VOL. 57 NO. 2 2016 JMSMA by Journal MSMA

VOL. LVII • NO. 2 • 2016

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VOL. LVII • NO. 2 • FEBRUARY 2016

EDITOR Lucius M. Lampton, MD ASSOCIATE EDITORS D. Stanley Hartness, MD Richard D. deShazo, MD

THE ASSOCIATION President Daniel P. Edney, MD President-Elect Lee Voulters, MD

MANAGING EDITOR Karen A. Evers

Secretary-Treasurer Michael Mansour, MD

PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD Leslie E. England, MD Ex-Officio and the Editors

Speaker Geri Lee Weiland, MD Vice Speaker Jeffrey A. Morris, MD Executive Director Charmain Kanosky

JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual). Periodicals postage paid at Jackson, MS and at additional mailing offices. CORRESPONDENCE: Journal MSMA, Managing Editor, Karen A. Evers, P.O. Box 2548, Ridgeland, MS 39158-2548, Ph.: 601-853-6733, Fax: 601-853-6746, www.MSMAonline.com.

SCIENTIFIC ARTICLES Top 10 Facts You Need to Know about Pneumococcal 32 Vaccination in Adults Tayyab Rehman, MD and Zarrish S. Khan, MD Validation of the Sonographic Ottawa Foot and Ankle Rules (SOFAR) Study in a Large Urban Trauma Center Brian Tollefson, MD; James Nichols, DO; Stephen Fromang, DO; Richard L. Summers, MD

Recurrent Diabetic Muscle Infarction Affecting Bilateral Thighs: Uncommon Presentation with Grave Prognosis William B. Horton, MD; Avnish Tripathi, MD; Timothy J. Ragland, MD; Tauqueer Yousuf, MD

Clinical Problem-Solving Case: I’ve Forgotten How to Pray Joanna Bayles, DO and John P.F.H. Vanderloo, MD

DEPARTMENTS From the Editor – The End of “Meaningless Use” Lucius M. Lampton, MD; Editor President's Page – Get Into the Groove Daniel P. Edney, MD; MSMA President

30 45

Letter /Editorial - Tribute to a Role Model Billy W. Long, MD

Editorial - The Unanticipated Consequences of “Meaningful Use” and Maintenance of Certification Requirements Robert T. Brodell, MD Editorial - Oh, No, Another Patient with Back Pain James A. Rish, MD, and Janet Maurer, MD

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49 53

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RELATED ORGANIZATIONS Mississippi State Department of Health– Reportable Disease Stats Currier Honored Dr. Nathan Davis Award Recipient

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POSTMASTER: send address changes to Journal of the Mississippi State Medical Association, P.O. Box 2548, Ridgeland, MS 39158-2548. The views expressed in this publication reflect the opinions of the authors and do not necessarily state the opinions or policies of the Mississippi State Medical Association. Copyright © 2016 Mississippi State Medical Association.

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ABOUT THE COVER

“Mushroom Flowers”– Dr. Martin Pomphrey of Mayhew discovered these fascinating funghi springing from a pile of wood chips. Mushroom species can be identified by their cap, gills, stem, spores, odor/taste and habitat. There are numerous websites dedicated to identifying wild mushrooms. These pictured might be a shaggy parasol variety but this managing editor couldn’t confirm it. n

VOL. LVII • NO. 2 • 2016

JOURNAL MSMA

F R O M

T H E

E D I T O R

The End of “Meaningless Use”

n early January, physicians across the country were both elated and surprised to hear of the coming end of the hated Meaningful Use (MU) program, often termed “Meaningless Use” by the more cynical among us. Centers for Medicare and Medicaid Services (CMS) Acting Administrator Andy Slavitt commented, “The CMS meaningful use program as it has existed will now effectively be over and replaced with something better.” Apparently responding to extensive concerns voiced by the AMA and other leading medical organizations, Slavitt was also quoted as saying, “We have to get the hearts and minds of physicians back. I think we’ve lost them.” Indeed, they have. MU, which has been in existence for six years, defines minimum government standards for using electronic health records (EHR) and for exchanging patient clinical data between healthcare providers, insurers, and patients. It also set specific objectives that physicians and hospitals had to achieve to qualify for CMS incentive programs and established financial penalties if they didn’t. Most complaints with MU were its layers of requirements and regulations which seemed to change daily

and rarely seemed relevant or evidence-based to practicing physicians. It was clear that the pace of change was too fast and that regulations increased the physician time-burden with useless demands. Many physicians are convinced MU worsened clinical patient care by focusing on computer outcomes rather than clinical outcomes. As well, MU’s failure to accomplish effective EHR interoperability was noteworthy. Although Slavitt’s bold comments are reassuring, our profession’s final judgement must be reserved until CMS rolls out the “something better.” Our elation with MU’s demise may be short-lived if what follows is worse. CMS’s current emphasis on the new Merit-based Incentive Payment System and alternate payment models will include their own versions of excessive and unnecessary regulations. Slavitt did imply that what is to follow will be more provider and patient centric, with focus on patient outcome. If CMS really wants the hearts and minds of physicians back, they must change more than just the name of their program. They must place the physician firmly in the EHR driver’s seat and enhance (and not diminish) the physician’s efficient delivery of quality and compassionate patient care. Contact me at LukeLampton@cableone.net. — Lucius M. Lampton, MD, Editor

JOURNAL EDITORIAL ADVISORY BOARD Timothy J. Alford, MD Family Physician, Kosciusko Medical Clinic Michael Artigues, MD Pediatrician, McComb Children’s Clinic Diane K. Beebe, MD Professor and Chair, Department of Family Medicine, University of Mississippi Medical Center, Jackson Rep. Sidney W. Bondurant, MD Retired Obstetrician-Gynecologist, Grenada Jennifer J. Bryan, MD Assistant Professor, Department of Family Medicine University of Mississippi Medical Center, Jackson Jeffrey D. Carron, MD Professor, Department of Otolaryngology & Communicative Sciences, University of Mississippi Medical Center, Jackson Gordon (Mike) Castleberry, MD Urologist, Starkville Urology Clinic Matthew deShazo, MD, MPH Assistant Professor-Cardiology, University of Mississippi Medical Center, Jackson Thomas E. Dobbs, MD, MPH State Epidemiologist, Mississippi State Department of Health, Hattiesburg Sharon Douglas, MD Professor of Medicine and Associate Dean for VA Education, University of Mississippi School of Medicine, Associate Chief of Staff for Education and Ethics, G.V. Montgomery VA Medical Center, Jackson Bradford J. Dye, III, MD Ear Nose & Throat Consultants, Oxford

30 VOL. 57 • NO. 2 • 2016

Daniel P. Edney, MD Executive Committee Member, National Disaster Life Support Education Consortium, Internist, The Street Clinic, Vicksburg Owen B. Evans, MD Professor of Pediatrics and Neurology University of Mississippi Medical Center, Jackson Maxie L. Gordon, MD Assistant Professor, Department of Psychiatry and Human Behavior, Director of the Adult Inpatient Psychiatry Unit and Medical Student Education, University of Mississippi Medical Center, Jackson Nitin K. Gupta, MD Assistant Professor-Digestive Diseases, University of Mississippi Medical Center, Jackson Scott Hambleton, MD Medical Director, Mississippi Professionals Health Program, Ridgeland J. Edward Hill, MD Family Physician, North Mississippi Medical Center, Tupelo W. Mark Horne, MD Internist, Jefferson Medical Associates, Laurel Daniel W. Jones, MD Sanderson Chair in Obesity, Metabolic Diseases and Nutrition Director, Clinical and Population Science, Mississippi Center for Obesity Research, Professor of Medicine and Physiology, Interim Chair, Department of Medicine Ben E. Kitchens, MD Family Physician, Iuka

Brett C. Lampton, MD Internist/Hospitalist, Baptist Memorial Hospital, Oxford Philip L. Levin, MD President, Gulf Coast Writers Association Emergency Medicine Physician, Gulfport Lillian Lien, MD Professor and Director, Division of Endocrinology, University of Mississippi Medical Center, Jackson William Lineaweaver, MD Editor, Annals of Plastic Surgery, Medical Director, JMS Burn and Reconstruction Center, Brandon Michael D. Maples, MD Vice President and Chief of Medical Operations, Baptist Health Systems Heddy-Dale Matthias, MD Anesthesiologist, Critical Care Internist, Madison Jason G. Murphy, MD Surgeon, Surgical Clinic Associates, Jackson Alan R. Moore, MD Clinical Neurophysiologist, Muscle and Nerve, Jackson Paul “Hal” Moore Jr., MD Radiologist, Singing River Radiology Group, Pascagoula Ann Myers, MD Rheumatologist , Mississippi Arthritis Clinic, Jackson Darden H. North, MD Obstetrician/Gynecologist , Jackson Health Care-Women, Flowood

Jack D. Owens, MD, MPH Neonatologist, Newborn Associates, Flowood Michelle Y. Owens, MD Associate Professor, Vice-Chair of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson Jimmy L. Stewart, Jr., MD Program Director, Combined Internal Medicine/ Pediatrics Residency Program, Associate Professor of Medicine and Pediatrics University of Mississippi Medical Center, Jackson Shou J. Tang, MD Professor and Director, Division of Digestive Diseases, University of Mississippi Medical Center, Jackson Samuel Calvin Thigpen, MD Hematology-Oncology Fellow, Department of Medicine, University of Mississippi Medical Center, Jackson Thad F. Waites, MD Clinical Cardiologist, Hattiesburg Clinic W. Lamar Weems, MD Urologist, Jackson Chris E. Wiggins, MD Orthopaedic Surgeon, Bienville Orthopaedic Specialists, Pascagoula John E. Wilkaitis, MD Chief Medical Officer, Brentwood Behavioral Healthcare, Flowood Sloan C. Youngblood, MD Assistant Medical Director, Department of Anesthesiology, University of Mississippi Medical Center, Jackson

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JOURNAL MSMA

Top 10 Facts You Need to Know about Pneumococcal Vaccination in Adults Tayyab Rehman, MD and Zarrish S. Khan, MD Introduction Streptococcus pneumoniae (pneumococcus) is an important cause of morbidity and mortality in adults. Adult pneumococcal disease may be categorized as either invasive or non-invasive: invasive disease is marked by the isolation of the organism from a normally sterile body site (blood, cerebrospinal fluid, pleural fluid, etc.) while non-invasive disease manifests as non-bacteremic pneumonia. Vaccination remains a proven strategy to reduce the burden of pneumococcal disease. In the last few years, several landmark studies have been conducted to elucidate the immunogenicity and effectiveness of pneumococcal vaccines in adults, prompting the Advisory Committee on Immunization Practices (ACIP) and the Centers for Disease Control and Prevention (CDC) to revise and update their recommendations. Salient feature of these recommendations are outlined below:

Two types of pneumococcal vaccines are currently approved for use in adults. The pneumococcal polysaccharide capsule is a major virulence factor and is the basic immunogen in all currently approved pneumococcal vaccines. The composition of the capsular polysaccharide varies from strain to strain. To date, more than 90 different strains (serotypes) have been identified that cause disease in humans. Presently available vaccine formulations aim to cover the most prevalent serotypes. These include: (a) the 23-valent pneumococcal polysaccharide vaccine (PPSV23 [Pneumovax 23, Merck & Co., Inc.]) containing capsular polysaccharides from 23 serotypes; and (b) the Box 1. 13-valent pneumococcal conjugate vaccine (PCV13 [Prevnar 13, Wyeth Presently Available Pneumococcal Vaccines Pharmaceuticals, Inc.]) containing capsular polysaccharides from 13 (1) 23-valent pneumococcal polysaccharide vaccine PPSV23 serotypes covalently attached to a carrier protein (Diphtheria CRM197). [Pneumovax 23, Merck & Co., Inc.] Of the 13 serotypes in PCV13, 12 are shared with PPSV23 while serotype (2) 13-valent pneumococcal conjugate vaccine PCV13 [Prevnar 13, Wyeth Pharmaceuticals, Inc.] 6A is unique to PCV131,2 (Box 1).

PPSV23 and PCV13 offer immunoprotection through distinct mechanisms. Box 2. The polysaccharide-based PPSV23 induces a T-cell independent response. However, the human immune system is not adept at Candidates for PPSV23 alone recognizing polysaccharide antigens. As a result, PPSV23 may not induce a robust response in children (≤2years), the elderly (≥65 Cigarette does smoking years) and individuals with immunocompromising conditions; moreover, PPSV23 not lead to immunologic memory formation so that subsequent re-exposure fails to induce an augmented response. Conjugation of polysaccharide with a protein may overcome these Alcoholism Box 1. that is robust, durable and anamnestic. In addition, limitations. The saccharide-protein complexes induce a T-cell dependent response Diabetes mellitus Presently Available Pneumococcal Vaccinescarriers, a feature not shared conjugated vaccines engender mucosal immunity that eradicates nasopharyngeal colonization in asymptomatic 3 with polysaccharide vaccines. Chronic heartpneumococcal disease (heartpolysaccharide failure, cardiomyopathies, etc.) (1) 23-valent vaccine PPSV23 [Pneumovax 23, Merck & Co., Inc.] Chronic lung disease (asthma, chronic obstructive pulmonary disease, etc.) (2) 13-valent pneumococcal conjugate vaccine PCV13 non-invasive disease; contrast, PPSV23 provides reliable [Prevnar 13, Wyethin Pharmaceuticals, Inc.] Chronic liver disease (cirrhosis)

PCV13 provides protection against both invasive and protection against only invasive disease. In clinical efficacy studies, PPSV23 consistently protected against invasive pneumococcal disease; however, protection against non-invasive pneumococcal pneumonia was not reliable.4,5 A 2009 meta-analysis concluded that PPSV23 was not effective in preventing pneumonia.4 This led to interest in PCV13 as an alternative or adjunct to PPSV23 in adults. The definitive evidence came from the recently concluded CAPiTA trial that showed that PCV13 afforded excellent protection against both invasive and non-invasive disease in the elderly.6

PPSV23 alone is indicated for adults 19-64 years of age who have certain underlying medical conditions associated with an increased risk for pneumococcal infection1,7 (Box 2).

