VOL. LIX • NO. 6/7 • 2018

VOLUME LIX • NO. 6/7 • 2018

Celebrating Years

150

House of Delegates MSMA ANNUAL SESSION 2018

FRIDAY AUGUST 17, 2018 8:00

MSMA Board of Trustees meeting [Time for specialty society meetings]

SATURDAY, AUGUST 18, 2018 Special History of Mississippi Medicine Program

7:00

10:00 House of Delegates 11:30

Candidate Forum (box lunch available @ 11:30)

8:00

12:30

Reference Committee Hearings

8:30

Caucuses

9:00

3:30 4:00

6:00

Rx CME. MSMA General Counsel Conner Reeves will outline the new prescribing rules passed by the medical board and submitted for approval by the occupational review board.

Shuttle from the Westin to the museum & from the Old Capitol Inn back to the Westin afterward.

10:00

150th Commemorative Reception at Museum of Mississippi History

10:15

Enjoy hors d’oeuvres and beverages while exploring the new Mississippi History Museum. Then, walk one block to the Old Capitol Inn for the Gala.

7:30

9:30

Presidential Awards Inaugural Gala The Old Capitol Inn

Gala Dinner Dance includes the official inauguration of MSMA’s 151st President Michael Mansour, MD; Leadership Awards program and dancing to music by the Raphael Semmes Jazz Ensemble.

10:45

Celebrating the 150th House of Delegates KICK OFF BREAKFAST Emcee J. Edward Hill, MD

CME: Arthur C. Guyton, MD Brought to you by the Mississippi Physicians Care Network. John Hall, PhD presenting.

CME: Civil War Medicine in Mississippi.

Brought to you by the physicians of Central Medical Society. Sid Bondurant, MD presenting.

CME: Mississippi Medicine and the Civil Rights Struggle. The Dr. Robert Smith Lecture brought to you by the UMMC Alumni Affairs.

Loretta Jackson-Williams, MD presenting.

CME: Yellow Fever in Mississippi Brought to you by The Physicians of Hattiesburg Clinic. Deanne L. Stephens, PhD presenting.

Break CME: Images in Mississippi Medicine Brought to you by the Journal of the Mississippi State Medical Association. Luke Lampton, MD presenting.

CME: Mississippi, M.A.S.H., and Arterial Repair: at the Intersection of Surgical History and Pop Culture. Michael C. Trotter, MD presenting.

11:15

CME: William Faulkner Nobel Laureate or Town Drunk? Brought to you by MACM. Randy Easterling, MD presenting.

11:45

CME: James D. Hardy, MD. Brought to you by Mississippi Chapter of the American College of Surgeons. Marc Mitchell, MD presenting.

12:15

KEYNOTE LUNCHEON The Honorable Haley Barbour

2:00 4:00

House of Delegates MSMA Board of Trustees Meeting

VOL. LIX • NO. 6/7 • JUNE/JULY 2018 SCIENCE OF MEDICINE

EDITOR Lucius M. Lampton, MD

THE ASSOCIATION President William M. Grantham, MD

Top 10 Facts You Need to Know: Sport-Related Concussion 276 Brian J. Tollefson, MD, CAQ-Sports Medicine; Richard L. Grantier, MD; Patrick O’Brien

President-Elect Michael Mansour, MD

MANAGING EDITOR Karen A. Evers

Secretary-Treasurer W. Mark Horne, MD

Smoke-Free Ordinances in Mississippi Predict Lower Hospital Admission Rates for Acute Cardiovascular, Stroke, and Pulmonary Events 285 Robert McMillen, PhD; Emily McClelland, MS; Amy Winter, MPH

PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD and the Editors

Speaker Geri Lee Weiland, MD

Non-syndromic Mitochondrial Hearing Loss Successfully Treated with Bilateral Cochlear Implantation: A Case Report 289 Kelsey L. Bounds, M3; Laura K. House, MD; Jeffrey D. Carron, MD

ASSOCIATE EDITORS D. Stanley Hartness, MD Richard D. deShazo, 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.

Top 10 Facts You Need to Know about Non-Alcoholic Fatty Liver Disease: A Review for the Primary Care Provider 280 Jared R. Beck, DO; Karin S. Gilkison, MD; John D. McKee, MD; Eric V. Plott, MD

The Hidden Repercussions of the Opioid Crisis in Mississippi’s Children: Neonatal Abstinence Syndrome/Neonatal Opioid Withdrawal Syndrome 293 Lauren Tucker, MD; Tara Nation, MSN, CPNP; Renate Savich, MD; Douglas Tucker, MD; Sujith Ramachandran, PhD; Dana Lindsay, RN; Chad Blackshear, MS; Robert D Annett, PhD

Malignant Solitary Fibrous Tumors of the Nasal Cavity Eric Tillotson, MD; Maria F. Gonzalez MD DEPARTMENTS From the Editor – There’s Always Next Month…

Lucius M. Lampton, MD

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274

President’s Page – We Are Back on Track William M. Grantham, MD

303

Editorials – Electronic Medical Records: It Takes a Forest!

Stanley Hartness, MD

304

To Cut or Not To Cut: Is Waiting the Best Solution to Many of Medicine's Problems?

305 Britt Cross, DO

SUBSCRIPTION RATE: $83.00 per annum; $96.00 per annum for foreign subscriptions; $7.00 per copy, $10.00 per foreign copy, as available.

Letters

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New Members

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ADVERTISING RATES: furnished on request. Jill Gordon, MSMA Director of Marketing. Ph. 601-853-6733, ext. 324, Email: JGordon@MSMAonline.com

Commentary – NPs and Elderly Care: We Can Do Better

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Images in Medicine – Washington County General Hospital, 1958 Lucius M. Lampton, MD

321

Poetry and Medicine – Backing into the Future John D. McEachin, MD

322

Una Voce – Walking with the Black Dog Dwalia S. South, MD

323

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 © 2018 Mississippi State Medical Association.

Official Publication

MSMA • Since 1959

ABOUT THE COVER Photo by Martin Pomphrey, MD; Mayhew Fireworks at Old Waverly – This photograph, by Dr. Martin Pomphrey of Mayhew, was taken on the 4th of July at the fireworks display held at Old Waverly Club in West Point, Mississippi. Dr. Pomphrey enhanced the image using Adobe Photoshop Lightroom. Every year there is an Independence Day celebration at Old Waverly which includes a salute to service members, talks by retired military, a kids’ parade, games, super supper, and finishing with fireworks. Host to Prairie Medical Society meetings, Old Waverly has been highly regarded as one of the truly unique, absolute premier private clubs in the U.S. Developed on the site of the historic Waverly Mansion, the club is a result of the vision of the George and Marcia Bryan Family, who sought to create a world-class destination for golf and hospitality on some of the most scenic acreage in the heart of the Mississippi Black Prairie. Since its founding in 1988, the golf course has been a fixture among various "Best of " lists, and has hosted several high-profile championship golf events over the years. Old Waverly has also been selected to host the 2019 US Women's Amateur.

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F R O M

T H E

E D I T O R

There’s Always Next Month…

T

he strength of our Journal is also its Achilles’ heel: it is a physician-run and physicianedited production, with its principal editors and editorial staff all physicians who manage full-time, demanding medical practices while also attending faithfully to their journal duties. A careful balance of monthly deadlines regarding submissions, editing, proofing, and printing keeps our beloved Lucius M. Lampton, MD publication on time and task. Falling Editor off track in the past has proven difficult to make up: working physicians frankly can’t edit more than one journal a month, or so we’ve found.

More than a year ago, due to health issues of critical staff, this journal slipped off track and despite our best efforts, was forced to combine several issues to return to timely production. Such is why recently you received an excellent combined issue dated last year. Beginning with the January special opioid issue (which received national acclaim), your Journal has been published on time, reestablishing its finite monthly submissions, proofing, and printing deadlines.

I early learned the importance of a deadline in publishing my weekly newspaper in Magnolia two decades ago. After once missing a printing deadline, my staff was told that whatever was on the page at 12 noon Wednesday went to press. “There’s always next week…” I told them when they would complain about the “drop-dead” deadline. I shared this long ago with our Managing Editor Karen Evers, and we’ve created our own mantra of “there’s always next month…” about our Journal work.

