedside Ultrasound in the Detection of a Ruptured Globe in a Porcine Model Amit Chandra, MD* Todd Mastrovitch, MD* Heidi Ladner, MD* Vincent Ting* Michael S. Radeos, MD* Sandeep Samudre, PhD, MPHâ&#x20AC;

* New York Hospital Queens, Department of Emergency Medicine â&#x20AC; Eastern Virginia Medical School, Norfolk, Virginia

Supervising Section Editor: J. Christian Fox, MD Submission history: Submitted October 30, 2008; Revision Received March 2, 2009; Accepted March 22, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Background: Recent case reports have shown that ultrasonography can be used to diagnose ocular pathology in an emergency setting. Ultrasound may be especially useful when periorbital edema and pain interfere with the examination of the post-traumatic eye.

Objective: This study evaluated the ability of emergency physicians to detect a ruptured globe in an ex-vivo porcine model.

Methods: Following a brief training lecture, 15 emergency medicine residents and 4 emergency medicine attending physicians used ultrasonography to evaluate 18 porcine eyes, randomized as normal, ruptured, or completely devoid of vitreous humor. The consequences of ultrasound applanation with this method were evaluated by measuring intraocular pressure changes with and without a 1mm clear plastic shield.

Results: Our study participants were able to identify abnormal eyes with a sensitivity of 79% (95% CI 73% to 84%) and a specificity of 51% (95% CI 41% to 61%). Intraocular pressure increased 5% with ultrasound applanation, though with a 1mm thick plastic shield there was no measurable change.

Conclusions: Ultrasound imaging may be a future modality to be used by trained emergency physicians to expedite the identification of a rupture globe, but it is unlikely to replace more definitive imaging techniques. The use of a clear plastic barrier in this porcine model prevents an increase in intraocular pressure without affecting image quality, and should be used in any future studies on this method.

[West J Emerg Med. 2009;10(4):263-266.]

Introduction Ocular trauma, including a ruptured globe, is associated with pain and surrounding soft tissue edema that can impede the direct physical examination of the affected eye in an emergency setting. Limited access to ophthalmologic specialists and equipment may lead to significant delays in the diagnosis and treatment of traumatic pathology.

Ultrasonography has been widely used in investigation of abnormal orbital pathology, especially in cases with lens or ocular media opacifications.1 Using variations like a-scan, b-scan, Doppler, and three-dimensional approaches, Western Journal of Emergency Medicine

ultrasonography is used to diagnose and follow up orbital diseases.2 The evaluation of ruptured globes with ultrasound presents an interesting dilemma, as management of the condition requires protection against any pressure to the globe.

Globe rupture occurs following blunt or penetrating ocular trauma and is considered an ophthalmologic emergency.

External signs of a ruptured globe include hyphema, irregular pupils, and a shallow anterior chamber.3 Immediate treatment when this diagnosis is suspected includes the placement of a metal shield over the eye. The potential of a ruptured globe 263

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Ultrasound Detection of a Ruptured Globe

Figure 1. Normal eye

Figure 3. Vitrectomy-complete vitreous loss

is therefore a relative contraindication to ultrasonographic applanation (i.e. the application of pressure over the cornea) due to the theoretical risk of intraocular content extrusion.

This study focused on the ability of emergency physicians to identify sonographic changes and detect a ruptured globe in a porcine model. Additionally, changes in intra-ocular pressure (IOP) during probe applanation with and without a clear plastic barrier were measured in order to evaluate the consequences of this technique.

ultrasound, including the identification of the lens, the optic nerve, and the retina. The individual eyes were randomized to be pretreated as normal, ruptured globes with abnormal anatomy and moderate vitreous loss (MVL or rupture), and complete vitreous loss (CVL or vitrectomy) conditions.

To simulate ruptured globes, we made a v-shaped incision approximately 2 mm from the lateral limbus in normal porcine eyes. For moderate injury, we aspirated 0.3 to 1.5 ml vitreous, and up to 4 ml for complete vitreous loss.

We covered the eyes with an opaque gelatin mold to blind the participants to the eye treatment, i.e. participants were unable to visually evaluate the eye itself. This mold also simulated a situation where periorbital edema precludes such an examination of the eye. Study participants filled out a questionnaire identifying their diagnosis for each eye as normal (Figure 1) , rupture-MVL (Figure 2), vitrectomy-CVL (Figure 3), or â&#x20AC;&#x153;unable to determine.â&#x20AC;?

After the initial study, a subset of normal (unruptured) eyes was cannulated and attached to a pressure sensor to

Methods Following a 15-minute lecture on the use of ultrasound in emergency eye conditions, 15 Emergency Medicine (EM) residents and four EM attendings performed ocular sonography with a10-MHz linear-array transducer on nine consecutive porcine heads (18 eyes). Both a Sonosite Titan and Micromaxx (Sonosite, Inc., Bothwell, WA, USA) ultrasound machines were used. The lecture presented an overview of normal eye architecture when viewed with

Figure 2. Rupture-moderate vitreous loss

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Ultrasound Detection of a Ruptured Globe

Table 1. Accuracy in identifying ocular conditions by year of training Identification of an “abnormal eye,” rupture Identification of a or vitrectomy (CI) ruptured globe (CI)

Figure 4. Pressure monitoring device

evaluate intraocular pressure (IOP) changes during the procedure (Figure 4). We selected normal eyes for this aspect of the study to detect the pressure applied on the closed (vs. open) system of an intact globe. The utility of a clear plastic barrier (1mm thick) to alleviate this pressure differential was also assessed. We cut a 2 x 4 inch acrylic plastic shield 1/16” thick (US Plastics, Lima, OH) to cover the bony superior and inferior orbit. Ultrasonography was then performed using the plastic barrier to alleviate additional pressure.

Prior to this study, the investigators received a letter of exemption from the NY Hospital Queens institutional review board.

Results Sonography of ruptured globes revealed a number of findings indicating the diagnosis, including loss of spherical shape, scalloping of posterior globe away from the orbital wall, and lens dislocation (Figure 2). The investigation noted that at least one third of the participants consistently verbalized a correct visualization of a rupture or vitrectomy yet noted the opposite finding on their questionnaire. This confusion reflected the participants’ misunderstanding of the definitions of rupture (MVL) versus vitrectomy (CVL). To preserve the source data, their inconsistency was not corrected during the study, but the final data was merged to allow any indication of an abnormal globe (moderate or complete vitreous loss) to be a positive finding if the experimental eye in question was indeed abnormal. In other words, a participant could identify an MVL eye as a vitrectomy or a CVL as a rupture.

The sensitivity of this technique to identify globe rupture, using this merged data set, was 79% (95% CI 73% to 84%). The specificity was 51% (95% CI 41% to 61%).

Using an unmerged data set, i.e. giving credit only for correct identification of a rupture, the sensitivity was 64% (95% CI 54% to 73%), and the specificity was 71% (95% CI 64% to 77%). Based on training level, attending emergency physicians (EPs) were consistently more accurate than Western Journal of Emergency Medicine

1st Year Resident Sensitivity Specificity

61% (44%, 77%) 83% (59%, 96%)

39% (17%, 64%) 86% (71%, 95%)

2nd Year Resident Sensitivity Specificity

83% (67%, 94%) 47% (30%, 65%)

69% (52%, 84%) 69% (56%, 80%)

3rd Year Resident Sensitivity Specificity

82% (70%, 91%) 23% (10%, 42%)

67% (47%, 83%) 58% (45%, 71%)

Attending Physician Sensitivity 81% (67%, 91%) Specificity 67% (45%, 85%

71% (49%, 87%) 77% (63%, 88%)

residents in identifying ocular conditions, although secondyear residents as a group had the highest scores. A breakdown of results (with 95% confidence intervals) by level of training is summarized in Table 1.

When maximal pressure was applied with the probe on normal eyes, IOP increased by 17%. IOP increased by only 5% when using the minimal amount of pressure to obtain a clear image. The probe did not cause a measurable increase in IOP nor was the ultrasound image quality altered when a plastic shield was used.

Discussion Ultrasonography provides a readily available, rapid, non-invasive imaging modality to evaluate the traumatic eye.

An ultrasound machine can be available for use where the diagnosis would otherwise be delayed by limited access to ocular computed tomography, magnetic resonance imaging, and ophthalmologic consultation.

Recent studies have shown that EPs can use ultrasound to diagnose ocular pathology. Blaivas et al.4 showed ultrasound’s capability in diagnosing ruptured globes, retinal detachments, lens dislocations, and central retinal artery occlusions in 26 out of 61 patients with acute visual changes or ocular trauma.

A subsequent study by Shriver5 in 2005 demonstrated the ability of ultrasonography to detect intraocular metallic foreign bodies. Other than the Blaivas article, this specific method of evaluation has not been described previously as a technique to identify a ruptured globe.

This study demonstrated that ultrasound may one day be used by appropriately trained EPs in the future to expedite the diagnosis of globe rupture; however, the sensitivity and specificity of this test indicate that it is unlikely to replace more definitive imaging modalities. The use of a clear plastic barrier prevents an increase in IOP without affecting image quality, and future research should employ this technique. The

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Chandra et al. higher sensitivity of second-year residents may be explained by an increased comfort level with ultrasonography as a result of a dedicated one-month ultrasound training course initiated for them over the previous year (and therefore not inclusive of first- or third-year residents). This study had several limitations: the porcine model; the limited pre-study training in ocular ultrasound; and the confusion on the study day between a rupture and vitrectomy. The porcine model allowed participants to identify abnormalities in the globeâ&#x20AC;&#x2122;s shape, the location of the lens, and the volume of vitreous humor; however, it did not allow for a simulation of vitreous hemorrhage, which is often associated with traumatic globe rupture.

Future research in a live animal or cadaveric human model, with a longer training lecture that stressed the difference between the positive control and experimental group, would be helpful in evaluating this diagnostic technique further before any practical recommendations can be made.

Ultrasound Detection of a Ruptured Globe Address for Correspondence: Amit Chandra, MD, Department of Emergency Medicine, New York Hospital Queens, 56-45 Main Street, Flushing, NY 11355. Email: Amitchandra2002@hotmail.com

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

References 1.

ophthalmology. J R Soc Med. 1980; 73:273-8.

2.

Volume X, no. 4 : November 2009

Fledelius HC. Ultrasound in ophthalmology. Ultrasound Med. Biol.

1997; 23:365-75.

3.

Mitchell J. Ocular emergencies. In Tintinalli JE, Kelen GD, Stapczynski, et al., eds. Emergency Medicine: A Comprehensive Study Guide, 6th ed. New York, NY: McGraw-Hill; 2004:1449-64.

4.

Acknowledgements The authors would like to thank Dr. Jim Ryan, Dr. Jay Gupta, Dr. William Manson, Ms. Lily Kwan, Dr. Michael Radeos, Dr. Frank Lattanzio Jr., and Dr. Fernando Silva for their contributions to this study.

Restori M, McLeod D, Wright JE. Diagnostic ultrasound in

Blaivas M, Theodoro D, Sierzenski P. A study of bedside ocular ultrasonography in the emergency department. Acad Emerg Med. 2002; 9:791-9.

5.

Shriver SA, Lyon M, Blaivas M. Detection of metallic ocular foreign bodies with handheld sonography in a porcine model. J Ultrasound Med. 2005; 24:1341-6.

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Images In Emergency Medicine

Cervical Spine Fracture in Ankylosing Spondylitis Jennifer Carnell, MD Jahan Fahimi, MD Charlotte Page Wills, MD

Alameda County Medical Center, Highland Hospital, Department of Emergency Medicine, Oakland, CA

Supervising Section Editor: Rick A McPheeters, DO Submission history: Submitted March 14, 2009; Revision Received June 11, 2009; Accepted June 15, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[WestJEM. 2009;10(4):267.]

A 66-year-old man with a history of ankylosing spondylitis presented to the emergency department as a trauma activation after a fall backward onto his sacrum from the bottom rung of a ladder. He initially complained of neck pain. On physical examination, midline lower cervical spine tenderness to palpation was present, but careful neurologic examination revealed no deficits. A CT scan of the cervical spine performed immediately after his arrival demonstrated an unstable fracture through areas of bony ankylosis with marked widening at C6-C7. He was admitted to the trauma service and subsequently underwent cervical spine fixation by the neurosurgical service.

Fractures occur most commonly in the cervical and thoracic spine, and fractures of the ankylosed spine are common as evidenced by a lifetime incidence of 14%.1 In this sagittal CT image of the cervical spine, both the typical bamboo spine appearance of ankylosing spondylitis and the fracture at C6-7 are evident. Because emergency medicine providers are often the first to evaluate patients after trauma or when they develop pain, it is important to recognize that the degree of trauma necessary to fracture the ankylosed spine is minimal. Many patients are unable to cite a specific causative trauma.2 Moreover, these fractures often result in neurologic complications and incomplete neurologic recovery. Imaging of the spine should be strongly considered in any patient with ankylosing spondylitis and new or unusual neck/back pain.

Timely identification of unstable fractures is instrumental in avoiding adverse neurologic sequelae.

Figure 1. CT of cervical spine fracture in ankylosing spondylitis.

REFERENCES 1.

Address for Correspondence: Jennifer Carnell, MD, Department of Emergency Medicine, Alameda County Medical Center, Highland Hospital, 1411 East 31st Street, Oakland, CA 94602. Email jencarnell@gmail.com

Western Journal of Emergency Medicine

Mundwiler M, Siddique K, Dym J, et al. Complications of the spine in ankylosing spondylitis with a focus on deformity correction.

Neurosurg Focus. 2008; 24:1-9.

2.

267

Vosse D, Feldtkeller E, Erlendsson J, et al. Clinical vertebral fractures in patients with ankylosing spondylitis. J Rheumatol. 2004; 31:1981-5.

Volume X, no. 4 : November 2009

Orignal Research

Emergency Department Patients with Psychiatric Complaints Return at Higher Rates than Controls Troy E. Madsen, MD Anne Bennett, MD Steven Groke, BSN Anne Zink, MD Christy McCowan, MD Alex Hernandez, MD Stuart Knapp, BS Deepthi Byreddy, MD Scott Mattsson, MD Nichole Quick, MD

University of Utah, Division of Emergency Medicine, Salt Lake City, UT

Supervising Section Editor: Jeffrey Druck, MD Submission history: Submitted November 6, 2008; Revision Received February 16, 2009; Accepted March 22, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Study objective: At our 35,000 visit/year emergency department (ED), we studied whether patients presenting to the ED with psychiatric complaints were admitted to the hospital at a higher rate than non-psychiatric patients, and whether these patients had a higher rate of reevaluation in the ED within 30 days following the index visit.

Methods: We reviewed the electronic records of all ED patients receiving a psychiatric evaluation from January to February 2007 and compared these patients to 300 randomly selected patients presenting during the study period for non-psychiatric complaints. Patients were followed for 30 days, and admission rates and return visits were compared.

Results: Two hundred thirty-four patients presented to the ED and were evaluated for psychiatric complaints during the study period. Twenty-four point seven percent of psychiatric patients were admitted upon initial presentation versus 20.7% of non-psychiatric patients (p = 0.258). Twentyone percent of discharged psychiatric patients returned to the ED within 30 days versus 13.4% of discharged non-psychiatric patients (p=0.041). Patients returning to the ED within 30 days had a 17.1% versus 21.6% admission rate for the psychiatric and non-psychiatric groups, respectively (p=0.485).

Conclusion: Patients presenting to this ED with psychiatric complaints were not admitted at a significantly higher rate than non-psychiatric patients. These psychiatric patients did, however, have a significantly higher return rate to the ED when compared to non-psychiatric patients.

[West J Emerg Med. 2009;10(4):268-272.]

INTRODUCTION Crowding is a significant problem facing emergency departments (EDs). Multiple factors contribute to this growing healthcare issue. Numerous studies have focused on the idea of â&#x20AC;&#x153;recidivists,â&#x20AC;? or high frequency ED users who are responsible for a disproportionate number of ED visits.1-7 In one study, 4% of the ED patients accounted for 18% of the Volume X, no. 4 : November 2009

total ED visits;8 another study found similar results with 3.5% of ED patients comprising 14.3% of all visits.4 These numbers and the described characteristics of recidivists are consistent even when studied in different healthcare systems in various countries, including France,9 the United States,5 Ireland,10 Canada,11 Sweden12 and the United Kingdom.13 Several studies focusing on the characteristics of

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Psychiatric Return Visits recidivists make it clear that the prevalence of psychiatric illness is very high in this population.9,14,16 One study, comparing 100 frequent attendees with 100 control patients, found that 11% of the study group presented with psychological problems compared to 1% of patients in the control group and reported alcohol or drug use in 38% of the frequent attendees compared to 6% of the control group.15 Consensus in the literature agrees on the following description of recidivists: men from poor socioeconomic background with marked psychosocial problems and/or complex medical problems. Furthermore, recidivists have a higher than expected mortality and morbidity.16-18 Such information only heightens the urgency to identify and appropriately intervene on behalf of psychiatric recidivists. Such measures may be life-saving and will certainly, though less importantly, be costsaving.

In this study we focus on a specific group of ED users namely patients who suffer from psychiatric illnesses, who are at increased risk to become recidivists, when compared to the baseline population. Suicidality and other psychiatric complaints are especially prone to recidivism.19,20,21 We addressed this issue of recidivism by comparing the 30-day return rate between patients presenting with a psychiatric complaint and those presenting with all other complaints of a non-psychiatric nature. We hypothesized that psychiatric patients returned to the ED at higher rates than non-psychiatric control patients, but were not admitted to an inpatient unit at a higher rate than these controls.

METHODS This study was conducted at the University of Utah Medical Center Emergency Department, the primary medical facility of the University of Utah Neuropsychiatric Institute and a unique research environment due to its expansive geographical catchment area, which includes Utah, Nevada, Wyoming, Idaho and western Colorado. The ED evaluates over 35,000 patients per year, and serves as the primary screening site for admission to the region’s largest psychiatric facility, which has 90 inpatient beds and approximately 3,000 inpatient admissions per year. The study was a retrospective chart review using the University of Utah Medical Center electronic medical record database, and was approved by the Institutional Review Board at the University of Utah on January 29, 2008.

The study group was comprised of all patients who presented between January and February 2007 with a psychiatric complaint for which an evaluation by a licensed clinical social worker (LCSW) was requested by an attending emergency physician (EP). The historical control population consisted of 300 randomly selected patients who presented to the ED with a non-psychiatric complaint during the months of January and February 2007. This number of control patients was selected based on power calculation to detect a 30% Western Journal of Emergency Medicine

difference in admission rates and return visits between groups, assuming 80% power and alpha of 0.05. Historical controls were selected from the ED patient log beginning January 1, which was the first day of the study period, and were selected from across the study period using a random number generator. Those who were evaluated by a LCSW at any point during their stay were excluded from the control population.

Psychiatric admission was defined as admission to an inpatient psychiatric unit. Medical students using a template form performed chart reviews. Investigators entered data into a standardized database. Twenty percent of the study charts were reviewed by one of the study’s primary investigators.