32 VOL. 57 • NO. 2 • 2016

Box 2. Box 3. Candidates for PPSV23 alone Candidates for dual PCV13 and PPSV23 vaccination Cigarette smoking Adults aged ≥65 Alcoholism Anatomic or functional asplenia (splenectomy, sickle cell disease, etc.) Diabetes mellitus Cerebrospinal ﬂuid leak Chronic heart disease (heart failure, cardiomyopathies, etc.) Cochlear implants Chronic lung disease (asthma, chronic obstructive pulmonary disease, etc.) Immunocompromising conditions: Chronic liver disease (cirrhosis) Congenital or acquired immunodeﬁciency HIV infection Chronic renal failure Box 3. Nephrotic syndrome Leukemia CandidatesLymphoma for dual PCV13 and PPSV23 vaccination

PCV13 and PPSV23, in a sequentially administered combination, are indicated for the elderly and for individuals with certain immunocompromising conditions or conditions associated with a very high risk of invasive pneumococcal disease1,2 (Box 3).

Pneumococcal vaccine-naïve individuals with a history or current diagnosis of pneumococcal disease should be vaccinated to reduce the risk of future infection. Infection with one pneumococcal strain does not confer blanket protection against all other strains. An individual who has suffered pneumococcal disease has already demonstrated susceptibility and remains at risk for future infection. Whether such individuals should receive vaccination (if they do not have any of the above-listed conditions to make them eligible for pneumococcal vaccination) has not been addressed in the most recent ACIP recommendations. In our opinion, such individuals should receive vaccination using both PCV13 and PPSV23 (i.e., PCV13 first, followed ≥8 weeks later by PPSV23). In a hospitalized patient with pneumonia, pneumococcal vaccine, if indicated, can be administered at any time prior to discharge.

The vaccination schedule requires particular attention when both PCV13 and PPSV23 are indicated. PCV13 and PPSV23 should be administered sequentially, not simultaneously. Whenever possible, PCV13 should be administered first. For pneumococcal vaccine-naïve individuals 19-64 years of age requiring dual vaccination, a single dose of PCV13 should be administered first followed ≥8 weeks later by PPSV23.1 A onetime repeat vaccination with PPSV23 is recommended ≥5 years after the last PPSV23 dose. For individuals 19-64 years of age who require dual vaccination but have a history of prior vaccination with PPSV23, a single dose of PCV13 should be given ≥1 year after the PPSV23. Repeat vaccination with PPSV23 is recommended ≥5 years after the last PPSV23 but no sooner than 8 weeks after the last PCV13 (Figure 1).

Box 3. Candidates for dual PCV13 and PPSV23 vaccination Adults aged ≥65 Anatomic or functional asplenia (splenectomy, sickle cell disease, etc.) Cerebrospinal ﬂuid leak Cochlear implants Immunocompromising conditions: Congenital or acquired immunodeﬁciency HIV infection Chronic renal failure Nephrotic syndrome Leukemia Lymphoma Hodgkin’s disease Multiple myeloma Generalized malignancy Iatrogenic immunosuppression Solid organ transplant

Figure 1. Schedule for dual vaccination, adults 19-64 with conditions listed in box 3: A) Pneumococcal vaccine-naïve:

PCV13

≥ 8 weeks

PPSV23

≥ 5 years

PPSV23

B) Individuals previously vaccinated with PPSV23: Previously received

PPSV23

≥ 1 year

PCV13

See below

PPSV23

≥ 8 weeks ≥ 5 years

Dual, sequential vaccination with PCV13 and PPSV23 is recommended for all individuals ≥65 years of age.8 Several scenarios may arise in this age group: (a) For immunocompetent, pneumococcal vaccine-naïve individuals ≥65 years of age, a single dose of PCV13, followed ≥1 year later by PPSV23, should be administered. (b) For individuals who previously received a dose Figure 2. Schedule for dual vaccination, adults ≥65: of PPSV23 at age ≥65 years, a single dose of PCV13 should be administered ≥1 year after the PPSV23. (c) For individuals who previously received PPSV23 before the age of 65 and are now ≥65 years of age, a single of PCV13vaccine-naïve: should be given ≥1 year after the PPSV23. Repeat A)dose Pneumococcal PPSV23 in this group should be administered ≥1 years after the PCV13 dose and ≥5 years after the last PPSV23. (d) For individuals aged ≥65 years with an immunocompromising condition, cerebrospinal fluid leak, cochlear implant or asplenia, the sequence of PCV13 followed by ≥ 1 yearbe ≥8 weeks(Figure PPSV23 is recommended with the proviso that the interval between the twoPCV13 vaccines should 2, next page). PPSV23

Concurrent administration of pneumococcal and influenza vaccines is acceptable. B) Individuals who previously received PPSV23 after age ≥ 65: has been In several clinical trials, simultaneous administration of pneumococcal (either PPSV23 or PCV13) and influenza vaccines 9,10 shown to be safe. Local reactions and post-vaccination fever may occur more commonly with co-administration; however, increased Previously received at age ≥65 incidence of serious side effects has not been reported. While antibody responses to both PPSV23 and PCV13 are diminished with co≥ 1 year PPSV23 administration of trivalent influenza vaccine, these reductions are modest and their impact on clinicalPCV13 efficacy has not been determined.10,11 Until further studies become available, it remains advisable to administer influenza and pneumococcal vaccines at the same visit in all scenarios where both vaccines are indicated. C) Individuals who received PPSV23 before age 65: Previously received at age <65

PPSV23

≥ 1 year

Current age ≥65

MSMA See below PCV13 JOURNAL PPSV23 33

Universal childhood PCV13 vaccination is likely to alter the epidemiology of adult pneumococcal disease. In 2000, PCV7 was introduced as a routine childhood vaccine. The following decade saw major declines in the rates of adult pneumococcal disease, attributable to indirect effects of childhood vaccination (herd immunity).12,13 In 2010, the ACIP recommended replacing PCV7 with PCV13 in childhood vaccination schedule.14 Initial evidence indicates that adult disease due to PCV13 serotypes is on the wane.15 However, since PCV13 does not cover all pathogenic serotypes, concern remains that non-vaccine serotypes may replace vaccine serotypes over time and become significant contributors to adult pneumococcal disease (serotype replacement).13,16 The epidemiology of pneumococcal disease in adults is likely to continue to evolve in coming years and ongoing surveillance will be needed to develop optimum vaccine strategies. n Corresponding Author: Tayyab Rehman, MD; Pulmonologist & Intensivist, Staff Physician, Delta Regional Medical Center, 1400 E Union St., Greenville, MS 38703. Cell: 504-491-4359. Email: tayyab208@yahoo.com.

Figure 2. Schedule for dual vaccination, adults ≥65: A) Pneumococcal vaccine-naïve:

PCV13

≥ 1 year

PPSV23

B) Individuals who previously received PPSV23 after age ≥ 65: Previously received at age ≥65

PPSV23

≥ 1 year

PCV13

C) Individuals who received PPSV23 before age 65: Previously received at age <65

PPSV23

≥ 1 year

Current age ≥65

PCV13

See below

PPSV23

≥ 1 year ≥ 5 years

D) Individuals ≥65 with asplenia, cerebrospinal ﬂuid leak, cochlear implant or an immunocompromising condition:

References 1. Centers for Disease C, Prevention. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine for adults with immunocompromising conditions: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. 2012;61(40):816-819. 2. Tomczyk S, Bennett NM, Stoecker C, et al. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine among adults aged >/=65 years: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. 2014;63(37):822-825. 3. Centers for Disease C, Prevention. Licensure of 13-valent pneumococcal conjugate vaccine for adults aged 50 years and older. MMWR. 2012;61(21):394-395. 4. Huss A, Scott P, Stuck AE, Trotter C, Egger M. Efficacy of pneumococcal vaccination in adults: a meta-analysis. CMAJ. 2009;180(1):48-58. 5. Moberley S, Holden J, Tatham DP, Andrews RM. Vaccines for preventing pneumococcal infection in adults. Cochrane Database Syst Rev. 2013;1:CD000422. 6. Bonten MJ, Huijts SM, Bolkenbaas M, et al. Polysaccharide conjugate vaccine against pneumococcal pneumonia in adults. N Engl J Med. 2015;372(12):1114-1125. 7. Centers for Disease C, Prevention, Advisory Committee on Immunization P. Updated recommendations for prevention of invasive pneumococcal disease among adults using the 23-valent pneumococcal polysaccharide vaccine (PPSV23). MMWR. 2010;59(34):1102-1106. 8. Kobayashi M, Bennett NM, Gierke R, et al. Intervals Between PCV13 and PPSV23 Vaccines: Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. 2015;64(34):944-947. 9. Honkanen PO, Keistinen T, Kivela SL. Reactions following administration of influenza vaccine alone or with pneumococcal vaccine to the elderly. Arch Intern Med. 1 1996;156(2):205-208. 2 10. Frenck RW, Jr., Gurtman A, Rubino J, et al. Randomized, controlled trial of a 13-valent pneumococcal conjugate vaccine administered concomitantly with an influenza 3 vaccine in healthy adults. Clinical and vaccine immunology : CVI. 2012;19(8):12964 1303. 5 11. Schwarz TF, Flamaing J, Rumke HC, et al. A randomized, double-blind trial to evaluate 6 immunogenicity and safety of 13-valent pneumococcal conjugate vaccine given 7 concomitantly with trivalent influenza vaccine in adults aged >/=65 years. Vaccine. 2011;29(32):5195-5202. 8 12. Lexau CA, Lynfield R, Danila R, et al. Changing epidemiology of invasive 9 pneumococcal disease among older adults in the era of pediatric pneumococcal 10 conjugate vaccine. JAMA. 2005;294(16):2043-2051. 34 VOL. 57 • NO. 2 • 2016

11 12 13 14

PCV13

≥ 8 weeks

PPSV23

13. Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis. 2010;201(1):32-41. 14. Nuorti JP, Whitney CG, Centers for Disease C, Prevention. Prevention of pneumococcal disease among infants and children - use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2010;59(RR-11):1-18. 15. Moore MR, Link-Gelles R, Schaffner W, et al. Effect of use of 13-valent pneumococcal conjugate vaccine in children on invasive pneumococcal disease in children and adults in the USA: analysis of multisite, population-based surveillance. Lancet Infect Dis. 2015;15(3):301-309. 16. Weinberger DM, Malley R, Lipsitch M. Serotype replacement in disease after pneumococcal vaccination. Lancet. 2011;378(9807):1962-1973.

Journal of the Mississippi State Med The University of Mississippi Medical Center Nephrology Division in Jackson, MS is seeking BC/BE two Nephrologists. Faculty candidates should submit a CV via fax to 601-984-5608. EOE, M/F/D/V.

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Validation of the Sonographic Ottawa Foot and Ankle Rules (SOFAR) Study in a Large Urban Trauma Center BRIAN TOLLEFSON, MD; JAMES NICHOLS, DO; STEPHEN FROMANG, DO; RICHARD L. SUMMERS, MD

Abstract Introduction: Differentiating the severity of acute ankle injuries is a common problem in the emergency department (ED). The Ottawa Foot and Ankle Rules (OFAR) were designed to obviate the need for unnecessary x-rays. Although these rules have been determined to be very sensitive, they lack the specificity necessary to make them practically useful for a condition in which a misdiagnosis could result in a significant disability. Our study objective was to determine if the addition of a bedside ultrasound (US) to the evaluation process could be used to significantly reduce the number of negative x-rays in OFAR positive patients. Methods: A prospective observational study was conducted in a Level I urban trauma center over a 12 month period in which bedside US was utilized to detect foot and/or ankle fractures in OFAR positive patients of age 18 years and older. All patients in the study received foot and/or ankle x-rays based on OFAR exam. Prior to viewing the x-rays, trained clinicians performed bedside US targeting the medial and lateral malleoli, navicular, and base of the 5th metatarsal and provided a diagnostic impression based on their US findings. The US findings were then compared to the formal x-ray interpretation. Results: A total of fifty patients was enrolled into the study of which twenty-one patients were discovered to have a fracture by US. The sensitivity of US in detecting foot and/or ankle fractures was 100% (95% Confidence Interval [CI] 78%-100%) and the specificity of OFAR increased from 50% (95% CI 37%-63%) to 100% (95% CI 87%-100%) with the addition of US. The negative predictive value was 100% (95% CI 89%-100%), and the positive predictive value was 100% (95% CI 81%-100%). Conclusions: Among OFAR positive patients, bedside US has high sensitivity and specificity for detecting foot and/or ankle fractures. Further studies should be conducted to determine if utilizing bedside US in addition to OFAR could significantly reduce the number of x-rays and improve the efficiency and costs associated with evaluating these injuries in the ED.

