Modern Resident - The newsletter of AAEM/RSA
January 2013
Volume 4: Issue 4  |  FacebookTwitterLinkedIn


Your 2012-2013 Leaders:

President
Leana S. Wen, MD MSc

Vice President
Stephanie Gardner, MD

Secretary-Treasurer
Taylor McCormick, MD

Immediate Past President
Teresa M. Ross, MD

At-Large Board Members
Rachael Engle, DO
Ali Farzad, MD
Megan Healy, MD
Sarah Terez Malka, MD
Meaghan Mercer, DO

Medical Student Council President
Mary Calderone

Publications Advisor - Ex-Officio Board Member
Joel Schofer, MD RDMS FAAEM

Modern Resident Contributors

Copy Editor: Rachael Engle, DO

Special thanks to this issue's contributors:
Kaitlin Fries, OMSII; Casey Grover, MD; Nathan Haas, MSIII; Brad Hansen, MSII; Elise Herringa, MSIII; David Hoffelder, MD; Valerie LeComte, MSIV; Shannon McNamara, MD; Meaghan Mercer, DO; Michael Moore, OMIV; Alexandra Murray, OMSIII; Mark Pittman, MD; Michael Pulia, MD FAAEM; Nestor Rodriguez, MD FAAEM; Jennifer Stancati, MSII; Pollianne Ward, MD; and Stephen Werner, OMSIII

Interested in writing?

Email submissions to: info@aaemrsa.org

Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM or AAEM/RSA.


Membership Update
Meaghan Mercer, DO
University of Nevada Las Vegas

There has been a steady increase in membership this year! We want to welcome our newest 100% residency program, the University of Arizona, as well as thank our long-standing 100% residency programs for their continued membership. We have had a strong increase in our international membership both at the resident and student level with large credit going to our new international committee’s hard work. AAEM/RSA’s ever-increasing benefits and continued dedication to education have resulted in a steady growth of our organization and we look forward to working with all of you to strengthen our membership.


Photo of the Month #1
Casey Grover, MD
Stanford/Kaiser Emergency Medicine Residency

Case Presentation:
A two-week-old infant is brought to the emergency department by her mother for “a rash” around her umbilicus. The child was born at 39 weeks via normal vaginal delivery and an uncomplicated pregnancy. The mother informs you that for the past week she has noted a “red thing” in the middle of the patient’s belly button that has been leaving a yellow stain on clothing and diapers.

The child has normal vital signs, is afebrile, and has a normal physical exam except for the umbilicus, which is displayed in the photo below.

What is the diagnosis?


Click to enlarge

Discussion
Diagnosis: Umbilical Granuloma
Umbilical granuloma is the most common cause of an umbilical mass, and is best described as a soft, pink, pedunculated, and friable lesion consisting of granulation tissue. It varies in size, but is most commonly three to 10mm. It forms in the first few weeks of life, and is more common when there is inflammation of the umbilical cord, such as with infection. Initial treatment is with silver nitrate, which is usually applied once or twice a week to the lesion for a few weeks. Management in the emergency department consists of identification of the condition followed by referral to pediatrics for further management. Emergency providers may decide, after discussion with the primary pediatric provider, to provide the first application of silver nitrate in the ED prior to discharge.

Reference

  1. Palazzi DL, Brandt ML. Care of the umbilicus and management of umbilical disorders. Up to Date. Version 20.10. Accessed via the web at uptodate.com on October 18, 2012.

On the Horizon: Shock - Administered Uninterrupted Chest Compressions
Meaghan Mercer, DO
University of Nevada Las Vegas

It is important to revisit and challenge dogma in medicine. When you think of defibrillation you hear the word "CLEAR" and know your primary job in that one instant is to make sure that none of the medical professionals participating in that code situation are at risk of receiving a life threatening shock. However, with the advent of gel adhesive pads is it still dangerous?