A significant source of information about the study population came from notes written by LCSWs. To more thoroughly evaluate psychiatric patients presenting to the ED, LCSWs complete a crisis note detailing their assessment and recommendations for admission versus discharge following the initial evaluation by an EP. Reason for evaluation by a LCSW included suicidal ideation, suicide attempt, psychosis, substance abuse, or any other psychiatric complaint for which the attending EP requested an evaluation. Detailed crisis notes follow a template format and include patient age, gender, presentation, history of suicide attempts, psychiatric history, living situation, and current sources of stress in the patient’s life. All patient-disposition decisions (admission vs. discharge) are made by the LCSW in discussion with the attending EP. LCSWs in the ED follow up on discharged patients through hospital records and community psychiatric facility records.

The control group consisted of patients who presented to the ED with a complaint of a non-psychiatric nature in the time period concurrent with the study group. These complaints represented the full spectrum of potential ED visits including trauma, abdominal pain, chest pain, infection, etc.

Patients were excluded from the control group if they had been evaluated by a LCSW for any reason during their stay, as the study group consisted of patients who had received an LCSW evaluation. These patients were found in the electronic database and selected randomly from the months of January through February 2007. We followed all patients included in the study for 30 days for return ED visit and hospitalization upon return visit. In the case of patients with multiple ED visits during the study period, the initial visit during this period was defined as the index visit, and additional visits were defined as repeat visits.

The admission rate, rate of return to ED within 30 days, and admission rate on return visits were compared for the two study groups. We performed statistical analysis using chisquare and Student’s t-test with p<0.05 considered statistically significant (SPSS v. 16.0).

RESULTS Two hundred thirty-four patients presented to the ED during the study period with a chief complaint of a psychiatric

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Psychiatric Return Visits Table 2. Presenting chief complaint among non-psychiatric patients

Table 1. Presenting chief complaint among psychiatric patients Visit reason Suicidal ideations/attempt

Visit reason

Number

Percent of total

Number

Percent of total

92

39.3%

Abdominal pain

60

20%

53

17.7%

Psychotic symptoms

33

14.1%

Trauma/burn

Substance abuse

29

12.4%

Chest pain

32

10.7%

32

10.7%

Behavior issues

25

10.7%

Neurologic

Depression

23

9.8%

Orthopedic

27

9%

Anxiety

21

9%

Weakness/malaise

25

8.3%

Medical

10

4.3%

Infection

20

6.7%

1­

0.4%

Respiratory

16

5.3%

ENT/dental

12

4%

Homicidal ideations

nature and were evaluated by a LCSW. Of these, 92 patients expressed suicidal ideation or confirmed having recently attempted suicide while 142 presented with non-suicidal psychiatric complaints. The most common non-suicidal psychiatric complaints were psychotic symptoms, substance abuse, behavioral issues, anxiety, and depression (Table 1).

As a comparison group, we selected 300 medical and trauma patients without psychiatric complaints who also presented during this same period. The most common visit reasons among the control group included abdominal pain, orthopedic complaints, trauma, neurologic symptoms, weakness/malaise, and chest pain (Table 2).

Psychiatric patient admission rates at the initial ED visit were higher than that of controls, but this was not statistically significant. Twenty-four point seven percent (58/234) of psychiatric patients were admitted upon initial presentation to the ED compared to 20.7% (62/300) of non-psychiatric patients (p = 0.258) (Figure 1).

The 30-day ED return visit rate for psychiatric patients who were discharged from the ED was significantly higher than that of the control group who were discharged: 21% (37/176) of psychiatric patients returned vs. 13.4% (32/238) of non-psychiatric patients (p=0.041). Among patients who were admitted to the hospital on initial ED visit, 7% (4/58) of psychiatric vs. 8% (5/62) of non-psychiatric patients returned to the ED within 30 days. Upon return ED visit, 17.1% (7/41) of psychiatric patients and 21.6% (8/37) of non-psychiatric patients were admitted to the hospital (Figure 1).

Overall, admitted psychiatric patients were less likely to return to the ED within 30 days of their index visit; 21% of discharged psychiatric patients vs. 6.9% of admitted psychiatric patients returned (p=0.014). There was not a significant difference in 30-day return rates between male (18.8%, 22/117) and female (16.2%, 19/117) psychiatric patients (p=0.606).

Among psychiatric patients, we compared return ED visits between those complaining of suicidal ideations and those with other psychiatric complaints. Thirty-one point five percent (29/92) of suicidal patients vs. 20.4% (29/142) of nonsuicidal patients were admitted at the time of the initial ED Volume X, no. 4 : November 2009

Dermatologic

6

2%

Obstetric/gynecologic

5

1.7%

Syncope

4

1.3%

GI bleed

3

1%

Toxicology

3

1%

Medication refill

2

0.7%

visit (p=0.055). Discharged suicidal patients were not more likely to return within 30 days (17.5% of suicidal vs. 23% of non-suicidal, p=0.386) nor to be admitted upon return ED visit (8.3% of suicidal vs. 20.7% of non-suicidal, p=0.339). There were no completed suicides during the study period.

As the LCSW evaluations included patients with substance abuse, we also compared return ED visits between patients who were evaluated for substance abuse to those with other psychiatric complaints. Seventeen point two percent (5/29) of those primarily evaluated with substance abuse were admitted to the hospital at the index ED visit vs. 25.9% of those with other psychiatric complaints (p=0.315). Return ED visit rates were nearly identical between groups: 17.2% (5/29) of substance abuse patients vs. 17.6% (36/205) of other psychiatric patients returned to the ED within 30 days (p=0.966).

270

Psychiatric

30

Non‐psychiatric

25 20 15 10 5 0 Initial hospital admission

Return ED visit

Admission upon return

Figure 1. Return emergency department visits and admissions among psychiatric and non-psychiatric patients

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Madsen et al.

Psychiatric Return Visits DISCUSSION Individuals presenting to EDs with psychiatric complaints represent a patient population for which recidivism is a common occurrence. Reasons for revisits are multi-factorial; however, because many patients face decreasing access to both inpatient and outpatient psychiatric services, the ED has become their sole safety net for obtaining needed care.

High recidivism in this population may be one of several factors that contribute to the growing problem of ED overcrowding. Recidivists may be judged by ED staff to have non-urgent concerns and given a lower priority, setting them up to have a serious problem overlooked.8 The increased use of medical care does not correlate with increased quality of care. Conflicting counsel and medications pose a threat to any frequent ED user.

High frequency ED users use other sources of medical care at a higher rate than the general population.15,8 While our data does not directly deal with this issue, it reinforces the necessity of finding care that works for this population.

The literature on this topic provides one such explanation for recidivists - simply that recidivists are a medically and psychosocially vulnerable group.1,5,16,18,26-28 Therefore, recidivists not only need more care but actually seek more care, suggesting that simply transferring care from the ED to primary care may not be the solution. Some continue this line of reasoning, stating that with increased severity of medical conditions, the ED may be a more appropriate place for recidivists than primary care facilities.5,29 When our data are evaluated within the sub-population of psychiatric recidivists, the issue becomes the high risk that this population presents to themselves. In this study we determined that psychiatric patients return to the ED at a significantly higher rate than those patients with a nonpsychiatric complaint. Past studies have highlighted the urgency of this problem by connecting excess mortality rates with recidivism.30-33 In a five-year follow-up study by Ostamo et al.,33 completed suicide was the cause of excess mortality in 37% of female deaths and 44% of male deaths among suicidal emergency patients. The risk of completed suicide is particularly high during the first year following an attempt,33-35 suggesting that immediate repeat visits must be handled with a heightened sense of caution and attention to the accuracy of assessment. Further analysis is needed to better characterize patients who return to the ED, require admission on repeat visit, or continue to demonstrate self-harm behavior upon discharge.

LIMITATIONS Limitations of this study are those common among all studies with a retrospective chart review design. The accuracy of the records may have been compromised by the author of the records, the interpretation of the reader or any of the intervening steps. The assessment of repeat visits was Western Journal of Emergency Medicine

determined by the availability of LCSW notes or ED physician notes rather than a hospital consensus database that may be more accurate. A limitation of this study is that the diagnosis of mental disorders was made by the clinical judgment of the attending EP rather than by the utilization of a standardized diagnostic tool.

Additionally, we included patients only from the months of January and February, 2007. This presents the potential for bias, as certain medical conditions may be more or less likely during this period, and seasonal condition may create the potential for variations in return visit rates. Lastly, because this is a single-institution study and the results may not be applicable or generalizable to other institutions. Our hospital serves as a regional referral center, which may skew the results due to the complexity of patients. We felt, however, that this would be at least partially counterbalanced by the medical control group, as our facility serves as a referral center for all medical complaints.

CONCLUSION Psychiatric patients are especially prone to recidivism.

In our study, this population was significantly more likely than medical controls to return to the ED within 30 days. Their recidivism makes this population amenable to preventive measures, while its severity highlights the critical need for prevention. Appropriately identifying patients for discharge versus inpatient treatment may both ease the burden on EDs as short-term repeat visits are prevented and more importantly, prevent the tragic outcomes of completed self-harm behaviors and continued suffering in this population.

Additional research is needed to identify those psychiatric patients best suited for admission versus discharge. Future research may also focus on alternatives to the ED that are available to psychiatric patients in need of care. Lastly, defining the role and interplay of roles among primary care physicians, psychiatrics, and EDs in the care of psychiatric patients may highlight potential solutions to the problem of psychiatric recidivists.

Address for Correspondence: Troy Madsen, MD, Division of Emergency Medicine, University of Utah, 30 N. 1900 E. 1C26, Salt Lake City, UT 84132. Email: troy.madsen@hsc.utah.edu Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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suicide. Br J Psychiatry. 1998; 173:531-5.

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The Clinical Differentiation of Cerebellar Infarction from Common Vertigo Syndromes James A. Nelson, MD* Erik Viirre MD, PhD†

* University of California at San Diego, Department of Emergency Medicine † University of California at San Diego, Department of Surgery, Division of Head and Neck Surgery

Supervising Section Editor: Kurt R. Denninghoff, MD Submission history: Submitted March 22, 2008; Revision Received March 31, 2009; Accepted June 1, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

This article summarizes the emergency department approach to diagnosing cerebellar infarction in the patient presenting with vertigo. Vertigo is defined and identification of a vertigo syndrome is discussed.

The differentiation of common vertigo syndromes such as benign paroxysmal positional vertigo, Meniere’s disease, migrainous vertigo, and vestibular neuritis is summarized. Confirmation of a peripheral vertigo syndrome substantially lowers the likelihood of cerebellar infarction, as do indicators of a peripheral disorder such as an abnormal head impulse test. Approximately 10% of patients with cerebellar infarction present with vertigo and no localizing neurologic deficits. The majority of these may have other signs of central vertigo, specifically direction-changing nystagmus and severe ataxia.

[West J Emerg Med. 2009;10(4):273-277.]

INTRODUCTION While most patients who present to emergency departments (ED) with isolated vertigo have benign disorders, approximately 0.7-3% have cerebellar infarction.1,2 Because the symptoms of cerebellar infarction overlap substantially with benign conditions it is commonly overlooked, with a misdiagnosis rate estimated at 35%2. Patients with missed cerebellar infarction in general are at higher risk for complications, with a mortality rate possibly as high as 40%.3 Physical diagnosis is the most important diagnostic modality for cerebellar infarction. Resorting to computed tomography (CT) is insufficient because it is only 26% sensitive for acute stroke.4 In contrast, important physical signs are present in the majority of patients with cerebellar infarction.

This review will first address differentiation of cerebellar infarction from the four most common vertigo syndromes: benign paroxysmal positional vertigo (BPPV), Meniere’s disease, migrainous vertigo, and vestibular neuritis.5 Then we will review the physical diagnosis of cerebellar infarction.

Finally, we will propose indications for neuroimaging.

Definition of Vertigo Vertigo is defined as a pathologic illusion of movement.6 Most commonly experienced as a spinning sensation, it Western Journal of Emergency Medicine

arises from a pathologic imbalance in the peripheral or central vestibular system. Patients will often merely report feeling dizzy, and further questioning is required to identify vertigo.7 Caution is advised in classifying the dizzy patient.

While differentiating vertigo from imbalance, presyncope and lightheadedness was traditionally taught, studies show that patients use overlapping terms to describe their experience and even change their minds during a single clinical encounter.8 The best way for a clinician to identify a vertigo syndrome is to realize that while most patients will report the classic rotational vertigo, approximately 17% will not.9 These patients may report episodic imbalance or dizziness that is made worse with head movement.

Benign Paroxysmal Positional Vertigo Benign paroxysmal positional vertigo is a distinct condition not typically confused with cerebellar infarction.

Central mimics of BPPV have been described, but they tend to be caused by tumors rather than strokes, and are recognized by association with other abnormalities.10 Patients present with brief episodes of intense vertigo, precipitated by a change in position. The paroxysms of intense symptoms lasting less than a minute are defining, as is positional provocation. Patients are well until a head movement, usually vertical, precipitates 273

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Cerebellar Infarction disease tend to have recurring episodes, so if the patient has not had previous episodes, labyrinthitis should be suspected instead. Labyrinthitis is thought to be the same disease process as vestibular neuritis, with the additional involvement of the auditory system.

Table 1. Red flags in vertigo 1.

Any neurologic deficit

2.

Total ipsilateral hearing loss

3.

Inability to walk without support

4.

Direction-changing nystagmus

the paroxysm of symptoms. In most cases BPPV is idiopathic, although 10% follow a bout of vestibular neuritis and 20% follow an episode of head trauma.11 The most common form of BPPV, caused by an otolith in the posterior semicircular canal, is diagnosed by finding torsional nystagmus on the Dix-Hallpike test.12 The examiner holds the seated patient’s head 45° to the left or right. This aligns the posterior semicircular canal in the vertical plane.

The patient should be asked to hold onto the examiner’s arm for stability. The examiner then drops the patient back to the supine position, with the head hanging down off the stretcher 10°-30°. This causes a large rotation of the posterior semicircular canal within its own plane, moving the loose otolith and reproducing the symptoms. The test is considered positive if it provokes the characteristic torsional and vertical nystagmus.13 The sensitivity of the Dix-Hallpike maneuver for BPPV has not been well-described in the ED setting. Even without a positive Dix-Hallpike test, patients with BPPV can be differentiated from those with cerebellar infarction by their episodic and positional symptoms. Those who do not fit this description require consideration of alternative diagnoses.

Meniere’s Disease Meniere’s disease is suspected in the patient who presents with simultaneous vertigo and cochlear complaints. Cochlear complaints can be hearing loss, tinnitus, or aural fullness. Also called endolymphatic hydrops, Meniere’s disease is thought to be caused by a buildup of fluid in the endolymphatic compartment of the inner ear. Episodes commonly last a few hours, although they can range from 20 minutes to a few days. Formal diagnosis requires hearing loss documented on audiologic examination on at least one occasion.14 Patients may have normal audiologic examination between episodes.

It is not common for a stroke to present with isolated vertigo and hearing loss, although case reports do exist.15 It occurs in only 0.3% of all brainstem infarctions and tends to present with complete ipsilateral deafness.16 In general, vertigo with hearing loss, unless it is with total ipsilateral deafness, indicates a peripheral disorder. The clinician should perform a thorough neurologic and neuro-otologic examination on these patients, as discussed below. Patients with a negative workup for stroke should be referred to an otolaryngologist for further testing and consideration of alternative diagnoses, such as labyrinthitis and schwannoma.6,17 Patients with Meniere’s Volume X, no. 4 : November 2009

Migrainous Vertigo Despite being the second most common cause of vertigo seen in clinical practice, migrainous vertigo remains underrecognized.5 Its clinical spectrum can be elusive. Half of patients present without headache.18 Its presenting features can vary, not only among different patients but in the same patient over time. Some have aura while others do not. Some have photophobia during attacks while others do not. For some, the migrainous vertigo appears to be like an aura that lasts for a few minutes (18%), but for others the vertigo lasts for longer than 24 hours (27%).19 Physical examination should reveal a normal neurologic examination, including coordination and gait. Video oculography has demonstrated findings of central nystagmus, but this has not yet been demonstrated on bedside physical examination.20 Formal diagnostic criteria for migrainous vertigo have been proposed.21 Strict criteria require: 1) recurrent episodes of vertigo; 2) a formal migraine diagnosis by International Headache Society (I.H.S.) criteria; 3) a migraine symptom during the attack (e.g. headache, photophobia, or aura); and 4) the exclusion of other causes. The category of “probable migrainous vertigo” is used for patients with some elements in the presentation to suggest migraine but no other identifiable cause.

Cerebellar infarction is not expected to present with migraine-associated symptoms, so most patients with criteria for migrainous vertigo and a normal neurologic examination can be treated for their migraine process without further work-up.

Vestibular Neuritis Vestibular neuritis is characterized by the acute vestibular syndrome, caused by decreased vestibular tone on one side.

Etiology is currently thought to be viral.22 Vestibular neuritis is recognized by characteristic findings on history and ocular examination. The history typically reveals a gradual onset, unlike for stroke where symptoms reach maximal intensity at onset. In vestibular neuritis, symptoms peak during the first day and begin to improve within a few days, although full recovery takes weeks to months.6 The associated vertigo is persistent and ongoing, although like all forms of vertigo, positional exacerbation is characteristic, as any head movement amplifies the disparity in bilateral vestibular tone.

Associated autonomic symptoms of nausea and vomiting are prominent.

General neurologic examination is normal, including motor, sensory, reflexes, cranial nerves and mental status.

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Cerebellar Infarction Most importantly, limb coordination is preserved on fingerto-nose, heel-to-shin, and rapid-alternating movement testing.

Although some mild incoordination is expected, the patient should retain the ability to ambulate. Their central nervous system continues to integrate its somatosensory, visual, and proprioceptive information, coordinating ambulation.

The vestibulopathic patient has decreased vestibular tone on the affected side. This imbalance in tone normally occurs when someone turns their head away from that side, so the vestibulopathic patient experiences the world as if they were continually turning their head away from the affected side.

The vestibulo-ocular reflex causes a compensatory slow drift of the eyes back toward the hypoactive ear, which is the slow phase of nystagmus. The fast phase of nystagmus is the corrective beating opposite the hypoactive ear.1 Its direction is both horizontal and torsional, and it is considered unidirectional, meaning regardless of where the patient looks, the direction of nystagmus will not change.22 It is accentuated when looking away from the hypoactive ear (Alexander’s Law). The patient feels this and will often shut her eyes when looking away from the hypoactive side. It should be remembered that unidirectional nystagmus can also occur in 46% of patients with cerebellar infarction so it cannot be used to confirm a peripheral disorder.23 However, there is one physical finding in particular that may provide some help.

The vestibulo-ocular reflex (VOR) hinges eye movement to head movement. When a normal person looks to one side, the labyrinth on that side signals the turn, and the eyes automatically move opposite to maintain fixed gaze. For example, the reader can turn the head alternately to each side yet continue to read, because of the VOR. For the vestibulopathic patient, when the head is rapidly moved toward the pathologic side, the eyes move with the head and visual fixation is broken. A refixation (“catch-up”) saccade is seen as the patient looks back to the original object. This is tested by the head thrust test, also called the head impulse test.24 The patient’s head is placed midline, and the patient is instructed to maintain visual fixation on the examiner’s nose. The examiner thrusts the patient’s head quickly to one side, and if a refixation saccade back to the nose is seen, canal paresis is present on the side to which the head was turned (Figure 1). The test should be done on both sides. A video of the test being performed is available online.25, 26 In other settings it has been described as only 34-39% sensitive for vestibular hypofunction.27,28 When studied in more highly selected ED populations a positive head impulse test was 100% sensitive for a peripheral disorder.26 A negative head impulse test was found in 91 to 96% of patients with cerebellar infarction.23, 26 Further studies need to address the role of the head impulse test in undifferentiated ED patients with vertigo syndromes. Until that time it can only be said that a positive head impulse test is more consistent with acute peripheral vestibulopathy, such as vestibular neuritis, and a negative head impulse test raises the concern for cerebellar infarction.