Also, many monthly national publications don’t publish every month, taking a month or two off annually to recharge and recover from the stressful pace of monthly deadlines. The New Criterion, a New York-based literary journal, does just that: it is published monthly but takes a breather in July and August. Thus, notice your Journal remains a timely, monthly journal, with 10 issues a year like The New Criterion and The Atlantic magazine, having two double issues a year: June/July and November/December. With our small staff and overly-stretched editors, this is a workable schedule to maintain our superior monthly scientific journal which serves as “the voice, the face, and the spirit of medicine in Mississippi.”n Contact me at LukeLampton@cableone.net.

— Lucius M. Lampton, MD, Editor

JOURNAL EDITORIAL ADVISORY BOARD ADDICTION MEDICINE Scott L. Hambleton, MD

EMERGENCY MEDICINE Philip Levin, MD

MEDICAL STUDENT John F. G. Bobo, M2

ALLERGY/IMMUNOLOGY Stephen B. LeBlanc, MD Patricia H. Stewart, MD

EPIDEMIOLOGY/PUBLIC HEALTH Mary Margaret Currier, MD, MPH Thomas E. Dobbs, MD, MPH

NEPHROLOGY Jorge Castaneda, MD Harvey A. Gersh, MD

ANESTHESIOLOGY Douglas R. Bacon, MD John W. Bethea, Jr., MD

FAMILY MEDICINE Tim J. Alford, MD Diane K. Beebe, MD Jennifer J. Bryan, MD J. Edward Hill, MD Ben Earl Kitchens, MD James J. Withers, MD

OBSTETRICS & GYNECOLOGY Sidney W. Bondurant, MD Darden H. North, MD

GENERAL SURGERY Andrew C. Mallette, MD

OTOLARYNGOLOGY Bradford J. Dye, III, MD

HEMATOLOGY Vincent E Herrin, MD

PEDIATRIC OTOLARYNGOLOGY Jeffrey D. Carron, MD

INTERNAL MEDICINE Daniel P. Edney, MD W. Mark Horne, MD Daniel W. Jones, MD Brett C. Lampton, MD Jimmy Lee Stewart, Jr., MD

PEDIATRICS Michael Artigues, MD Owen B. Evans, MD

CARDIOVASCULAR DISEASE Cameron Guild, MD Thad F. Waites, MD CHILD & ADOLESCENT PSYCHIATRY John Elgin Wilkaitis, MD Nisha S. Withane, MD, Fellow CLINICAL NEUROPHYSIOLOGY Alan R. Moore, MD DERMATOLOGY Robert T. Brodell, MD Adam C. Byrd, MD

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ORTHOPEDIC SURGERY Chris E. Wiggins, MD

PLASTIC SURGERY William C. Lineaweaver, MD Chair, Journal Editorial Advisory Board PSYCHIATRY Beverly J. Bryant, MD June A. Powell, MD PULMONARY DISEASE Sharon P. Douglas, MD John R. Spurzem, MD RADIOLOGY P. H. (Hal) Moore, Jr., MD RHEUMATOLOGY C. Ann Myers, MD UROLOGY W. Lamar Weems, MD

Do Not Enter the Courtroom Without the Protection of MACM Regardless of merit, thousands of medical malpractice claims are filed each year. Some say it is not a question of IF you will be sued; it is a question of WHEN. Call MACM today for your professional liability needs and to join so many others who have placed their trust with a company that has been physician owned and physician governed for over 40 years.

macm.net 601-605-4882 | macm.net JOURNAL MSMA

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Top 10 Facts You Need to Know: Sport-Related Concussion BRIAN J. TOLLEFSON, MD, CAQ-SPORTS MEDICINE; RICHARD L. GRANTIER, MD; PATRICK O’BRIEN It is estimated that there are as many as 3.8 million sport-related concussions (SRC) annually in the United States.1 This number may actually be much higher as many SRC go undiagnosed or unreported. It is important for all primary care providers to become familiar with the current literature, management guidelines, and state laws pertaining to SRC. Sports-related concussion is a potentially serious injury that requires prompt identification and proper management to ensure a safe return to play.

1

The Consensus Statement on Concussion in Sport is a peerreviewed publication considered by many to be the gold standard for the diagnosis and management of sport-related concussion.

The Consensus Statement on Concussion in Sport is the product of an international group of clinicians and researchers considered to be experts in the field of SRC. This Concussion in Sport Group (CISG) meets every four years to collaborate on a review of current literature and expert opinion related to SRC. The most recent meeting was held in Berlin in October 2016. The CISG consensus statement from that meeting was published in April 2017. The CISG consensus statement builds on the previously published Consensus statements.2-5 The CISG consensus statement is not intended to be a legal standard of care. It is intended to be a guide consistent with the “reasonable practice of a healthcare professional”.6

2

The definition of sport-related concussion is complex. The 2017 CISG consensus statement defines SRC as a traumatic brain injury induced by biomechanics forces with the following common features:

• Caused by a direct blow to the head or an impulsive force transmitted to the head from elsewhere on the body.

• Typically results in rapid onset and resolution of impaired neurological function.

• E xhibits clinical signs and symptoms due to functional disturbance rather than structural injury—no abnormality seen on standard neuroimaging.

• Results in a range of clinical signs and symptoms that often do not include loss of consciousness.

Although it is often done in practice and seen in literature, the CISG consensus statement guards against using the terms ‘sport-related concussion’ and ‘mild traumatic brain injury’ interchangeably.6,7

3

Medical providers caring for athletes must be up-to-date on the diagnosis and management of Sport-Related Concussion.

The diagnosis of SRC is not always straightforward, and the misdiagnosis or mismanagement of SRC can have devastating consequences for the injured athlete. The clinical signs and symptoms are often subtle and may even be delayed for hours or days after the initial injury.8 It is important to be familiar with the signs and symptoms of SRC and maintain a strong index of suspicion for this often under recognized condition.

Medical providers can gain valuable up-to-date SRC training by reviewing the 2017 Consensus Statement on Concussion in Sports referenced above6 and by completing the CDC HEADS UP to Health Care Providers online training modules.9

4

Sport-Related Concussion should be suspected in an athlete that displays any of the following signs and symptoms after a direct or indirect impact to the head:

• O bservable Signs—loss of consciousness, slowness to get up after a play, disorientation, blank stare, balance or coordination difficulties, head or facial injury, vomiting, emotional lability.

• R eported Symptoms—headache, dizziness, blurred vision, sensitivity to noise or light, irritability, anxiousness, drowsiness, feeling slowed down or “in a fog”.

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Headache and dizziness are the most common post-SRC symptoms.6

5

The Sports Concussion Assessment Tool version 5 (SCAT 5) should be used to help diagnose SRC. SRC is one of the most challenging injuries in sports medicine to accurately diagnose. Acutely, a SRC is an evolving injury with rapidly changing signs and symptoms.

Adding to the diagnostic complexity, the athlete will often downplay or deny symptoms for fear of being pulled from the game.

Currently, there is no definitive test or marker for the diagnosis of SRC. The SCAT 5 used for individuals 13 years and older and child SCAT 5 used for individuals 12 years and younger represents the most well-established instrument for the sideline evaluation of concussion. A copy of the SCAT 5 and child SCAT 5 can be downloaded for free and without copyright infringement for use by the healthcare professional on the sideline.11,12

6

An athlete displaying any signs or symptoms of sport-related concussion must be removed from play immediately. SRC is a clinical diagnosis. The sideline provider must maintain a high index of suspicion for this sometimes elusive diagnosis. Once a player is suspected of having sustained an SRC, the player must be removed from play immediately. Further evaluation can be conducted on the sideline or in the locker room using the SCAT 5. If, after further evaluation, the player is diagnosed with a SRC, the player is not allowed to return to play that day. Depending on the severity of symptoms, the concussed player should either be transported to the emergency room for further evaluation or observed on the sideline for progression of symptoms. At no time should the injured athlete be left alone. After a 1-2 day period of physical and cognitive rest, the athlete is allowed to enter the return-to-sport protocol which is described later in this article.6,13

7

Look for “red flags” of more serious injury in athletes with suspected sports-related concussion. Any athlete suspected of having an SRC after a direct or indirect blow to the head must be quickly identified on the field. The injured athlete must be immediately evaluated for “red flags” that could indicate other potentially more serious injuries. Red flags with suspected SRC include:

• Significant neck pain or tenderness—suspect possible cervical spine injury.

• Double vision, weakness or tingling/burning in arms or legs—suspect intracranial hemorrhage or cervical spine injury.