When clearing the patient for defibrillation, this causes an interruption in chest compressions causing the central perfusion pressure (CPP) to drop, and it can take more than one minute of good-quality chest compressions to restore them to pre-pause levels.1 CPP has been found to be the best single predictor of ROSC, with values less than 15mmHg predicting a failure. Therefore, we are greatly increasing the morbidity and mortality of our patients with each second off the chest. Circulation published the article “Hands-On Defibrillation, An Analysis of Electrical Current Flow Through Rescuers in Direct Contact with Patients During Biphasic External Defibrillation,” in which they investigate the amount of leakage voltage and current to a rescuer receives during defibrillation. They found that the current measured in the rescuer’s body ranged from 19 to 907µA. In most cases, the leakage current measured below recommended safety standards and none of the rescuers felt a shock.2

The emergence of pregelled self-adhesive pads has greatly decreased the risk of current transmission due to contained gel, reliable pad placement, and decreased operator error. Risk is heightened if the rescuer is in contact with a highly conductive material such as fluids including sweat, gel, or other bodily fluids; however, this can be minimized by placing a dry towel or blanket between the patient and rescuer. Also, the investigators in the study wore gloves, which provide insulation against electrical current.3

Hands-off defibrillation should still be practiced if hand-held paddle electrodes are being used or if there is a highly conductive substance between the provider and patient. More research needs to be done but it is on the horizon and could alter the way we do CPR in the future. The phrase "I'm clear, you're clear, we are all clear" may soon be a memory.

References

  1. Steen S, Liao Q, Pierre L, et al: "The critical importance of minimal delay between chest compressions and subsequent defibrillation: a haemodynamic explanation." Resuscitation. 2003;58(3):249–258.
  2. Hands-On Defibrillation. An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External Defibrillation. Michael S. Lloyd, MD; Brian Heeke, BS; Paul F. Walter, MD; Jonathan J. Langberg, MD. Circulation. 2008;117:2425-2427, doi:10.1161/CIRCULATIONAHA.107.189727.
  3. Kerber, RE. "I'm Clear, You're Clear, Everybody’s Clear": A Tradition No Longer Necessary for Defibrillation? Circulation 2008;117:2435-2436.

Toxicology Review: Chronic Salicylate Poisoning
Pollianne Ward, MD
Temple University Hospital

A 46-year-old female presented to an urban emergency department with complaints of a fall and altered mental status per family. It was reported that the patient had begun to experience nausea and vomiting followed by somnolence one day prior. She had no medical problems and did not take any medications regularly. Vital signs were heart rate 125, BP 130/86, temperature 99.6˚ F, respiratory rate 22 and oxygen saturation 99% on room air. The patient had some minor facial fractures from a fall, but no other injuries after trauma evaluation. EKG showed a sinus tachycardia with a widened QRS and peaked T waves. Basic metabolic panel revealed creatinine 8.5, potassium 7.3, and an anion gap metabolic acidosis. Treatment of hyperkalemia was initiated. A comprehensive drug screen was sent, which showed a salicylate level of 75mg/dl.

Salicylate overdose is a not uncommon chief complaint that emergency physicians encounter. Either intentional or accidental, acute toxicity is usually easily recognizable with symptoms of nausea, vomiting, tinnitus, tachypnea and lethargy in a known or suspected ingestion. However, chronic toxicity can often be indolent and present with non-specific symptoms.

Chronic salicylate toxicity can often mimic other conditions. Non-cardiogenic pulmonary edema occurs in about of 35% of chronic ingestions and may steer the provider down a different path, delaying diagnosis. Hyperpyrexia and altered mental status can be mistaken for sepsis or hyperglycemia and acidosis for DKA. This leads to a higher mortality rate of about 25% for chronic toxicity. Death occurs from cerebral edema and cardiovascular collapse, which is often already significant if the patient presents with acidosis, coma, or renal failure.

Furthermore, serum salicylate levels are lower than with acute poisonings. Acute poisonings can occur at doses of over 150mg/kg of aspirin, leading to serum levels of greater than 30mg/dl. Chronic toxicity can be seen at serum levels of 10-30mg/dl. A normogram was once developed to predict toxic concentrations of aspirin, but is not used because serum levels have been found to be unreliable, especially in chronic toxicity. This phenomenon is due, in part, to the absorption and distribution of the drug. Acidemia and renal failure also inhibit excretion, further potentiating toxicity.

The patient in the case above was promptly dialyzed and recovered without complications. When her mental status normalized, she admitted to taking several doses per day of aspirin for low back pain that had started two weeks earlier. The mainstay of treatment in chronic salicylate toxicity remains rehydration and urine alkalinization. Hemodialysis should be considered in chronic toxicity at lower plasma levels than acute, about 60mg/dl or if there is any evidence of cardiovascular, CNS, or renal dysfunction.

Although uncommon, a high index of suspicion for chronic salicylate toxicity should be maintained in the patient with altered mental status or acidosis, especially the elderly. Early recognition can facilitate appropriate treatment and decrease mortality.