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Figure 1. Head impulse test. A: The right ear has intact peripheral vestibular function. When the head is turned to the right, the vestibulo-ocular reflex moves the eyes to maintain visual fixation.

B: The right ear now has impaired vestibular function. When the head is turned to the right, the eyes move with it, breaking visual fixation, and a refixation saccade is seen as the eyes dart back to the examiner’s face. This indicates a peripheral vestibular disorder on the right side. Reprinted from The Lancet Neurology, Vol. 7, Edlow JA, Newman-Toker DE, and Savitz SI, Diagnosis and initial management of cerebellar infarction”, Page No. 959, Copyright 2008, with permission from Elsevier.

Cerebellar Infarction Cerebellar infarction represents approximately 2.3 % of acute strokes overall.29 These can result from occlusion of the superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA), or the posterior inferior cerebellar artery (PICA). Larger cerebellar infarcts produce symptoms and signs localizing to the brainstem, such as diplopia, dysarthria, limb ataxia, dysphagia, and weakness or numbness.

Approximately 10% of patients with cerebellar infarction can present with isolated vertigo, that is, vertigo with no localizing findings on motor, sensory, reflex, cranial nerve, or limb coordination examination. Most of these are infarcts of the medial branch of the PICA (96%).23 Patients with isolated vertigo due to cerebellar infarction pose a significant diagnostic challenge to the

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emergency physician (EP). It is known for being frequently misdiagnosed, often with consequent disability.3 While its infrequency precludes good ED studies on its presenting signs, the literature is sufficient to offer some historical and physical clues that may alert the clinician to the possibility of a cerebellar infarction.

First, stroke in general tends to present with the sudden and immediate onset of symptoms, usually reaching maximal intensity at once. Second, vascular risk factors raise the prior probability of disease. Hypertension and cardioaortic diseases are found in the majority of patients with cerebellar infarction, and an embolic source is found in 24-40%.23,29 Finally, two easily overlooked physical signs have been shown to indicate cerebellar infarction.

The first is severe ataxia, which has classically been considered a sign of central vertigo.6 Seventy-one percent of patients with cerebellar infarction and isolated vertigo will present with the inability to walk without support.23 Graded by two independent observers, this appears to be an objective and reproducible finding, although the observers were not blinded to the diagnosis. The other 29% have mild to moderate imbalance with ambulation, which would not in itself permit differentiation from vestibular neuritis.

The second important physical sign of cerebellar infarction is direction-changing nystagmus, also called multidirectional nystagmus, or gaze-evoked nystagmus. Such patients have nystagmus that changes directions according to the patientâ&#x20AC;&#x2122;s gaze. For example, if the patient looks to the right it beats to the right, and when the patient looks left it beats to the left. This was found to be 56% sensitive for cerebellar infarction, although the clinicians were not blinded to the diagnosis.23 The clinician should avoid the mistake of extreme lateral strain, as this produces end-point nystagmus, which is normal and reflects only muscle fatigue.30 Certain medications, especially anti-epileptics and alcohol, can cause nystagmus as well.

The inability to walk without support and directionchanging nystagmus are important signs because they are commonly present even when no other findings of brainstem ischemia are present. At least one of these two signs was seen in 84% (21 of 25) of the patients with cerebellar infarction and isolated vertigo.23 Indications for Neuroimaging Evidence-based recommendations for neuroimaging in the vertiginous patient have not been established. Based upon currently available evidence, clear indications for neuroimaging include any focal neurologic deficit, the inability to walk without support, and direction-changing nystagmus.

When neuroimaging is indicated, diffusion-weighted magnetic resonance imaging (MRI) with magnetic resonance angiography is currently considered the optimal study. For

hemorrhagic strokes, computed tomography (CT) and MRI are both excellent studies.31 However, for ischemic strokes, MRI is clearly superior with an 83% sensitivity compared to 26% for CT.4 Physicians should therefore not rely on CT scanning to rule out cerebellar infarction.

CONCLUSION Cerebellar infarction is present in 3% of patients presenting with vertigo.1 Of these, only 10% lack focal neurologic deficits. Evidence cited in this review suggests that even when there are no neurologic deficits, most cases of cerebellar infarction will present with either the inability to walk without support or direction-changing nystagmus.23 In a patient with a low prior probability of stroke, the emergency physician will usually have good justification for discharging the patient who has isolated vertigo and a completely normal neurologic and neuro-otologic examination. One study of 15 cases of missed cerebellar infarction showed that all 15 lacked documented performance of standard neurologic examination and gait.3 Prompt evaluation by a neurologist or otolaryngologist is recommended for patients who have not received a definite diagnosis.

Address for Correspondence: James A. Nelson, MD, Department of Emergency Medicine, University of California, San Diego, 200 W Arbor Drive, San Diego, CA 92103. Email jamesnelsonmd@gmail.com Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

REFERENCES 1.

Seemungal BM. Neuro-otological emergencies. Curr Opin Neurol.

2007; 20:32-9.

2.

Kerber KA, Brown DL, Lisabeth LD, et al. Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population-based study. Stroke. 2006; 37:2484-7.

3.

Savitz SI, Caplan LR, Edlow JA. Pitfalls in the diagnosis of cerebellar infarction. Acad Emerg Med. 2007; 14:63-8.

4.

Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison.

Lancet. 2007; 369:293-8.

5.

Neuhauser HK. Epidemiology of vertigo. Curr Opin Neurol. 2007; 20:40-6.

6.

Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998; 339:680-5.

7.

Drachman DA, Hart CW: An approach to the dizzy patient.

Neurology. 1972; 22:323-34.

8.

Newman-Toker DE, Cannon LM, Stofferahn ME, et al. Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting. Mayo Clin Proc. 2007; 82:1329-40.

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Neuhauser HK, von Brevern M, Radtke A, et al. Epidemiology of

20. von Brevern M, Zeise D, Neuhauser H, et al. Acute migrainous

vestibular vertigo: a neurotologic survey of the general population.

vertigo: clinical and oculographic findings. Brain. 2005; 128:365-74.

Neurology. 2005; 65:898-904.

21. Olesen J. Classification and diagnostic criteria for headache disorders,

10. Baloh RW. Differentiating between peripheral and central cause of

cranial neuralgias and facial pain. Cephalalgia. 1988; 8:9-96.

vertigo. Otolaryngol Head Neck Surg. 1998; 119:55-59.

22. Baloh RW. Vestibular neuritis. N Engl J Med. 2003; 348:1027-32.

11. Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J

23. Lee H, Sohn SI, Cho YW, et al. Cerebellar infarction presenting

Med. 1999; 341:1590-6.

isolated vertigo: frequency and vascular topographical patterns.

12. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis

Neurology. 2006; 67:1178-83.

of certain common disorders of the vestibular system. Proc R Soc

24. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch

Med. 1952; 45:341-354.

Neurol. 1988; 45:737-9.

13. Viirre E, Purcell I, and Baloh RW. The Dix-Hallpike test and the

25. Lewis RF and Carey JP. Abnormal eye movements associated with

canalith repositioning maneuver. Laryngoscope. 2005; 115:184-7.

unilateral loss of vestibular function. N Engl J Med. 2006; 355:e26.

14. Committee on Hearing and Equilibrium, American Academy of

26. Newman-Toker DE, Kattah JC, Alvernia JE, et al. Normal head

Otolaryngology-Head and Neck Foundation, Inc. Guidelines for the

impulse test differentiates acute cerebellar strokes from vestibular

diagnosis and evaluation of therapy in Meniereâ&#x20AC;&#x2122;s disease. Otolaryngol Head Neck Surg. 1995; 113:181-5.

neuritis. Neurology. 2008; 70:2378-85.

27. 27.Beynon GJ, Jani P, Baguley DM. A clinical evaluation of head

15. Son EJ, Bang JH, Kang JG. Anterior inferior cerebellar artery

impulse testing. Clin Otolaryngol. 1998; 23:117-22.

infarction presenting with sudden hearing loss and vertigo.

28. Harvey SA, Wood DJ. The oculocephalic response in the evaluation

Laryngoscope. 2007; 117:556-8.

of the dizzy patient. Laryngoscope. 1996; 106:6-9.

16. Lee H, Baloh RW. Sudden deafness in vertebrobasilar ischemia:

29. Tohgi H, Takahashi S, Chiba K, et al. Cerebellar infarction. Clinical

clinical features, vascular topographical patterns and long-term

and neuroimaging analysis in 293 patients. The Tohoku Cerebellar

outcome. J Neurol Sci. 2005; 228:99-104.

Infarction Study Group. Stroke. 1993; 24:1697-701.

17. Kentala E. Characteristics of six otologic diseases involving vertigo.

30. Leigh RJ, Rucker JC. Nystagmus and related ocular motility

Am J Otol. 1996; 17:883-92.

disorders. In: Miller NR, Newman NJ, eds. Walsh and Hoytâ&#x20AC;&#x2122;s

18. Brantberg K, Trees N, Baloh RW. Migraine-associated vertigo. Acta

Clinical Neuro-Opthalmology. Baltimore, MD: Lippincott, Williams &

Otolaryngol. 2005; 125:276-9.

Wilkins; 2004.

19. Neuhauser H, Lempert T. Vertigo and dizziness related to migraine: a

31. Kidwell CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for

diagnostic challenge. Cephalalgia. 2004; 24:83-91.

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detection of acute intracerebral hemorrhage. JAMA. 2004; 292:1823-30.

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Case Report

The Back Alley Revisited: Sepsis after Attempted Self-Induced Abortion Teresa A Saultes, DO Diane Devita, MD Jason D. Heiner, MD

Madigan Army Medical Center, Department of Emergency Medicine, Tacoma, WA

Supervising Section Editor: Laleh Gharahbaghian, MD Submission history: Submitted March 11, 2009; Revision Received June 17, 2009; Accepted June 19, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

While unsafe abortions have become rare in the United States, the practice persists. We present a 24-year-old female with a 21-week twin gestation who presented to the emergency department with complications of an attempted self-induced abortion. Her complicated clinical course included sepsis, chorioamnionitis, fetal demise, and a total abdominal hysterectomy with bilateral salpingo-oophorectomy for complications of endomyometritis. We discuss unsafe abortions, risk factors, and the management of septic abortion. Prompt recognition by the emergency physician and aggressive management of septic abortion is critical to decreasing maternal morbidity and mortality.

[West J Emerg Med. 2009;10(4):278-280.]

INTRODUCTION Internationally, approximately 42 million pregnancies are terminated each year with an estimated 20 million terminations in unsafe conditions.1 The World Health Organization estimates that 68,000 women die annually due to the complications of unsafe abortions, with sepsis as the primary cause of death.1,2 Although 97% of unsafe abortions occur in developing countries, todayâ&#x20AC;&#x2122;s emergency physician (EP) may still encounter this rare entity and its complications, which have persisted despite the legalization of abortion here.3 While unsafe abortions in the U.S. are now rare occurrences for which little research exists, recent literature reports of self-induced abortions have predominantly involved adolescents.4,5,6 A 2008 Centers for Disease Control and Prevention (CDC) Morbidity and Mortality Weekly Report (MMWR) regarding U.S. abortion surveillance estimated the number of deaths for legal and illegal abortions from 19722004 to be 393 and 95, respectively.7 Although recognized as an underestimation, the CDC has reported between zero and two annual maternal deaths from 1979-2004 in the U.S. due to complications of abortion.7 Roughly 40% of all unsafe abortions are performed on women ages 15-24, and adolescents account for 19% of all reported legal abortions.1,6 Young women choosing to abort may face barriers that lead them to a self-induced or otherwise unsafe termination of pregnancy. In the U.S. the number Volume X, no. 4 : November 2009

of abortion providers has decreased and about one-third of women live in a county with no abortion provider. States are increasingly mandating parental involvement in a minorâ&#x20AC;&#x2122;s decision to have an abortion. In 2001 the inflation-adjusted cost of an abortion rose, with the national average ranging from $350-$900 for a first trimester abortion.6,8 These issues are likely to influence the young women who will eventually seek care by an EP for complications associated with an unsafe abortion.

We report a case of an attempted self-induced abortion via the intrauterine insertion of a metal coat hanger that was complicated by sepsis. This patientâ&#x20AC;&#x2122;s presentation illustrates both the major complication of septic abortion and the diagnostic challenge for the EP when a patient conceals the preceding events. We briefly review self-induced abortions and discuss diagnostic strategies as well as the management of the patient presenting with a septic abortion. Finally, we address the role that the EP may play in identifying patients who may be at particular risk for this dangerous entity.

CASE REPORT A 24-year-old previously healthy female (gravida 3, para 2) arrived by ambulance to the emergency department (ED) with sudden onset of diffuse, severe abdominal pain. She endured emesis and vaginal spotting for one day and a history of irregular menses making her unsure if she were pregnant.

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Sepsis After Self-Induced Abortion Her blood pressure was 82/51 mmHg; heart rate, 113 beats/ min; respiratory rate, 22 breaths/min; temperature, 36.4oC (97.5oF); and O2 saturation, 97% on room air. She was given two liters normal saline bolus. She was in obvious discomfort, with a diffusely tender, gravid abdomen, with the contracting fundus just below the umbilicus. Laboratory tests revealed a hematocrit of 25%, white blood cell count (WBC) of 12,000 mm3 and a positive urine pregnancy test. Serum electrolytes, and renal and liver functions were normal. Markers of disseminated intravascular coagulation, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and D-dimer were all normal, as was urine toxicology screen.

Fetal heart tones were 177 beats/minute.

Once the obstetrics and gynecology (OB) service was consulted the patient admitted to prior knowledge of her gravid state with no prenatal care. A transabdominal ultrasound revealed a twin pregnancy at 21 weeks gestation, no obvious evidence of abruption, and a significant amount of abdominal free fluid. She then confessed to attempting to end her pregnancy earlier that day by passing a coat hanger deep into her vagina until she felt a â&#x20AC;&#x153;pop,â&#x20AC;? followed by a gush of fluid and the onset of her abdominal pain. Speculum exam noted no evidence of lower genitourinary injury.

Given the patientâ&#x20AC;&#x2122;s persistent hemodynamic instability and acute abdomen, the general surgery service performed exploratory laparotomy, where one liter of blood was found in her abdomen with a hemostatic wound at the uterine fundus. Broad spectrum antibiotics (ampicillin, gentamicin, and clindamycin) were given. Her postoperative course included sepsis, chorioamnionitis, fetal demise, acute respiratory distress syndrome (ARDS), and a total abdominal hysterectomy with bilateral salpingo-oophorectomy for complications of endomyometritis.

DISCUSSION Methods to terminate pregnancy have existed since ancient times. The Chinese Emperor Shen Nung described the use of mercury for inducing abortion 5000 years ago.9 Over 100 methods have been described to induce abortion and can be divided into four categories: oral and injectable medicines, vaginal preparations and cervical dilators, uterine instrumentation, and trauma to the abdomen (Table 1).3,10 All of these can impose a serious threat to the life and wellbeing of the mother, with abortions later in the pregnancy associated with greater maternal morbidity and mortality.3 Uterine insertion of rigid foreign objects increases the risk of perforation, and intrauterine instillation of soap solutions increases the risk of uterine necrosis, renal failure, central nervous system toxicity, cardiac depression, and respiratory arrest.11 Information about potential methods of unsafe abortions are found in the Internet, lay publications, and common cultural knowledge. For example, a survey of primarily Hispanic women in New York City found that a Western Journal of Emergency Medicine

Table 1. Common methods of unsafe abortion3,10 Oral and injectable medications: Metal salts, phosphorus, lead, kerosene, turpentine, detergent solutions, uterine stimulants (misoprostol or oxytocin), chloroquine, oral contraceptives Vaginal preparations and cervical dilators: Potassium permanganate, herbal preparations, douching with soap, dried asparagus, compressed balsa wood Uterine instrumentation: Coat Hanger, knitting needle, stick, crochet hook, douching, rubber catheter, air blown in by a syringe or turkey baster Trauma to the abdomen: Self-inflicted blows, abdominal pressure, jumping from a height

substantial number were familiar with the use of misoprostol as an abortifacient and 5% had used the method themselves.6 In the U.S. serious complications from abortions requiring hospitalization are estimated to occur less than one per 1,000 abortions.12 Septic abortion, the major complication associated with both legal and illegal abortions, is associated with fever, endometritis, and parametritis, with treatment aimed at eliminating the infectious process.13 While there is a paucity of research regarding the current mortality of sepsis associated with abortion or in pregnant patients, the overall mortality of sepsis in these patients may be as high as 20% to 50%.14 The signs and symptoms, similar to those of pelvic inflammatory disease, include fever, malodorous vaginal discharge, cervical motion tenderness, and pelvic or abdominal pain. In addition, trauma to the cervix or upper vagina may be recognized if there has been an unsafe abortion.15 Infections from septic abortion are usually polymicrobial and include anaerobes (streptococcus, bacteroides), aerobes (Escherichia coli), and sexually transmitted pathogens. Infection from Clostridium perfringens carries a particularly high morbidity and mortality, and in Third World countries tetanus may cause death from septic abortion.2,13 The diagnosis of septic abortion is made clinically and must be considered when any woman of childbearing age presents with vaginal bleeding, abdominal pain, and fever.

Typically the patient is young or unmarried and hesitant to reveal that she has had or attempted an abortion; she delays seeking care until she is very ill.13 A positive pregnancy test may indicate either a present pregnancy or a recent pregnancy if the uterus is empty. Other laboratory tests in the evaluation should include a complete blood count, blood type with Rh status, tests of hepatic and renal function, serum electrolytes, prothrombin time, partial thromboplastin time, platelet count, disseminated intravascular coagulation panel, and gram stain and culture of any uterine discharge.16 Ultrasound may reveal retained intrauterine material, intra-abdominal free fluid, and possibly pelvic abscesses. Other imaging modalities include computed tomography and magnetic resonance imaging, 279

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which may demonstrate uterine emphysema or intraperitoneal air from uterine perforation.

Because the majority of obstetrical infections are polymicrobial, broad-spectrum antibiotics should be given until the causative organisms are identified. A standard regimen includes ampicillin, gentamicin, and either clindamycin or metronidazole.10,15 The patient’s status of tetanus immunization should also be addressed. Currently there are no evidence-based recommendations specific to the obstetric patient who is critically ill or septic. Early goaldirected therapy has shown to improve survival, although these goals were established in nonpregnant patients. Either crystalloids or colloids may be used for volume expansion, and both inotropes and vasopressors are given by protocol to these ill patients who may also be gravid.17 In general, a transfusion threshold at a hemoglobin of 7.0 to 9.0 g/dL is reasonable, and if time allows, type-specific and CMV-safe (leukoreduced) transfusions are preferred.17 Finally, early consultation with OB and general surgery is imperative as laparatomy may be indicated if there is suspicion of uterine perforation, bowel injury, abscess formation, or clostridial infections.