• S evere or increasing headache, seizure, prolonged loss of consciousness, deteriorating conscious state, vomiting, and increasing restlessness, agitation or combativeness—suspect intracranial hemorrhage.6 An injured athlete displaying any of these “red flags” should be immediately transported to the emergency room, potentially in full spinal injury precautions.

8

All 50 states now have a youth concussion law that mandates education and management of sport-related concussion. The law in Mississippi was enacted on July 1st, 2014, and is known called the “Mississippi Youth Concussion Law”. The law is a three-page document that should be read in its entirety by all healthcare providers who care for young athletes in Mississippi. The law applies to all private and public school athletes in grades 7-12 involved in school-sponsored activities. Although most legislation is similar, each state has its own law with subtle differences. If caring for an athlete in another state, you must follow that State’s specific Law. In summary, the Mississippi youth concussion law mandates the following:13 • School organization shall adopt and implement a concussion management and return-to-play policy.

• Parents or guardians shall receive and sign a copy of the school’s concussion policy before the start of the sport season.

• A thlete with a suspected SRC shall be removed from practice or game immediately; not allowed to return the same day; evaluated by a healthcare provider.

• Athlete diagnosed with SRC shall be referred to a licensed physician, preferably one with experience in managing SRCs. • Athlete diagnosed with SRC may return to play only after full recovery and clearance by a healthcare provider.

• State Department of Health shall endorse online concussion recognition education course.

9

Following a sport-related concussion, the athlete must complete a supervised graduated return-to-sport (RTS) protocol. The graduated RTS protocol is ideally supervised by the team physician or athletic trainer. The RTS protocol consists of 6 progressive stages of activity that culminates in the athlete returning to full unrestricted play. The RTS protocol begins after a 24-48 hour period of physical and cognitive rest only if the athlete is completely asymptomatic. There should be at least 24 hours between each stage of the protocol. If any sign or symptom recurs during the progressive stages of exercise, the athlete should go back to the previous stage. The following table is a generic example of a graduated RTS protocol as detailed in the 2017 CISG consensus statement.6 A more sport specific strategy should be tailored to the individual athlete and sport.

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individual athlete and sport.

Table. Six Progressive Steps of Return-­‐to-­‐sport (RTS) Protocol Figure. Six Progressive Steps of Return-to-sport (RTS) Protocol

Stage

Aim

Ac9vity

Goal of each step

1

Symptoms limited acIvity

Non-­‐strenuous daily acIviIes

Work/school acIviIes

2

Light aerobic acIvity

Walking or staIonary biking

Increase heart rate

3

Sport-­‐specific exercise

Running drills. No head impact.

Add progressive movement

4

Non-­‐contact training drills

More strenuous training; Add resistance training

Exercise, coordinaIon, and increased thinking

5

Full-­‐contact pracIce

ParIcipate in normal pracIce

Restore confidence and assess funcIonal skills

6

Return to sport

Normal game play

1010

There are several potential long-term risks associated with repeated sport-related concussions. These sometimes devastating complications should be discussed with the athletes and guardians prior to returning to sports with high risk for repeat There are several poten9al long-­‐term risks associated with repeated sport-­‐related concussions. concussion.

• SThese someImes devastaIng complicaIons should be discussed with the athletes and guardians prior to econd impact syndrome (SIS)—SIS is a rare and devastating consequence of returning to play too early after suffering a sportreturning to sports with high risk for repeat concussion. related concussion. It is thought that the initial concussion leaves the protective auto regulatory mechanisms of the brain vulnerable to subsequent trauma. A second impact on the incompletely healed brain results in massive cerebral edema and herniation. The injured • Second impact syndrome (SIS)—SIS is a rare and devastaIng consequence of returning to play too athlete often dies on the field within minutes of the injury or may survive with profound neurologic deficits.14 early afer suffering a sport-­‐related concussion. It is thought that the iniIal concussion leaves the • Post-concussive syndrome (PCS)—After a sport-related concussion, symptoms typically resolve within 1-2 weeks. A small percentage A second protecIve auto regulatory mechanisms of the brain vulnerable to subsequent trauma. (less than 10%) go on to develop PCS remaining symptomatic for several weeks or months following the injury. Risk factors for PCS 15,16 impact on the incompletely healed brain results in massive cerebral edema and herniaIon. The Although treatment guidelines commonly advocate include repeated concussions, history of psychiatric illness, and migraine. complete rest following an SRC, there is no evidence that completely avoiding physical activity while symptomatic expedites recovery. injured athlete ofen dies on the field within minutes of the injury or may survive with profound 14 A recent study suggests that physical activity within 7 days of the SRC may reduce the risk of PCS.17 Ideally, management of PCS neurologic deficits. should take place in a multidisciplinary collaborative setting experienced in treating this condition.18 • C hronic traumatic encephalopathy (CTE)—CTE is a progressive neurodegenerative brain disease associated with repeated head trauma. Pathologically, CTE results from a buildup of abnormal tau protein in the brain that disrupts neuropathways.19,20 The resulting clinical symptoms may include aggression, memory loss, depression, anxiety, and suicidal behavior. A recent well-publicized study examined the brains of more than 100 former NFL football players and found that 99% of those examined had pathological evidence of CTE.21 n

References 1. Mullally, W, Concussion. Am J of Med. 2017:130;885-892.

2. Aubry M, Cantu R, Dvorak J, et al; Concussion in Sport (CIS) Group. Summary and agreement statement of the 1st international symposium on concussion in sport, Vienna 2001. Clin J Sport Med. 2002;12:6–11.

3. McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd international conference on concussion in sport, Prague 2004. Br J Sports Med. 2005;39:i78–i86.

4. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport - the third international conference on concussion in sport held in Zurich, November 2008. Phys Sportsmed. 2009;37:141–59.

5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th international conference on concussion in sport held in Zurich, November 2012. Br J Sports Med. 2013;47:250–8.

6. McCrory P, Meeuwisse W, Dvorak J, et al. consensus statement on concussion in sport – the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;0:1-10.

7. McCrory P, Feddermann-Demont N, Dvořák J, et al. What is the definition of sports-related concussion: a systematic review. Br J Sports Med. 2017;51:877-887.

8. Morgan, C., Zuckerman, S., Lee, Y., King, L., Beaird, S., Sills, A., & Solomon, G. (2015). Predictors of postconcussion syndrome after sports-related concussion in young athletes: a matched case-control study. J Neurosurg Pediatr. 1-10 DOI: 10.3171/2014.10.PEDS14356.

9. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, Division of Unintentional Injury Prevention, HEADS UP to Health Care Providers. www.cdc.gov/headsup/providers/index.html. Accessed July 20, 2017.

10. Davis GA, et al. Br J Sports Med 2017;0:1–8. doi:10.1136/bjsports-2017-097506SCAT5 BJSM Online First, Concussion in Sport Group 2017. Sport Concussion Assessment Tool — 5th Edition http://bjsm.bmj.com/content/bjsports/early/2017/04/26/bjsports-2017-097506SCAT5.full.pdf. Accessed July 20, 2017.

11. Davis GA, et al. Sport concussion assessment tool - 5th edition. Br J Sports Med. 2017;0:1-8.

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12. Davis GA, et al. Child sport concussion assessment tool – 5th edition. Br J Sports Med. 2017;0:1–8.

13. Mississippi Legislature Regular Session 2014 Committee Substitute for House Bill No. 48. By: Representatives Mims, Crawford. http://billstatus.ls.state.ms.us/ documents/2014/pdf/HB/0001-0099/HB0048SG.pdf. Accessed July 20, 2017.

14. Bey T, Ostick B. Second impact syndrome. Western J of Emerg Med. 2009;10(1):610.

15. Morgan C, Zuckerman S, Lee Y, et al. Predictors of postconcussion syndrome after sports-related concussion in young athletes: a matched case-control study.

J Neurosurg Pediatr. 2015;15:589-98.

16. Bleiberg J, Cernich AN, Cameron K, et al. Duration of cognitive impairment after sports concussion. Neurosurgery. 2004;54:1073–78–78–80.

17. Grool A, Aglipay M, Momoli G, et al. Association between early participation in physical activity following acute concussion and persistent postconcussive symptoms in children and adolescents. JAMA. 2016;316(23):2504-2514.

18. Makdissi M, Schneider K, Feddermann-Demont N, et al. Approach to investigation and treatment of persistent symptoms following sport-related concussion: a systematic review. Br J Sports Med. 2017;51(12):958-68.

19. McKee AC, Stern RA, Nowinski CJ, et al. The spectrum of disease in chronic traumatic encephalopathy. Brain. 2013;136:43-64.