References

  1. Seger, DL, Murray, L. Aspirin. Marx: Rosen’s Emergency Medicine, 7th ed. St Louis, Mo: Mosby; 2009:1954-56.
  2. Kerr, F, Krenzelock, EP. Salicylates. Shannon: Haddad and Winchester’s Clinical Management of Poisoning and Overdose, 4th ed. Philadelphia, PA: Saunders.; 2007:845-847.

Recognition and Management of West Nile Virus in the Emergency Setting
Mark Pittman, MD
Valerie LeComte, MSIV
Elise Heeringa, MSIII
Georgetown University Hospital/Washington Hospital Center

Background
With increasing globalization and ease of travel, diseases once forgotten and relegated to the developing world are again emerging in our population and EDs. Physicians must now be able to effectively recognize these formerly “tropical” diseases and initiate management, particularly given the role of the ED as an epidemiologic bellwether.

This summer, one of these emerging tropical diseases — West Nile Virus (WNV) — captured headlines as record-breaking numbers of people became ill. As of September 18th, 134 deaths and 3,142 total cases had been reported to the CDC, the second highest incidence since WNV first appeared in the US in 1999. Given the recent epidemic proportions, it has become even more important for emergency physicians to feel comfortable identifying West Nile in order to steer treatment decisions, contribute to surveillance data, and ultimately guide prevention programs.

Transmission
As a zoonotic arbovirus, WNV is typically spread by the bite of a mosquito, which itself acquires the virus by feeding on infected birds, the primary reservoir. In a small number of cases WNV has also reportedly been spread through blood transfusions, organ transplants, breastfeeding, and transplacental routes. In general, however, humans and other mammals are felt to be incidental or “dead-end” hosts, as they usually do not develop the infectious-level viremias that would permit spread to others.

Signs & Symptoms
About 80% of those infected with WNV will remain completely asymptomatic, but up to one in five people infected will experience milder symptoms often termed “West Nile fever.” The signs and symptoms of West Nile fever include fever, headache, malaise, back pain, myalgias, and anorexia for 3-6 days, with the majority having mild residual symptoms for over 30 days. Variable symptoms include maculopapular rash, ocular manifestations (chorioretinitis), pharyngitis, nausea, vomiting, diarrhea, and abdominal pain. Approximately one in 150 people infected with WNV will develop a more severe, neuroinvasive version, which may present as encephalitis, meningitis, flaccid paralysis, or a mixed pattern.

Work-Up & Treatment
In patients with West Nile fever, serologic testing with ELISA for detection of IgM antibody to WNV is recommended, but cross-reactivity to related flaviviruses such as dengue and yellow fever may occur, even from recent vaccination. In those with suspected neuroinvasive WNV, lumbar puncture and testing of CSF for IgM antibody is recommended in addition to the serologic testing. CSF usually shows a pleocytosis with a predominance of lymphocytes, elevated proteins, and normal glucose. Head CT is generally normal, but abnormal MRI findings are possible and variable.

Treatment is mainly supportive. Interferon, ribavirin, and IV immunoglobulin have been used in neuroinvasive disease, but evidence to support their use has not been demonstrated.

Prognosis & Risk Factors
West Nile fever is a self-limiting disease without life-threatening sequelae. Serious adverse outcomes are limited to patients with neuroinvasive disease, with fatality ranging from 3-15%. Data on the long-term prognosis for survivors of neuroinvasive disease is quite variable.

Age is by far the greatest risk factor for the development of neuroinvasive WNV infection, and there should be a high index of suspicion in any patient older than 50 years who presents with meningitis or encephalitis in summer or early fall. The disease can occur year-round in temperate climates, so obtaining a recent travel history is valuable, particularly regarding the six states where about 70% of the cases have occurred this year — Texas, South Dakota, Mississippi, Oklahoma, Louisiana, and Michigan.

References

  1. cdc.gov
  2. Cook RL, Xu X, Yablonsky EJ, et al. Demographic and clinical factors associated with persistent symptoms after West Nile virus infection. Am J Trop Med Hyg. 2010;83:1133-6.
  3. Loeb M, Hanna S, Nicolle L, et al. Prognosis after West Nile Virus Infection. Ann Int Med. 2008;149(4):232-41.
  4. O'Leary DR, Marfin AA, Montgomery SP, et al. The epidemic of West Nile virus in the United States, 2002. Vector Borne Zoonotic Dis. 2004;4:61-70.
  5. Sejvar JJ, Haddad MB, Tierney BC, et al. Neurologic manifestations and outcome of West Nile virus infection. JAMA. 2003;290:511-15.