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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estimates of the incidence of unsafe abortion and associated mortality in 2000. 4th ed. Geneva, Switzerland: World Health Organization; 2004.

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Grimes DA, Benson J, Singh S, et al. Unsafe abortion: the preventable pandemic. Lancet. 2006; 368:1908-19.

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Honigman B, Davila G, Petersen J. Reemergence of self-induced abortions. J Emerg Med. 1993; 11:105-12.

5.

Smith JP. Risky choices: the dangers of teens using self-induced abortion attempts. J Pediatr Health Care. 1998; 12:147-51.

6.

Coles MS, Koenigs LP. Self-induced medical abortion in an adolescent. J Pediatr Adolesc Gynecol. 2007; 20:93-95.

7.

Strauss LT, Gamble SB, Parker WY, et al. Abortion surveillance— United States, 2005. MMWR Surveillance Summaries. Nov 28, 2008; 57:1-32. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/ ss5713a1.htm. Accessed March 6, 2009.

8.

Alan Guttmacher Institute. Source Presentation: Trends in abortion in the United States, 1973-2005. January 2008. Available at http://www. guttmacher.org/presentations/trends.pdf. Accessed March 6, 2009.

9.

Glenc F. [Induced abortion—a historical outline]. Pol Tyg Lek. 1974; 29:1957-8 (polish).

10. Singh S. Hospital admissions resulting from unsafe abortion: estimates from 13 developing countries. Lancet. 2006; 268:1887-92.

11. Burnhill MS. Treatment of women who have undergone chemically induced abortion. J Reprod Med. 1985; 30:610-14.

12. Grimes DA, Creinin MD. Induced abortion: an overview for internists.

Ann Intern Med. 2004; 140:620-6.

13. Stubblefield PG, Grimes DA. Current concepts: septic abortion. N Engl J Med. 1994; 331:310-14.

Address for Correspondence: Teresa Saultes, DO, Dept. of Emergency Medicine, Madigan Army Medical Center, Tacoma, WA 98431. Email: teresasaultes@gmail.com

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Finkielman JD, De Feo FD, Heller PG, et al. The clinical course of patients with septic abortion admitted to an intensive care unit.

CONCLUSION We present a case of a woman with an unwanted pregnancy who attempted self-induced abortion with a coat hanger. The ease of air travel, cultural and educational barriers, and diminishing providers who perform legal abortions all contribute to this disease process. Patients often delay treatment and may present to the ED in florid septic shock. A female presenting with abdominal pain, fever, vaginal bleeding, and a positive pregnancy test mandates the consideration of septic abortion. Early goal-directed therapy and broad-spectrum antibiotics should be given with prompt consultation with OB and general surgery. Early recognition and aggressive management of septic abortion is critical to decrease maternal morbidity and mortality.

This manuscript was written as part of official Department of Defense duties and is in the public domain, and therefore copyright cannot be assigned. The views expressed herein are solely those of the authors and do not represent the official views of the Department of Defense or Army Medical Department.

World Health Organization. Unsafe abortion: global and regional

14. Fernández-Pérez ER, Salman S, Pendem S, et al. Sepsis during pregnancy. Crit Care Med. 2005; 33:S286-93.

15. DeCherney AH, Nathan L. Current diagnosis and treatment obstetrics and gynecology. 10th ed. New York, NY: McGraw-Hill; 2007.

16. Stone CK, Humphries R. Current diagnosis and treatment emergency medicine. 6th ed. East Norwalk, CT: McGraw-Hill; 2008.

17. Guinn DA, Abel DE, Tomlinson MW. Early goal directed therapy for sepsis during pregnancy. Obstet and Gynecol Clin N Am. 2007; 34:459-79.

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Review Article

Non-Traumatic Urologic Emergencies in Men: A Clinical Review Chad S Kessler, MD*† Julie Bauml†

* Jesse Brown VA Medical Center, Department of Emergency Medicine, Chicago, IL † University of Illinois at Chicago, Chicago, IL

Supervising Section Editor: Chris Mills, MD, MPH Submission history: Submitted January 20, 2009; Revision Received April 14, 2009; Accepted April 26, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

Although true urologic emergencies are extremely rare, they are a vital part of any emergency physician’s (EP) knowledge base, as delays in treatment lead to permanent damage. The four urologic emergencies discussed are priapism, paraphimosis, testicular torsion, and Fournier’s gangrene.

An overview is given for each, including causes, pathophysiology, diagnosis, treatment, and new developments. The focus for priapism is on diagnosis and distinguishing high-flow from low-flow forms, as the latter requires emergent treatment. For paraphimosis, we describe various methods of relieving the stricture, from manual reduction to surgery in extreme cases. For testicular torsion, the most important factor in salvaging the testicle is decreasing time to treatment. This is accomplished through experience and understanding which signs and symptoms strongly suggest it, so that time-consuming tests are avoided. Lastly, Fournier’s gangrene is potentially fatal. While aggressive medical and surgical therapy will improve chances of survival and outcome, it is vital for the emergency department (ED) physician to diagnose Fournier’s. It often presents in the elderly, immunocompromised, or those with depressed mental status. The goal of this paper is to arm EPs with information to recognize urological emergencies and intervene quickly to preserve tissue, fertility, and life.

[West J Emerg Med. 2009;10(4):281-287.]

PRIAPISM Overview Priapism is a persistent and painful erection lasting more than four hours that is not related to sexual arousal or relieved by sexual intercourse.1 There are two types of priapism: low-flow and high-flow. Low-flow priapism, or ischemic priapism, results from decreased venous and lymphatic drainage of the corpus cavernosum. Highflow priapism is less likely to be ischemic and is most often caused by a traumatic arterial laceration. The main complication of priapism is erectile dysfunction, especially in recurrent ischemic priapism, due to inflammation and fibrosis of the corpus cavernosum.

Causes Most cases of low-flow priapism in adults are secondary to medication or drug use. Drugs of abuse, such as alcohol and cocaine, are important contributors to priapism, especially in heavy users.2 Blood pressure medications such Western Journal of Emergency Medicine

as hydralazine, prazosin, and calcium channel blockers are common causes. Psychiatric medications, also notorious for causing priapism, include trazodone, chlorpromazine, thioridazine, and other selective serotonin re-uptake inhibitors (SSRIs). Oral erectile dysfunction medications like sildenafil, vardenafil, and tadalafil can also lead to priapism (Table).3 Furthermore, blood dyscrasias and hypercoagulable states, such as sickle cell disease, thalassemias, polycythemia, and vasculitis, often cause low-flow priapism.1 The most common cause of high-flow priapism, regardless of age, is arteriovenous fistula formation secondary to perineal trauma, most commonly straddle-type injuries.4 Pathophysiology Several underlying mechanisms cause priapism.

In low-flow priapism, the most common mechanism is sludging of red blood cells, which clogs the spaces of the corpus cavernosum leading to impaired drainage of blood.5 Impaired venous outflow can also lead to thrombosis and 281

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Urologic Emergencies priapism is definitively known. Moreover, a urine toxicology screen for illicit drugs is useful when suspected.2

Table 1. Pathogenesis of priapism MEDICATIONS

NEUROLOGIC

OTHER

Antihypertensives Hydralazine CCBs

Spinal stenosis

Spider bites

Psychiatric Trazadone Chloropromazine Thioridazine

Spinal cord lesions or trauma

Erectile Dysfunction

Total parenteral nutrition (TPN)

Sildenafil/valdenafil Recreational drugs Alcohol Cocaine

Carbon monoxide poisoning

Multiple sclerosis

Blood dyscrasias

CCB, calcium channel blocker.

further ischemia from remaining stagnant blood.3 Highflow priapism is usually caused by an arteriovenous shunt following perineal trauma, which causes abnormally high flow of blood through the caverosum.5 Diagnosis Patients present with an erect, tender penis and soft glans, unrelated to sexual arousal.5 When comparing low- and high-flow states, it should be noted that the highflow state is usually less painful and carries a smaller risk of ischemia.3 Since the recognition of priapism is fairly straightforward, the diagnostic challenge lies in differentiating high- from low-flow states through patient history, as the treatment differs greatly. Generally, highflow priapism patients will have a recent history of perineal trauma, often times a straddle injury. These patients usually seek treatment later in the course as they do not typically experience intense pain, as opposed to low-flow patients.1 The definitive distinction between high- and low-flow states can also be made by penile blood gas, aspirated from the corpus cavernosum. Low-flow priapism is a hypoxic state, so blood appears dark and dusky. Non-ischemic priapism aspirate is well oxygenated and bright red.

An ischemic penile blood gas typically reveals a partial pressure of oxygen (PO2) < 30 mmHg, a partial pressure of carbon dioxide (PCO2) > 60 mmHg, and a pH < 7.25, whereas a non-ischemic state will closely mimic normal arterial blood. Color duplex ultrasonography may also be used to differentiate the two by visualizing flow patterns.

Additionally, a fistula or pseudoaneurysm may be discovered by ultrasound in the high-flow state.2 Complete blood count (CBC), coagulation studies, and a sickle cell screen should be performed.1 Hemoglobin electrophoresis and reticulocyte count can reveal sickle-cell abnormalities or thalassemias and are indicated for all priapism patients unless the cause of Volume X, no. 4 : November 2009

Treatment The first step in the management of priapism, regardless of the cause, is always hydration and analgesia. If the patient has an acute sickle-cell crisis, fluids and analgesia with supplemental oxygen may lead to detumescence.1 For ischemic priapism, subcutaneous terbutaline sulfate (0.25 to 0.5 mg) every 30 minutes as needed is often effective.3 The next step in treatment involves aspiration of cavernosal blood and direct caversonal injection of phenylephrine (100200 mg every 5-10 minutes with a max of 1000 mg).2 A three-way stopcock is recommended so that irrigation can be alternated with aspiration.3 Blood pressure monitoring is vital if attempting to treat with phenylephrine, and often these patients need continuous cardiac telemetry. If there is immediate recurrence after aspiration, the next step is a surgical shunt between the corpora spongiosa and cavernosum.

For high-flow priapism, the treatment strategy is much different. This type of priapism is non-ischemic as arterial blood flow is intact. Thus, it is usually non-emergent and can be observed before deciding upon invasive treatment.

Preserving penile function is of primary concern. Treatment with selective arterial embolization using an autologous clot is highly effective with normal sexual function restoration in 86% of cases.4 Evidence-Based Updates Previously, priapism caused by sickle-cell anemia was treated by transfusing packed red blood cells (RBCs).5 However, that therapy has not been shown to change shortor long-term outcomes and may even cause neurological sequelae.6 Although it is important to screen for sickle cell disease as a cause of priapism, its treatment is currently not different from that of other causes. Sickle-cell priapism should be treated in the same manner as other ischemic priapisms with supplemental oxygen, analgesia and hydration. Eventual exchange transfusions can be performed, but direct blood transfusions are now controversial.3,6 New research focuses on treatment options targeting the underlying pathology of priapism. Phosphodiesterase 5 (PDE5), a molecular effector, has been implicated in recurrent priapism. PDE5 is important in breaking down nitric oxide and restoring normal blood flow to the penis after an erection. In addition, drugs which limit the fibrotic response in priapism, and therefore limit potential erectile dysfunction, are being studied. Notably, antioxidants are being investigated as a possible treatment, although effectiveness has not been established.2,7,8 The theory is that antioxidants will relieve some of the post-ischemic reperfusion injury, thus limiting cavernosal fibrosis and muscle damage.

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trauma, and hair tourniquets can all have similar presentations to paraphimosis. When considering paraphimosis, it is important to distinguish between various infections and strictures of the penis. To clarify, balanitis is an infection of the glans only, whereas balanoposthitis is an infection of the glans and the foreskin.

Figure 1. Paraphimosis with non-retractable foreskin and distal swelling (reprinted with permission)10

PARAPHIMOSIS Overview Paraphimosis occurs when the foreskin becomes fixed in the retracted position and cannot be reduced, therefore constricting venous return from the glans. Without immediate treatment this causes edema, induration, ischemia, and eventually necrosis of the glans.

Causes The most common cause of paraphimosis is previous phimosis (fibrosis and constriction of the prepuce distal to the glans preventing retraction).9 This leads to a circular scar, which can then form a tourniquet when the foreskin is retracted, preventing proper venous and lymphatic drainage.

Another significant cause of paraphimosis is iatrogenic, when medical staff fails to reduce the foreskin after urethral catheterization or genital exam. Other causes of paraphimosis include poor urogenital hygiene, chronic balanoposthisis, and genital piercing.5

Diagnosis Typically, patients present with edema and pain of the glans and the inability to pull back the retracted foreskin.

Diagnosis is usually straightforward as the stricture caused by the prepuce of the non-retractable foreskin and the resulting edema is easily visualized (Figure 1). Allergic reactions, Western Journal of Emergency Medicine

Treatment The primary concerns with regard to treatment of paraphimosis are to relieve any significant pain and prevent further ischemia to the glans. First, manual reduction of the foreskin should be attempted. A penile nerve block or ice can often minimize patient discomfort and lead to a successful decompression. The glans should be compressed to reduce the edema during the attempt to replace the foreskin. If the foreskin cannot be reduced within a few attempts this effort should be terminated so as not to cause more irritation and swelling. Needle punctures into the inflamed portion of the penis to remove blood can help decrease the size of the glans and help facilitate manual reduction as well. If these measures fail, a urologist should be consulted to perform a dorsal slit procedure. A dorsal slit procedure entails incising the fibrotic ring of the prepuce to relieve the constriction and reduce the foreskin. Circumcision is the definitive treatment and will prevent any future episodes.3,5 Evidence-Based Updates Alternative treatments for paraphimosis, especially popular in Europe, involve creative ways of decreasing the edema to the glans and facilitating reduction. The first concept is based on applying a high concentration of sugar to the outside of the glans in order to osmotically draw water out and reduce swelling. Granulated sugar can be directly applied, but it is not always on hand in the ED. An alternative is to soak gauze in 50mL of 50% dextrose and apply. At this time, there are no randomized controlled studies documenting the efficacy of this procedure, and evidence exists only in case reports. Another way of decreasing edema is to inject 1mL of hyaluronidase (250 U/mL) into the prepuce.11 Hyaluronidase can break down hyaluronic acid in the extracellular fluid, decreasing tissue resistance and increasing solute diffusion between tissues.12 The risk with these procedures is that they delay resolution of the ischemia to the glans by one to two hours. Therefore, although these procedures are safe, they should be attempted only after reduction with penile block alone fails and the patient wishes to avoid dorsal slit procedure or circumcision. Another method to decrease swelling that can be effective up to 90% of the time is to soak the penis in a glove full of ice for five minutes before attempting manual reduction.13 It should be noted that sufficient evidence does not exist for any of these treatments of paraphimosis. The largest case studies for these methods are as follows: use of sugarâ&#x20AC;&#x201D; three patients,14 iced gloveâ&#x20AC;&#x201D;10 patients,13 and multiple needle 283

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Urologic Emergencies position, this is called a “bell-clapper deformity” (Figure 2), which predisposes to torsion.3 This deformity is present in up to 12% of the male population.18 In adults, incomplete attachment of the gubernacula is a more common predisposing malformation.5 Both malformations leave the testicle free to rotate. Furthermore, torsion might also be caused by strong cremasteric reflex during nocturnal erections, although this has yet to be well established in the literature.1

Figure 2. “Bell-clapper” deformity predisposing to testicular torsion17

punctures—39 patients.15 Prospective, randomized controlled studies would be invaluable in identifying the best method(s) of treating paraphimosis.

TESTICULAR TORSION Overview Testicular torsion results from a twisting of the spermatic cord, which impedes blood flow to the testis and impairs venous drainage, resulting in edema, ischemia, and necrosis.

Testicular torsion has a bimodal age distribution with the first peak at age 1-2 years old and the second higher peak in adolescence. Torsion is fairly uncommon in adults over 40.5 Speed of diagnosis and time to treatment is vital in preserving patients’ testes and fertility. If detorsion occurs within four hours, the salvage rate is 96%, which drops precipitously to 10% after 24 hours.3 Although not always the cause of an acute scrotum, testicular torsion needs to remain high on the differential until proven otherwise as “time is testicle.”

Important complications of testicular torsion include infertility and possible autoimmune attack of the contralateral testicle, as a response to the destruction of necrotic tissue and breakdown of the blood-testicular barrier in the affected testicle.16 Pathophysiology The basic pathophysiology behind testicular torsion is a malformation in which the testicle is allowed to rotate more freely around the spermatic cord. The most common abnormality is a malformed tunica vaginalis. The tunica vaginalis normally attaches the superior pole of the testes to the posterior scrotum, fixing it in place. When the vaginalis instead extends over the whole testicle, fixing it in a horizontal Volume X, no. 4 : November 2009

Diagnosis The most common presentation is that of acute scrotal pain and swelling, often with a high-riding testicle and an absent cremasteric reflex. History is extremely important in differentiating testicular torsion from other common causes of acute scrotum, such as appendiceal torsion and epidydimitis.1 Testicular torsion has a quicker onset of pain, whereas epidydimitis and appendiceal torsion typically have more subacute presentations.3 Patients with testicular torsion often have experienced previous bouts of pain indicating intermittent torsion. Testicular appendages are embryologic remnants of ductal structures. Torsion of these structures causes local hemorrhage, which often presents with a bluish discoloration on the skin. The presence of localized tenderness over the superior pole of the testis along with this “blue dot sign” is highly suggestive of appendiceal torsion. Early appendiceal torsion may be differentiated by history and exam from testicular torsion, but as it progresses, swelling obscures the blue dot sign and makes point tenderness of the superior pole more difficult to appreciate.18 Moreover, epidydimitis is more common after puberty (due to sexual activity) and torsion of the appendage is more common in prepubertal boys. Additionally, palpation of the spermatic cord usually reveals tenderness in epidydimitis but not in torsion.19 A positive Prehn’s sign (relief of pain upon elevation of the scrotum) points away from torsion and suggests epidydimitis but is an unreliable test with poor sensitivity.5 The cremasteric reflex is intact in epidydimitis but absent in testicular torsion.

Absent cremasteric reflex is the most sensitive sign of testicular torsion with two retrospective studies20,21 showing 100% sensitivity for testicular torsion in boys older than 30 months.22 Urinalysis showing pyuria and leukocytosis suggests epidydimitis as do urinary symptoms such as dysuria, urgency, and frequency. Further symptoms such as nausea and vomiting are more common in testicular torsion than in appendiceal torsion or epidydimitis. In conjunction with scrotal pain, nausea and vomiting in children or adolescents has a 96% positive predictive value for torsion.1,23 In the past, nuclear scintigraphy had been used to distinguish between testicular torsion, epidydimitis, and torsion of the appendix. However, it has largely been replaced by color flow doppler where available, as it is quicker to use and simultaneously analyzes the anatomy of the spermatic cord and testicle.19 Color flow doppler is both sensitive

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Salvage rate (%)

Urologic Emergencies

zinc aspartate, and caffeic acid phenethyl ester (CAPE).