20. Omalu BI, DeKosky ST, Minster RL, et al. Chroinc traumatic encephalopathy in a national football league player. Neurosurgery. 2005;57(1):128-133.

21. Mez J, Daneshvar DH, Kiernan PT, et al. Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football. JAMA. 2017;318(4):360-370.

Author Information Program Director of the Primary Care Sports Medicine Fellowship at the University of Mississippi Medical Center (UMMC) in Jackson (Tollefson). PGY-2 emergency medicine resident at UMMC (Grantier). Primary Care Sports Medicine Fellowship Coordinator at UMMC (O’Brien).

Pen > Sword

E

xpress your opinion in the JMSMA through a letter to the editor or guest editorial. The Journal MSMA welcomes letters to the editor. Letters for publication should be less than 300 words. Guest editorials or comments may be longer, with an average of 600 words. All letters are subject to editing for length and clarity. If you are writing in response to a particular article, please mention the headline and issue date in your letter. Also include your contact information. While we do not publish street addresses, e-mail addresses, or telephone numbers, we do verify authorship, as well as clarify ambiguities, to protect our letterwriters. You can submit your letter via email to: KEvers@MSMAonline.com or mail it to the Journal office at MSMA headquarters: P.O. Box 2548, Ridgeland, MS 39158-2548.

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Top 10 Facts You Need to Know about Non-Alcoholic Fatty Liver Disease: A Review for the Primary Care Provider JARED R. BECK, DO; KARIN S. GILKISON, MD, MPH; JOHN D. MCKEE, MD; ERIC V. PLOTT, MD Nonalcoholic fatty liver disease (NAFLD) is found worldwide and is the leading cause of hepatic disorders in Western industrialized countries.

Even more alarming is the prevalence of NAFLD; it is higher than originally thought with some studies reporting upwards of 40% of the middleaged population.1 This figure is even more prevalent in the Southern United States in which 70% of the obese and diabetic population were found to have NAFLD.1 NAFLD is now the second leading indication for liver transplant in the United States and based on current trends, recent studies have reported that NAFLD will become the leading cause of liver transplant both in Europe and in the United States.2 Despite these egregious statistics, NAFLD often times goes unnoticed leading to increased overall mortality and morbidity in aged matched populations.3 Here are the top 10 things primary care providers should know about NAFLD in order to help identify and treat these patients.

1

NAFLD is defined as the presence of hepatic steatosis in individuals who consume little or no alcohol after exclusion of other causes of liver disease. As the name implies, nonalcoholic fatty liver disease is a clinical pathological entity in which the liver’s histological appearance demonstrates accumulation of fat within hepatocytes, or “steatosis.” This fatty accumulation of NAFLD can range from simple hepatic steatosis, to steatohepatitis (fat with inflammation), to end stage fibrosis, or “cirrhosis,” and is the leading cause of cryptogenic cirrhosis after other probable causes have been ruled out.4 The histologic appearance of NAFLD is very similar to alcohol induced liver injury, and can be difficult to exclude from a varying spectrum of hepatic insults. Therefore, the vital distinguishing feature of NAFLD, even though it is the most common liver disease in the United States, is that it can only be diagnosed after other causes of liver disease have been eliminated.

2

The primary pathogenesis of NAFLD includes insulin resistance and fat accumulation. The exact pathogenesis and mechanism of fatty liver disease has yet to be fully elucidated. There are a handful of proposed mechanisms, but the most commonly accepted theories involve insulin resistance and triglyceride accumulation leading to hepatocellular injury. One proposed “two-hit” theory proposes a first hit of insulin resistance which promotes hepatic steatosis. The fatty liver becomes less capable of coping with oxidative stress leading to the second hit: inflammation.5

3

The risk factors for NAFLD are unfortunately common. The most common risk factor for NAFLD is obesity, which affects greater than 35% of the US population.6 Other risk factors include insulin resistance, type 2 diabetes, metabolic syndrome, dyslipidemia, systemic hypertension, and cardiovascular disease.7 Males are two times more likely to have NAFLD than their female counterparts. Cohort studies have also found that Hispanic individuals have a significantly higher prevalence when compared to the general population.8 The prevalence of NAFLD increases with age with peak between 40 and 65 years old.8 There is evidence to suggest that NAFLD is a heritable condition in which family members of children with NAFLD should be considered at high risk for NAFLD even in the absence of obesity.8

4

The signs and symptoms of NAFLD are non-specific. Unfortunately, most patient with NAFLD are neither asymptomatic nor presenting with specific complaints. The most common symptoms are fatigue and malaise. Patients can complain of vague, colicky, right upper quadrant pain. On physical exam, they may have evidence of hepatomegaly, but this may be difficult to discern in an obese patient.

Patients are more likely to come to the attention of a provider from lab abnormalities, such as low platelets, or elevation in AST, ALT, bilirubin, creatinine, or INR, or evidence on imaging studies suggesting steatosis, which is often an incidental finding. Patients who have progressed to cirrhosis may demonstrate physical stigmata of chronic liver disease, displaying signs of splenomegaly, ascites, caput medusae, palmar erythema, jaundice, asterixis and/or spider telangiectasias,9 or have no signs and symptoms at all. Patients with decompensated cirrhosis may present with hepatic encephalopathy, gastrointestinal tract bleeding, spontaneous bacterial peritonitis, acute renal failure, or shortness of breath indicative of hepatorenal or hepatopulmonary syndrome.10

5

Nonalcoholic fatty liver (NAFL) and Nonalcoholic steatohepatitis (NASH) are not the same entity. These terms are not the same.

NAFLD is the larger umbrella term that encompasses two very distinct subdivisions: nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). The primary distinguishing factor between the two is inflammation. In NAFL, there is hepatic steatosis only, without evidence of inflammation. In NASH, there is hepatic steatosis with inflammation, and hence the designation “hepatitis.” NASH is commonly associated with an increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) above normal, generally defined as greater than 19 in women and 30 in men, regardless of assigned lab “normal” ranges.11 These lab values are commonly elevated two-to threefold upper limit of normal, but can oscillate between normal and elevated levels even with persistently active disease. Ultimately, a liver biopsy is needed to differentiate between the two entities.12 280 VOL. 59 • NO. 6/7 • 2018

6

NAFLD is a diagnosis of exclusion. It is paramount to differentiate NAFLD from other etiologies. This requires a thorough evaluation to identify potential risks for, or presence of, other etiologies that can cause similar presentations as treatment can vary dramatically.

These include alcohol abuse, toxin-mediated injury, medication insult, infectious hepatitis, and genetic-related liver disease such as hemochromatosis, alpha-1 antitrypsin deficiency, and Wilson’s disease. Auto-immune etiologies and pregnancy-related liver disease must also be considered. In the right clinical setting, the diagnosis of NAFLD can often be made after these disease processes have been ruled out. Laboratory tests such as the serum aminotransferases, alkaline phosphatase and ferritin can be helpful but are neither required nor sufficient for making the diagnosis. Imaging in the right clinical setting is sufficient to support the diagnosis of NAFLD. Ultrasound is relatively sensitive and specific for NAFLD and should be the first mode of imaging obtained when suspicion exists. Liver biopsy is the gold standard for definitive diagnosis, but often not required. Biopsy is the only way, however, to differentiate between the two histologic subtypes of NAFLD: NAFL and NASH.13

7

To treat NAFLD, treat the underlying risk factors. The cornerstone for managing patients with NAFLD is to treat the underlying risk factors for this liver disease, with primary target of weight loss through lifestyle interventions including reduced caloric intake, a regular exercise regimen, and increasing muscle mass to increase the metabolic potential at rest. This is the foundation of treatment. Weight loss of 3-5% has been shown to provide significant improvement in steatosis. A greater weight loss goal of at least 10% can improve and reverse steatohepatitis, and has even been shown to reverse and resolve fibrosis!3 Metformin remains a foundational treatment for type 2 diabetes but is not currently recommended as a NAFLD-specific treatment. Pioglitazone was shown to improve steatohepatitis, but in a predominantly nondiabetic population. A more recent randomized trial has further demonstrated that long-term pioglitazone treatment is safe and effective in patients with prediabetes, type 2 diabetes and NASH.14 Vitamin E has also shown to improve liver histology in patients with NASH, but required a high dose of 800 units daily, and was unfortunately associated with an increased risk of prostate cancer in men and a controversial increase in all-cause mortality.15 Ultimately, it is important to continue to treat and manage the patient’s underlying chronic comorbidities to include diabetes mellitus type 2, dyslipidemia, and obesity with primary treatment focus on 10% weight loss.3

8

Consider a liver biopsy in patients diagnosed with NAFLD. Timing liver biopsy in patients with NAFLD should be thoughtfully deliberated. It may even be deferred until after a gastroenterology or hepatology consult is obtained. This outpatient procedure of liver biopsy is fairly straight-forward, but carries risks of morbidity and even rare mortality. The primary indications for liver biopsy in these patients include: confirmation of diagnosis, differentiation between NAFL and NASH, and staging of fibrosis. Outside of diagnostic question, however, it will rarely change active management, because primary treatment for all NAFLD patients is weight loss. Patients who are found to have NASH, and are at increased risk of advancing to fibrosis and cirrhosis, may have the most benefit from liver biopsy. Liver biopsy data may also provide a needed incentive to reach their weight loss goal. Studies have indicated that patients with increased risk of NASH include uncontrolled diabetes, severe obesity, advanced age and elevated AST/ALT ratio.16 Alternatives to biopsy available to assess the severity of NAFLD and fibrosis include the NAFLD fibrosis score, fibrotest, magnetic resonance elastography and transient elastography depending on available resources.