Implication for health policy/medical education/research/ practice Utilizing bedside ultrasonography in addition to Ottawa Foot and Ankle Rules in acutely injured patients could significantly reduce the number of ordered x-rays and length of stay in the emergency department. Key Words: SOFAR, ankle fracture, Ottawa foot and ankle rules, validation, trauma Introduction Acute foot and ankle injuries are common reasons for emergency department visits. Most of these patients receive x-rays of the foot and ankle and are ultimately diagnosed with a sprain. The clinical Ottawa Foot and Ankle Rules (OFAR) were created to reduce the number of unnecessary x-rays and radiation exposure used in the evaluation of patients in the emergency department (ED).1 Although these rules are very sensitive in identifying foot and ankle fractures, they lack the specificity needed to make them practically useful. The initial OFAR studies reported a sensitivity of 94.6% and 100% and a specificity of 15.5% and 11.5% for foot and ankle fractures respectively.1-3 Lucchesi et al found that clinical gestalt alone had a sensitivity of 69% for predicting ankle fractures and 76% for mid-foot fractures. Even with the application of the OFAR, less than 22% of the patients that present to the ED with ankle and foot injuries are found to have a fracture.2 Approximately 80% of foot and ankle injuries that meet criteria for x-ray imaging by OFAR do not have a fracture. The table lists the Ottawa foot and ankle rules originally described by Stiell et al.1 Table 1â&#x20AC;&#x201D;Ottawa Foot andand Ankle Rules:Rules TABLE. Ottawa Foot Ankle Ankle XR required only if pain in malleolar region and any of the following: - Tenderness over posterior aspect or tip of lateral malleolus (distal 6 cm) - Tenderness over posterior aspect or tip of medial malleolus (distal 6 cm) - Unable to bear weight 4 steps both immediately after injury and in the ED Foot XR required only if pain in midfoot region and any of the following: - Tenderness over navicular bone - Tenderness over base of 5th metatarsal - Unable to bear weight 4 steps both immediately after injury and in the ED

Figure 1: AP ankle x-ray with non-displacedJOURNAL oblique fracture through lateral MSMA 35 malleolus

Ultrasound has been shown to be a valuable tool for evaluating osseous and soft tissue injuries. Advantages of US include absence of radiation, lower cost, ease of use, availability, and portability. Furthermore, ED visit times could be significantly decreased by triaging injuries to needed diagnostic studies and appropriate treatment. Using bedside US, a quick and detailed assessment of the musculoskeletal components of the foot and ankle are easily obtained by experienced sonographers.4 Although the advantages of US for accessing foot and ankle injuries are known, a definitive clinical validation has yet to be established.5-7 Several relatively small studies have been conducted to examine the utility of bedside US in OFAR positive patients.8-12 In a prospective cohort study involving 110 patients, Canagasabey et al. identified 10 of 11 fractures using bedside ultrasound for a sensitivity of 90.9% and specificity of 90.9%.9 Another study conducted in Sweden by Hedelin et al. suggested that US-guided triage could safely decrease x-ray utilization by 70% compared to only 23% when using OFAR alone.10 A prospective study conducted by Ekinci et al found all 20 fractures in 131 OFAR positive patients for a sensitivity and specificity of 100%.11 Finally, a recent ED study conducted in Turkey by Atilla et al. involving 246 patients found a sensitivity and specificity of 87.3 and 96.4%, respectively.12 The purpose of our study is to add to the mounting evidence supporting the use of ED bedside US in the evaluation of OFAR positive patients with foot and ankle injuries. We postulate that an US augmented foot and ankle exam can substantially and safely decrease the number of negative foot and ankle x-rays performed in the ED. Previously, this augmented exam has been cleverly termed the Sonographic Ottawa Foot and Ankle Rules (SOFAR).9 It is our contention that the use of bedside US to evaluate OFAR positive patients be thought of as an extension of the physical exam with the sole purpose of improving the specificity of the clinical OFAR and further eliminating the need for unnecessary and costly x-rays. Methods This prospective validation and observational study was conducted at the University of Mississippi Medical Center (UMMC) from March 1, 2011, to March 31, 2012. This study was designed as an external validation of the SOFAR study.9 Prior to beginning this study, the protocol was approved by the UMMC’s institutional review board. Study investigators were two PGY3 emergency medicine residents and a board certified emergency medicine attending with primary care sports medicine subspecialty certification. A brief systematic instruction was given to the residents who performed satisfactory return demonstration of a focused foot and ankle US exam. Total instructional period for the foot and ankle exam was less than one hour. A Sonosite ultrasound machine with a 15-6 MHz linear probe, as described in foot and ankle US techniques by Fessell et al, was used for all instruction and patient examinations.13 Patients enrolled in our study were a convenience sample of patients identified in triage with a chief complaint of foot and/or ankle pain related to injury. Patients 18 years of age and older that had screened positive by the OFAR were included in the study. Exclusion criteria

36 VOL. 57 • NO. 2 • 2016

for our study included patients that were less than 18 years old, pregnant, prisoners, or unable to give consent. Those that had obvious dislocations, open fractures, multiple injuries, or preexisting ankle pathology were also excluded. After a potential study participant was identified, a study investigator discussed enrollment with the patient and obtained written consent. The investigator then proceeded to perform a focused foot and ankle physical exam and US exam on the study patient. After recording the results of the physical exam and US exam, routine trauma series x-rays were obtained of the foot and/or ankle. In all cases the US exam of the foot and ankle was performed and interpreted prior to obtaining and reviewing x-rays. The results recorded by the study investigator were then correlated with final x-ray reports interpreted by a board certified radiologist. Findings on the US exam were not used to clinically manage any of the patients. Patient management was based on clinical Table exam and1—Ottawa x-ray findings.Foot and Ankle Rules:

SPSS statistics for Windows used in to malleolar analyze the region data collected Ankle XR required onlywas if pain and any of th in our- study. Test characteristics of sensitivity, specificity, positive Tenderness over posterior aspect or tip of lateral malleolus (d predictive value, and negative predictiveaspect value were used determine - Tenderness over posterior or tip oftomedial malleolus (d the validity of using US to4detect exclude foot andafter ankleinjury and - Unable to bedside bear weight stepsorboth immediate fractures. Foot XR required only if pain in midfoot region and any of the fo - Tenderness over navicular bone An example of a typical lateral malleolus fracture is demonstrated th Tenderness over base of 5 metatarsal on the x-ray in Figure 1 and the corresponding ultrasound image in Unable to bear the weight 4 steps(normal) both immediately after injury a Figure- 2. For comparison, contralateral lateral malleolus is shown in Figure 3.

FIGURE 1. AP ankle x-ray with non-displaced oblique Figure AP ankle x-ray with non-displaced oblique fracture thr fracture1:through lateral malleolus

Figure 2: Longitudinal US image of non-displaced lateral malleolus fracture:

The ultrasound examination was well tolerated by all study participants. FIGURE 2. Longitudinal US image of non-displaced lateral None of the patients reported significant discomfort or requested that Figure 2: Longitudinal US image of non-displaced lateral malleolus fracture: malleolus fracture the US examination be terminated. The findings of our study suggest that using bedside US to examine patients that screen positive by the OFAR would decrease the number of unnecessary x-rays by 64%. Discussion In our study, we observed a sensitivity and specificity for detecting fractures using bedside US in OFAR positive patients of 100%. The negative predictive value and the positive predictive value were 100%, as well, demonstrating substantial improvements over clinical Ottawa Foot and Ankle Rules (OFAR) alone. These results further support the use of bedside US as a viable option for assessing patients with acute foot and ankle injuries.

FIGURE 3. Longitudinal US image of normal malleolus Figure 3: Longitudinal US image of normal lateral lateral malleolus: Figure 3: Longitudinal US image of normal lateral malleolus:

Results

It is important to consider how US might be used as an ancillary study in addition to the OFAR. The OFAR are already nearly 100% sensitive in diagnosing foot and ankle fractures. In order to demonstrate an improvement in this sensitivity, an extremely large multi-center study would be necessary, which would be very difficult to achieve, and the results of such a study would be unlikely to change practice. Furthermore, if a fracture is found via US, x-ray will be necessary as it remains the cornerstone for orthopedic planning and monitoring. However, there are some situations by which ultrasound may be helpful both in decreasing radiographic use as well as potentially decreasing patient length of stay in the emergency department. First, the specificity of the OFAR is very low, and previous studies indicate that the reduction in radiographs in OFAR positive patients is only about 36%.3 Combined with the highly sensitive OFAR, bedside US raises the specificity to a useful level. In our study, US was 100% specific for fracture, with a lower 95% confidence interval of 87%. If a sufficiently large study was powered to have a lower 95% CI of nearly 100%, a larger proportion of patients would not require x-rays and could quickly be assessed and discharged without the need for further workup. Figure 4 outlines a potential evaluation algorithm for patients that present to the ED with isolated midfoot and/ or ankle injuries.

There were a total of 50 participants (23 female and 27 male) enrolled into the study with the average age being FIGURE 4. SOFAR algorithm for evaluation of isolated foot and ankle injuries 35-years-old. A combined 21 of the 50 patients (36%) were discovered to have a single isolated fracture or a combination of fractures on US. There were four isolated fifth metatarsal fractures identified, and seventeen patients had isolated malleolus fractures or a combination of lateral and medial malleoli fractures. No navicular fractures were found in this study. The specificity of the Ottawa Foot and Ankle Rules (OFAR) in our study was 50% (95% CI 37%-63%). The sensitivity of US in detecting foot or ankle fractures on OFAR positive patients was 100% (95% Confidence Interval [CI] 78%-100%). The specificity of US on OFAR positive patients was also 100% (95% CI 87%100%). The negative predictive value was 100% (95% CI 89%-100%), and the positive predictive value was 100% (95% CI 81%-100%).

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Second, one of the barriers to the use of standardized decision rules is patient expectations of receiving diagnostic imaging. The use of bedside ultrasound provides safe and cost-effective diagnostic imaging that may alleviate some of these patient concerns. Performance of US studies would also allow a physician to spend additional time at the bedside and likely improve patient satisfaction. This remains an area that could be addressed by future investigations. Finally, ultrasound may play a valuable role in more unconventional environments. Ultrasound use in triage could rapidly diagnose foot and ankle fractures. This would allow more rapid x-ray ordering and specialty consultation. Those patients with negative US studies could potentially be discharged directly from triage thus dramatically improving ED length of stay. The use of US in a primary care clinic or sporting event sideline setting also has potential applications worth investigating. In the clinic setting, a negative US exam could decrease the need to refer patients for unnecessary offsite x-rays. The use of US on the sideline could assist the sports medicine physician in making real-time return to play decisions. The portability of modern US machines makes both of these options a viable practice. There are several limitations of our study that deserve consideration. One of the limitations is that the sample size only included 50 patients, which led to the lower 95% confidence of 78% for sensitivity and 87% for the specificity. Another potential limitation was that the population studied was essentially a convenience sample. Patients were enrolled in the study only during the times that one of the three primary investigators was available. Furthermore, musculoskeletal US requires considerable training and practice to use efficiently and effectively in the clinical setting. However, as our study indicates, one can learn the focused US exam technique required to evaluate for ankle and foot fractures quickly with very little training or experience. Ultrasound training is required in all emergency medicine residency programs, and emergency medicine physicians are becoming more comfortable using bedside US to make treatment decisions. We did not enroll a sufficient number of patients to comment on the utility of ultrasound in obese patients. Morbidly obese patients can be more difficult to examine adequately with US. Future studies could focus on this patient population. Finally, our study represented a relatively young cohort of patients. It is possible that older patients (with decreased bone density) may have lower specificity for fracture with ultrasound. On the other hand, ultrasound may actually prove superior to traditional x-rays in this setting, and it is another area of potential investigation. Conclusion This validation study showed that US is highly sensitive and specific in identification of foot and ankle fractures when combined with the Ottawa Foot and Ankle Rules (OFAR). With a sensitivity and

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specificity of near 100%, the use of bedside US may be effectively implemented to rule out acute foot and ankle fractures in OFAR positive patients. Ultrasound has the potential to drastically decrease the number of negative x-rays obtained on OFAR positive patients. Although the results of our study and other similar studies are promising, larger studies in more diverse patient populations should be conducted to validate these findings prior to implementing bedside ultrasound to definitely rule out foot and ankle fractures. n References 1.

Stiell IG, Mcknight RD, Greenberg GH, et al. Implementation of the Ottawa ankle rules. JAMA 1994;271:827-32.

Lucchesi GM, Jackson RE, Franklin Peacock W, et al. Sensitivity of the Ottawa rules. Ann Emerg Med 1995; 26;1-5.