Image of the Month #2: Nine-year-old Male with Unilateral Thigh Pain
Nate Haas, MSIII
Loyola University Chicago Stritch School of Medicine

A nine-year-old caucasian male presents to the ED with his mother after six days of worsening left thigh and knee pain. The mother reports she could not see her pediatrician for two more weeks and decided to come to the ED today due to her child’s worsening pain. Both the child and his mother deny any history of trauma, injury, or recent illness. The boy’s mother reports that he woke up with vague complaints of thigh or knee discomfort six days ago, and that his pain has since increased to a current 8/10. Upon further questioning, the mother recalls a similar episode of vague mild pain in the left leg two months ago, at which time she did not seek medical attention due to the perceived mild nature of the pain.

The child has no significant past medical or surgical history aside from "being on the small side of the growth chart his whole life" per his mother. The child lives at home with his mother and father, and both parents smoke frequently inside the home. Family history is significant for "lots of blood clots" on the maternal side of the family.

On exam, the child appears to be in moderate pain, but in no acute distress. He is awake, alert, and oriented, and displays an antalgic gait. His height and weight are each at the eighth percentile for his age. He is afebrile, and vital signs are all within normal limits. There is no erythema, warmth, swelling, or visible deformity in the lower extremities bilaterally, including all joints. There is mild tenderness to palpation over the left femoroacetabular joint, but none elsewhere. Active and passive ranges of motion are mildly decreased in left hip internal and external rotation, but normal in the right hip and normal bilaterally elsewhere.

A CBC, ESR, and CRP were all within normal limits. The following plain film was obtained:


Image source: http://www.peds-ortho.com/perthes.html

What is your diagnosis?

Answer: Legg-Calvé-Perthes disease
Legg-Calvé-Perthes disease (LCP) is a syndrome of idiopathic avascular necrosis of the femoral head that presents most frequently in children ages 3-12 years-old. Males are affected more often than females, and Caucasians more often than African-Americans.1 The exact pathophysiology remains unclear, but several predisposing factors and conditions have been postulated to play a role in the development of LCP. Inherited coagulopathies, especially Factor V Leiden, have been thought to be more prevalent in children with LCP, although this claim remains controversial.2 Second-hand smoke exposure is another proposed risk factor.3 Children whose bone development lags behind that of their peers have demonstrated an increased susceptibility to LCP.4

This is in contrast to slipped capital femoral epiphysis (SCFE), which is more likely to occur in an obese female child after minor trauma. A common presentation of SCFE is simultaneous external rotation and abduction of the hip to relieve the discomfort.

The above image demonstrates advanced disease, and the characteristic avascular necrosis of the femoral head seen above is often not present on plain films initially. It is important to remember that children with early stage LCP often present with pain and with no radiologic evidence of damage to the boney structures of the hip. Thus, a high index of suspicion for LCP must remain when evaluating children with lower extremity pain or limp.

Current treatment for LCP consists of making the child non-weight-bearing, splinting, and referral to a pediatric orthopedic surgeon.

References

  1. Sherry DD, Malleson PN. Nonrheumatic musculoskeletal pain. In: Textbook of Pediatric Rheumatology, 4th, Cassidy JT, Petty RE (Eds), WB Saunders, Philadelphia 2001. p.362.
  2. Glueck CJ, Crawford A, Roy D, et al. Association of antithrombotic factor deficiencies and hypofibrinolysis with Legg-Perthes disease. J Bone Joint Surg Am 1996; 78:3.
  3. Glueck CJ, Freiberg RA, Crawford A, et al. Secondhand smoke, hypofibrinolysis, and Legg-Perthes disease. Clin Orthop Relat Res 1998; :159.
  4. Wenger DR, Ward WT, Herring JA. Legg-Calvé-Perthes disease. J Bone Joint Surg Am 1991; 73:778.

Occult Pneumothorax in Blunt Trauma
David Hoffelder, MD
Nestor Rodriguez, MD FAAEM
University of Wisconsin

Part 1: The Questions
Clinical scenario: You are the emergency physician taking care of a 25-year-old intoxicated male who is brought in via EMS fully immobilized on a backboard and c-collared following a high speed MVA. On primary survey the patient is alert, talking, and breathing normally with intact pulses and no neurologic deficits. Vital signs: HR 114, BP 136/88, RR 18, SaO2 96% on 2L nasal cannula. Secondary survey reveals mild left-sided chest wall tenderness without any obvious evidence of chest trauma. The abdominal exam reveals a seatbelt sign across the lower abdomen with mild associated tenderness to palpation. Otherwise, the patient’s exam is normal. FAST exam, supine chest and pelvis X-rays are unremarkable. Based on the patient’s presentation and examination findings, you order CT scans of his head, cervical spine, abdomen and pelvis. A few minutes later, the radiologist notifies you that all of the CT scans are normal other then a non-displaced left eighth rib fracture and a moderate sized left sided pneumothorax.