9

Current guidelines do not recommend screening for NAFLD. Current guidelines do not recommend screening for NAFLD in primary care, including the high-risk obese and diabetic patients. This is primarily due to remaining uncertainties regarding the best method of diagnosis and treatment of NAFLD. However, there is supporting evidence from multiple studies that screened for NAFLD in high risk patients with non-invasive methods which could potentially lead to a change in future guideline recommendations.17,18 As mentioned previously, liver chemistries can be within normal range despite having NAFL or NASH, thus does not make for an adequate screening test. Liver ultrasound is relatively more sensitive compared to liver chemistries, but this test can be expensive and time consuming as a screening test. However, incidental findings on imaging of hepatic steatosis does warrant further evaluation and should be worked up accordingly.3

10

Refer to a specialist when you have exhausted your resources. Currently there are no definitive recommendations that delineate when to refer to a specialist. In general, if a patient has failed attempts of trying to manage their chronic comorbidities, or you are unsure of what to do next, it is reasonable to refer the patient to a specialist within that field. For NAFLD, it is generally recommended that a patient with evidence of steatohepatitis on biopsy, severely elevated aminotransferases, or suspicion of cirrhosis be referred to a gastroenterologist or hepatologist for further risk stratification and management,3 and very reasonable to refer earlier in the course of disease to assess for liver diseases, need for liver biopsy, and treatment recommendations.

NAFLD is seen worldwide and is the leading cause of liver disorders in developed countries. In the Southern United States, among the middleaged population, it is thought that greater than 40% have NAFLD, which could lead to increased morbidity and mortality in a significant number of patients if left untreated. Therefore, it is important as primary care physicians to recognize NAFLD and the risk factors associated with NAFLD. Primary care physicians and mid-level providers are at the front lines of health care. Primary care providers have regular interaction with general patients in which the identification of lab abnormalities and incidental findings on imaging are first encountered. If identified, these findings are what will lead to the workup and subsequent diagnosis of NAFLD, which then allows for intervention, and hopefully prevention of advanced liver disease and transplant. Regular office visits provide a platform for patient education and counseling with a focus on weight loss and lifestyle modifications which are the cornerstones of treatment for NAFLD. If needed, primary care providers can then also appropriately refer patients to a specialist for further evaluation or continued surveillance of NAFLD. n

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References 1. Williams CD, Stengel J, Asike MI, et al. Prevalence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among a largely middle-aged population utilizing ultrasound and liver biopsy: a prospective study. Gastroenterology. 2011;140(1):124. doi: 10.1053/j.gastro.2010.09.038.

2. Pais R, Barritt AS, Calmus Y, et al. NAFLD and liver transplantation: Current burden and expected challenges. J Hepatol. 2016;65(6):1245-1257. doi:10.1016/j. jhep.2016.07.033.

3. Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. Hepatology. 2012;55:2005-2023. doi: 10.1038/ajg.2012.217.

4. Caldwell SH, Oelsner DH, Iezzoni JC, et al. Cryptogenic cirrhosis: clinical characterization and risk factors for underlying disease. Hepatology. 1999;29(3):664. doi: 10.1002/hep.510290347 5. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology. 2003;37: 917–923. doi:10.1053/ jhep.2003.50161.

6. https://www.cdc.gov/obesity/data/adult.html. Accessed June 22, 2017.

7. Sheth SG, Gordon FD, Chopra S. Nonalcoholic Steatohepatitis. Ann Intern Med. 1997;126:137-145. doi: 10.7326/0003-4819-126-2-199701150-00008.

8. Schwimmer JB, Celedon MA, Lavine JE, et al. Heritability of Nonalcoholic Fatty Liver Disease. Gastroenterology. 2009;136(5):1585-1592. doi: 10.1053/j.gastro.2009.01.050.

9. Heidelbaugh, JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am Fam Physician. 2006;1;74(5):756-62.

10. Heidelbaugh JJ, Bruderly, M. Cirrhosis and chronic liver failure: part 2. Complications and treatment. Am Fam Physician. 2006;1;74(5):756-62.

11. Kwo P, Cohen S, Lim J. ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. Am J Gastroenterol. 2017;112(1):18-35. doi: 10.1038/ajg.2016.517.

12. Lall C, Aisen A, Bansal N, Sandrasegaran K. Nonalcoholic Fatty Liver Disease. Am J Roentgenol. 2008;190:4, 993-1002. doi: 10.2214/AJR.07.2052 13. Cusi K, Orsak B, Bril F, Lomonaco R, Hecht J, Ortiz-Lopez C, et al. Long-Term Pioglitazone Treatment for Patients With Nonalcoholic Steatohepatitis and Prediabetes or Type 2 Diabetes Mellitus: A Randomized Trial. Ann Intern Med. 2016;165:305-315. doi: 10.7326/M15-1774.

14. Miller ER, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality.

Ann Intern Med. 2005;142:37-46. doi: 10.7326/0003-4819-142-1-200501040-00110.

15. Bedogni G, Nobili V, Tiribelli C. Epidemiology of fatty liver: An update. World J Gastroenterol. 2014;20(27):9050-9054. doi:10.3748/wjg.v20.i27.9050.

16. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: From steatosis to cirrhosis. Hepatology. 2006;43: S99–S112. doi:10.1002/hep.20973.

17. Doycheva I, Cui J, Nguyen P, et al. Non-invasive screening for NAFLD and advanced fibrosis in diabetes in primary care setting by MRI and MRE. Alimen Pharmcol Ther.

2016;43(1):83-95. doi:10.1111/apt.13405.

18. Kwok R, Choi KC, Wong GL, et al. Screening diabetic patients for non-alcoholic fatty liver disease with controlled attenuation parameter and liver stiffness measurements: a prospective cohort study. Gut. 2016;65:1359-1368. doi: 10.1136/gutjnl-2015-309265.

Author Information Internal Medicine Resident, ACP resident/fellow, Division of Internal Medicine, Captain, United States Air Force, Keesler Medical Center, Biloxi (Beck). Staff Gastroenterologist and Internal Medicine Teaching Faculty, Department of Gastroenterology, Hepatology, and Internal medicine, Major, United States Air Force, Keesler Medical Center, Biloxi (Gilkison).

Post doctorate trained at Harvard Medical School, President of the Mississippi Chapter of the Gastroenterology Society, Partner of Digestive Health Center of Ocean Springs (McKee).

Staff Gastroenterologist and Internal Medicine Teaching Faculty, Department of Gastroenterology, Hepatology, and Internal medicine, Lt. Colonel, United States Air Force, Keesler Medical Center, Biloxi (Plott).

Corresponding Author: Internal Medicine Resident, ACP resident/fellow, Division of Internal Medicine, Captain, United States Air Force, Keesler Medical Center, Biloxi, MS becksta3@gmail.com..

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Smoke-Free Ordinances in Mississippi Predict Lower Hospital Admission Rates for Acute Cardiovascular, Stroke, and Pulmonary Events ROBERT MCMILLEN, PHD; EMILY MCCLELLAND, MS; AMY WINTER, MPH Abstract Purpose: Although Mississippi does not have statewide smoke-free legislation, 157 municipalities in Mississippi have smoke-free ordinances.