Stiell IG, Greenberg GH, McKnight RD, et al. Study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med 1992; 21: 384-90.

Jacobson JA. Musculoskeletal sonography and MR imaging. A role for both imaging methods. Radiol Clin North Am 1999;37:713e35

Mellerowicz H, Stelling E, Kefenbaum A. Diagnostic ultrasound in the athleteâ&#x20AC;&#x2122;s locomoter system. Br J Sports Med 1990;24:31e9.

Singh AK, Malpass TS, Walker G. Ultrasonic assessment of injuries to the lateral complex of the ankle. Arch Emerg Med 1990;7:90e4.

Simanovsky N, Hiller N, Leibner E, et al. Sonographic detection of radiographically occult fractures in paediatric ankle injuries. Paedtr Radiol 2005;35:1062e5.

Hsu CC, Tsai EC, Chen CP, et al. Ultrasonographic examination for inversion ankle sprains associated with osseous injuries. Am J Phys Med Rehabil 2006; 85; 785-92.

Canagasabey MD, Callaghan MJ, Carley S. The Sonographic Ottawa Foot and Ankle Rules Study (the SOFAR Study). Emerg Med J 2011;28:838-840.

10.

Hedelin H, Goksor L, Karlsson J et al. Ultrasound-assisted triage of the ankle trauma can decrease the need for radiographic imaging. Am J Emerg Med 2013;31:1686-9.

11.

Ekinci S, Polat O, Gunalp M, et al. The accuracy of ultrasound evaluation in foot and ankle trauma. Am J Emerg Med 2013;31(11):1551-5.

12.

Atilla OD, Yesilaras M, Kilic TY, et al. The accuracy of bedside ultrasonography as a diagnostic tool for fractures in the ankle and foot. Academic Emerg Med 2014;21(9):1058-61.

13.

Fessell DP, Vanderschueren GM, Jacobson JA, et al. US of the ankle: technique, anatomy, and diagnosis of pathological conditions. Radiographics. 1998 Mar-Apr;18(2):325-40.

Author Information: Director of emergency ultrasound and associate professor of emergency medicine at the University of Mississippi Medical Center (UMMC) in Jackson, MS (Dr. Tollefson). Emergency physician at Merit Health River Oaks in Flowood, MS, and a former emergency medicine chief resident and sports medicine fellow at UMMC (Dr. Nichols). Emergency physician at St. Lucie Medical Center in St. Lucie, FL, and a former emergency medicine chief resident at UMMC (Dr. Fromang). Dean of Research at the University of Mississippi Medical Center in Jackson, MS (Dr. Summers).

Corresponding Author: Brian J. Tollefson, MD Department of Emergency Medicine University of Mississippi Medical Center 2500 North State Street Jackson, MS 39216 Phone: 601-984-5582 Fax: 601-984-5583 (btollefson@umc.edu)

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Recurrent Diabetic Muscle Infarction Affecting Bilateral Thighs: Uncommon Presentation with Grave Prognosis WILLIAM B. HORTON, MD; AVNISH TRIPATHI, MD; TIMOTHY J. RAGLAND, MD; TAUQUEER YOUSUF, MD Abstract Introduction Diabetic muscle infarction is a rare microangiopathic complication of poorly-controlled diabetes mellitus. Here we present the case of a female with a thirteen year history of poorly-controlled diabetes mellitus who presented with severe right leg pain and swelling and was eventually diagnosed with this condition. Case Presentation A 24-year-old female with a thirteen year history of poorly-controlled diabetes mellitus presented with intense right thigh pain and swelling. Initial labs revealed elevated hemoglobin A1c, CK, ESR, and CRP. White blood cell count was within normal limits and patient was afebrile with normal vitals at time of presentation. Magnetic resonance imaging of the right lower extremity demonstrated T1 isohypointensity in the vastus medialis and sartorius with diffuse fascial and subcutaneous edema. Bilateral lower extremity dopplers revealed no evidence of deep vein thrombosis and autoimmune workup was negative. The patient was diagnosed with diabetic muscle infarction given the combination of her clinical presentation and imaging findings. She was started on low-dose aspirin and glycemic control was achieved with a rigorous insulin regimen prior to discharge. She returned six weeks after discharge with persistent right thigh pain and swelling. MRI at this time revealed findings consistent with diabetic muscle infarction in left and right thighs. Discussion Clinicians should include diabetic muscle infarction in the differential of any diabetic patient who presents with lower extremity pain and swelling and history of poor glycemic control. Maintaining a high index of suspicion can help confirm the diagnosis early and avoid unnecessary tests and interventions that can lengthen recovery time. Introduction Diabetic muscle infarction (DMI), also termed diabetic myonecrosis, is a rare microangiopathic complication associated with poorly-

controlled diabetes mellitus (DM). First described by Angervall and Stener in 1965,1 DMI presents clinically as acute pain and swelling of the affected muscle without preceding trauma or fever.2 Bilateral involvement has been reported in 8.4% of cases.3 Patients with DMI usually exhibit other complications of poor glycemic control, including nephropathy, retinopathy, and/or neuropathy. The most commonly affected muscles are quadriceps, hip adductors, and hamstrings.4 Although diabetes is a very common disease, DMI is an uncommon complication. Less than 200 cases have been reported since it was initially described over 45 years ago.5 Here we present the case of a female with a thirteen year history of poorly-controlled DM who presented with severe right leg pain and swelling and was eventually diagnosed with DMI. Case Presentation A 24-year-old African-American female presented with complaints of intense right leg pain and swelling that had progressively worsened over the preceding week. Mild erythema with significant edema and tenderness were noted on examination of the medial aspect of the right thigh. The patient had a thirteen year history of insulindependent DM and an extensive history of poor glycemic control with multiple admissions for diabetic ketoacidosis. She also carried diagnoses of diabetic retinopathy and neuropathy. Initial labs were notable for glucose of 294 mg/dL, hemoglobin A1c 12.6%, and CK 374 U/L. ESR and CRP were elevated at 110 mm/hr and 8.0 mg/dL, respectively. Urinalysis demonstrated ketonuria and 4+ proteinuria. Patient was afebrile and all vital signs were within normal limits at time of presentation. Magnetic resonance imaging (MRI) of the right lower extremity demonstrated T1 iso-hypointensity in the vastus medialis and sartorius with diffuse fascial and subcutaneous edema, initially considered suggestive of cellulitis (Figure 1). Bilateral lower extremity dopplers were negative for deep vein thromboses. She was started on vancomycin and piperacillin-tazobactam for suspected cellulitis, but her right lower extremity pain/swelling failed to improve and orthopedic surgery was consulted. She underwent irrigation and debridement for suspected cellulitis. In the operating room, necrotic JOURNAL MSMA

FIGURE 1. Axial proton density fat saturated image (A) and noncontrasted axial T1 fat saturated image (B) at the same level show diffuse swelling throughout the anterior thigh musculature (white arrows) with ill-defined central T1 iso-hypointensity in the vastus medialis and sartorius (black arrows). There is diffuse fascial and subcutaneous edema (dashed arrows).

musculature was noted in the vastus medialis and cultures were sent. Gram-stain was negative for bacteria and cultures returned no growth after 5 days. Blood cultures were also negative. She noted little improvement in her right lower extremity pain/swelling over the remainder of hospitalization, despite antibiotics and pain medication. Infectious Disease was consulted and recommended discharging home with six weeks of intravenous vancomycin and ertapenem. Glycemic control improved on NPH insulin 12 units BID and regular insulin 3 units TID AC while hospitalized and was continued at discharge. She returned six weeks later complaining of persistent right lower extremity pain/swelling that had not improved after completing antibiotic therapy. She now noted a one-week history of intense pain/ swelling in the left lower extremity as well. Initial labs were notable for glucose of 442 mg/dL along with ESR and CRP that had actually increased to 126 mm/hr and 22.6 mg/dL. Antinuclear, Smith, SSA, SS-B, double-stranded DNA, SCL-70, and JO-1 antibodies were all ordered and returned negative. Repeat MRI of the right lower extremity with and without contrast demonstrated diffuse muscle swelling and enhancement with central necrosis, consistent with diabetic muscle infarction. Similar findings were now also observed in the left thigh (Figure 2). She was offered muscle biopsy but refused. With the patient remaining afebrile with normal white blood cell count (WBC) throughout two hospitalizations plus no evidence of infection found in the operating room along with negative cultures, she was diagnosed with bilateral DMI. We discussed this diagnosis with the patient and informed her that the best treatment was improved glycemic control along with rest and NSAID therapy. She was started on low-dose aspirin along with NPH insulin 15 units BID and insulin lispro 3 units TID AC. Glycemic control and lower

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FIGURE 2. Pre-contrasted T1 weighted fat saturated image (A) and post-gadolinium axial T1 weighted fat saturated image (B) six weeks after initial presentation shows diffuse muscle swelling (white arrows) and enhancement with central necrosis (black arrows); there is only a small enhancing rim which suggests necrosis rather than abscess. Findings are of diabetic muscle infarction. Similar findings are now also demonstrated in the left thigh (dashed arrows).

extremity pain gradually improved and she was discharged home on the insulin regimen initiated while hospitalized. She was scheduled for close primary care follow-up as well. Discussion DMI is a rare complication of long-standing uncontrolled DM. A review of 166 episodes in 115 DM patients by Trujillo-Santos found that most patients had long-standing DM (> 15 years) with associated microvascular complications including retinopathy (71%), nephropathy (57%), and/or neuropathy (55%).3 Patients typically present with abrupt onset of unilateral pain, tenderness, and edema of the thigh, though bilateral and upper extremity involvement have been reported.3 The pain is usually severe, persisting during rest and increasing with activity.6 Muscles most commonly affected include quadriceps (60-65%), hip adductors (13%), hamstrings (8%), and hip flexors (2%).7 Table 1 summarizes the demographic, clinical, and laboratory features of 116 DMI patients from a review by Kapur et al.8 In the workup of DMI, routine laboratory investigations are relatively nonspecific. WBC and serum CK levels may be normal or mildly elevated. Elevated inflammatory markers are classically seen.9 Sonographic examination typically demonstrates focal or diffuse muscle edema of the affected limb(s) and is particularly useful in excluding deep venous thrombosis.10 Magnetic resonance imaging (MRI) has a high tissue contrast resolution and is the ideal imaging modality to detect muscular edema and intramuscular pathological changes. Typical MRI findings include diffuse enlargement of involved muscle groups, partial loss of normal fatty intermuscular septa, and small, focal rim-enhancing fluid collections with a characteristic feature of an increased signal from the affected muscle area in T2-weighted images and isointense or hypointense areas on T1-weighted images.11

Diagnosis can usually be made combining clinical and radiological findings. Biopsy confirms the diagnosis in over 90% of cases12 but is currently not recommended as evidence suggests it prolongs course of pain and recovery secondary to poor wound healing and also carries risk of complications such as hematoma, infection, and nerve palsy.6

resection of infarcted muscles increased recovery time to 13 weeks and should generally be avoided.14 Once a patient with DM develops DMI, the likelihood of recurrence in the same muscle or contralateral limb is greater than 50%, with as many as 1 to 2 episodes per year reported after the initial event.14 DMI carries a good short-term prognosis as it is often a self-limiting disease; most patients see recovery in 3-4 weeks Treatment is mainly supportive and consists of rest, analgesia, lowonce glycemic control is achieved.14 However, long-term prognosis dose aspirin, and rigorous glycemic control.13 A review by Kapur and is poor and overall survival appears comparable to the prognosis of McKendry demonstrated low-dose aspirin shortens recovery time myocardial infarction, with a 55% one-year survival rate noted.15 Most to 5.5 weeks as compared to 8.1 weeks in those treated with rest and patients die within 5 years of diagnosis as DMI suggests significant analgesia alone.14 Figure 3 details time to recovery for conservative, vascular compromise and represents a very late stage of terminal medical, and surgical treatments in the same review.14 Surgical diabetic complication.14 There is limited data available in the literature on ultimate cause of death in patients diagnosed with DMI. Based upon our literature review for this case FIGURE 3. Time to recovery from symptom onset and treatment onset in patients report, it appears that most DMI patients ultimately with DMI. succumb to cardiac ischemia or infection.15

Conclusion

Adapted from: Kapur S, McKendry RJ. Treatment and outcomes of diabetic muscle infarction. J Clin Rheumatol 2005;11(1):8-12.

Table 1.Demographic, Demographic,clinical, clinical, and and laboratory laboratory features DMI TABLE. featuresofof DMIinin116 116patients. patients.

We have presented the case of a 24-year-old female with poorly-controlled DM who presented with acute right leg pain and swelling and was eventually diagnosed with bilateral DMI of the right and left thighs. Our patient’s presentation compared similarly to the clinical characteristics of DMI identified in the Table. She had a thirteen year history of DM (compared to mean duration of 15 years in the Table), had been diagnosed with two other DM complications (retinopathy and neuropathy), presented with acute onset of painful swelling in her lower extremity, and demonstrated elevated ESR and CK values with normal WBC. All of these characteristics coupled with her lack of systemic signs of infection pointed towards a diagnosis of DMI.