Allopurinol has mixed results in rat trials with one study showing no histological improvements after reperfusion versus control25 and another showing significant improvement in tissue damage when using lipid peroxidation byproducts as a surrogate marker for oxidative injury.26 Another study illustrated biochemical changes and decreased injury with allopurinol compared with melatonin that demonstrated histological improvement as well.27 N-acetylcysteine has been shown to decrease post-reperfusion apoptosis of germ cells in rats,28 and zinc aspartate and CAPE have shown decreased histological damage.29,30 All of the preceding studies are relatively new and require further animal and human testing before clinical use.

100 90 80 70 60 50 40 30 20 10 0 0

5

10

15

20

25

30

Time (hours)

Figure 3. Testicular torsion salvage rates over time24

and specific, 89.9% and 98.8% respectively.18 Computed tomography (CT) scans provide detailed anatomical information but carry a radiation exposure risk for the testicles and also fail to provide information about blood flow to the testes. Of note, obtaining diagnostic tests should not delay surgical exploration and repair. These tests are used only when history and physical provide equivocal findings.5 No one sign or symptom establishes the diagnosis of torsion. Ultimately, clinical judgment is always best in evaluating testicular pain and swelling.

Treatment Time is of the essence in attempting to salvage an ischemic testicle, as salvage rates rely heavily on a speedy diagnosis (Figure 3). Treatment consists of emergent surgery to detorse the affected testicle and attach it properly to the scrotal wall. This procedure is also done on the unaffected testicle as malformations which contribute to testicular torsion are often bilateral.23 When suspicion of torsion is high, the only appropriate step is immediate surgical consultation to save as much tissue as possible. While waiting for surgical intervention, manual detorsion of the testicle by using a medial to lateral rotation or “dialing out” can be attempted.

If successful, this can restore some blood flow and provide temporary pain relief. However, it is not definitive treatment and surgical consultation is still required.3,5 Evidence-Based Updates In most instances, surgical repair is the best and most appropriate treatment for testicular torsion. However, there is new research focused on the post-surgical setting looking at medical treatments that may limit reperfusion injury and help preserve testicular function. The list of proposed medications is exhaustive with more than 40 researched agents, usually investigated in rats. The most frequently discussed medications include allopurinol, melatonin, N-acetylcysteine, Western Journal of Emergency Medicine

Fournier’s Gangrene Overview Fournier’s gangrene is a necrotizing fasciitis of the perineum which can quickly spread to the skin of the entire scrotum and penis. It is usually caused by a polymicrobial infection. Fournier’s affects all ages and both genders. This condition is life-threatening with a mortality rate of 13-22% despite timely and aggressive therapy.5,31 Causes In Fournier’s gangrene, 50-60% of infections stem from a gastrointestinal (GI) or genitourinary (GU) source.

Immunocompromised patients, especially diabetics and alcoholics, with or without trauma or instrumentation are at significant risk. Additionally, the infection is most aggressive when both aerobic and anaerobic bacteria are involved.3 The most commonly cultured organisms include E. coli, bacteroides, and staphylococci. The most likely culprit for an infection of colorectal origin is clostridium.5 Pathophysiology The process begins locally with infection in the skin and spreads down the fascial plane where inflammation, ischemia, and necrosis result. The low oxygen content and necrosis potentiate the effects of the anaerobic bacteria and cause rapid dissemination of the infection.3 Diagnosis Patients typically present with genital induration, pain, erythema, and crepitus. A plain radiograph or CT may demonstrate air in the perineal tissues.1 Although diagnosis is straightforward when the lesions are found (Figure 4), failure to examine the genitals, especially in the elderly or obtunded patient, can result in misdiagnosis. Additionally, finding the nidus of infection, if one exists, is important. If a periurethral source is suspected, a retrograde urethrogram should be performed. If a perirectal source is suspected, proctoscopy may be revealing.5 It is also important to elicit a history of

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Urologic Emergencies for quick, decisive action, require that EPs be vigilant and knowledgeable. For priapism the major difficulty lies in differentiating high-flow from low-flow states as low-flow requires more immediate treatment. For paraphimosis, it is important to understand the various methods of reduction: manual with analgesia, dorsal slit procedure, and circumcision. Testicular torsion diagnosis relies heavily on history and physical. With high clinical suspicion, an EP should never wait for a confirmatory test to consult with an urologist. Lastly, in Fournier’s gangrene, a thorough physical exam, especially in the elderly and immunocompromised, can lead to diagnosis and prompt treatment of this potentially fatal infection. In order to decrease permanent tissue damage, reduce infertility and save lives, a vigilant EP will always be mindful of these four non-traumatic urologic emergencies.

Acknowledgements The authors would like to thank Dr. Henry Pitzele and Dr. Wesley Eilbert for their time and help in reviewing this manuscript.

Figure 4. Fournier’s gangrene with spreading necrosis along fascial planes (reprinted with permission)32

perineal trauma, as even superficial scratches or burns can be the initiating event.

Address for Correspondence: Chad Kessler, MD, FACEP, Department of Emergency Medicine, Jesse Brown VA Hospital, 820 S. Damen Ave., Chicago, IL 60612. Email Chad.kessler@va.gov.

Treatment Treatment of Fournier’s gangrene relies on an aggressive medical and surgical approach. Medical treatment includes rapid fluid resuscitation and broad spectrum antibiotics to cover gram positive, gram negative, clostridium and anerobes.3 Surgical debridement is the most important treatment and should be followed by aggressive wound care with frequent dressing changes and re-debridement if required.31 Genital skin is highly elastic and grafts are not required unless over 60% of the skin is removed. A cosmetically acceptable scrotum can generally be restored post-debridement. Suprapubic catherterization may be necessary depending on the extent of the damage.1

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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Am. 2004; 88: 495-518.

2.

Evidence-Based Updates Hyperbaric oxygen (HBO) has traditionally been used as adjunctive therapy for Fournier’s, although randomized controlled trials of effectiveness are lacking. Studies preformed as recently as 2005 have failed to show a significant difference in morbidity or mortality associated with hyperbaric oxygen. Moreover, in one study, the author showed that patients required an average of six treatments at $600$1300 each.33 A small trial in 2008 from a regional burn center with expertise in HBO echoed these findings and was also not able to show improved outcome. The generalized use of HBO for Fournier’s gangrene cannot be routinely recommended.

Conclusion True urologic emergencies presenting to the ED are rare. However, the difficulty in differentiating these emergencies from more common conditions and the need Volume X, no. 4 : November 2009

Rosenstein D, McAninch J. Urologic Emergencies. Med Clin North Burnett AL, Bivalacqua TJ. Priapsim Current Principles and Practice.

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Wagner MJ. PEER VII: Physician’s evaluation and educational review in emergency medicine. ACEP; 2006 (revised 2007).

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Numan F, Cantasdemir M, Ozbayrak M, et al. Posttraumatic Nonischemic Priapism Treated with Autologous Blood Clot Embolization. J Sex Med. 2008; 5:173-9.

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Merritt AL, Haiman C, Henderson SO. Myth: Blood transfusion is effective for sickle-cell anemia associated priapism. CJEM. March 2006; 8:119-22.

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Muneer A, Cellek S, Ralph DJ, et al. The investigation of putative agents, using an in vitro model, to prevent cavernosal smooth muscle dysfunction during low-flow priapism. BJU Int. 2008; 102:988-92.

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Burnett, AL. Molecular pharmacotherapeutic targeting of PDE5 for preservation of penile health. J Andrology. 2008; 29:3-14.

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Filippone, LM. Diagnosis: Paraphimosis. Emerg Med News.

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resource. Available at: http://www.surgical-tutor.org.uk/default-home.

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11. Little B, White M. Treatment options for paraphimosis. Int J Clin

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26. Silva AC, Ortiz V, Silva RA, et al. Effect of allopurinol on rat testicles

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paraphimosis. Ann Roy Coll Surg. 2001; 83:126-7.

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14. Gonzalez FM, Sousa EMA, Parra ML. Sugar: treatment of choice in

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15. Houghton GR. The “iced-glove” method of treatment of paraphimosis.

BJS. 1973; 60:876-7.

Surg. 2004; 39:1238-41.

28. Payabvash S, Salmasi AH, Kiumehr S, et al. Salutary effects of

16. Kapoor S. Testicular torsion: a race against time. Int J Clin Pract.

N-acetylcysteine on apoptotic damage in a rat model of testicular

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17. Shah BR, Lucchesi M. Atlas of Pediatric Emergency Medicine. New

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18. Gatti, JM. Current management of the acute scrotum. Semin Pediatr

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19. Galejs LE, Kass EJ. Diagnosis and treatment of the acute scrotum.

30. Atik E, Görür S, Kiper AN. The effect of caffeic acid phenethyl

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20. Kadish HA, Bolte RG. A retrospective review of pediatric patients with epididymitis, testicular torsion, and torsion of testicular appendages.

reperfusion injury. Pharmocol Res. 2006; 54:293-7.

31. Cohen MS. Current experience and management of Fournier’s

Pediatrics. 1998; 102:73-6.

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21. Rabinowitz R. The importance of the cremasteric reflex in acute scrotal swelling in children. J Urol. 1984; 132:89-90.

Assoc; 1983.

32. Parks J. Buckeye Surgeon: Fournier’s Gangrene. Available at:

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Case Report

Bilateral Psoas Abscess in the Emergency Department Eric B. Tomich, DO David Della-Giustina, MD

Madigan Army Medical Center, Department of Emergency Medicine, Tacoma, WA

Supervising Section Editor: Chris Mills, MD Submission history: Submitted June 13, 2008; Revision Received August 4, 2008; Accepted November 10, 2008 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

We present the case of a 45-year-old female who presented multiple times to the emergency department with acute low back pain and was subsequently diagnosed with bilateral psoas muscle abscess. Psoas abscess is an uncommon cause of acute low back pain that is associated with high morbidity and mortality. The onset of symptoms is frequently insidious and the clinical presentation vague. Proper diagnosis requires vigilance of the physician to recognize signs in the history and physical examination that are suggestive of a potentially serious spinal condition and initiate further workup.

While most patients with acute low back pain have a benign etiology, this case report demonstrates the challenge of diagnosing a patient with bilateral psoas abscess who had few known risk factors and symptoms typical of mechanical low back pain.

[West J Emerg Med. 2009;10(4):288-291.]

CASE REPORT A 45-year-old white female initially presented to the emergency department (ED) with a chief complaint of a traumatic severe left lower back pain for three days. The pain was sharp and radiated down her left anterior thigh. The pain worsened with movement and improved with rest, but persisted when lying still. Associated symptoms included dysuria and mild generalized abdominal pain. Past medical and surgical history was significant for genital herpes, iron deficient anemia, and hemorrhoidectomy. She took no prescription medicine. Social history was positive for tobacco use, but she denied alcohol or recreational drug use.

Her job was labor intensive and involved heavy lifting. She first noticed the pain with associated stiffness upon waking the morning after a work shift. She denied trauma, fevers, rigors, weight loss, nausea, vomiting, diarrhea, constipation, vaginal bleeding or discharge, weakness or numbness in the lower extremities, and urinary incontinence. On physical examination she was afebrile with normal vital signs. She was in obvious discomfort and unable to sit up straight due to pain.

Her gait was antalgic. She had tenderness to palpation and increased tone over her left lumbar paraspinal musculature.

Her strength, reflexes and sensation of the lower extremities were normal. The remainder of the physical exam was unremarkable. She was diagnosed with lumbosacral strain and discharged home with a prescription of opiate analgesics.

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The patient returned to the ED via ambulance four days later, tearful and writhing in pain. Her vital signs were normal.

The physical examination was essentially unchanged from her previous encounter. Specifically, there was no midline spinal tenderness or neurologic deficits in the lower extremities.

Straight leg testing was negative with reproduction of the back pain but without radiation. Plain spinal radiographs showed degenerative changes but no acute process. She was treated with intravenous (IV) opiates and antiemetics and was discharged to home when she stated her pain had diminished.

Four days later, or eight days after her initial presentation, she returned to the ED with worsening back pain and intermittent fevers up to 103째F. The pain was now located across the whole lower back with associated radiation down both anterior thighs. Heart rate and blood pressure were normal. On examination she had tenderness to palpation of the lumbar region with exacerbation of the pain upon flexion and extension of the trunk. Laboratory exam revealed a hemoglobin of 10.3 g/dl; white blood cell count of 8300 cells/mm3; and a negative urinalysis. IV opiates and benzodiazepines provided little relief. A non-contrast CT scan of the lumbar spine showed several small areas of low attenuation with peripheral enhancement in the medial margins of both psoas muscles (Figure 1). The largest of these collections measured 1.4 cm x 1.2 cm on the right and was consistent with psoas abscess collection. There was also

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with those of the iliacus to form the iliopsoas, which functions as the chief flexor of the hip. Innervation arises from the lumbar plexus via branches of the L2-L4 nerves. The psoas is surrounded by a rich venous plexus, which could explain its predisposition to infection from hematogenous spread.2

Figure 1. Non-contrast CT scan of lumbar spine with arrow pointing to abscess in right psoas muscle. Note presence of abscess in the left psoas muscle along the medial border.

abnormal enhancement of the paravertebral soft tissue near L3-L5, which was suspicious for diskitis. She was admitted to the hospital and started on IV ceftriaxone, metronidazole, and clindamycin for broad spectrum coverage, including anaerobes. A triple-contrast CT of the abdomen and pelvis to rule out an abdominal source of infection resulting in secondary extension to the psoas muscle was negative. MRI of the lumbar spine showed no signs of diskitis or vertebral osteomyelitis. On the second hospital day she underwent CT-guided drainage of the largest abscess in the right psoas muscle. This procedure resulted in approximately 1 mL of purulent fluid that revealed many white and red blood cells, and gram positive cocci. The fluid culture was positive for methicillin-sensitive Staphylococcus aureus (MSSA). The antibiotic regimen was changed to oral cephalexin. Two days following abscess drainage she was discharged home in stable condition. In follow up with her primary physician two weeks later she tested negative for HIV and a urine toxicology screen was positive for cocaine.

DISCUSSION Anatomy The psoas muscle originates from the lateral borders of the 12th thoracic to the 5th lumbar vertebrae in the retroperitoneal space and inserts at the lesser trochanter of the femur. In 70% of people it is a single structure known as the psoas muscle, but 30% have the psoas minor that lies anterior to the major.1 The fibers of the psoas muscle blend Western Journal of Emergency Medicine

Etiology and Epidemiology Back pain is second only to upper respiratory infections as a cause for symptom-related visits to primary care physicians.3 Acute low back pain is defined as pain present for six weeks or less.4 Psoas abscess can be classified as either primary or secondary. The etiology of primary psoas abscess remains uncertain. Current literature suggests that it results from either hematogenous spread from occult infection or local trauma with resultant intramuscular hematoma formation, which predisposes to abscess formation.5,6 Primary psoas abscess occurs most commonly in patients with a history of diabetes, injection drug use, alcoholism, AIDS, renal failure, hematologic malignancy, immunosuppression, or malnutrition.

Additional risk factors include age under 20 years, males (3:1 predominance), and low socioeconomic status.5-8 In the United States, primary psoas abscess makes up 61% of cases.

The predominant organism is Staphylococcus aureus (over 88%), followed by Escherichia coli and Streptococcus.1,5,8,9 Secondary psoas abscess is often caused by a mixed flora of enteric bacteria, commonly E. coli and Bacteroides.9 Mycobacterium tuberculosis infection of the spine, known as Pott’s disease, is the most frequent cause of secondary psoas abscess in developing countries.8 Conditions associated with secondary psoas abscess include Crohn’s disease, diverticulitis, appendicitis, colorectal cancer, urinary tract infection, vertebral osteomyelitis, mycotic abdominal aortic aneurysm, endocarditis, and history of instrumentation in or around the spine.1,5 It is noteworthy that bilateral psoas abscess occurs in just 3% of all cases, primary or secondary.10 History and Physical Symptoms are often nonspecific, which makes it difficult to make the diagnosis at the initial visit. The classic triad of fever, back pain, and psoas spasm is present in only 30% of patients.11 Other common symptoms include malaise, weight loss, nausea, anorexia, and pain that radiates to the flank, groin, or anterior thigh.5,6,8 Back pain is the most frequently encountered symptom, with a mean duration of 10.6 days before presentation.11 On examination, the presence of a limp, palpable mass in the inguinal region, severe pain upon passive hyperextension of the hip or active flexion of the psoas against the examiner’s hand can be specific for psoas abscess.5 Correct and early diagnosis is difficult, with arthritis, vertebral osteomyelitis, lumbar strain, and abdominal/urologic disorders being the most common alternative diagnoses.11,12 Patients that present with symptoms of septic shock or those with a Mycobacterium

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tuberculosis etiology are even less likely to have classic signs and symptoms which may delay definitive diagnosis and treatment.13,14 Laboratory and Radiological Testing In general, laboratory testing is nonspecific in diagnosing psoas abscess; however, abnormal results may prompt one to pursue infection as a source of the patientâ&#x20AC;&#x2122;s symptoms.

If there is any concern of infection, whether it be diskitis or psoas abscess, then a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), blood cultures, and urinalysis (UA) may be helpful.1,6,8 In a retrospective review of 11 cases, leukocytosis was the most common laboratory finding.15 Blood cultures are positive in about 50% of patients.8 ESR and CRP will generally be elevated and may be useful in following the disease course.

Pyuria and anemia are also common.6 Plain radiographs are typically unremarkable unless there is underlying diskitis or vertebral osteomyelitis that has been present for several weeks. Because ultrasound is diagnostic in only 60% of cases and MRI appears to have no better than the 90% sensitivity and 80% specificity of CT for diagnosing psoas abscess,1 IV contrast-enhanced spiral CT has become the gold standard in imaging.8 However, MRI is better than CT at imaging the spinal canal and provides a more complete evaluation for all potential sources of back pain. CT of the abdomen and pelvis with oral and IV contrast should also be considered, especially in cases where secondary psoas abscess is suspected.

Ultimately, definitive diagnosis and treatment is achieved with CT-guided drainage and culture of fluid.6 Management and Outcomes The initial treatment of primary psoas abscess involves the empiric use of IV anti-staphylococcal antibiotics since nearly 90% are due to S. aureus. These should have coverage against most gram positive organisms, including MRSA, with vancomycin, linezolid or clindamycin being appropriate choices. In secondary psoas abscess a mixed flora of enteric pathogens predominate. Antibiotics need to have coverage for both gram negative and anaerobic bacteria. Fluroquinolones, anti-psuedomonal penicillins, late generation cephalosporins, plus or minus metronidazole should be used empirically for maximal coverage.11,16 The antibiotic regimen can later be changed to reflect the results of the culture and sensitivity profile and in general is continued for two weeks after abscess drainage.2 CT-guided percutaneous drainage (PCD) or surgical drainage are the two definitive treatment modalities. PCD is less invasive and is currently the treatment of choice, especially in primary psoas abscess.17 Surgical drainage is indicated when PCD fails, or if there is a contraindication to PCD or abdominal pathology that requires intervention. Surgical drainage has been associated with shorter hospital stays when compared to PCD in secondary abscess due to the higher incidence of concurrent Volume X, no. 4 : November 2009

intra-abdominal pathology.18 Mortality rates for primary and secondary psoas abscess are 2.4% and 18.9% respectively.16 Death is usually due to inadequate or delayed treatment, with mortality close to 100% in patients who did not undergo drainage, most often from sepsis.6,16 CONCLUSION Psoas abscess is an unusual cause of back pain that is often missed initially, as illustrated by this case. Perhaps if our patient had admitted to illicit drug use, as was discovered at a subsequent outpatient visit, the diagnosis could have been made sooner. It is still unknown whether she was using injection drugs, but with her ultimate diagnosis of primary psoas abscess secondary to MSSA coupled with a negative HIV test and no history of diabetes or immunosuppressed state, it seems plausible. Our patientâ&#x20AC;&#x2122;s management was consistent with the literature as to antibiotic choices and abscess drainage, resulting in a favorable outcome. It is important for emergency physicians to be aware of signs and symptoms suggestive of a serious spinal condition and initiate further workup. One should consider psoas abscess as a cause of back pain in the patient who presents with known risk factors: fever, unremitting pain, pain on hyperextension of the hip, and evidence of psoas spasm.