This study compares hospital admission rates for acute cardiovascular, stroke, and pulmonary events for counties with and without smoke-free county seats.

Methods: The Mississippi Inpatient Outpatient Data System provided admission data. Admission rates for tobacco smoke related events were compared using ANCOVAs, adjusting for county demographics.

Admission rates for events not associated with tobacco smoke were also compared.

Results: Admission rates for tobacco smoke related events were lower in counties with smoke-free seats (152.5) that those without smoke-free seats (173.7), p<.05. There were no differences in admission rates for events not associated with tobacco smoke (18.0 vs 16.4, ns).

Conclusions: The findings of this study suggest that smoke-free ordinances predict lower hospital admissions for tobacco smoke related health events. Broader protections from tobacco smoke at the state-level could improve health and reduce healthcare costs.

Key Words: Tobacco smoke pollution, hospital admissions, smoke-free ordinances There are more than 7,000 chemicals in tobacco smoke. Among the 250 chemicals that are known to be harmful to health, at least 69 are carcinogenic.1 The harms of tobacco smoke exposure to non-smokers are well documented, and include both acute and chronic diseases.2-4 These health risks from exposure also generate substantial healthcare costs to the state. Annual Medicaid direct costs due to exposure to secondhand smoke exceed $36 million.5 In order to improve health and reduce healthcare costs, twenty-five states and the District of Columbia have implemented statewide smokefree legislation for indoor public places, including restaurants, bars, and workplaces. Mississippi has not yet implemented statewide legislation.

However, 157 municipalities in Mississippi have enacted local smokefree ordinances (as of 1 February 2018) in order to protect their citizens from tobacco smoke in indoor public spaces (although 13 of these municipalities have exemptions for bars or other establishments).

Numerous studies have shown that smoke-free legislation is associated with decreased hospital admissions for myocardial infarction and other cardiovascular events,6-14 strokes,15 and respiratory events.7,16-19 To illustrate, admissions for coronary heart disease in Bowling Green,

KY, decreased by 39% the year after the city implemented a smoke-free ordinance, whereas admission rates did not change in a matched control city (Kent, OH).20 These studies examined admissions for numerous types of acute events, in very different types of places, from small cities to states, and even entire countries. Although the methods and the size of reductions in admissions have varied across studies, the general finding of a reduction in admissions for acute events related to tobacco smoke exposure has remained consistent.

Within Mississippi, our previous research from controlled observational studies demonstrated that hospital admissions for heart attacks in both Starkville and Hattiesburg decreased substantially following the implementation of the smoke-free ordinances.21 Starkville residents experienced a 27.7% reduction in heart attack admissions compared to the 14.8% reduction observed among those who did not live in Starkville, while Hattiesburg residents experienced a 13.4% reduction in heart attack admissions compared to the 3.8% reduction observed among those who did not live in Hattiesburg. In both municipalities, the observed decrease in heart attack admissions was much higher than that observed in control communities that did not have a smoke-free ordinance.

This study expands this body of observational research by using a state-wide database of hospital admissions in Mississippi to examine the relationship between local smoke-free ordinances and hospital admissions for acute myocardial, stroke, and pulmonary events.

Methods This study applied a controlled observational approach to objectively examine hospital admission rates for adverse health events related to tobacco smoke, such as acute myocardial, stroke, and pulmonary events.

Specifically, we compared admission rates in counties with a county seat that had implemented a smoke-free ordinance to counties that had not.

Admission data are currently available for the years 2013 to 2016 from the Mississippi Inpatient Outpatient Data System (IODS), maintained by the Mississippi Hospital Association and the Mississippi State Department of Health.

Unit of Analysis Admission rates within Mississippi counties were selected as the unit of analyses. Rates per 10,000 residents rather than total admissions were examined in order to standardize admissions across counties with different population sizes. Counties were selected as the unit of analyses because the IODS does not provide data on patientsâ&#x20AC;&#x2122; municipality of residence Although the IODS includes zip code data for patients, the US Census does not provide the population data by zip codes necessary to calculate rates.

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Mississippi’s 82 counties are classified based on whether or not the county seat had a smoke-free ordinance in place during the study period (2013-2016). For the ten counties with two county seats, classification was based on the municipality with the higher population. Within Mississippi, 28 counties were classified as not having a smoke-free county seat and 36 had a smoke-free county seat for all four years of the study period. Sixteen counties became smoke-free during the study period and two did so after 2016 (Table 1).

Table 1. Mississippi counties County County Seat Smoke-Free Ordinance Adams County Natchez None Alcorn County Corinth 2007 Amite County Liberty None Attala County Kosciusko 2007 Benton County Ashland None Bolivar County Cleveland None Calhoun County Pittsboro 2015 Carroll County Vaiden 2012 Chickasaw County Houston None Choctaw County Ackerman None Claiborne County Port Gibson None Clarke County Quitman After 2016 Clay County West Point None Coahoma County Clarksdale 2014 Copiah County Hazlehurst None Covington County Collins 2008 DeSoto County Hernando 2007 Forrest County Hattiesburg 2007 Franklin County Meadville 2015 George County Lucedale 2013 Greene County Leakesville 2016 Grenada County Grenada 2009 Hancock County Bay Saint Louis None Harrison County Gulfport 2008 Hinds County Jackson 2010 Holmes County Lexington 2016 Humphreys County Belzoni 2010 Issaquena County Mayersville 2005 Itawamba County Fulton None Jackson County Pascagoula 2013 Jasper County Bay Springs None Jefferson County Fayette 2015 Jefferson Davis County Prentiss 2010 Jones County Laurel 2008 Kemper County De Kalb None Lafayette County Oxford 2006 Lamar County Purvis None Lauderdale County Meridian 2010 Lawrence County Monticello 2012 Leake County Carthage None Lee County Tupelo 2006 Leflore County Greenwood 2007 Lincoln County Brookhaven 2011 Lowndes County Columbus 2010 Madison County Canton 2012 Marion County Columbia None Marshall County Holly Springs 2016 286 VOL. 59 • NO. 6/7 • 2018

County County Seat Smoke-Free Ordinance Monroe County Aberdeen 2007 Montgomery County Winona None Neshoba County Philadelphia None Newton County Decatur None Noxubee County Macon 2016 Oktibbeha County Starkville 2006 Panola County Batesville 2010 Pearl River County Poplarville 2015 Perry County New Augusta 2012 Pike County Magnolia After 2016 Pontotoc County Pontotoc 2008 Prentiss County Booneville 2012 Quitman County Marks 2011 Rankin County Brandon 2015 Scott County Forest 2012 Sharkey County Rolling Fork 2011 Simpson County Mendenhall 2014 Smith County Raleigh None Stone County Wiggins 2013 Sunflower County Indianola 2012 Tallahatchie County Charleston 2015 Tate County Senatobia 2015 Tippah County Ripley None Tishomingo County Iuka 2015 Tunica County Tunica None Union County New Albany 2011 Walthall County Tylertown None Warren County Vicksburg None Washington County Greenville 2007 Wayne County Waynesboro None Webster County Walthall None Wilkinson County Woodville 2014 Winston County Louisville 2014 Yalobusha County Water Valley None Yazoo County Yazoo None Admission Classification Findings are based on the principle diagnosis for each hospital admission. This code is for the condition established after study to be chiefly responsible for occasioning the admission of the patient to the hospital for care.22 That is, the code is for the primary reason that the patient was admitted to the hospital. We identified admissions with principle diagnosis ICD-9/10 codes to select admissions for cardiovascular, respiratory, and control conditions in Mississippi. Based on prior research, we selected three cardiovascular conditions (acute myocardial infarction, angina, and ischemic stroke; I20-I25, I63-I66, G45, G46,),6,7,9,10,23-27 and three respiratory conditions (asthma, chronic obstructive pulmonary disease, and bronchitis or pneumonia; J40, J41, J32, J43, J44, J45, J46, J12-J18, J20).7,16,17 Previous research demonstrates a relationship between smoking bans and rates of admission to hospital for these acute conditions. We selected acute cholecystitis (K81), bowel obstruction (K56), and appendicitis (K35, K36, K37) as control conditions.7 Hospital admissions because of these conditions should be independent of any changes in smoking legislation, given that no known relationship exists between these conditions and smoke exposure.

County Admission Rates Admissions with a primary diagnosis code meeting inclusion criteria

were aggregated at the county level for each year of the study. The resulting data set included the annual total number of admissions for tobacco-related and control diseases for each county. Rates per 10,000 for each year were calculated for each county by dividing the total number of admissions by the county population, and then multiplying by 10,000.