Clinical Features

Cases Reported (total n = 116)

Mean Age (years)

Male/Female

55/61

Mean Duration of DM (years)

Type 1 DM, n (%)

77/104 (74)

Diabetic R, K, or N, n (%)

69/71 (97)

Retinopathy, n (%)

53/90 (60)

Nephropathy, n (%)

73/92 (80)

Neuropathy, n (%)

66/104 (64)

Acute Onset of Symptoms, n (%)

85/95 (90)

Painful Swelling, n (%)

109/110 (99)

References

Palpable Muscle Mass, n (%)

47/108 (44)

1. Angervall L, Stener B. Tumoriform focal muscular degeneration in two diabetic patients. Diabetologia 1965;1(1):39-42.

WBC > 11 x 10 /l, n (%)

21/60 (35)

ESR > 50 mm/h, n (%)

26/35 (74)

CK > 150 U/l, n (%)

20/47 (45)

R: Retinopathy

K: Nephropathy

N: Peripheral Neuropathy

Clinicians should include DMI in the differential of any DM patient who presents with intense lower extremity pain/swelling and a history of poor glycemic control. Patients who present without history of preceding fever or trauma should raise clinical suspicion for DMI and sensitive diagnostic tools like MRI should be used to help make the diagnosis. Maintaining a high index of suspicion can help confirm the diagnosis early and avoid unnecessary tests and interventions that can lengthen recovery time, as happened in our patient.

2. Sran S, Sran M, Ferguson N, Anand P. Diabetic myonecrosis: uncommon complications in common diseases. Case Rep Endocrinol 2014;2014:175029. n: Number

Adaptedfrom: from:Kapur KapurS,S,Brunet BrunetJA, JA, McKendry Diabetic muscle infarction: case report review. Adapted McKendry RJ.RJ. Diabetic muscle infarction: case report andand review. J J Rheumatol 2004;31(1):190-194. Rheumatol 2004; 31(1): 190-194.

3. Trujillo-Santos AJ. Diabetic muscle infarction: an underdiagnosed complication of long-standing diabetes. Diabetes Care 2003;26(1):211-215. 4. Rocca PV, Alloway JA, Nashel DJ. Diabetic muscular infarction. Semin Arthritis Rheum 1993; 22(4):280-287.

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5. Iyer SN, Drake AJ 3rd, West RL, Tanenberg RJ. Diabetic muscle infarction: a rare complication of long-standing and poorly controlled diabetes mellitus. Case Rep Med 2011;2011:407921. 6. Morcuende JA, Dobbs MB, Crawford H, Buckwalter JA. Diabetic muscle infarction. Iowa Orthop J 2000;20:65-74. 7. Rashidi A, Bahrani O. Diabetic myonecrosis of the thigh. J Clin Endocrinol Metab 2011; 96(8):2310-2311. 8. Kapur S, Brunet AJ, McKendry RJ. Diabetic muscle infarction: case report and review. J Rheumatol 2004;31(1):190-194. 9. Bhasin R, Ghobrial I. Diabetic myonecrosis: a diagnostic challenge in patients with long-standing diabetes. J Community Hosp Intern Med Perspect 2013;3(1):20494. 10. Delaney-Sathy LO, Fessell DP, Jacobson JA, Hayes CW. Sonography of diabetic muscle infarction with MR imaging, CT, and pathologic correlation. Am J Roentgenol 2000; 174(1):165-169. 11. Jelinek JS, Murphey MD, Aboulafia AJ, Dussault RG, et al. Muscle infarction in patients with diabetes mellitus: MR imaging findings. Radiology 1999;211(1):241-247. 12. Chester CS, Banker BQ. Focal infarction of muscle in diabetics. Diabetes Care 1986; 9(6):623-630. 13. De Vlieger G, Bammens B, Claus F, Vos R, Claes K. Diabetic muscle infarction: a rare cause of acute limb pain in dialysis patients. Case Rep Nephrol 2013; 2013: 931523. 14. Kapur S, McKendry RJ. Treatment and outcomes of diabetic muscle infarction. J Clin Rheumatol 2005;11(1):8-12. 15. Chow KM, Szeto CC, Wong TY, Leung FK, et al. Diabetic muscle infarction: myocardial infarct equivalent. Diabetes Care 2002;25(10):1895.

Author Information PGY-3 trainee in Internal Medicine at the University of Mississippi Medical Center (Dr. Horton); PGY-4 Cardiology fellow at the University of Louisville School of Medicine in Kentucky (Dr. Tripathi); PGY-5 Radiology trainee at the University of Mississippi Medical Center (Dr. Ragland); Assistant professor in hospital medicine in the Department of Medicine at the University of Mississippi Medical Center (Dr. Yousuf). Corresponding Author: William B. Horton, MD; 2500 North State St.; Jackson, MS 39216 (wbhorton@umc.edu)

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I’ve Forgotten How to Pray JOANNA BAYLES, DO AND JOHN P.F.H. VANDERLOO, MD A 55-year-old African American male presented to the Emergency Department with confusion and bradykinesia. According to his sister, he suddenly was unable to pray while standing before his congregation 8 days prior to this presentation. Over the next several days he became increasingly confused and complained of “losing my mind.” A co-worker reported that the patient had been acting differently for approximately 2 weeks. There were no witnessed seizures and no witnessed falls. The initial differential diagnosis for altered mental status is broad and includes infectious, neurologic, metabolic, and psychiatric causes. Cerebrovascular accident (CVA), intracranial hemorrhage and a central nervous system tumor are neurologic considerations. Hypothyroidism is a consideration given the patient’s overall slowed thought processes and movements. Potential psychiatric causes of altered mental status include depression, Alzheimer’s disease, catatonic schizophrenia and malingering. Last, possible infectious causes include a urinary tract infection and pneumonia. More history is needed to refine the diagnosis. The patient’s review of systems was positive only for subjective fevers and confusion. His past medical history included vitamin D deficiency and severe, long-standing hypertension. He was told approximately 1 year prior to this presentation that he had life-threatening hypertension. Systolic blood pressure at that time was greater than 200 mmHg. He also admitted to going for long periods without medication refills. His surgical history included a hernia repair. His family history included diabetes, hypertension, and stroke. He denied alcohol consumption and the use of illicit drugs but did admit to smoking a half a pack of cigarettes daily for 2-3 decades. The patient had no known drug or food allergies. In addition to being a preacher, his sister stated he worked for a city government. Given the limited review of symptoms, it is still difficult to discern what exactly is causing the patient’s symptoms. Given his subjective fevers, infectious causes cannot be excluded. His history of poorly controlled hypertension, smoking history and word-finding difficulty allow for the consideration of a CVA. Metabolic causes including hypothyroidism or diabetes,given his positive family history, could be contributing to his symptoms, but he does not complain of polyuria or polydipsia. Perhaps a finding from the physical examination will help narrow this broad differential.

His initial vital signs were within normal limits except for a slightly elevated blood pressure of 150/91 mmHg. His cardiac, pulmonary, and abdominal examination results were normal. The patient was awake but lethargic and answered questions slowly and with difficulty, only responding “yes” or “no.” He was unable to state his full name, his location or the date when being questioned, thus his orientation to person, place and time was unable to be assessed. He appeared to have good muscle tone but no nuchal rigidity. Sensation was normal, but strength could not be assessed as he had difficulty following commands. His limited movements appeared to be in slow motion. At this point, because he is afebrile, I am moving infectious causes lower on the differential diagnosis list, but I cannot exclude them entirely. His pending urinalysis, chest radiograph, rapid plasma regain, and complete blood count with differential should help further exclude or include infectious causes. A urinary tract infection or neurosyphilis could be the primary culprit, since meningitis or pneumonia are less likely as he has no positive meningeal signs or pulmonary findings on physical examination. A urine drug screen was added to investigate for ingestion or usages of illicit substances that could affect his mental status and neurological examination results. His psychomotor retardation is still concerning for metabolic or neurologic causes. In all patients whose clinical presentation is suspicious for stroke, computed tomography (CT) of the head without contrast is the first step in the diagnostic pathway.1 I also need to order a metabolic panel, thyroid stimulating hormone, folate and B12 studies to investigate for electrolyte abnormalities, hypo- or hyperthyroidism and B12 and folate deficiencies. Initial lab results revealed normal electrolytes except for a low potassium concentration of 3 mEq/L. His thyroid stimulating hormone concentration was normal at 0.96 mIU/L. Folate and vitamin B12 concentrations were normal at 13.4 ng/mL and 462 pg/mL, respectively. A complete blood count was within normal limits. CT of the head without contrast showed no acute intracranial abnormality. His chest radiograph showed no evidence of pneumonia. The urinalysis showed no signs of a urinary tract infection. The patient was subsequently admitted to the inpatient service and intravenously hydrated with normal saline with potassium chloride while given nothing by mouth as CVA had not been fully excluded and he may not have been able

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to swallow. A magnetic resonance imaging (MRI) scan of the brain was ordered to evaluate for subacute CVA. Bed rest with fall precautions was ordered, as his altered mental status made him a risk for falls. His home blood pressure medications were continued. The next morning, the MRI revealed chronic small vessel disease and a left frontal lobe infarction. A neurologist was consulted, and the hospital stroke protocol was activated. An ischemic frontal lobe stroke! Despite the patient’s somewhat unusual presentation, damage to the frontal lobe is a logical cause of his presenting symptoms. The frontal lobe contains most of the dopamine-sensitive neurons in the cerebral cortex.The dopamine system is associated with reward, attention, short-term memory tasks and executive functions such as planning for the future, judgement and decision-making skills. These functions can decrease significantly in someone whose frontal lobe is damaged.2 Lesions in the dominant hemisphere can result in aphasia, and lesions in the non-dominant hemisphere can result in apraxia or a loss of ability to perform purposeful movement. This patient is right handed, making the left brain his dominant side; therefore, he has a lesion in the dominant hemisphere. This makes sense, as he can attempt purposeful movement but is severely aphasic. CT scans use radiographs to compute the image. Blood, bony abnormalities and metallic fragments are best visualized on CT versus other imaging modalities, but some strokes, mainly ischemic, can be missed. MRI is better in general for visualization of soft tissue structures because it relies on the magnetic stimulation of hydrogen protons that are ubiquitous in nearly all cells.3In this patient who presented with ischemic stroke, MRI allowed visualization of the left frontal lobe ischemic infarct when CT did not. Additional orders placed by the neurologist included antiplatelet therapy in the form of aspirin, initiation of a statin and discontinuation of patient’s scheduled antihypertensives to allow for permissive hypertension. A CT angiogram of the head and neck revealed stenosis of the supraclinoid segment of the left internal carotid artery. The left internal carotid arterybranches into the anterior and middle cerebral arteries, both of which supply blood to the frontal lobe. Therefore, this patient was at a higher risk for a left-sided infarct due to turbulent and overall decreased blood flow through this vessel. In patients with acute ischemic stroke, platelets become activated. When aspirin (160-300 mg) is started within 48 hours of acute ischemic stroke, there is a significant decrease in mortality and morbidity.4 Antiplatelet therapy and statin therapy are recommended in all patients with carotid artery stenosis who have suffered a transient ischemic attack or CVA,5 which definitely includes this patient. Guideline consensus statements note that antihypertensive medications should be withheld except in patients with a systolic blood pressure over 220 mmHg or diastolic blood pressure over 120 mmHg.6 In a patient undergoing IV thrombolysis for acute ischemic stroke, the recommended upper limit of systolic blood pressure is 185 mmHg for the first 24 hours. If blood pressure exceeds these thresholds, shortacting, titratable medications such as labetalol (Trandate), nicardipine (Cardene), nitroprusside (Nitropress) or esmolol (Brevibloc) may be

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used. Blood pressure should not be reduced by more than 15% in a 24-hour period.6 Cerebral autoregulation maintains cerebral blood flow within normal limits (55-60 ml/100 g/min) at systemic blood pressures between 60 mmHg and 125 mmHg. After acute stroke, however, cerebral autoregulation becomes impaired, leaving cerebral blood flow dependent upon systemic blood pressure. In this case, reducing systemic blood pressure will reduce cerebral blood flow in the ischemic penumbra, which increases the risk of neuronal death and brain hypoxia.7 On day 2 of admission, this patient appeared more alert and was more verbal. He was able to report that he had also suffered from right sided weakness in the few days prior to admission. As part of his management, physical therapy, occupational therapy and speech therapy were consulted. He improved daily throughout his admission and was almost at his baseline level of functioning by the day of discharge. After several days, he was able to return home supported by home health and outpatient physical and occupational therapy. In summary, this patient’s signs, symptoms, and diagnostic studies clearly indicated that this patient suffered from an ischemic CVA. The mainstay of treatment for patients who have suffered an ischemic CVA is permissive hypertension during hospitalization, antiplatelet, and statin therapy during and after hospitalization and physical therapy during and after hospitalization for treatment of any strength deficits. In addition to these interventions, outpatient neurology follow-up was arranged.n Key Words: Acute neuroimaging, ischemic CVA, frontal lobe, antiplatelet therapy References 1. Wardlaw JM, Seymour J, Cairns J, Keir S, Sandercock P. Immediate computed tomography scanning of acute stroke is cost-effective and improves quality of life. Stroke. 2004; 35(11):2477-2483. 2. Roca M, Parr A, Thompson R, Woolgar A, et al. Executive function and fluid intelligence after frontal lobe lesions. Brain. 2010;133(1):234-247. 3. Berger, A. Magnetic resonance imaging. British Medical Journal. 2002;324(7328):35 4. Sandercock PA, Counsell C, Gubitz GJ, Tseng MC. Antiplatelet therapy for acute ischemic stroke. Cochrane Database Syst Rev. 2008;16(3):CD000029. 5. Merwick A, Albers GW, Arsaya EM, et al. Reduction in early stroke risk in carotid stenosis with transient ischemic attack associated with statin treatment. Stroke. 2013 Oct.; 44(10):2814-20 6. Jain AR, Bellolio MF, Stead LG. Treatment of hypertension in acute ischemic stroke. Current Treatment Options in Neurology. 2009;11(2):120-125. 7. Bhalla A, Wolf CD, Rudd AG. Management of acute physiological parameters after stroke.QJM. 2001; 94(3):167-172.