Laboratory testing is helpful but not sufficient to confirm or rule out the diagnosis; therefore spinal imaging with CT or MRI is the test of choice to make the diagnosis. All patients with psoas abscess require hospitalization for surgical or percutaneous drainage and treatment with antibiotics.

Address for Correspondence: Eric B. Tomich, DO, Madigan Army Medical Center, Department of Emergency Medicine, Bldg 9040 Fitzsimmons Ave, Tacoma, WA 98431. Email: eric.tomich@ us.army.mil The opinions or assertions contained herein are the private views of the authors and not to be construed as official or reflecting the views of the Department of the Army, the Department of Defense or the U.S. Government.

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

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Riyad MN, Sallam MA, Nur A. Pyogenic psoas abscess: discussion of its epidemiology, etiology, bacteriology, diagnosis, treatment and prognosis-case report. Kuwait Med J. 2003; 35:44-47.

2.

Taiwo B. Psoas abscess: a primer for the internist. South Med J. 2001; 94:2-5.

3.

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Bratton RL. Assessment and management of acute low back pain.

12. Muckley T, Schultz T, Kirschner M, et al. Psoas abscess: the spine as

Am Fam Physician. 1999; 60:1-9.

5.

a primary source of infection. Spine. 2003; 28:106-13.

Mallick IH, Thoufeeq MH, Rajendran TP. Iliopsoas abscess. Postgrad

13. Perez-Fernandez S, de la Fuente J, Fernandez FJ, et al. Psoas

Med J. 2004; 80:459-62.

6.

abscesses: an updated perspective. Enferm Infecc Microbiol Clin.

Thongngarm T, McMurray RW. Primary psoas abscess [letter]. Ann

2006; 24:313-8.

Rheum Dis. 2001; 60:173-6.

7.

14. Hamono S, Kiyoshima K, Nakatsu H, et al. Pyogenic psoas abscess:

Walsh TR, Reilly JR, Hanley E, et al. Changing etiology of iliopsoas

difficulty in early diagnosis. Urol Int. 2003; 71:178-83.

abscess. Am J Surg. 1992; 163:413-16.

8.

15. Lee YT, Lee CM, Su SC, et al. Psoas abscess: a ten year review. J

Isdale AH, Nolan DF, Butt WP, et al. Psoas abscess in rheumatoid

Microbiol Immunol Infect. 1999; 32:40-46.

arthritis-an inperspicuous diagnosis. Br J Rhuemato. 1994; 33:853-8.

9.

16. Gruenwald I, Abrahamson J, Cohen O. Psoas abscess: case report

Vandenberge M, Marie S, Kuipers T, et al. Psoas abscess: report of a series and review of the literature. Neth J Med. 2005; 63:413-6.

and review of the literature. J Urol. 1992; 147:1624-6.

17. Dinc H, Onder C, Turhan AL et al. Percutaneous drainage of

10. Bresee JS, Edwards MS. Psoas abscess in children. Pediatr Infect

tuberculosis and nontuberculosis psoas abscess. Eur J Radiol.

Dis J. 1990; 9:201-6.

11. Chern CH, Hu SC, Kao WF, et al. Psoas abscess: making an early

1996; 23:130-4.

18. Procaccino JA, Laury IC, Fazio VW, et al. Psoas abscess: difficulties

diagnosis in the ED. Am J Emerg Med. 1997; 15:83-8.

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encountered. Dis Colon Rectum. 1991; 34:784-9.

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Case Report

Lidocaine Toxicity Misinterpreted as a Stroke Benjamin Bursell, MD Richard M. Ratzan, MD Alan J. Smally, MD

University of Connecticut School of Medicine, Division of Emergency Medicine, Hartford, CT

Supervising Section Editor: Teresita M. Hogan, MD Submission history: Submitted May 25, 2008; Revision Received October 17, 2008; Accepted May 10, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

For more than 50 years lidocaine has been used to treat ventricular arrhythmias. Neurologic dysfunction, manifested as a stroke, occurred acutely in an 87-year-old woman after she had been administered repeated doses of lidocaine, a lidocaine infusion, then an intravenous amiodarone infusion for ventricular tachycardia. This was ultimately diagnosed as lidocaine toxicity with a serum lidocaine level of 7.9 mg/L (1.5 - 6.0 mg/L). We discuss lidocaine toxicity and risk factors leading to its development, which include particularly hepatic dysfunction, cardiac dysfunction, advanced age and other drug administration.

[West J Emerg Med. 2009;10(4):292-294.]

INTRODUCTION Sudden cardiac death, most commonly caused by ventricular tachycardia or fibrillation, affects over half a million people in the United States each year.1 Intravenous lidocaine has been administered for the treatment of ventricular arrhythmias for over 50 years and is still commonly used to treat these arrhythmias, although it is no longer considered first line therapy.2 Newer antiarrhythmics are replacing lidocaine for many indications and are sometimes concomitantly administered with potential drug interactions. If prescribers are aware of the presentation of lidocaine toxicity and its precipitants they can better avoid complications. We describe a patient in whom a lidocaine bolus and drip successfully abolished ventricular arrhythmias who was then administered concurrent amiodarone. This precipitated severe neurologic deterioration suggesting stroke.

We will review the dosing, metabolism, and other factors that contribute to decreased metabolism of lidocaine with severe neurologic toxicity.

CASE REPORT Near midday an 87-year-old woman activated 911 complaining of shortness of breath. The patientâ&#x20AC;&#x2122;s past history was significant for myocardial infarction. A recent echocardiogram showed left ventricular hypokinesis consistent with an ischemic cardiomyopathy with an ejection fraction of 20 to 25%. Previous magnetic resonance imaging showed a 9x11x16 mm meningioma, without metastasis, edema or hydrocephalus. Her medications included verapamil, Volume X, no. 4 : November 2009

timolol, and diazepam.

The initial assessment by paramedics at 1320 described an alert and appropriate patient with pupils equal, round and reactive; the breathing was not labored, lungs were clear, and finger stick glucose was 139. The rhythm was ventricular tachycardia. Paramedics gave 50mg lidocaine intravenous (IV) push, with resolution of the tachycardia to a narrow complex sinus rhythm at a rate of 80 beats per minute. The rhythm was stable for one to two minutes, then recurred.

They administered a second dose of lidocaine 50mg IV push, resulting in resolution of the tachycardia to a sinus rate of 78 beats per minute. The patient reported a decrease in shortness of breath and some mild dizziness. Paramedic personnel initiated a lidocaine drip at 2mg/minute for transport to the emergency department (ED).

In the primary ED, 28 minutes later, the patient had a ventricular rate of 152 beats per minute. She received a third 50mg dose of lidocaine IV. Her electrocardiogram (EKG) revealed normal sinus rhythm with left ventricular hypertrophy and an anteroseptal infarct of indeterminate age.

At 1413 the physician increased the lidocaine drip to 4mg/ minute, and administered aspirin 325mg by mouth. Shortly thereafter, the patient received a loading dose of amiodarone 150mg IV, followed by an amiodarone drip at 1mg/minute.

She then came via EMS to our hospital.

En route emergency medical service personnel noted the patient to be in normal sinus rhythm with ventricular ectopy. The lidocaine drip remained at 4mg/minute and the amiodarone drip at 1mg/minute. The IV pump delivering

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Lidocaine Toxicity as a Stroke amiodarone failed 20 minutes into the transfer and the medication discontinued. During transfer the report notes that the patient complained of “being sleepy” but was alert and appropriate. Six minutes prior to arrival the patient’s mental status changed abruptly. She became non-verbal, her eyes remained open with a fixed gaze, but she was able to flex her hands on command.

Upon arrival to our ED the patient’s vitals signs were: heart rate 76 beats/min, respiratory rate 22 per minute, blood pressure 135/65, tympanic temperature 96.4°F, and oxygen saturation 92% on 15-liter flow nonrebreather mask.

Her weight was 49 kilograms. Her airway was patent. The EKG monitor showed normal sinus rhythm. The patient was unresponsive to painful stimuli with pupils 4mm and nonreactive with intact gag reflex. Plantar reflexes were neutral. Given the patient’s abrupt change in mental status, brainstem stroke was considered and we consulted neurology.

We ordered an expedited computerized tomographic scan (CT) of the head 19 minutes after arrival. Two minutes later she received 0.4mg naloxone intraveniously and the lidocaine drip was discontinued. The patient’s National Institute of Health (NIH) stroke score was 24, indicating severe neurologic impairment.

Initial imaging studies included a chest x-ray with the only abnormality being an enlarged cardiac silhouette. CT scan of the head revealed mild microvascular ischemic changes. An 11 mm partially calcified right falcine mass was consistent with a stable meningioma. CT angiography examination in the ED 51 minutes after arrival demonstrated no evidence of vaso-occlusive change affecting the cervical or intracranial arterial vessels. Laboratory values drawn 19 minutes after arrival at our facility were as follows: Sodium 135 mmol/L, potassium 3.7 mmol/L, chloride 103 mmol/L, bicarbonate 19 mmol/L, creatinine 0.7 mg/dL, blood urea nitrogen 19 mg/dL, glucose 164 mg/dL, Mg 1.6 mg/ dL, phosphorus 4.8 mg/dL, ionized calcium 1.10 mmol/L (reference 1.17-1.33 mmol/L). Cardiac enzymes, creatinine kinase (CK), CKMB and Troponin-T were normal. The initial arterial blood gas obtained on room air showed a pH of 7.28; the pCO2 was 44 mmHg, pO2 63 mmHg, and oxygen saturation 87%. The serum lidocaine level drawn 51 minutes after arrival, 30 minutes after the lidocaine drip was discontinued, resulted 7.9 mg/L with a reference range in our laboratory of 1.5-6.0 mg/L. Following termination of the lidocaine drip the patient’s mental status gradually and steadily improved. By 60 minutes after termination of the drip her NIH stroke scale score was three, indicative of minimal impairment. During the ensuing hospitalization no more abnormalities of mental status or other neurologic complaints were encountered.

DISCUSSION Lidocaine is a class Ib anti-arrhythmic drug used Western Journal of Emergency Medicine

intravenously for ventricular dysrhythmias and subcutaneously for local anesthesia. The 2005 (most recent) guidelines of the American Heart Association suggest that it is a second line drug after amiodarone for ventricular arrhythmia.

Amiodarone is now the primary recommendation for medical cardioversion because it is believed that aqueous amiodarone is more effective than lidocaine in the treatment of shockresistant ventricular tachycardia. An alternative treatment is intravenously administered lidocaine.2 The two major categories of the adverse effects of lidocaine are neurologic and cardiac, with the former being more common. Lidocaine’s mechanism of action is depression of neuronal excitability by blockage of voltage-dependent sodium channels in the cell membrane. This produces the therapeutic effects of myocardial stabilization and local anesthesia and causes lidocaine’s toxicity.3 Neurologic manifestations include paresthesias, confusion, dizziness, and respiratory depression, which can progress to psychosis, loss of consciousness and seizure. Cardiac manifestations of lidocaine toxicity are many, including dysrhythmia, sinus bradycardia, and QRS widening.4 There have also been reports of sino-atrial node suppression by lidocaine particularly in conjunction with other sodium channel blockers such as phenytoin. Toxicity may be associated with cardiovascular collapse and complete loss of blood pressure, even in younger patients.4 The atrioventricular node can be adversely affected by inadvertent overdose. Severe bradycardia and asystole have been described in patients with myocardial infarction and in patients with high grade atrioventricular block.5 Initial doses of lidocaine range from 0.5 up to 1.5 mg/kg.

One may repeat 0.5 to 0.75 mg/kg every five to 10 minutes to a maximum total dose of 3 mg/kg. In the patient with normal hepatic function, maintenance infusion of 1 to 4 mg/ min should be initiated.2 This administration is necessary due to lidocaine’s biphasic elimination with an initial half-life of approximately seven to 30 minutes (due to plasma protein binding and redistribution into adipose and muscle tissue) and a terminal half-life of approximately 1.5 to two hours which is prolonged with alterations in liver function. The parent compound is rapidly metabolized in the liver by dealkylation to active metabolites, monoethylglycine xylidide (more toxic than the parent compound) and glycine xylidide which have extended half-lives of two and 10 hours.4 This may account for prolonged neurologic symptoms. Less than 10% is excreted in the urine, so a history of renal failure or dialysis do not alter ED dosing.

At the time our patient’s mental status was recognized to be a manifestation of lidocaine toxicity and when the lidocaine drip stopped, the patient had received a total of 811 mg of lidocaine in three hours and 20 minutes, a total dose of approximately 13 mg/kg over two half-lives of the drug.

Similar impairments have been reported with larger doses of lidocaine over shorter periods.5

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Pfeifer et al.6 looked at 750 recipients of intravenous lidocaine. The mean age of these patients was 65 years, and almost 75% of these patients had received the drug for a cardiovascular disorder. Adverse reactions were described in 47 patients; 31 were central nervous system disturbances, and eight had cardiovascular complications. Significant adverse reactions were more frequent in patients with acute myocardial infarction and congestive heart failure. Toxicity was increasingly frequent in patients with decreased body weight and with increasing age but not with serum albumin or blood urea nitrogen. This study was performed before the widespread use of amiodarone.

Other studies have sought to understand the interaction of lidocaine and amiodarone both in vitro and in vivo. In laboratory experiments lidocaine metabolism was slowed with the inhibition of cytochrome P-4503A4 by amiodarone and its metabolite. In six test patients the mean lidocaine clearance was decreased by nearly 20 percent when the drugs were coadministered.7 This interaction would be especially relevant when lidocaine accumulates in patients with congestive heart failure or hepatic dysfunction.

Our patient appears to fit all the major determinants of lidocaine toxicity found in these studies. She was a thin elderly woman with previous myocardial infarction, documented poor ventricular function, and secondarily decreased hepatic clearance. Amiodarone was co-administered, which decreased the systemic clearance of lidocaine, leaving this patient extremely vulnerable to overdose.

CONCLUSION Although amiodarone has replaced lidocaine as the medication of choice for stable wide complex tachycardia, lidocaine is still widely used. Physicians should be familiar with the neurologic and cardiac toxic effects. Risk factors for lidocaine toxicity include previous evidence of myocardial infarction, congestive heart failure, decreased body weight, increased age, and other conditions that affect hepatic clearance (Table). Co-administration of amiodarone and lidocaine decreases the clearance of lidocaine and may increase the risk of toxicity.

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Table. Factors increasing the likelihood of lidocaine toxicity •

Older age

•

Decreased body weight

•

Acute myocardial infarction

•

Congestive heart failure

•

Decreased hepatic function

•

Concomitant use of drugs decreasing P-450 activity (including amiodarone)

Address for Correspondence: AJ Smally, Hartford Hospital Dept. of Traumatology and Emergency Medicine, 80 Seymour Street, Hartford, CT 06102. Email: asmally@harthosp.org Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

REFERENCES 1.

State-specific mortality from sudden cardiac death--United States, 1999. MMWR Morb Mortal Wkly Rep. 2002; 51:123-6.

2.

ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005; 112(24 Suppl):IV1-203.

3.

Walker IA, Slovis CM. Lidocaine in the treatment of status epilepticus.

Acad Emerg Med. 1997; 4:918-22.

4.

Jonville AP, Barbier P, Blond MH, et al. Accidental lidocaine overdosage in an infant. J Toxicol Clin Toxicol. 1990; 28:101-6.

5.

Bryant CA, Hoffman JR, Nichter LS. Pitfalls and perils of intravenous lidocaine. West J Med. 1983; 139:528-30.

6.

Pfeifer HJ, Greenblatt DJ, Koch-Weser J. Clinical use and toxicity of intravenous lidocaine. A report from the Boston Collaborative Drug Surveillance Program. Am Heart J. 1976; 92:168-73.

7.

Ha HR, Candinas R, Stieger B, et al. Interaction between amiodarone and lidocaine. J Cardiovasc Pharmacol. 1996; 28:533-9.

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Case Report

Molar Pregnancy in the Emergency Department Lori Masterson, MD Shu B. Chan, MD, MS Bryan Bluhm, MD

Emergency Medicine Residency Program, Resurrection Medical Center, Chicago, Illinois

Supervising Section Editor: J. Christian Fox, MD Submission history: Submitted November 3, 2008; Revision Received April 29, 2009; Accepted May 1, 2009Reprints available through open access at http://escholarship.org/uc/uciem_westjem

A 15-year-old female presented to the emergency department with complaints of vaginal bleeding.

She was pale, anxious, cool and clammy with tachycardic, thready peripheral pulses and hemoglobin of 2.4g/dL. Her abdomen was gravid appearing, approximately early to mid-second trimester in size.

Pelvic examination revealed 2 cm open cervical os with spontaneous discharge of blood, clots and a copious amount of champagne-colored grapelike spongy material. After 2L boluses of normal saline and two units of crossmatched blood, patient was transported to the operating room. Surgical pathology confirmed a complete hydatidiform mole.

[West J Emerg Med. 2009;10(4):295-296.]

CASE REPORT A 15-year-old female patient presented via emergency medical services to the ED with complaints of vaginal bleeding and weakness. The patient had been bleeding for the past seven days and had mild cramping abdominal pain. She admitted to sexual activity but was unsure if she was pregnant.

She believed her last menstrual period was approximately one month prior. Her past medical history and family history were unremarkable. She denied allergies to medications, smoking, drinking alcohol or any drug use.

The patient was alert and oriented and in obvious distress.

She was pale, anxious, and weak. Her temperature was 98.2˚F, blood pressure 129/64mmHg, heart rate 133bpm, respiratory rate of 16 breaths per min with a pulse oximetry of 100% on supplemental oxygen. On physical exam she was cool and clammy with mildly labored breathing. She was tachycardic with thready peripheral pulses and no murmurs. Her abdomen was gravid appearing, approximately early to mid-second trimester in size. She was soft and mildly tender to palpation in the lower quadrants bilaterally. Her lower extremities were nontender and moderately edematous. Pelvic examination revealed spontaneous discharge of blood, clots and a copious amount of champagne-colored grapelike spongy material. No fetal parts were identifiable (Figure 1). The cervical os was open to approximately 2cm with moderate cervical motion tenderness.