This case highlights an increasingly familiar scenario among emergency department trauma patients: the elusive occult pneumothorax (OPTX); which is defined as a pneumothorax (PTX) not suspected based on clinical examination or initial supine chest x-ray, yet detected on CT scan. OPTX is most commonly associated with rib fractures. The detection of OPTX has increased dramatically with the widespread use of CT scanning in trauma patients, and this has raised the question of how the stable patient with an OPTX should be optimally managed.1

Medical decision making time
Do you place a chest tube in this otherwise asymptomatic patient? Do you simply observe this patient with a pneumothorax? Can you use positive pressure ventilation (PPV) if simply observing this patient?

Things to consider: On one hand, there is a concern that a PTX may progress in size and even develop into a tension pneumothorax, exposing the patient to worse consequences. On the other hand, tube thoracostomy (TT) is a procedure with associated risk, including complications of pneumonia, empyema, and lung and vascular injuries. In addition, the current ATLS guidelines state that TT should be performed prior to initiating positive pressure ventilation (PPV) in patients with traumatic PTX, but that observation may be appropriate in asymptomatic patients.2

The next edition will cover in-depth evidence behind use of tube thoracostomy in occult pneumothorax and controversy behind using positive pressure ventilation in occult pneumothorax management.

References

  1. Injury. Int. J. Care Injured. 2009; 928-931.
  2. ATLS 2008

Fungal Meningitis Overview
Alexandra Murray, OMSII
Ohio University Heritage College of Osteopathic Medicine

In early September 2012, three batches of improperly purified methylprednisolone acetate were distributed from the New England Compounding Center (NECC) in Framingham, Massachusetts, to 23 states across America.1 Over the past three months these nonsterile steroid vials have caused a nationwide outbreak of fungal meningitis and joint infections that have infected 438 people in 19 states, and killed 32 people as of November 9, 2012.1 The NECC issued a recall for the three tainted lots of steroid injections on September 26th and the CDC estimates that there was an estimated 42-day risk period that ended on November 7, 2012.1 Although the risk period has ended, this outbreak provides a unique opportunity to review some of the signs, symptoms, and recommended treatment related to fungal meningitis.

The signs and symptoms of fungal meningitis are identical to other forms of meningitis. Predominant symptoms include fever, headache, stiff neck, nausea, vomiting, photophobia, and altered mental status.2,3 Unlike viral or bacterial meningitis, fungal meningitis is not contagious and can only cause infection if the fungus enters the bloodstream and directly accesses the central nervous system, or if there is an infected site near the CNS.2,3 Historically, fungal meningitis has primarily been found to infect immunocompromised individuals; however, there are specific species of fungus that are found in particular environments.2,4

Common Fungal Meningitis Causes
Cryptococcus neoformans Thought to be acquired through inhaling soil contaminated with bird droppings; AIDS and immune suppression
Coccidioides immitis Found in the soil of endemic areas, particularly in Southwestern US and parts of Central and South America; increased virulence in dark-skinned races
Candida sp.  Hospital settings; IV drug abuse; post-surgery; prolonged intravenous therapy; disseminated candidiasis
Histoplasma capsulatum  Found in environments with heavy contamination of bird or bat droppings, particularly in the Midwest near the Ohio and Mississippi Rivers; AIDS; mucosal lesions
Blastomyces dermatitidis  Thought to exist in soil rich in decaying organic matter in the Midwestern and southeastern USA; usually systemic infection; abscesses; draining sinus; ulcers
Aspergillus sp.  Sinusitis; granulocytopenia or immunosuppression
Sporothrix schenckii  Traumatic inoculation; IV drug use; ulcerated skin lesion
Exserohilum rostratum Predominant species found in 2012 fungal meningitis outbreak