Author Information: Former resident in the Department of Family Medicine at the University of Mississippi Medical Center (UMMC), now in practice at Hancock Medical Center in Long Beach, MS (Dr. Bayles jdbayles@umc.edu); Assistant Professor, Department of Family Medicine, UMMC, Jackson, MS Telephone: (601) 984-6800 (Dr. Vanderloo).

P R E S I D E N T ’ S

P A G E

Getting Into the Groove

hat a great job you have blessed me with. Being MSMA president just these short few months has shown me the importance of the good work of our association as we all work to defend the profession. I’m working to get “into the groove” as your president. It has been truly humbling to have the honor and duty to serve as the spokesperson for the “physicians who care for Mississippi.” I take this duty extremely seriously and am careful to stay on message regarding the positions and policies of MSMA as our House of Delegates and Board of Trustees has developed them. I remain aware of the hard work done by our members, our councils, our staff, our Board, and our House as I meet with the various heads of state government, state agency heads, medical interest groups, various boards representing medical interest and discuss our agenda. This job is quite busy and somewhat demanding but it also is extremely rewarding thus far. We have several 2016 legislative session big issues that we are preparing for: Scope of practice with nurse practitioners, Any Willing Provider legislation, and working with the Mississippi State Board of Medical Licensure regarding the interstate “Compact” are just a few of the very important issues we will need your help with this year, and we will keep you informed. Please stay abreast of the major issues in medicine by reading each issue of our Joumal and the “Physicians Position” e-mail updates. A major issue on the national stage recently that continues to gather media attention has to do with the prescription opioid epidemic. Based on actions of the HOD, the BOT has endorsed my appointing three work groups to study and seek solutions for the various aspects of this public health crisis. The first group will be studying best practices and how to best fit these into the practice lives of hard working Mississippi physicians. This group will be studying how to help our doctors as they are striking the delicate balance of proper pain management and protecting the public from unintentional overdoses and addiction. Their mandate is to develop appropriate prescribing guidelines that will work best for our state by reviewing the literature, reviewing the various guidelines at the national level and applying this knowledge to help us practice pain management wisely. The second group will be reviewing the needs and further development for our very own MPHP as it continues to serve us well in rescuing physician lives and careers from the destructive disease of addiction and other psychiatric disorders. The third group will serve as the “Blue Ribbon” panel which will pull the work product of the other two groups plus incorporate experts and leaders in our state from the fields of pain management, addiction treatment, primary care and surgical specialties, law enforcement, and state regulators to develop a reasoned study of the entire subject with all of its complexities. Our desire is to develop a white paper discussing the issue and the solutions as we see them as Mississippi’s doctors. These groups are being formed now and will begin work soon. We will keep you informed on these and other important MSMA issues. So, let’s all “get into the groove” of working together through our MSMA: defending the profession for 148 years. n

Daniel P. Edney, MD MSMA President

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L E T T E R S

Homage to a Small Town Doc Dear JMSMA Editor, Dr. Luke Lampton and I were recently together in a meeting at the MHA. I complimented him on his stewardship of our JMSMA and how, in my opinion, it has improved. Also, I believe the Journal has become more relevant and is dealing with important issues in society as well as medicine. As we parted, Dr. Lampton suggested that I should submit an essay to the Journal. I am not sure whether the enclosed, short essay will find compatibility in the Journal. Upon my reflection, it is evident that none of us is solely responsible for any success achieved in life. We all owe much to our parents, teachers, and other role models we meet along life’s journey. This is my feeble attempt to offer homage to a small town doctor who opened my eyes to possibilities I may have never considered. Sincerely, Billy W. Long, MD, Madison

Tribute to a Role Model

grew up in the Appalachian foothills of Northeast Mississippi on a farm in Blue Springs. We raised cotton, soybeans, hay and Black Angus cattle. From an early age I worked in the fields alongside our sharecroppers choppin’ cotton {hoeing out the weeds) and later in the year picking cotton by hand. Since I was terribly unproductive as a cotton picker (workers were paid by the pound picked), my dad sent me to work in our cotton gin, covering the graveyard shift. All of this was during my early teenage years, and I recall this period of my life fondly. My comaraderie with the farm hands allowed me to gain insights into their lives and struggles. The life lessons learned working on our land proved to be very useful as I tackled higher education and the challenges of my future career as a physician. My father was a high school graduate, while my mother had completed the eleventh grade. None of my grandparents, aunts or uncles had attended college. But, as a young boy I was exposed to our family doctor. Dr. John Mitchell Ford of Baldwyn was a close friend of my father, Bonner Long, and he was an exceptional family doctor. We went to his Baldwyn clinic with our asthma attacks, farm accidents, and common colds. Also, he made house calls. His visits to care for my mother’s father, my grandfather Scott (Papaw), was my first awareness of how medicine could provide so much comfort and relief. Scott Moore had suffered a devastating stroke leaving him paralyzed, bedridden, and aphasic. This made office visits for Scott impractical. Because of Dr. Ford’s example, I began to think about becoming a doctor. Years later, one of his sons, Tim Ford, would rise to be Speaker of the House of Representatives in Mississippi. After medical school at the University of Mississippi and during my internal medicine residency, Dr. Ford had admitted my father to the local hospital in Baldwyn. During a phone conversation about my dad’s health status, Doc inquired about my future plans. I replied that I was interested in gastroenterology and had enjoyed doing a few research projects at UMMC. He shared with me that a Baldwyn native, Dr. Phillip Gorden, was on the staff at the National Institutes of Health (NIH) in Bethesda. Dr. Ford had likely been a role model for Dr. Gorden, having encouraged him to pursue medical school while he was growing up in Baldwyn. Dr. Gorden reported that there was an opening in the Digestive Diseases section at NIH. After my interview at NIH, I was selected for a two-year program as a Clinical Associate while serving in the U.S. Public Health Service. This was a particularly attractive opportunity since serving in the Viet Nam war was an alternate possibility. Following my two years in Bethesda, I was fortunate to enter a gastroenterology fellowship at the University of Pennsylvania in Philadelphia. Using the knowledge gained at NIH, I applied for an NIH grant and a VA grant. Luckily both grants were awarded, and I served on the Penn faculty as an Assistant Professor of Medicine for two years. During medical school, I had married a beautiful Alabama girl, and we had our first child in Philadelphia. The pull to return to our families and roots was enough for us to move back to Jackson where I practiced for 33 years at Gastrointestinal Associates as one of the three founding physicians. I am sure Dr. Ford, who died many years ago, chuckles above when he remembers that naive country boy who for a short time was an Ivy League professor. n

Billy W. Long, MD, Madison 46 VOL. 57 • NO. 2 • 2016

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The Unanticipated Consequences of “Meaningful Use” and Maintenance of Certification Requirements

recent opinion editorial in the in The New York Times Sunday Review [Wachter, R.M. (2016, January 16)” How Measurement Fails Doctors and Teachers”] suggests that the federal governments over-reach into the practice of medicine may be waning. In fact, testing is everywhere. It has become a national obsession. From grade school to graduate school, standardized tests offered the potential to improve education by emphasizing areas of weakness among individual students and entire school systems. However, unintended consequences intruded as students and teachers began to “teach to the test” and the time devoted to preparation intruded on the educational mission of schools leading to worsening test scores. Similarly, physicians, hospitals, and medical centers are being assessed to death. Scores of digital ratings now look at every aspect of clinical practice in the name of “quality.” Recognizing the real potential to improve service and prevent harm to patients, the outcome measures utilized often have no scientific basis with doctors being judged by small numbers of patients, non-random samples, and overall scores representing a combination of random factors with no equivalence. Companies are popping up to game the system and improve the digital reputation of physicians. The unanticipated consequences are real. Patients may choose a physician based on erroneous data. Maintenance of Certification may require use of expensive, ineffective and time-consuming systems that represent “busy work” and fail to impact quality of care. “Meaningful Use” requirements add countless “mouse clicks” to the physicians day, place their back squarely in the patient’s face, and bulk up charts with unimportant information that makes it harder to identify the key history and physical findings that would positively impact patient care. I agree with Dr Wachter’s op-ed piece that it is time for quality measurement “to be scaled back and allowed to mature.” It is time for the government to measure the unintended consequences of systems they put into place. It is time for the public to recognize that the ubiquitous systems that purport to judge the quality of physicians and hospitals are easily gamed and often fail to reflect true quality care. Physicians should not dismiss quality measurement altogether. For instance, we need efficient and effective systems to insure that children receive appropriate vaccinations. Developing such systems and putting them in place is an approach that will truly improve patient care rather than frustrating physicians who see themselves increasingly spinning wheels while seeing no hope of gaining traction. An immediate halt to the application of inefficient and ineffective meaningful use criteria would be a good first step in a sane approach to patient care. n

Robert T. Brodell, MD, FAAD Professor and Chair, Department of Dermatology University of Mississippi Medical Center 601-815-8000 rbrodell@umc.edu

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Oh, No, Another Patient with Back Pain JAMES A. RISH, MD, PHYSICIAN CLINICAL REVIEWER, NIA MAGELLAN JANET MAURER, MD, ASSOCIATE CHIEF MEDICAL OFFICER AND VP OF QUALITY, NIA MAGELLAN

t seems like every other patient you see in your office has back pain. And that isn’t far from true. It is estimated that at any point in time 26% of the population has back pain and that almost 80% will have back pain at some point during their adult lives.1 And back pain accounts for 2 - 3% of all physician visits.2 But, unlike upper respiratory tract infections or ear infections, this is not an easy problem to treat. In fact, more than 10 % of patients with back pain report that they consider their condition chronic.3 So what do you do when a person, often in obvious distress, comes into your office with back pain? Of course, you offer them analgesics— preferably NSAIDS or similar drugs. Some cases may require short term opioids if the pain is severe and the patient cannot tolerate NSAIDS or is not responsive to them. He or she also may benefit from modifications in activity and either physical therapy, chiropractic care or carefully planned home exercise programs. Corticosteroid injections may be an option in a small percent of patients who do not improve over the first two weeks with these conservative measures. But what about an MRI? Well, there are certainly some circumstances where an early MRI is important. These are called ‘red flag’ clinical signs. For example, if you suspect your patient has a tumor, an infection, has a fracture, is immunosuppressed, or has a progressive neurological deficit you need an MRI to determine if urgent surgical or other intervention is necessary. However, only about 10% of patients present with this type of problem; that means 90% present with issues related to disc or other degenerative disease How does an MRI help them? Studies have shown that about 80% of patients who present with this type of problem have resolution of their pain in about six weeks with conservative care. Does ordering an MRI early help in the management? Rarely. If the patient doesn’t have a significant or progressive neurological deficit, he/she is not a surgical candidate. And he/she would need to complete at least six weeks of conservative care without improvement before an assessment could be made about any surgical intervention . This is the official position of the North American Spine Society (NASS) who published as one of their five Choosing Wisely things physicians and patients should discuss: ‘Don’t recommend advanced imaging (e.g., MRI) of the spine within the first six weeks in patients with nonspecific acute low back pain in the absence of ‘red flags.’ 4 The reason for this recommendation is that symptoms and findings on MRI don’t necessarily correlate with one another. And even if there is obvious disc disease on the MRI, the symptoms will resolve about 80% of the time regardless of what the MRI shows.5 There is plenty of time to get an MRI after conservative care has been completed if the patient continues to be symptomatic-and the number of MRIs actually ordered and completed will be reduced by 80%. This eliminates many unnecessary tests, frees up the MRI machines for other patients and significantly reduces health care costs. What is the best clinical approach? So what do you do when the patient, in obvious distress, is sitting in front of you wanting you to make it better? First do a complete history and physical examination and make sure there are no ‘red flag’ issues. Then explain that the symptoms will likely resolve on conservative care in 4 to 6 weeks. Finally, provide a comprehensive treatment plan focused on adequate analgesia, heat, the importance of staying active, and physical therapy or a home exercise program. If the patient is asking for an MRI, explain that an MRI does not treat back pain and may not even elucidate his/her back problem. An MRI will be considered if he/she does not respond to conservative care or develops neurological deficits. At that point, the MRI becomes a valuable diagnostic tool. n Corresponding Author- James A. Rish, MD, PO Box 2483, Tupelo, MS 38803 References 1. Frymoyer JW, Pope MH, Clements JH, Wilder DG, MacPherson B, Ashikaga T. Risk factors in low back pain: An epidemiological survey. J Bone Joint Surg Am 1983; 65(2):213-8. 2. Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: estimates from US national surveys 2002. Spine 2006;31(23):2724-7. 3. Freburger JK, Holmes GM, Agans RP, Jackman AM, Darter JD, Wallace AS, Castel LD, Kalsbeek WD, Carey TS. The rising prevalence of chronic low back pain. Arch Intern Med 2009;169(3); 251-8. 4. Choosing Wisely North American Spine Society. October 2013. http://www.choosingwisely.org/societies/north-american-spine-society. Accessed July 12, 2015. 5. Maus T. Imaging the back patient. Phys Med Rehabil Clin N Am 2010; 21(4):725-66.