ED laboratory results showed hemoglobin of 2.4 g/dL, hematocrit of 7.3%, white blood count at 16,700 with 74% Western Journal of Emergency Medicine

Figure 1. “Bag of grapes” appearance to a molar pregnancy

neutrophils and 4% bands, platelets at 133,000, international normalized ratio of 1.3, and bicarbonate of 12 mmol/L. Bun was elevated at 36 mg/dL and creatinine was 0.6 mg/dL. Free T4 was 2.79 ng/dL (normall range: 0.93-1.7) and TSH was 0.01 mcu/mL (normal range: 0.27-4.2). Beta HCG was 460,318 mIU/mL, 64 times the upper limit of normal for an estimated gestational age of a five-week fetus. EKG revealed sinus tachycardia.

Obstetrics was emergently consulted and the patient transported urgently to the operating room for dilation and

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curettage. While in the ED, the patient received 2L boluses of normal saline and two units of crossmatched blood.

Surgical pathology confirmed a complete hydatidiform mole.

The patient suffered postoperative complications including respiratory distress requiring intubation, cardiomyopathy (ejection fraction of 25%) and hyperthyroidism. She was medically managed in the intensive care unit and discharged one week later with improved ejection fraction, recovering thyroid function and no evidence of malignant gestational trophoblastic disease.

transvaginal ultrasound and increasingly sensitive β-hcg assays. Numerous studies evaluating the efficacy of ultrasound in detecting molar pregnancy demonstrate a 57-95 percent sensitivity for the detection of CM compared to only 18-49 percent sensitivity for PM.11 This case is of particular interest due to its late presentation and classic features. It is unusual for this type of patient to expel diagnostic tissue in the ED, and it serves as a reminder that patients who delay medical attention may not present as expected.

DISCUSSION Hydatidiform mole (molar pregnancy) is a relatively rare complication of fertilization with an incidence in the United States of 0.63 to 1.1 per 1000 pregnancies, although rates vary geographically.1 It is included in the spectrum of gestational trophoblastic diseases and is comprised of both complete molar pregnancies (CM) and partial molar pregnancies (PM).

Pathologically, CM demonstrate diffuse villous edema and trophoblastic proliferation with absence of a fetus, whereas with PM villous edema and trophoblastic proliferation are variable and the fetus typically demonstrates congenital abnormalities and growth retardation.2 The most well characterized risk factor for CM is extreme of maternal age. Maternal ages less than 20 or greater than 40 years have been associated with relative risks for CM as high as 10- and 11-fold greater respectively.3,4 However, the majority of molar pregnancies occur within the 20-40 year range, as these represent the most common reproductive years. History of prior molar pregnancy is another important risk factor for both CM and PM, with repeat molar pregnancies occurring 0.6 to 2.6 percent of the time.1 Other potential risk factors include oral contraceptive use, maternal type A or AB blood groups, maternal smoking, and maternal alcohol abuse.1,3 Molar pregnancy typically presents in the first trimester and may be associated with a wide array of findings, including vaginal bleeding (most common), uterine size larger than expected according to pregnancy date (CM), uterine size smaller than expected according to pregnancy date (PM), excessive beta-human chorionic gonadotropin (β-hcg) levels, anemia, hyperemesis gravidum, theca lutein cysts, preeclampsia, and respiratory distress.2,5,6 β-hcg is a glycoprotein hormone structurally similar to thyroid-stimulating hormone, and for this reason many patients will present with clinical hyperthyroidism.7 This patient’s peripheral edema is most likely related to her significant peripartum cardiomyopathy, although differential diagnosis also includes preeclampsia, hyperthryoidism, high output failure, or a hypoalbuminemic state. Studies comparing modern clinical presentations of CM with historical presentations have demonstrated a significant reduction in many of the classic presenting signs and symptoms such as vaginal bleeding and excessive uterine size.8,9,10 This reduction is attributed to early detection by Volume X, no. 4 : November 2009

Address for Correspondence: Shu B. Chan MD, MS , Resurrection Medical Center, Emergency Medicine, 7435 West Talcott Avenue, Chicago, Illinois 60631. Email: schan@reshealthcare.org Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none.

REFERENCES 1.

Smith HO. Gestational trophoblastic disease epidemiology and trends. Clin Obstet Gynecol. 2003; 46:541-56.

2.

Soper JT. Gestational trophoblastic disease. Obstet Gynecol. 2006; 108:176-87.

3.

Altieri A, Franceschi S, Ferlay J, Smith J, La Vecchia C. Epidemiology and aetiology of gestational trophoblastic diseases. Lancet Oncol.

2003; 4:670-8.

4.

Garner EI, Goldstein DP, Feltmate CM, Berkowitz RS. Gestational trophoblastic disease. Clin Obstet Gynecol. 2007; 50:112-22.

5.

Niemann I, Petersen LK, Hansen ES, Sunde L. Differences in current clinical features of diploid and triploid hydatidiform mole. BJOG. 2007; 114:1273-7.

6.

Soper JT, Mutch DG, Schink JC; American College of Obstetricians and Gynecologists. Diagnosis and treatment of gestational trophoblastic disease: ACOG Practice Bulletin No. 53. Gynecol Oncol. 2004; 93:575-85.

7.

Hershman JM. Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid. Best Practice & Research. Clinical Endocrinology & Metabolism. 2004; 18:249-65.

8.

Soto-Wright V, Bernstein M, Goldstein DP, Berkowitz RS. The changing clinical presentation of complete molar pregnancy. Obstet Gynecol. 1995; 86:775-9.

9.

Mangili G, Garavaglia E, Cavoretto P, Gentile C, Scarfone G, Rabaiotti E. Clinical presentation of hydatidiform mole in northern Italy: has it changed in the last 20 years? Am J Obstet Gynecol. 2008; 198:302.

10. Coukos G, Makrigiannakis A, Chung J, Randall TC, Rubin SC, Benjamin I. Complete hydatidiform mole. A disease with a changing profile. J Reprod Med. 1999; 44:698-704.

11. Kirk E, Papageorghiou AT, Condous G, Bottomley C, Bourne T. The

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accuracy of first trimester ultrasound in the diagnosis of hydatidiform mole. Ultrasound Obstet Gynecol. 2007; 29:70-5.

Western Journal of Emergency Medicine

Images In Emergency Medicine

Scrotal Swelling After Penetrating Chest Trauma Jason D. Heiner, MD, MC* Elizabeth C Skeins, MDâ&#x20AC; Diane DeVita, MD* Joseph S Litner, MD, PhD*

* Madigan Army Medical Center, Department of Emergency Medicine, Tacoma, WA â&#x20AC; LSU Interim Hospital, Department of Emergency Medicine, New Orleans, LA

Supervising Section Editor: Sean Henderson, MD Submission history: Submitted February 18, 2009; Accepted March 9, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):297.]

A 16-year-old male was brought to the emergency department by ambulance after being found lying unresponsive on an overturned motorcycle. He was orotracheally intubated. He had palpable subcutaneous crepitus over the chest and abdomen with massive scrotal swelling, and his back exam revealed multiple penetrating wounds (Figure 1). Autopsy results found five rightsided posterior thoracic gunshot wounds. The path of one bullet shattered the right seventh rib, entering the right lung and exiting though the main pulmonary artery before ending at the left clavicle.

The presence of intra-scrotal air or gas is a rare clinical entity formed when air reaches the scrotum through tissue planes and cavities via the path of least resistance. The air source may be remote from the scrotum. Known causes include infections from gas-producing organisms, intestinal or gastric perforation and pneumothorax.1,2 Three common routes could allow air to track into the scrotum: 1) intra-abdominal air through a patent process vaginalis; 2) retroperitoneal air through the inguinal canal superficial to the fascia covering the spermatic cord; and 3) direct extension of subcutaneous emphysema of the trunk.2 While imaging studies can aid in the diagnosis of pneumoscrotum, it does not require specific treatment. Instead, diagnosis and treatment should focus on identification and resolution of the underlying cause. Antibiotics are recommended when pneumoscrotum arises after intestinal perforation or infection. Spontaneous resolution generally occurs three to five days after eliminating the source of gas.1,3 In the case presented here, the cause of pneumoscrotum was life threatening. Penetrating trauma violating the pleura resulted in the introduction of air within the subcutaneous tissues. An expanding scrotum with crepitus may provide a valuable clue to an underlying serious etiology that is not immediately obvious.

Address for Correspondence: Jason Heiner, MD. Address for Correspondence: Jason Heiner, MD, Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, WA, 98431, USA. Email: jason.heiner1@us.army.mil.

Figure 1. Markedly swollen scrotum with no other visible signs of anterior trauma (top) and multiple right scapular gunshot entrance wounds posteriorly (bottom).

REFERENCES 1.

Firman R, Heiselman D, Lloyd T, et al. Pneumoscrotum. Ann Emerg Med. 1993; 8:1353-6.

Disclaimer: The views expressed are those of the authors and do not reflect the official policy of the Department of the Army, the Department of Defense or the U.S. Government

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2.

Wakabayashi Y, Bush WH Jr. Pneumoscrotum after blunt chest trauma. J Emerg Med. 1994; 5:603-5.

3.

297

Sharma TC, Kagan HN. Scrotal emphysema. Am Surg. 1980; 11:652-3.

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Images In Emergency Medicine

Supraglottic Laryngeal Mass Laura Andrews Sean O. Henderson, MD

Keck School of Medicine of the University of Southern California, Department of Emergency Medicine, Los Angeles, CA

Supervising Section Editor: Matthew Strehlow, MD Submission history: Submitted June 26, 2008; Revision Received December 10, 2009; Accepted January 10, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):298-299.]

A

B

Figure 1. Computed tomography results revealed A) the absence of a visible airway compared to B) an open airway taken below the level of the mass.

A 60-year-old Hispanic male with a history of smoking presented to the emergency department with complaint of dysphagia for the past two months. Additional symptoms included progressive shortness of breath and stridor. CT results from an outside institution showed 80% airway obstruction. Despite the findings, the patientâ&#x20AC;&#x2122;s vitals were normal, with respirations of 20 and an initial room air oxygen saturation of 98%. Palpable neck masses or lymphadenopathy were not noted at the time of physical exam. A CT revealed the absence of a visible airway (Figure 1a; compare with Figure 1b taken below the level of the mass) and an expansive soft-tissue mass roughly spanning spinal cord levels C1 to C6 (Figure 2). An emergent ENT consult was called and the patient was given dexamethasone to control edema and prevent further obstruction. He was taken to the operating room where he could not be intubated and underwent an emergency tracheotomy. Direct laryngoscopy and biopsy revealed significant epiglottic destruction by squamous cell carcinoma, with lymphangitic metastasis to the cervical soft Volume X, no. 4 : November 2009

Figure 2. Soft-tissue mass roughly spanning spinal cord levels C1 to C6

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Supraglottic Laryngeal Mass tissues. Patient was given dexamethasone to control edema and prevent further obstruction.

Squamous cell carcinoma of the larynx occurs up to 30 times more frequently in men and is associated with a history of smoking and alcohol consumption, which together can increase the risk of laryngeal cancer by a factor greater than 100.1,2,3 Compared to glottic, supraglottic tumors have greater risk of lymphogenous metastasis due to greater vascularity and later presentation due to fewer symptoms.4 As a result, many patients presenting with advanced disease have palpable neck metastases.

The extensive obstruction that this patient presented with warrants mention of the management options available in such a case. The emergency physician needs to be aware of alternatives for salvaging the airway in these rare instances.

The standard landmark-based cricothyrotomy would have been ineffective as the tumor obstructed this region entirely. While jet ventilation below the level of the obstruction could have been used as a temporizing measure, the only practical approach to establishing a definitive airway would have been to move the “cric” down several rings to a level free of obstruction.

Western Journal of Emergency Medicine

Address for Correspondence: Sean O. Henderson, MD, Department of Emergency Medicine, LAC+USC Medical Center, Unit #1, Room 1011, 1200 N. State Street, Los Angeles, CA 90033. Email: sohender@hsc.usc.edu REFERENCES 1.

Hoffman HT, Porter K, Karnell LH, et al. Laryngeal cancer in the United States: changes in demographics, patterns of care, and survival. Laryngoscope. 2006; 116:1-13.

2.

Gronbaek M, Becker U, Johansen D, et al. Population based cohort study of the association between alcohol intake and cancer of the upper digestive tract. British Medical Journal. 1998; 317:844-47.

3.

Cosetti M, Yu GP, Schantz SP. Five-year survival rates and time trends of laryngeal cancer in the US population. Archives of Otolaryngology – Head & Neck Surgery. 2008; 134:370-79.

4.

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Raitiola H, Pukander J, Laippala P. Glottic and supraglottic laryngeal carcinoma: differences in epidemiology, clinical characteristics and prognosis. Acta Oto-Laryngologica. 1999; 119:847-51.

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Images In Emergency Medicine

Non-Communicating Hydrocephalus Keith J. Yablonicky, MD Stuart P. Swadron, MD

Keck School of Medicine of the University of Southern California, Department of Emergency Medicine, Los Angeles, CA

Supervising Section Editor: Sean Henderson, MD Submission history: Submitted March 24, 2009; Revision Received May 12, 2009; Accepted May 21, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

← ←

←

[West J Emerg Med. 2009;10(4):300-301.]

Figure 1. Hydrocephalus with enlarged lateral and third ventricles on computed tomography.

Figure 2. Normal fourth ventricle on computed tomography suggesting the hydrocephalus being related to acquired stenosis of the aqueduct of Sylvius.

A 28-year-old male presented to the emergency department with acute onset of confusion, slurred speech, disequilibrium, and right-sided facial droop. He had no headache, fever, chills, recent trauma, recent travel, or similar symptoms in the past. He was previously healthy with no history of drug, alcohol or tobacco use. His family history and review of systems were unremarkable. Although his vital signs were normal, his mental status fluctuated widely, from completely cogent to having difficulty following basic instructions. He had a slight right-sided facial droop and right upper extremity weakness with

pronator drift. His right lower extremity had normal strength and function. His deep tendon reflexes and sensation were intact. His balance was poor and he fell toward his right side.

The remainder of his exam was unremarkable.

Non-contrast head computed tomography demonstrated hydrocephalus with enlarged lateral and third ventricles, no focal lesions and no hemorrhage (Figure 1). Complete blood count, serum chemistry and coagulation studies were all normal. The patient received consultation from the neurology and neurosurgical services, and was admitted for an MRI and possible ventriculostomy. An MRI confirmed

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Acquired Non-Communicating Hydrocephalus the diagnosis of hydrocephalus but revealed no additional pathology. In the absence of other findings and a normal fourth ventricle (Figure 2), the hydrocephalus in this case appears to be related to acquired stenosis of the aqueduct of Sylvius, the narrow channel of cerebrospinal fluid (CSF) that connects the third and fourth ventricles.1 It may result from any process that narrows or occludes the flow of CSF, including infections, tumors or hemorrhage. On further review of the patientâ&#x20AC;&#x2122;s history, it was discovered that he had suffered from bacterial meningitis as a child.2 The patient improved clinically over the next two days and did not require a ventriculostomy. He was discharged with close neurology and neurosurgical follow up.

Western Journal of Emergency Medicine

Address for Correspondence: Stuart P. Swadron, MD, Department of Emergency Medicine, LAC+USC Medical Center, Unit #1, Room 1011, 1200 N. State Street, Los Angeles, CA 90033. Email: swadron@usc.edu REFERENCES 1.

Marx JA, Hockberger RS, Walls RM, et al. Rosenâ&#x20AC;&#x2122;s Emergency Medicine: Concepts and Clinical Practice, 6th Edition. St. Louis, MO: Mosby Inc.; 2006.

2.

Baustian GH, McIntire S, Heinzman D. Hydrocephalus. MD Consult.

First Consult. August 24 2007. Available at: http://www.mdconsult. com/das/pdxmd/body/169396854-2/0?type=med&eid=9-u1.0-_1_ mt_1010369. Accessed March 24, 2009.

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Rhabdomyolysis-Induced Severe Hyperkalemia Clark Rosenberry, MD Franco Stone, NREMT-P Kristine Kalbfleisch, MD

Madigan Army Medical Center, Department of Emergency Medicine, Fort Lewis, WA

Supervising Section Editor: Sean Henderson, MD Submission history: Submitted May 24, 2009; Accepted June 1, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):302.]

A 22-year-old male was brought in by paramedics who found him unresponsive at home surrounded by drug paraphernalia. He had a blood pressure of 84/50 mm Hg; oxygen saturation of 88%; irregular pulse; and Glasgow Coma Scale of 3. His skin was cool, diaphoretic and ashen in color, except for a grossly erythematous right arm. Lab work demonstrated an initial creatine kinase of 5,414 U/L that increased to 165,300 U/L by the next day. His potassium was 8.6 mmol/L. Hyperkalemia, defined as a potassium level greater than 5.5 mmol/L, is a potentially fatal disorder that occurs in as many as 10% of hospitalized patients.1,2 Causes include rhabdomyolysis, hemolysis, renal failure, acidosis, and medications.2 Cardiac conduction can be impaired, resulting in dysrhythmias. Electrocardiography (ECG) is important because it may be diagnostic and dictate emergent treatment.

The first ECG changes seen are shortening of the QT interval, peaked T waves, and ST segment depression, followed by widening of the QRS complex, increased PR interval, and decreased P wave amplitude. Lastly, the P wave disappears and the QRS widens until it resembles a sine wave. Ventricular fibrillation or asystole may follow. Emergent treatment with calcium gluconate or calcium chloride is indicated to stabilize the myocardium if ECG changes are present.2,3 Serial doses of calcium are given until the ECG normalizes.2 Inhaled albuterol, intravenous sodium bicarbonate, and intravenous insulin with glucose should be used to temporarily shift potassium back into cells.3 Furosemide and sodium polystyrene should also be administered to increase the excretion of potassium. Hemodialysis may be required in the setting of renal failure or severe cases. The ultimate treatment goal of hyperkalemia is to identify and correct the underlying etiology.

Figure 1. Rhythm strip of lead II demonstrating severe hyperkalemia.

REFERENCES 1.

Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol.

2008; 3:324-30.

2.

Garth D. Hyperkalemia. eMedicine Web site. Available at: http:// emedicine.medscape.com/article/766479-overview. Accessed May

Address for Correspondence: Clark Rosenberry, MD, Department of Emergency Medicine, Madigan Army Medical Center, Fort Lewis, WA. Email: crosenberry04@jcu.edu.

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3, 2009.

3.

Weisberg LS, Dellinger RP. Management of severe hyperkalemia.

Crit Care Med. 2008; 36:3246-51.

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Ultrasound-Confirmed Frontal Bone Fracture Jeremy N. Johnson, DO Daniel F. McBride, MD, MPH Steve Crandall, MD Christopher Kang, MD

Madigan Army Medical Center/University of Washington Emergency Medicine Residency, Fort Lewis, WA

Supervising Section Editor: J. Christian Fox, MD Submission history: Submitted October 13, 2007; Revision Received January 25, 2009; Accepted January 26, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):303.]

A 21-year-old man walked into the ED complaining of mild headache after colliding with another player during a baseball game. The patient denied loss of consciousness and noted numbness over his left forehead. He denied vision change, fluid from his nose or ears, dizziness or other injury. He had normal mentation, no neck pain, and an otherwise non-focal exam. He declined pain medication.

A visible depression is noted overlying the left frontal bone.

(Figure 1.) An ultrasound (US) at the bedside demonstrates an isolated comminuted fracture of the left frontal sinus with depression of one segment into the sinus and an overlying flap created by the other fragment. The CT image confirmed this (Figure 2).