Analyses Analyses are based on annual hospital admission rates for each of the 82 Mississippi counties from 2013 to 2016. Over this four year period, there are 328 county-years for these counties. Among these, 180 county-years had a smoke-free county seat and 148 did not. We conducted one-way ANCOVAs to compare rates of hospital admissions in counties with and without smoke-free ordinances implemented in the county seat. County demographics serving as covariates in the ANCOVA included percent of residents with health insurance, ratio of primary care providers to resident, percent of residents with college degrees, median income, and prevalence of cigarette smoking among adults. None of the covariates had a correlation coefficient greater than 0.8 with another covariate.

Results Admission rates for tobacco-related health events ranged from 37.40 to 316.54 per 10,000 residents, with an average rate of 160.62. Admission rates for health events unrelated to tobacco smoke exposure ranged from 0.0 to 44.88, with an average rate of 17.00.

Hospital admissions for health events related to tobacco smoke were significantly higher in counties without smoke-free ordinances in the county seat (173.7 per 10,000 residents) than counties with a smokefree ordinance (152.5 per 10,000 residents) [F(1,312)=4.8, p=0.029].

Admissions for the health events serving as controls were the same in counties without smoke-free ordinances in the county seat (18.0 per 10,000 residents) than those with a smoke-free county seat (16.4 per 10,000 residents) [F(1,314)=2.8, ns].

Follow-up analyses compared admission rates for the sub-categories of tobacco smoke related health events; acute coronary, stroke, asthma, COPD, and pneumonia events. Admission rates for pneumonia (50.5 vs 60.2) [F(1,312)=4.8, p=0.029] and stroke (35.7 vs 33.7) [F(1,312)=4.6, p=0.032] were statistically lower in counties with smoke-free ordinances.

Admission rates were also lower for acute coronary, asthma, and COPD, but the differences were not statistically significant.

Discussion The Institute of Medicine is an independent, nonprofit organization that works outside of the government. Their mission is to provide unbiased and authoritative advice to the federal government on policy matters pertaining to the health of the public. Based on an independent review of all of the relevant research this institute concluded that the consistent findings from these studies confirms that smoking bans decrease the rate of heart attacks.28 Consistent with the IOM report and previous research, admission data from Mississippi hospitals revealed that smoke-free ordinances were associated with lower admission rates for health events related to tobacco smoke exposure. Fewer hospital admissions for tobacco related health events were found to be associated with the implementation of a smokefree ordinance. Moreover, there were no differences in admission rates for health events unrelated to tobacco smoke. When considered in the context of the growing body of research linking smoke-free policies to reductions in hospital admission, this demonstrates that

Mississippi could experience a substantial decrease in heart attacks, as well as substantial cost savings, if more communities and/or the state implemented smoke-free legislation.

Despite the increasing evidence that smoke-free legislation has immediate and long-term health benefits, states and municipalities may be reluctant to implement smoke-free legislation due to concerns about public support or loss of tax revenue from the hospitality sector.

However, public support for a state-wide smoke-free law is robust.

According to our 2016 Mississippi Social Climate Survey of Tobacco Control, more than three-quarters of Mississippi adults (75.2%) favor a state law prohibiting smoking in most indoor places, including workplaces, public buildings, offices, restaurants, & bars. Support is nonpartisan, Republicans (79.5%) and Democrats (75.5%) are equally supportive of a state law.29 In addition to strong public support, prior research reveals no harmful economic consequences of smoke-free legislation. Numerous studies have found that tax revenue from restaurants and bars remained stable or increased slightly after implementation of smoke-free legislation.30-35 Within Mississippi, our analysis of Tourism and Economic Development (TED) Tax revenue found no evidence that smoke-free ordinances had an adverse effect on the local hospitality industry. Analyses of TED tax revenue indicated that inflation-adjusted tax revenues increased slightly during the 12 months following implementation of the smokefree ordinance, whereas there was no change in revenue in aggregated control municipalities.36 Limitations There are several limitations to this research. First, most of the smokefree ordinances that impacted our more populated areas of the state occurred before the IODS was in existence. There were not substantial changes in the percentage of the Mississippi population protected from 2013 to 2016. Thus, it is not possible to conduct pre/post analyses of admissions in these areas. Second, counties were the unit of analysis and were categorized by their county seat. Although more geographically precise data on residence are available in the IODS, the Census does not provide population data at the zip code level. The number of people residing in a geographic area is needed in order to compute admission rates. Third, a small number of county seats did not have a smokefree ordinance, but other municipalities in the county did have one.

These counties were classified as not having a smoke-free ordinance.

However, if this classification strategy biased the results, it would have been against our hypothesis. Finally, although admission rates were also lower for acute coronary, asthma, and COPD, these differences were not statistically significant.

Conclusions Consistent with the IOM report and previous research, the findings of this study suggest that smoke-free ordinances predict lower hospital admissions for tobacco smoke related health events. Broader protections from tobacco smoke at the state-level could improve health and reduce healthcare costs. Moreover, the public strongly supports these protections and smoke-free legislation has not been found to hurt tax revenues. n

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7. Naiman A, Glazier RH, and Moineddin R. Association of anti-smoking legislation with rates of hospital admission for cardiovascular and respiratory conditions. CMAJ. 2010;182(8):761-7. doi:10.1503/cmaj.091130.

8. Abe TM, Scholz J, de Masi E, Nobre MR, and Kalil Filho R. Decrease in mortality rate and hospital admissions for acute myocardial infarction after the enactment of the smoking ban law in São Paulo city, Brazil. Tob Control.

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10. Agüero F, Dégano IR, Subirana I, Grau M, Zamora A, Sala J, Ramos R, Treserras R, Marrugat J, and Elosua R. Impact of a partial smoke-free legislation on myocardial infarction incidence, mortality and case-fatality in a population-based registry: the REGICOR Study. PLoS One. 2013;8(1):e53722. doi:10.1371/ journal.pone.0053722.

11. Villalbí JR, Castillo A, Cleries M, Saltó E, Sánchez E, Martínez R, Tresserras R, and Vela E. Acute myocardial infarction hospitalization statistics: apparent decline accompanying an increase in smoke-free areas. Revista Española de Cardiología (English Edition). 2009;62(7):812-815.

12. Bartecchi C, Alsever RN, Nevin-Woods C, Thomas WM, Estacio RO, Bartelson BB, and Krantz MJ. Reduction in the incidence of acute myocardial infarction associated with a citywide smoking ordinance. Circulation. 2006;114(14):14906. doi:10.1161/CIRCULATIONAHA.106.615245.

13. Centers for Disease Control and Prevention (CDC). Reduced hospitalizations for acute myocardial infarction after implementation of a smoke-free ordinance-City of Pueblo, Colorado, 2002-2006. MMWR Morb Mortal Wkly Rep. 2009;57(51):1373-7.

14. Juster HR, Loomis BR, Hinman TM, Farrelly MC, Hyland A, Bauer UE, and Birkhead GS. Declines in hospital admissions for acute myocardial infarction in New York State after implementation of a comprehensive smoking ban. Am J Pub Health. 2007;97(11):2035-9. doi:10.2105/AJPH.2006.099994.

15. Herman PM, and Walsh ME. Hospital admissions for acute myocardial infarction, angina, stroke, and asthma after implementation of Arizona's comprehensive statewide smoking ban. Am J Pub Health. 2011;101(3):491-496.

16. Mackay D, Haw S, Ayres JG, Fischbacher C, and Pell JP. Smoke-free legislation and hospitalizations for childhood asthma. NEJM. 2010;363(12):1139-1145.

17. Millett C, Lee JT, Laverty AA, Glantz SA, and Majeed A. Hospital admissions for childhood asthma after smoke-free legislation in England. Pediatrics.

2013;131(2):e495-501. doi:10.1542/peds.2012-2592.

18. Lee SL, Wong WH, and Lau YL. Smoke-free legislation reduces hospital admissions for childhood lower respiratory tract infection. Tob Control.

2016;25(e2):e90-e94. doi:10.1136/tobaccocontrol-2015-052541.

19. Rayens M, Burkhart P, Zhang M, Lee S, Moser D, Mannino D, and Hahn E. Reduction in asthma-related emergency department visits after implementation of a smoke-free law. J Allergy Clin Immun. 2008. doi:10.1016/j.jaci.2008.06.029.