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I N

M E M O R I A M

The JMSMA encourages families, friends, and our readers to submit obituaries and photos of Mississippi physicians for inclusion in the pages of our Journal. Email to KEvers@MSMAonline.com or slow mail to JMSMA. —Ed.

Thomas F. Adams, Sr., MD, 60, of Columbus, died on March 25, 2015. He was born December 26, 1954 in Calera, AL. Dr. Adams attended Fisk University in Nashville, TN. In 1977, he entered Morehouse College and then Howard University in the fall of 1980 where he completed a Doctorate of Medicine Degree in 1982 and a residency in internal medicine and pediatrics. Dr. Adams entered the medical profession in 1986 as an internist/ pediatrician. He was Board Certified in Pediatrics. His areas of practice included: Adams Internal Medicine/Pediatrics Clinic, Columbus; Delta Health Center, Greenville; Greater Meridian Health Center, Shuqualak; Adams Family Medical Clinic, West Point and Aberdeen; North Mississippi Medical Center, West Point; and Bolivar County Hospital, Cleveland. He retired from medicine in June 2014. Fred Allison, Jr., MD, 92, Professor of Medicine Emeritus at Vanderbilt University and a former Mississippi physician, died on May 8, 2015. Reared in Auburn, AL, Dr. Allison graduated from Auburn University. He served as a member of the Army Specialized Training Corps and graduated from the Vanderbilt University School of Medicine in 1946. Dr. Allison trained in internal medicine at Vanderbilt Hospital, Barnes Hospital in St. Louis, and the Peter Bent Brigham Hospital in Boston. After specializing in virology and infectious diseases at Louisiana State University Medical Center in New Orleans, he began research into cellular immunity at Washington University School of Medicine in St. Louis. In 1955 he became one of the original faculty of the new School of Medicine at the University of Mississippi in Jackson. In 1968, after a sabbatical year of study at the Rockefeller University in New York City, Dr. Allison was appointed as the Edgar Hull Professor and Head of the Department of Medicine at L.S.U. School of Medicine in New Orleans and Chief of Medicine at the L.S.U. Division of Charity Hospital. Upon retiring from L.S.U. in 1987, he returned to his alma mater, Vanderbilt University, as a professor of medicine and Physician-In-Chief of the Nashville Metropolitan General Hospital. In 1993 he was appointed Chief of the Division of General Internal Medicine at Vanderbilt, a position he held until 1996 before serving as a consultant in internal medicine for the Zerfoss Student Health Service at Vanderbilt.

Willard Henry Boggan, Jr., MD, of Jackson, died on February 14, 2015. While he was born in Memphis, TN, his family moved to Mississippi and he graduated from Clinton High School. Upon graduation, he enrolled at Mississippi College where he graduated with honors. After college, Willard enrolled in medical school at the University of Tennessee in Memphis and entered the US Navy Reserves during World War II. He completed his residency in internal medicine at Kennedy Teaching Hospital in Memphis and then was called to active duty during the Korean War. Dr. Boggan practiced medicine for 47 years. He was an internal medicine physician with a subspecialty in cardiology. He was elected a Fellow of the American College of Physicians in 1956 and was a Professor of Medicine at the University Medical Center in Jackson for 35 years. He helped found Doctor’s, River Oaks, and Charter Hospitals, and served as Chief of Staff at Doctor’s and River Oaks Hospitals. Richard Carlton Boronow, MD, 81, died on March 28, 2015. Dr. Boronow was born in Appleton, Wisconsin, December 18, 1933. He attended Northwestern University. In 1959, he received his MD from Northwestern University School of Medicine, Chicago. After a rotating internship at Cook County Hospital and a residency in obstetrics and gynecology at Evanston, IL, Hospital, he completed general surgical training at Memorial Sloan Kettering Cancer Center in New York and a fellowship at MD Anderson Cancer Center in Houston. Dr. Boronow was Board Certified in Obstetrics and Gynecology and in Gynecologic Oncology and served as an examiner for the Gynecologic Oncology Boards. In 1965, Dr. Boronow joined his mentor, Dr. David N. Danforth, OB/ GYN Chairman, at Northwestern for private practice and a part-time faculty appointment. In 1967, he joined the University of Mississippi Medical Center in Jackson, MS, where he served for 10 years at Director, Division of Gynecologic Oncology, the last year and a half as Acting Chair of the UMC Department of Obstetrics and Gynecology. He achieved the rank of full professor and in 2007 was named “Honorary Physician” in the department. In 1977, Dr. Boronow entered private practice, partnering in 2004 with Dr. Paul Seago. Dr. Boronow was a founding member and president of the Society of Gynecologic Oncologists, president of the Society of Pelvic Surgeons, founding member of the International Gynecologic

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Cancer Society, founding member and president of the Felix Rutledge Society (an M. D. Anderson alumni group), and president of the Society of Memorial (Sloan-Kettering) Gynecologic Oncologists. Other society memberships included American College of Obstetricians and Gynecologists, American College of Surgeons, American Radium Society, Society of Surgical Oncology, American Gynecological and Obstetrical Society, Central Association of Obstetricians and Gynecologists, Mississippi State Medical Association, and Jackson Gynecic Association. Wallace Earl “Mike” Caldwell, MD died on May 6, 2015. He was born August 11, 1923, in Baldwyn. After graduating from Baldwyn High School in 1941, Dr. Caldwell attended Memphis State College. He entered the Navy V-12 program at Mississippi College in Clinton before attending Officer Training School in 1944 at Northwestern University in Chicago. He was transferred to the USS Burleson (APA67) as a landing craft officer in San Pedro, California. After serving in the Pacific, he was discharged from the Navy in 1946. He then attended the University of Mississippi Medical School in Oxford and transferred in 1948 to the University of Texas Southwestern Medical School in Dallas, Texas, for his final two years, graduating in 1950 with an MD and then interning at Shreveport Charity Hospital. In 1951, Dr. Caldwell returned to Baldwyn to practice medicine with his father, Dr. R.B. Caldwell, and his brother, Dr. R.E. Caldwell. From 1977 to 1978 Dr. Caldwell was District 1 Health Officer for the State Department of Health. He moved to Jackson in 1978 to serve as medical director of Blue Cross and Blue Shield of Mississippi from 1978 to 1988. After retirement he worked first part time and later full time as chief medical officer of the Jackson Military Entrance Processing Station, retiring in 2002. Dr. Caldwell was active in the Ole Miss Medical Alumni Association, serving one year as president and one year as chair of the Guardian Society. Dewitt Grey Crawford, MD, 80, died on January 17, 2016. He was born in Greenwood and moved to Louisville at age 5 where he graduated from high school with honors. He attended Georgia Tech and then transferred to the University of Mississippi. He graduated from medical school in 1960 and interned at John Gaston Hospital, Memphis, TN. He returned to Louisville to practice family medicine with his father. Dr. Crawford was active in the Mississippi State Medical Association and the Mississippi Academy of Family Physicians where he served as president and was named Family Physician of the Year. He was a member and past president of the MS Board of Medical Licensure. He was also involved in the MS Health Care Association of Nursing Homes. Dr. Crawford served as a Battalion Surgeon for the MS Army National Guard.

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Charles Michael “Mike” “Timer” Currie, MD, 61, of Tupelo, died on May 12, 2015. A Poplar Bluff, MO, native, he was born May 22, 1953 and grew up in Orlando, FL. He received his Bachelor of Science in physics at Florida Technological University (now University of Central Florida) and his Masters in biomedical electrical engineering from Washington University in St. Louis, MO, and went on to receive his Medical Degree from St. Louis University. Mike completed his residency in radiology and his fellowship in neuroradiology both at Vanderbilt University in Nashville, Tennessee. He was also an assistant professor of neuroradiology at Vanderbilt. In 1987, he joined Radiology of Tupelo, and in 2000, he founded Imaging Associates of North Mississippi, which later became RPG Medical Imaging. He also owned the Imaging Center. Dr. Currie was involved in many professional and community organizations. He had served as president of Northeast Mississippi Medical Society, a member of the American Medical Association, the Mississippi State Medical Association, and the South East Neuroradiological Society. Walter Gough, Jr., MD, 72, died on February 16, 2016. Dr. Gough graduated from the Meharry Medical College School of Medicine in 1970. Dr. Gough came to the Delta in April of 1970 to study at Taborian Hospital in Mound Bayou. He specialized in family medicine and emergency medicine. He practiced medicine at Gough’s Family and Pediatric Clinic in Drew and was also a staff physician at North Sunflower Medical Center in Ruleville. Dr. Gough was the first black president of the Mississippi State Chapter of Emergency Room Physicians. He was a member of the Mississippi State Medical Association and the Mississippi Academy of Family Physicians. He also served on the Mississippi State Board of Health. John E. Green, MD died on March 17, 2015. He was born on November 17, 1934 and he graduated from Hattiesburg High School in 1952. He attended Vanderbilt University from 1952 to 1955 and received his MD from Tulane University Medical School in 1959. He completed a rotating internship at the University of Mississippi Medical Center in 1960 and spent the fall of 1960 attending Harvard University’s Basic Sciences in Ophthalmology. He completed a three-year preceptorship with Gulf States Eye Surgery Foundation in New Orleans. He joined his father and others in Green Clinic (later Green Eye Institute) in Hattiesburg on October 1, 1963, where he practiced ophthalmology until his retirement from the clinic on June 30, 2000.

Clyde H. Gunn, Jr., MD, FACS, 88, of Moss Point, MS, died on January 16, 2016. He was born May 17, 1927, in Poplarville. Because his father was a Methodist minister, Clyde Jr. spent most of his childhood living in various places in Mississippi, including Biloxi and Meridian, where he graduated in 1944. He studied one year at Millsaps College in Jackson, MS, before training with the United States Navy for 18 months. Returning to Millsaps, he graduated with honors in 1948. Clyde entered medical school at Emory University in Atlanta, GA, where he received his Doctor of Medicine degree in 1952. Following an internship at Crawford Long Hospital in Atlanta, he moved their family to Moss Point. Clyde and Wallace E. Calhoun, Jr., MD, formed a general medical practice, working together for ten years, both in Moss Point and at Singing River Hospital in Pascagoula. In 1963, Clyde returned to Atlanta to complete a general surgery residency at Emory University Hospital and Grady Memorial Hospital, serving both facilities as Chief Resident in 1967. Subsequently, he became a Diplomate of the American Board of Surgery and a Fellow in the American College of Surgeons. Moving back to Mississippi in 1967, Clyde began practicing general surgery in Moss Point and at Singing River Hospital. In 1982, he enlisted for a two-year period in the United States Navy Reserve as a Captain assigned to the Naval Hospital in Pensacola, FL, serving periodically as Ship Surgeon aboard the USS America. In 1984, Clyde returned to his general surgery practice at Singing River Hospital and retired in 1988. Mary Elizabeth Hawkins, MD, 78, of Flora, died on April 7, 2015. She was born July 6, 1936, in New Orleans and attended Robert E. Lee Grammar School and Fourchette High School. Dr. Hawkins received her B.S. Degree from MSCW (now MUW) in 1957 before earning her MD from LSU School of Medicine (New Orleans) in 1963. Following internship and residency at the University of Mississippi Medical Center, Dr. Hawkins entered OB/GYN private practice in Jackson. Dr. Hawkins was one of the founders of Woman’s Hospital, as well as Chief of Staff. She retired from active practice in 1999 and became an OB/GYN Assistant Professor at UMMC, staffing the Specialty Clinics in the Jackson Medical Mall. She was a member of the American College of OB/GYN as well as numerous local and national societies. Thomas R. Howell, MD, 79, of Laurel, born February 15, 1936, died on Tuesday, February 9, 2016. Following graduation from Jones County Junior College, he attended The University of Southern Mississippi earning a Bachelor of Science degree before graduating from The University of Tennessee with his Doctor of Medicine degree in 1965. He returned to Laurel and was one of the