The force required to fracture the frontal sinus ranges from 800-2200 lbs, more than enough to cause associated injuries.1 Complications include: CSF leak, osteomyelitis, meningitis, brain abscess or mucopyocele, and cavernous sinus thrombosis.

Operative repair is best performed by an ENT specialist using endoscopic techniques to assure good cosmetic outcome.2 Currently CT, which is the criterion reference for diagnosis of skull fractures, is most important to evaluate for inner table fractures or co-existing mid-face fractures.3 Despite the superiority of CT, US can be used in remote or austere environments. Research comparing CT to US for superficial facial fractures needs to be done to determine test characteristics.

A

Figure 1. Facial view showing depression of the left frontal bone Address for Correspondence: Jeremy N. Johnson, DO, Department of Emergency Medicine, Madigan Army Medical Center, Fort Lewis, WA. Email: jeremy.n.johnson@amedd.army.mil The opinions and assertions contained herein are the private views of the authors and should not be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

REFERENCES 1.

Nahum AM. The biomechanics of maxillofacial trauma. Clin Plast Surg. 1975; 2:59-64.

2.

Strong EB, Kellman RM. Endoscopic repair of anterior table--frontal sinus fractures. Facial Plast Surg Clin North Am. 2006; 14:25-9.

3.

Sun JK, Lemay DR. Imaging of Facial Trauma. Neuroimaging Clin N Am. 2002; 12:295-309.

B

Figure 2. A) CT-facial bones, depicting depression of left frontal bone into the frontal sinus with blood in the frontal sinus. B) UltrasoundFrontal bones, depicting depression of the left frontal bone and a normal right frontal bone.

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Non-traumatic Shoulder Dislocation Jacob Manteuffel, MD

Henry Ford Hospital, Department of Emergency Medicine, Detroit, MI

Supervising Section Editor: Sean Henderson, MD Submission history: Submitted March 20, 2009; Accepted April 6, 2009 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):304.]

A 42-year-old female with a past medical history significant for intravenous drug abuse presented to the emergency department complaining of a two-week history of worsening left shoulder pain. She denied any trauma to the shoulder but noted it had become increasingly difficult to move secondary to pain. On physical exam she was afebrile and the rest of her vital signs were within normal limits.

Asymmetry was noted between the right and left shoulders and the left shoulder was warm, erythematous and tender to palpation. Her left arm was held in adduction and internal rotation, with extremely limited range of motion secondary to pain. We obtained a radiograph of the shoulder and laboratory tests that revealed an elevated white blood cell count of 12.9, erythrocyte sedimentation rate of 66 mm/hr and a C-reactive protein level of 5.4 mg/dl. Orthopedic surgery was then consulted. A needle tap of the left shoulder yielded 30 ml of purulent fluid. Lab cultures grew methicillin-resistant Staphylococcus aureus, and the patient was started on empiric intravenous vancomycin. In the operating room orthopedic surgery found that the patient had an extracapsular subdeltoid abscess.

A review of the literature indicates this is a rare case of an extracapsular abscess causing marked radiographic evidence of dislocation in the shoulder. There are case reports of septic arthritis in the shoulder represented with radiographic evidence of dislocation.1 Atlanto-axial subluxation secondary to retropharyngeal abscess is described; however, there are no reports of similar dislocations outside of the axial skeleton.2 This case reinforces the point that every dislocation is not secondary to trauma. It also emphasizes the importance of a detailed history and physical examination to discern the causes of pain, with corroboration of radiographic findings.

Figure 1. Radiograph of dislocation in the shoulder caused by extracapsular abscess.

REFERENCES 1.

Gomplels BM, Darlington LG. Septic arthritis in rheumatoid disease causing bilateral shoulder dislocation: diagnosis and treatment assisted by grey scale ultrasonagraphy. Ann Rheum Dis. 1981; 40:609-11.

Address for Correspondence: Jacob Manteuffel, MD, Department of Emergency Medicine, Henry Ford Hospital, 2799 W. Grand Blvd, Detroit, MI 48201. Email jmanteu1@hfhs.org

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2.

Welinder NP, Hoffmann P, Hakansson S. Pathogenesis of nontraumatic atlanto-axial subluxation (Griselâ&#x20AC;&#x2122;s syndrome). Eur Arch Otorhinolaryngol. 1997; 254:251-4.

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All That Wheezes Is Not Asthma Andrew C. Miller, MD* Rashid M. Rashid, MD, PhD† Elamin M. Elamin, MD, MSc‡

* State University of New York Downstate Medical Center and Kings County Hospital Center, Departments of Emergency Medicine and Internal Medicine, Brooklyn, NY † MD Anderson Cancer Center, Department of Dermatology, University of Texas.

Houston, TX ‡ University of Florida, Departments of Pulmonary, Critical Care, and Anesthesiology, Gainsville, FL

Supervising Section Editor: Eric R. Snoey, MD Submission history: Submitted September 4, 2008; Revision Received September 23, 2008; Accepted November 28, 2008 Reprints available through open access at http://escholarship.org/uc/uciem_westjem

[West J Emerg Med. 2009;10(4):305-306.]

Figure 1. Upper extremity cutaneous plaque sarcoidosis

A 34-year-old African American woman presented with shortness-of-breath, wheezing, pedal edema, and a rash. On examination she had reddish-purple indurated plaques and nodules on the nasal rim and cheeks, and raised plaques on the trunk and extremities (Figures 1 and 2). Jugular venous distension, diffuse wheezing, rales, and bilateral pitting pedal edema were present. Her chest x-ray and CT scan demonstrated bilateral hilar lymphadenopathy. A 2-D echo revealed a 10% ejection fraction. Serum was ANA-negative with elevated angiotensin-converting enzyme levels and lymphocytopenia. Cutaneous biopsies showed non-caseating granulomas. The attending physician diagnosed disseminated sarcoidosis and initiated systemic steroid treatment. The Western Journal of Emergency Medicine

Figure 2. Lower extremity cutaneous sarcoidosis

patient was to have an automatic implantable cardioverter defibrillator (ICD) placed due to advanced cardiomyopathy and, as per protocol, underwent routine cardiac catheterization one day prior. The patient died post-catheterization from unstable ventricular tachycardia.

This patient’s skin findings are characteristic of plaque sarcoidosis with nasal lupus pernio. This chronic granulomatous disorder is characterized by activated T-lymphocytes and macrophages and may involve any organ system. Cutaneous lesions were the first recognized manifestations of sarcoidosis.1 The ACCESS study characterized sarcoidosis in 736 patients in the U.S.2 Sarcoidspecific cutaneous lesions were observed in 15.9% of all 305

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Cutaneous Sarcoidosis

sarcoid patients.2 Plaque sarcoid heralds long-standing disease, and lupus pernio is highly predictive of upper airway involvement. The ACCESS study criteria for diagnosing cardiac involvement rely on the presence of cardiomyopathy or electrocardiographic or scintigraphic abnormalities in patients with known sarcoidosis.3 Conversely, the Japanese Ministry of Health and Welfare criteria take into account symptoms, electrocardiographic, echocardiographic, and scintigraphic findings.3 Corticosteroids remain the cornerstone of treatment.1 Current guidelines for ICD implantation are the same as for those with other nonischemic cardiomyopathies.3 Emergency physicians must remember that “all that wheezes is not asthma.” Multi-system disorders such as sarcoidosis must be considered in patients with shortness-of-breath, rash, and signs of heart failure.

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Address for Correspondence: Andrew C. Miller, MD, Department of Emergency Medicine, 450 Clarkson Avenue, Box 1228, Brooklyn, NY 11203-2098. Email: andrewcmiller@optonline.net; taqwa1@gmail.com

REFERENCES 1.

Rose AS, Tielker MA, Knox, KS. Hepatic, Ocular, and Cutaneous Sarcoidosis. Clin Chest Med. 2008; 29:509-524.

2.

Baughman RP, Teirstein AS, Judson MA, et al. Clinical characteristics of patients in a case–control study of sarcoidosis. Am J Respir Crit Care Med. 2001; 164(10 Pt 1):1885-9.

3.

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Lubitz SA, Goldbarg SH, Mehta D. Sudden Cardiac Death in Infiltrative Cardiomyopathies: Sarcoidosis, Scleroderma, Amyloidosis, Hemachromatosis. Prog Cardiovasc Dis. 2008; 51:58-73.

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Kessler et al.

Urologic Emergencies

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25. Akgur FM, Killinc K, Aktug T, et al. The effect of allopurinol

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pretreatment on ischemia-reperfusion injury and early changes

York, NY: McGraw Hill; 2006.

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18. Gatti, JM. Current management of the acute scrotum. Semin Pediatr

testicular torsion-detorsion. J Pediatr Surg. 2004; 39:91-5.

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20. Kadish HA, Bolte RG. A retrospective review of pediatric patients with epididymitis, testicular torsion, and torsion of testicular appendages.

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Pediatrics. 1998; 102:73-6.

Assoc; 1983.

21. Rabinowitz R. The importance of the cremasteric reflex in acute scrotal swelling in children. J Urol. 1984; 132:89-90.

Faculty Positions Available in Emergency Medicine

University of California, Irvine School of Medicine The University of California, Irvine is recruiting three new full-time faculty members, either in the Health Sciences Clinical Series or Clinical Scholar (Clinical X) Series at the Assistant or Associate Professor level. The HS Clinical Series includes substantial patient care, medical student and resident teaching, and optional clinical research. Candidates for the Clinical Scholar Series will develop an independent research program, and already have or develop a track record in scholarly activity. Board preparation or certification in EM required.

Fellowship or advanced degree, or both, strongly desired. Appropriate Rank and Series commensurate with qualifications.

UC Irvine Medical Center is a 472-bed tertiary care hospital with all residencies.

The ED is a progressive 35-bed Level I Trauma Center with 38,000 patients, in urban Orange County. Collegial relationships with all services. Excellent salary and benefits with incentive plan. Send or email CV to: Mark Langdorf, MD, MHPE, FACEP UC Irvine Medical Center Route 128, 101 City Drive Orange, CA 92868 Email: mark.langdorf@uci.edu

http://ohiosurgery.blogspot.com/2008/04/fourniers-gangrene.html.

Accessed January 13, 2009.

74:1739-46.

33. Mindrup SR, Kealey G, Fallon B. Hyperbaric oxygen for the treatment of Fournier’s gangrene. J Urol. 2005; 173:1975-7.

1:485-96.

in

Emergency Medical Services and Disaster Medicine

University of California, Irvine School of Medicine University of California, Irvine, Department of Emergency Medicine is seeking an HS Clinical Instructor for July, 2010. UC Irvine Medical Center is a Level I Trauma center with 2200 runs/year, 40,000 ED census. The fellowship in Emergency Medical Services and Disaster Medicine, beginning July 1, 2010, combines the traditional emphasis on EMS research with the disciplines of emergency management/ disaster medicine and public health. A key focus of the fellowship is health policy and health services systems research including mass casualty management and triage. Completion of American Council of Graduate Medical Education (ACGME) accredited Emergency Medicine Residency required prior to start. The two-year combined program, with an integrated Masters of Public Health, will be jointly administered

by Director, EMS and Disaster Medicine. Salary commensurate with level of clinical work. Send CV, statement of interest and three letters of recommendation to: Carl Schultz, MD Department of Emergency Medicine, Route 128, UC Irvine Medical Center, 101 City Drive, Orange, CA 92868.

Or apply online at https://recruit.ap.uci.edu The University of California, Irvine is an equal opportunity employer committed to excellence through diversity.

Emergency Medicine Education Fellowship University of California, Irvine School of Medicine

University of California, Irvine, Department of Emergency Medicine (EM) is seeking a HS Clinical Instructor- Education Fellow for July, 2011. University of California, Irvine Medical Center is a Level I Trauma center with 2200 runs/year, 40,000 ED census with a three-year residency program since 1989. Fellowship concentration areas include education, medical school curriculum design, simulation, peer-reviewed journal editing and publishing. This two-year research fellowship includes a requirement for completion of a Masters in Education.

Possibility exists for a one-year fellowship for candidates with a Masters degree or those starting one during their fellowship. Completion of an ACGME accredited EM Residency is required. Salary is commensurate with the level of clinical work.

Send CV and statement of interest to: Dr. Shahram Lotfipour at SHL@uci.edu or Department of Emergency Medicine UC Irvine Medical Center, Route 128-01 101 The City Drive Orange, CA 92868 or Call 714-456-5239

Western Journal of Emergency Medicine

Fellowship

The University of California, Irvine is an equal opportunity employer committed to excellence through diversity.

32. Parks J. Buckeye Surgeon: Fournier’s Gangrene. Available at:

22. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician. 2006; 23. Coley B. The acute pediatric scrotum. Ultrasound Clinics. 2006;

Classified Academic Faculty and Fellowship Positions

287

Volume X, no. 4 : November 2009

FACULTY POSITIONS IN EMERGENCY MEDICINE

American University of Beirut, Faculty of Medicine and Medical Center, Beirut, Lebanon The Faculty of Medicine and Medical Center of the American University of Beirut, Beirut, Lebanon, is establishing a high quality Academic Department of Emergency Medicine. We are actively seeking experienced Emergency Medicine physicians for this development.

Candidates must be board-certified or -eligible in Emergency Medicine by the American Board of Emergency Medicine or the American Board of Osteopathic Emergency Medicine and must have at least three years successful experience in Emergency Medicine. Excellent opportunities exist for faculty development, research and teaching. The compensation is competitive, and the position offers excellent benefits.

To apply please send a cover letter, CV and names of three references to: Amin Antoine N. Kazzi, MD, FAAEM Chief of Service & Medical Director, Emergency Department AUB Faculty of Medicine and Medical Center American University of Beirut P.O.Box 11-0236 / Medical Dean’s Office Riad El-Solh / Beirut 1107 2020, Lebanon

See the Department of Emergency Medicine’s website available at http://www. emergencymed.uci.edu/ for more details.

For additional information, e-mail: ak63@aub.edu.lb

The University of California, Irvine is an equal opportunity employer committed to excellence through diversity.

The American University of Beirut is an affirmative action, equal opportunity employer.

Western Journal of Emergency Medicine

Volume X, no. 4 : November 2009

Newly Published Textbook Announcement

Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices As societies become more complex and interconnected, the global risk for catastrophic disasters is increasing. Demand for expertise to mitigate the human suffering and damage these events cause is also high. A new field of disaster medicine is emerging, offering innovative approaches to optimize disaster management. Much of the information needed to create the foundation for this growing specialty is not objectively described or is scattered among multiple different sources. Now, for the first time, a coherent and comprehensive collection of scientific observations and evidence-based recommendations with expert contributors from around the globe is available in Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices. This definitive work on disaster medicine identifies essential subject matter, clarifies nomenclature, and outlines necessary areas of proficiency for healthcare professionals handling mass casualty crises. It also describes in-depth strategies for the rapid diagnosis and treatment of victims suffering from blast injuries or exposure to chemical, biological, and radiological agents.

• •

A fresh new approach to disaster preparedness and response, written for both emergency physicians and nurses Covers a wide range of disaster situations, with strategies for rapid diagnosis and treatment of victims, as well as scene management Contributed by experts from all over the world, supplemented with photos and diagrams of each aspect of disaster response

•

Available for purchase at the American College of Emergency Physicians bookstore, Cambridge University Press and Amazon.com.

29th Annual Mammoth Mountain Emergency Medicine Conference March 7-12, 2010

e h t e v

Sa

e t Da

*Alaskan Airlines from $178 round trip http://www.emconference.org/mammoth

Giant Steps In Emergency Medicine 2010 Hilton San Diego Resort & Spa, San Diego

Su nda y - Wed ne sda y, Ju n

1 0 2 , 0 3 e 27 -

The CME course you have been waiting for. Known for their interactive, enthusiastic, and effective teaching styles, Drs. Joe Lex, Amal Mattu and Ghazala Sharieff routinely participate in CME courses nationally and internationally.

They don’t lecture and then disappear. They are committed to audience education and promote interaction and questions.

Special Guest Faculty Peter M. C. DeBlieux, MD, FAAEM, FACEP

0

Course highlights • • • • • •

20.25 Cme credits High-yield topics Optional pediatric workshop Optional ECG workshop Optional LLSA workshop Afternoons free for family activities

For further details & to register www.giantsteps-em.com 503-635-4891 or 1-866-924-7929

Newly Published Textbook Announcement

Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices As societies become more complex and interconnected, the global risk for catastrophic disasters is increasing. Demand for expertise to mitigate the human suffering and damage these events cause is also high. A new field of disaster medicine is emerging, offering innovative approaches to optimize disaster management. Much of the information needed to create the foundation for this growing specialty is not objectively described or is scattered among multiple different sources. Now, for the first time, a coherent and comprehensive collection of scientific observations and evidence-based recommendations with expert contributors from around the globe is available in Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices. This definitive work on disaster medicine identifies essential subject matter, clarifies nomenclature, and outlines necessary areas of proficiency for healthcare professionals handling mass casualty crises. It also describes in-depth strategies for the rapid diagnosis and treatment of victims suffering from blast injuries or exposure to chemical, biological, and radiological agents.

• •

A fresh new approach to disaster preparedness and response, written for both emergency physicians and nurses Covers a wide range of disaster situations, with strategies for rapid diagnosis and treatment of victims, as well as scene management Contributed by experts from all over the world, supplemented with photos and diagrams of each aspect of disaster response

•

Available for purchase at the American College of Emergency Physicians bookstore, Cambridge University Press and Amazon.com.

29th Annual Mammoth Mountain Emergency Medicine Conference March 7-12, 2010

e h t e v

Sa

e t Da

*Alaskan Airlines from $178 round trip http://www.emconference.org/mammoth

Giant Steps In Emergency Medicine 2010 Hilton San Diego Resort & Spa, San Diego

Su nda y - Wed ne sda y, Ju n

1 0 2 , 0 3 e 27 -

The CME course you have been waiting for. Known for their interactive, enthusiastic, and effective teaching styles, Drs. Joe Lex, Amal Mattu and Ghazala Sharieff routinely participate in CME courses nationally and internationally.

They don’t lecture and then disappear. They are committed to audience education and promote interaction and questions.

Special Guest Faculty Peter M. C. DeBlieux, MD, FAAEM, FACEP

0

Course highlights • • • • • •

20.25 Cme credits High-yield topics Optional pediatric workshop Optional ECG workshop Optional LLSA workshop Afternoons free for family activities

For further details & to register www.giantsteps-em.com 503-635-4891 or 1-866-924-7929

Save the Date

February 15 â&#x20AC;&#x201C; 17, 2010

C a e s a r s P a l a c e , L a s Ve g a s , N V

Save the Date

February 15 â&#x20AC;&#x201C; 17, 2010

C a e s a r s P a l a c e , L a s Ve g a s , N V

The Power of Partnership CEP America is redefining the performance of EDs across the country. We’re a democratic partnership of emergency physicians where leadership, innovation and autonomy are encouraged. If you’re looking for an opportunity to find the right balance of practice and lifestyle, partnering with CEP America could be the right choice.

• A democratic partnership of ED physicians offering honest, transparent ownership • Consistently achieve top rankings for patient and physician satisfaction • Excellent health/retirement programs and management support • 63 emergency sites in six states Contact us today about Partnership opportunities!