Adapted from Table 382-2 Infectious Causes of Chronic Meningitis4

Fungal meningitis is treated with long courses of high dose IV antifungal medications. The length of treatment depends on the patient's immune status and the type of fungal species causing the infection.2,3 Longer courses of treatment are required for individuals with comorbid conditions such as AIDS, HIV, diabetes, cancer, etc.2,3 The CDC currently recommends that infections of Exserohilum rostratum be treated with IV Voriconazole or Liposomal Amphotericin B.1

The prognosis for fungal meningitis includes high mortality rates, frequent treatment complications, and neurologic sequelae.5 Patients should be monitored closely and counseled regarding the importance of adherence to antifungal maintenance therapy because of the high incidence of relapse if treatment is discontinued

References

  1. Multistate Fungal Meningitis Outbreak Investigation. Centers for Disease Control and Prevention. 2012. Available at: http://www.cdc.gov/hai/outbreaks/meningitis.html. Accessed November 12, 2012.
  2. Fungal Meningitis. Centers for Disease Control and Prevention. 2012. Available at: http://www.cdc.gov/meningitis/fungal.html. Accessed November 12, 2012.
  3. Roos KL, Tyler KL. Chapter 381. Meningitis, Encephalitis, Brain Abscess, and Empyema. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
  4. Koroshetz WJ. Chapter 382. Chronic and Recurrent Meningitis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
  5. Greenberg DA, Aminoff MJ, Simon RP. Chapter 4. Confusional States. In: Greenberg DA, Aminoff MJ, Simon RP, eds. Clinical Neurology. 8th ed. New York: McGraw-Hill; 2012.

ACGME Unified Accreditation
Kaitlin Fries, OMSII
Ohio University Heritage College of Osteopathic Medicine

The ACGME’s recent announcement regarding a unified accreditation program in graduate medical education will provide exciting changes for future physicians. While the system’s framework has been laid, there are still many details to be ironed out. Over the upcoming months the ACGME will work closely with the AOA and AACOM to outline these specific details in hopes of reaching the end goal of unified accreditation for Graduate Medical Education.

The AOA began pursuing this unified system a little over a year ago, in response to policies that the ACGME had proposed. These proposals, if enacted, would have drastically impacted osteopathic students by limiting their abilities to enter an ACGME fellowship unless an ACGME residency had been completed. Another proposed policy, would have prevented DOs from entering an ACGME training program once completing an AOA accredited internship year.

The unified accreditation system will address three main topics. First, AOA specialty board certifications would be accepted toward the requirements of being ACGME program directors and faculty. Second, all AOA programs would also be accredited by the ACGME. Finally, AOA and AACOM would become organizational members of ACGME and do all of their accrediting through the joint body in the future.

The current goal is to reach a unified match by July of 2015. This would benefit the osteopathic physicians by ensuring their access to ACGME approved fellowships, as well as allowing DO’s with AOA certification to become ACGME program directors/faculty. While osteopathic residency programs will continue their OMM and OPP competencies, there is discussion of allowing MD’s to enter osteopathic training programs if certain prerequisites in regard to OPP and OMM are met. There will be no changes to licensure examinations (USMLE/COMLEX), however, there is hope that this unified system will further push ACGME residency program directors to understand and interpret COMLEX scores.

This is a very exciting time in graduate medical education. Chief executive officer of ACGME, Thomas Nasca, MD MACP, referred to the unified accreditation system as a “watershed moment for medical training in the U.S.” AOA President Ray E. Stowers, DO, added “Americans deserve a health care system where continuously improving the quality of care and the health of our patients is the driving force. A unified accreditation system creates an opportunity to set universal standards for demonstrating competency with a focus on positive outcomes and the ability to share information on best practices.”

References

  1. "FAQs - ACGME Unified Accreditation System." American Osteopathic Association. N.p., 24 Oct. 2012. Web. 10 Nov. 2012. http://www.osteopathic.org/.
  2. "M.D.s and D.O.s Moving toward a Single, Unified Accreditation System for Graduate Medical Education." ACGME. N.p., 24 Oct. 2012. Web. 10 Nov. 2012. www.acgme.org.

Management of Atraumatic Thigh Pain in a Patient on Bisphosphonate Therapy
Brad Hansen, MSII
Jennifer Stancati, MSII
Loyola University of Chicago Sritch School of Medicine
Michael Pulia, MD FAAEM
University of Wisconsin School of Medicine and Public Health

A 79-year-old woman presents to the emergency department (ED) complaining of atraumatic right thigh pain with weight bearing. This pain has been progressive over several weeks. Past medical history is remarkable for osteoporosis which has been treated with long-term bisphosphonates. Upon examination, there is mild tenderness over her lateral proximal right thigh with no redness, no deformity, and normal ROM. An x-ray of her right femur demonstrates lateral cortical thickening with associated stress fracture in the proximal diaphysis. What is the diagnosis and appropriate management?