original founders of Laurel Family Clinic. He then completed his surgery residence in Birming-ham, AL and practiced general surgery for many years at South Central Regional Medical Center. He also proudly served his country as a Sergeant in the United States Army Reserve earning an Honorable Discharge in 1962. Leon Lenoir, MD, 89, of Greenville died on February 8, 2016. He was born on February 10, 1926 in Lumberton, then lived in Kiln, MS; Ferriday, LA and Barth, MS. A 1942 graduate of Hattiesburg High School, Dr. Lenoir continued his edu-cation at Mississippi Agricultural and Mechanical College in Starkville, now known as Mississippi State University. He enlisted in the United States Navy in 1944 where he served as a Hospital Corpsman. Upon being discharged in 1947, he enrolled in Tulane University in New Orleans, LA where he graduated from medical school in 1952. He completed his internship and residency in internal medicine and a cardiology fellowship at Charity Hospital in New Orleans in 1956, when he opened his practice in the May Building in downtown Greenville. He and his cousin, Dr. Robert E. Lee opened Lenoir and Lee Clinic in 1961. The partnership of Lenoir, Lee and Cirilli was formed in 1986 when Dr. Michael J. Cirilli joined the practice. William Campbell Little, MD, 65, of Madison, died on Thursday, July 9, 2015. He was born on May 1, 1950, in Cleveland, OH. Dr. Little was a graduate of Oberlin College, and the Ohio State University College of Medicine. He served his residency at University of Virginia School of Medicine and his cardiology fellowship at University of Alabama at Birmingham. Dr. Little was on the faculty of the University of Texas San Antonio and retired from Wake Forest University as the Vice Chair of the Department of Internal Medicine and Professor of Cardiology. Most recently, he was the Patrick Lehan Professor of Cardiovascular Medicine and chair of the Department of Medicine at the University of Mississippi Medical Center. Among many professional activities, he was chair of the American Board of Internal Medicine’s Subspecialty Board on Cardiovascular Diseases. S. H. “Mac” McDonnieal, Jr. , MD, 95, a longtime Jackson physician, died on December 10, 2015. Born in Mize, he grew up in Summerland, MS. Dr. McDonnieal practiced internal medicine at Baptist Medical Center in Jackson from 1955 until 1989. At age 70, he began a second career as a medical consultant with the Department of Rehabilitation Services for the State of Mississippi. In 2013, he retired once again, at age 93. Dr. McDonnieal received a bachelor’s degree with honors from Mississippi College before serving in WWII as an Army ordnance chemist. He earned a master’s degree in chemistry at Vanderbilt University, and an MD with honors at Tulane University, followed by an internship at Charity Hospital in New Orleans, a residency in internal medicine at Southern Baptist Hospital in New Orleans, and a teaching fellowship in internal medicine at Tulane.

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After training at Tulane, Dr. McDonnieal came to Jackson as a clinical professor of medicine at University Medical Center before opening his practice in 1955. His memberships also included the Mississippi State Medical Association, American College of Chest Physicians, American Society of Internal Medicine, American College of Physicians and American College of Angiography. William “Bill” Alfred Middleton, Sr., MD, 90, of Winona, died May 31, 2015. Dr. Middleton was born on December 8, 1924. He served in the United States Army during World War II in New Guinea and the Philippines. Following his service to his country, he attended Mississippi College in Clinton and then Tulane School of Medicine in New Orleans, where he completed his medical degree. Dr. Middleton then returned to Winona to begin his 50-plus year medical career as a general practitioner and surgeon. He was an active member of the American Medical Association and the Mississippi State Medical Association throughout his career. For more on Dr. Middleton, see JMSMA, “Asclepiad,” January 2012, 32. David McIntosh Owen, MD, 79, of Hattiesburg, died on April 27, 2015. Dr. Owen was born in Gulfport on October 6, 1935. He was an Eagle Scout and a 1953 graduate of Gulfport High School. In 1957, he graduated from the University of Mississippi. A 1960 graduate of the University of Mississippi Medical Center. Dr. Owen completed his residency in internal medicine and a fellowship in hematology and oncology. He moved to Hattiesburg in 1966 where he joined the Hattiesburg Clinic and practiced medicine at both Forrest General Hospital and Methodist Hospital. He was board certified in internal medicine and medical oncology. Dr. Owen was Hattiesburg’s first hematologist-oncologist and pioneered cancer treatment at Forrest General Hospital. He was responsible for setting up Forrest General’s cancer registry, serving as its chairman from creation until his retirement in 2000. He was a founding member of the Ochsner Community Clinical Oncology Program and was actively involved in cancer clinical research. He served as president of the South Mississippi Medical Society. He also served on numerous medical boards including as chairman of the Board of Trustees of the Mississippi State Medical Association and president of the Mississippi division of the American Cancer Society. Kenneth Noel Reed, MD, of Ridgeland, died on March 7, 2015. Kenneth was born November 29, 1938, and graduated from Belzoni High School, the University of Mississippi in pre-med, the University of Mississippi Medical School, followed by a residency at the University of Tennessee in otolaryngology. He completed a fellowship in facial 52 VOL. 57 • NO. 2 • 2016

plastic surgery at McDill Air Force Base in Tampa, FL. He then returned to Jackson in 1971 and was a founding member of the Ear, Nose, and Throat Surgical Group in Jackson. Gail E. Rasmussen, MD, of Meridian, died on June 3, 2015, after a sixteen month battle with melanoma. Dr. Rasmussen received a Doctor of Medicine from the University of Miami in 1987 and served her anesthesiology residency training at Yale-New Haven Hospital. Gail joined Meridian Anesthesiology Group in December1998 and became a member of the Board of Directors in 2004. She served as president from 2009 until 2011. She also served as a Medical Staff Officer for Anderson Regional Medical Center (ARMC) from 2010 to 2013. Serving as Chief of Staff in 2012 and Chief Quality Officer in 2013 for ARMC, Dr. Rasmussen was instrumental in upgrading and overseeing the Pediatric Anesthesiology program. Dr. Robert B. Townes, Jr., MD, 89, of Grenada, died, October 23, 2015. He was born June 5, 1926 in Grenada. He attended Grenada’s public school, and graduated from John Rundle High School. During World War II, he enlisted in the Navy in March, 1944, and served overseas as a hospital corpsman in Okinawa. He attended the University of Mississippi where he earned his Bachelor of Arts and Master of Science degrees. He attended Tulane University Medical School and graduated with an MD in 1955. After one year of internship at Charity Hospital in New Orleans, he returned to Grenada and joined Dr. W. B. Hunt in the general practice of medicine. After 51 years of practice, he retired in 2008. Dr. Townes was a member of the Mississippi State Medical Association, Mississippi Academy of Family Physicians, and a charter member of the American Academy of Family Physicians where he was board certified. He was a clinical associate professor of Family Medicine at the University of Mississippi for 30 years. Dr. Townes was appointed by Governor William Winter to serve on the Mississippi State Board of Medical Licensure. Cecil Theodore Williams, Jr., MD, 81, of Laurel, died on May 24, 2015. Born on March 23, 1934 in Laurel, Dr. Williams graduated from George S. Gardner High School in 1952. He attended the University of Southern Mississippi where he received a degree in geology. He went to work for Continental Oil Company before receiving a special calling to become a physician. Dr. Williams entered medical school and received his medical degree from the University of Mississippi. After specializing in cardiology, Dr. Williams returned to his hometown of Laurel where he practiced cardiology for over 25 years.

N E W

BEVARD, BRENT D., Hattiesburg; Physical Medicine & Rehabilitation

M E M B E R S

OSBORNE, SUSANNE V., Picayune; Obstetrics & Gynecology

BROWN, KIMBERLY LATISHA, Ocean Springs; Pediatrics

PELLERANO, EDWARD, Hattiesburg; Critical Care Medicine (Int Med)

COBB, JAMES ROBERT, McComb; Internal Medicine

PORTIS, RAYMOND L., Jackson; Critical Care Medicine (Int Med)

GLEASON, SARA HANAK, Jackson; Psychiatry

RAUSH, NICHOLAS C., Hattiesburg; General Surgery

HARRIS, ROBERT B., McComb; General Surgery

ROBERSON, ROWLAND M., Tupelo; Orthopedic Surgery

HEINDL, BRITTAIN F., Hattiesburg; Internal Medicine

ROKA, ATTILA, Meridian; Internal Medicine

HILL-CHANCE, GERRI L., Hazlehurst; Child & Adolescent Psychiatry

SHIPP, JAMES BYRON, Oxford; Ophthalmology

ISLAM, KHONDKER, Meridian; Internal Medicine

STOUT, JEFFERY B., Oxford; Cardiovascular Disease

JAIN, NITESH KUMAR, McComb; Internal Medicine

TUCKER, JOSHUA ERIC, Pascagoula; Physical Medicine & Rehabilitation

JOHNSON, DARYL A., Hattiesburg; Neurosurgery

WANEE, NEIL R., Smithville; Family Medicine

MARKS, TYLER G., Tupelo; Orthopedic Surgery

WINFIELD, TAMARA C., Jackson; Family Medicine

MORAN, MICHAEL E., McComb; Urology

ZAFAR, SALMAN, Hattiesburg; Internal Medicine

Show lawmakers the face of organized medicine.

DOCTOR

OF THE DAY

Every day during the legislative session, the Capitol Medical Unit is staffed by a full time nurse and an MSMA volunteer physician who provides basic health care services to legislators and capitol staff. As a Doctor of the Day, you’ll see firsthand the everyday operations of the Mississippi Legislature and be recognized on both the Senate and House floors at the opening of each day’s session. Volunteers can choose from a half day on Monday or Friday or a full day on Tuesday, Wednesday or Thursday.

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54 VOL. 57 • NO. 2 • 2016

S T A T E

D E P A R T M E N T

O F

H E A L T H

Currier Honored Dr. Nathan Davis Award Recipient

tate Health Officer Dr. Mary Currier was honored with the 2016 Dr. Nathan Davis Award for Outstanding Government Service by the American Medical Association (AMA) at an awards ceremony in Washington, D.C. The Mississippi State Medical Association (MSMA) nominated Currier late last year.

“The AMA’s Nathan Davis Award is recognized nationally as one of the most prestigious honors extended to elected officials and career government employees for outstanding endeavors that advance public health. MSMA nominated Dr. Currier to highlight her work to protect the public by requiring immunizations for school attendance. The Mississippi law is a model law that is recognized nationally as the strongest and best immunization law in America,” said MSMA President Dr. Daniel P. Edney. Dr. Edney adds, “Dr. Currier’s leadership and dedication to this fight justly identifies her as our country’s outstanding public health official for 2016.” Mississippi State Board of Health Chairman Dr. Lucius M. “Luke” Lampton congratulated Dr. Currier during its last quarterly board meeting. “No one in the United States is more deserving of this award than Dr. Mary Currier. She has spent the last 30 years in state service with a tireless commitment to improve the health of all Mississippians. This honor speaks not only to her exemplary leadership, but also to the impressive dedication and work of all Department of Health employees who make a positive difference each day in the lives of our citizens,” Inaugurated in 1989, the honor bears the name of the doctor who founded the AMA in 1847. “I am extremely honored and humbled by this recognition. I believe this award really goes to all those who work together, in this state, to improve health,” said Dr. Mary Currier.” Dr. Currier, who in January was appointed to her second term as State Health Officer, has served in numerous capacities with the state since 1984, including two terms as State Epidemiologist from 1993 to 2003 and again from 2007 to 2010.

Joe Scarborough, from “Morning Joe” on MSNBC who served as master of ceremonies, Mary Currier, MD, MPH and Stephen R. Permut, MD, JD, Chair of the AMA Board of Trustees

In 2015, Dr. Currier’s stand on mandatory immunizations which only allow for medical exemptions pushed Mississippi into the national spotlight with the highest vaccination rate for kindergarten students during the 2013-2014 school year at 99.7 percent. The national average is 93.3–95 percent for the measles, mumps, and rubella (MMR) vaccine; the diphtheria, tetanus, and pertussis (DTap); and the varicella vaccine. A senate resolution further honored the Mississippi State Department of Health.

Also during her tenure, Mississippi received a national award from the March of Dimes for successfully lowering the preterm birth rate by 11 percent since 2009, giving more babies a healthy start in life. The Virginia Apgar Award recognized states that accepted and met a challenge to lower their preterm birth rates by at least 8 percent between 2009 and 2014. Dina Ray, Executive Director for the MS Chapter of the March of Dimes said, “Dr. Mary Currier’s leadership in Mississippi is without equal. She has made a lifelong impact on the rate of prematurity and infant mortality in our state. Where others see hurdles, Dr. Currier sees opportunity. Dr. Currier has been a valuable volunteer for the March of Dimes, and champion of our cause, as well as a tireless advocate for healthier moms and babies in Mississippi.” A graduate of the University of Mississippi School of Medicine, Dr. Currier received her Master’s degree and preventive medicine residency training in Public Health from the Johns Hopkins School of Hygiene and Public Health. Currier’s Bachelor’s degree is from Rice University, and she attended Trinity College in Dublin, Ireland.

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She is a member of the Mississippi State Medical Association, the Mississippi Public Health Association, and is the Southeast Regional Representative to the Board of the Association of State and Territorial Health Officials. Currier is Board certified in General Preventive Medicine and Public Health. Only one other Mississippian has won the Dr. Nathan Davis Award. Former State Attorney General Mike Moore received the honor in 1997 for his work in achieving Mississippi’s legal settlement with national tobacco companies. n

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