Diagnosis
Incomplete atypical femur fracture

Management Recommendations about treatment and prevention of these types of fractures were given in a recently published review by the American Society for Bone and Mineral Research (ASBMR). The ASBMR defines atypical femur fracture as:

  • located just distal to the lesser trochanter to just proximal to the supracondylar flare
  • associated with no trauma or minimal trauma
  • transverse or short oblique in configuration
  • non-comminuted
  • complete fractures extend through both cortices and may be associated with a medial spike; incomplete fractures involve only the lateral cortex

Atypical femur fractures can occur in patients with no exposure to bisphosphonates, but they are more common in patients on bisphosphonate therapy. In the review article by the ASBMR, 70% of the case studies found prodromal thigh pain to be present prior to complete atypical femur fracture. In patients presenting with thigh pain who are undergoing bisphosphonate or other potent anti-resorptive therapy, it is important to order x-ray imaging. With high clinical suspicion for atypical femur fracture, a technetium bone scan or MRI of both legs should also be considered.

If an incomplete fracture is found, and pain is present, there is the option of fixing or treating conservatively by limiting weight bearing activity and following up with x-rays to look for improvement. If an incomplete fracture is found and there is no pain present, weight bearing activity should be limited and close follow up should be kept. If a complete fracture is found, it should be fixed with intramedullary nail fixation. Additionally, in cases of incomplete and complete fracture, bisphosphonate therapy should be discontinued. These fractures may need more aggressive intervention than what is traditionally taught, as a small stress fracture can quickly turn into a complete fracture. Bisphosphonates are a commonly utilized therapy in the treatment of osteoporosis and we must be keenly aware of their association with atypical femur fractures.

Reference

  1. Shane E, Burr D, Ebeling PR, et al. Atypical subtrochanteric and diaphyseal femoral fractures: Report of a task force of the American Society for Bone and Mineral Research. J Bone Miner Res. 2010;25:2267–2294. DOI: 10.1002/jbmr.253.

New Technology in EM: What's Up with FOAM?
Shannon McNamara, MD
Temple University Hospital

You may have come across the term “FOAM” lately in EM content online and scratched your head wondering if people were talking about a rabies outbreak or a nerve gas attack. The term FOAM (Free Open Access Medical Education) describes all collaborative, interactive, open access medical education resources distributed on the web.

Online education in emergency medicine isn’t new. Blogs like EMCrit, Academic Life in EM, Free EM talks, and Life in the Fast Lane have been around for years. FOAM is more than just a new name for these resources. FOAM is a movement by a rapidly growing community of physicians around the world to come together online to teach, to learn, and to debate the art and practice of medicine. In the past, residents learned through clinical teaching and formal didactics, reading textbooks and published literature in peer reviewed journals, and attending annual conferences. Online resources don’t replace these traditional learning modalities, but rather provide a complementary outlet to discuss and debate our practice in a timely, accessible, international forum. This is a powerful opportunity to participate in vibrant dialogue about our constantly changing field.

The next challenge for the FOAM movement will be to figure out the most practical and productive way to integrate online resources with traditional physician learning. How do we organize the explosion of online content into a comprehensive, quality curriculum? What are the most accessible ways for the average physician to find and use quality online resources?

You’re already reading FOAM with AAEM’s Modern Resident, and can access selected articles on MedScape. The Life in the Fast Lane Review is a comprehensive overview of new, quality FOAM content every week. The best part about FOAM is the collaborative dialogue, much of which happens on Twitter, 140 characters at a time. @AAEMRSA and the #FOAMed hashtag are good places to start. @FOAMStarter created a succinct list of the top 25 people in FOAM to follow for beginners new to the forum.

As part of the first generation of digital natives in medicine, we will be instrumental in determining how our medical education system evolves in order to take advantage of new technology. FOAM is an exciting example of people making that happen.


Wilderness Medicine Guideline Update for Preventing Lightening Injuries
Stephen Werner, OMSII
Ohio University Heritage College of Osteopathic Medicine

According to the National Weather Service, lightening causes an average of 400 injuries and 50 deaths each year.1 Due to these data and the risk posed to outdoor enthusiasts, the Wilderness Medical Society (WMS) recently convened an expert panel to update previously published guidelines for the prevention and treatment of lightening injuries.

Lightening is capable of carrying up to two billion volts over a period of about three milliseconds.2 The energy from a lightening strike can discharge directly onto an individual, called a direct strike. It can also travel through the air or traverse the ground following discharge onto a nearby object. This scattering of energy can injure multiple victims in one strike.

The most life-threatening lightening injury is sudden death due to simultaneous cardiac and pulmonary arrest. Studies suggest this is a result of the spontaneous depolarization of cardiac myocytes and the medullary respiratory center. The new WMS guidelines recommend a reverse triage system for lightening victims.3 Priority should be given to victims without vital signs based on multiple case reports of successful resuscitation following lightening induced cardiopulmonary arrest. Finally, the WMS update reinforces the findings that lightening strike victims do not carry residual charge, and should be resuscitated according to current advanced life-support guidelines as soon as the scene can be deemed safe.

To avoid lightening injury, the WMS recommends a number of precautionary measures. While the safest place to be during a lightening storm is indoors, those individuals in outdoor environments should seek refuge in a deep cave, ravine or dense forest. Taking shelter in a tent or picnic area is not recommended due to the risk of current transmission. Other high-risk areas like ski lifts, ridgelines or summits should be avoided, especially in the afternoon hours when lightening strikes are most common. To further minimize injury, one should sit on a backpack (metal frame removed) or foam-sleeping pad in a crouched position with legs and arms close together. Groups should stay at least 20 feet apart to minimize mass casualty situations. Before continuing outdoor activity, a minimum of 30 minutes should be allotted after the last thunderclap to allow for an adequate buffer zone between the storm and the individual.

Overall, lightening storms are an unpredictable danger in a wilderness environment. Being aware of basic lightening preventative measures is an important part of any safe journey into the great outdoors. Happy hiking!

References

  1. Cooper, M. The National Weather Service Lightening Safety. http://www.lightningsafety.noaa.gov/medical.htm. Accessed September 27, 2012.
  2. Fish RM. Chapter 213. Lightning Injuries. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. P. 1391-1392
  3. Davis C, Engeln A, Johnson E, et al. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Lightning Injuries. Wilderness & Environmental Medicine. 2012; 23: 260–269. Accessed September 27, 2012.

NextGenU Emergency Medicine Clerkship
Mike Moore, OMIV
Pacific Northwest University of Health Sciences

As a medical student working in a variety of different locations, it can be difficult to find a standardized rotation in emergency medicine as would be found in an academic medical center. In addition, you may be looking for a way to distinguish yourself as a future emergency medicine resident, and find a way to enhance your CV as you prepare for ERAS. An initiative based at the University of British Columbia in Vancouver, BC, may be a useful addition to your studies.

Called "NextGenU" and located at NextGenU.org on the internet, it is the work of a number of partners lead by a small staff located in Vancouver. It started as a portal for medical information provided for low-middle resource/income countries. As the use of this portal grew, the need for a location to collect medical education resources became apparent. This lead to a partnership between several organizations, notably the Society for Academic Emergency Medicine (SAEM) and the International Federation for Emergency Medicine, to develop what became the first offering of NextGenU, a module in emergency medicine, designed to be used as a core experience for an emergency medicine clerkship.

Developed in conjunction with SAEM, there are eight modules to complete, providing a framework for learning a diagnostic and treatment approach to common emergency department presentations through online study and peer-to-peer activities, as well as a way for a mentor to provide interaction and feedback for your studies. Many online activities added to the clinical year curriculum tend to be case studies or case reviews that are artificial and not synchronized with what you may be seeing in clinic or the hospital on a day-to-day basis. The online activities in the NextGenU emergency medicine clerkship are instead organized by the core content of an ideal emergency medicine clerkship and allow the student and mentor to work through the material together with minimal burden on the preceptor’s time.

This partnership with a mentor provides a much needed mechanism for medical student and preceptor interaction that enhances the educational experience. In addition, it provides a unique way of recognizing your individual effort in learning emergency medicine that certainly would enhance a CV as well as provide an opportunity to explore the rapidly expanding world of free open access medical education. In addition, I would highly recommend the outstanding EMBasic podcast, which is specifically oriented to core topics in emergency medicine for medical students.

Online Resources

  1. http://nextgenu.org "NextGenU.org – Portal to Free, Accredited Higher Education"
  2. http://embasic.org "EM Basic – Your Boot Camp Guide for Emergency Medicine"