20. Khuder SA, Milz S, Jordan T, Price J, Silvestri K, and Butler P. The impact of a smoking ban on hospital admissions for coronary heart disease. Prev Med. 2007;45(1):3-8. doi:10.1016/j.ypmed.2007.03.011.

21. McMillen R, Hill A, and Collins R. The Starkville & Hattiesburg Heart Attack Studies: Reductions in Heart Attack Admissions Following the Implementation of Local Smoke-Free Ordinances; 2010. Available at: https://mstobaccodata. org/wp-content/uploads/2015/08/HeartAttackReport_Oct10.pdf. Accessed October 27, 2017.

22. Mississippi Hospital Association and the Mississippi State Department of Health. Inpatient Outpatient Data System: Inpatient Data Dictionary 2017.

23. Ferrante D, Linetzky B, Virgolini M, Schoj V, and Apelberg B. Reduction in hospital admissions for acute coronary syndrome after the successful 288 VOL. 59 • NO. 6/7 • 2018

implementation of 100% smoke-free legislation in Argentina: a comparison with partial smoking restrictions. Tob Control. 2011. doi:10.1136/tc.2010.042325.

24. Abe TM, Scholz J, de Masi E, Nobre MR, and Filho RK. Decrease in mortality rate and hospital admissions for acute myocardial infarction after the enactment of the smoking ban law in São Paulo city, Brazil. Tob Control. 2016. doi:10.1136/ tobaccocontrol-2016-053261.

25. Rodu B, Peiper N, and Cole P. Acute myocardial infarction mortality before and after state-wide smoking bans. J Community Health. 2012;37(2):468-72. doi:10.1007/s10900-011-9464-5.

26. Sims M, Maxwell R, Bauld L, and Gilmore A. Short term impact of smokefree legislation in England: retrospective analysis of hospital admissions for myocardial infarction. BMJ. 2010;340(jun08 1):c2161-c2161. doi:10.1136/ bmj.c2161.

27. Dove M, Dockery D, Mittleman M, Schwartz J, Sullivan E, Keithly L, and Land T. The impact of Massachusetts' smoke-free workplace laws on acute myocardial infarction deaths. Am J Pub Health. 2010;100(11):2206-2212. doi:10.2105/ AJPH.2009.189662.

28. Institute of Medicine. Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence. The National Academies Press; 2010. Available at: https://doi.org/10.17226/12649. Accessed February 1, 2018.

29. Mississippi Tobacco Data. 2016 Mississippi Social Climate Survey of Tobacco Control: Support for Smokefree Air; 2017. Available at: https://mstobaccodata. org/wp-content/uploads/2015/08/support-for-smoke-free-air-2016.pdf.

Accessed February 1, 2018.

30. Alamar B. Smoke-free ordinances increase restaurant profit and value. Contemp Econ Policy. 2004;22(4):520-525.

31. Bartosch W. Economic effect of smoke-free restaurant policies in Massachusetts.

J Pub Health Manage Pract. 1999;5(1):53-62.

32. Bartosch W, and Pope G. The Economic Effect of Smoke-Free Restaurant Policies on Restaurant Business in Massachusetts. J Pub Health Manage Pract.

9(5):53-62.

33. Dai C. The Economic Impact of Florida’s Smoke-free Workplace Law. 2004.

34. Engelen, Farrelly M, and Hyland A. The health and economic impact of New York’s clean indoor air act. New York State Department of Health; 2006.

Available at: http://www.health.ny.gov/prevention/tobacco_control/docs/ ciaa_impact_report.pdf.

35. Hahn EJ. Smokefree legislation: a review of health and economic outcomes research. Am J Prev Med. 2010;39(6 Suppl 1):S66-76. doi:10.1016/j. amepre.2010.08.013.

36. McMillen R, and Shackelford S. Tax Revenue in Mississippi Communities Following Implementation of Smoke-free Ordinances: An Examination of Tourism and Economic Development Tax Revenues. msma.pdf. 2012;53:319321.

Acknowledgement: This paper summarizes independent research based on the Inpatient Outpatient Data System (IODS). The Mississippi Hospital Association and the Mississippi State Department of Health maintain the IODS. The information, views, and opinions contained herein are those of the authors and do not necessarily reflect the views and opinions of these organization.

Funding Source: This work was supported by the Office of Tobacco Control, Mississippi State Department of Health. The information, views, and opinions contained herein are those of the authors and do not necessarily reflect the views and opinions of this organization.

Author Information Professor, Department of Psychology, Mississippi State University and Associate Director of the Tobacco Control Unit, Social Science Research Center, Mississippi State University (McMillen). Data Management Coordinator, Social Science Research Center, Mississippi State University (McClelland). Director, Office of Tobacco Control Director, Mississippi State Department of Health (Winter).

Conflict of Interest/ Financial Disclosure: None.

Corresponding Author: Robert McMillen, One Research Blvd, Suite 103, Starkville, MS, 39759. robert.mcmillen@ssrc.msstate.edu

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Non-syndromic Mitochondrial Hearing Loss Successfully Treated with Bilateral Cochlear Implantation: A Case Report KELSEY L. BOUNDS, M3; LAURA K. HOUSE, MD; JEFFREY D. CARRON, MD Introduction Less than 1% of all profound hearing loss in infancy is caused by a mitochondrial mutation. There have been only 2 mitochondrial genes identified that have been associated with non-syndromic mitochondrial hearing loss. The less common of these 2 gene mutations causes a childhood-onset, bilateral sensorineural hearing loss. There is limited literature about the treatment and management of this condition; however, this disorder should be recognized as a treatable entity. Here we present a case in which bilateral cochlear implants successfully treated a child with non-syndromic mitochondrial hearing loss.

Key Words: Mitochondrial mutations, sensorineural hearing loss, non-syndromic, cochlear implantation Case Presentation This patient is a 6-year-old male born with bilateral profound sensorineural hearing loss discovered during newborn hearing screening. His mother had no risk factors known to cause congenital hearing loss such as antibiotic exposure, viruses, or family history of hearing loss. He was born full term with an uncomplicated delivery.

Physical exam revealed normal pinnae, external auditory canals, and tympanic membranes bilaterally.

Auditory Brainstem Response (ABR) testing revealed absent waves at 90 dB as well as with tone burst stimuli from 250-4000 Hz. Tympanometry results indicated normal middle ear compliance bilaterally. These results were consistent with profound bilateral sensorineural hearing loss. Audiologic testing also included the InfantToddler Meaningful Auditory Integration Scale, which estimates patients’ spontaneous responses to sound in daily environments, in which he had a very low score (3/40).

It was recommended that he undergo genetic testing, which revealed a mitochondrial mutation in MTTS1 consistent with non-syndromic mitochondrial hearing loss.

At 8 weeks of age the patient was fit for bilateral hearing aids. After a standard audiologic battery of tests was performed and hearing aid trial completed, he was deemed a cochlear implant candidate. Computed tomography and magnetic resonance imaging of the bilateral temporal bones revealed normal middle and inner ear anatomy, with no contraindications to cochlear implantation.

The patient ultimately underwent bilateral cochlear implantation at 6 months of age. Cochlear implantation was performed using the standard facial recess approach. Intraoperative neural testing

confirmed stimulation of all electrodes on the left side and all except the most proximal 4 electrodes on the right side. Initial post-operative testing showed excellent response to sound with recorded head turns at 20 dB for both processors. Speech awareness reliably was seen at 20 dB HL. The patient ultimately did well with the cochlear implant. His speech and language skills have progressed to above average range for his age group. After 5 years of age, the patient no longer required speech therapy. At his most recent follow up, he was doing well in a mainstream classroom without any issues relating to the cochlear implant. He has not shown any signs or symptoms of systemic mitochondrial disease.

Discussion Cochlear implantation has been a safe and effective treatment for bilateral profound sensorineural hearing loss since the 1980’s.

Historically, the ideal candidate for cochlear implantation was a patient over 18 years of age with hearing loss secondary to ototoxic drugs, Meniere’s disease, otosclerosis, trauma, or sudden sensorineural hearing loss.1 Cochlear implants are now routinely performed in children, with excellent results similar to adult candidates and minimal complications.2 We present a case of a patient with mitochondrial nonsyndromic deafness. Recent studies estimate that congenital hearing loss occurs in 1-3:1000 neonates. 50% of congenital hearing loss is hereditary and 50% of hearing loss is acquired. Mitochondrial related hearing loss is very rare, representing only one percent of hereditary forms of congenital hearing loss. Most cases of mitochondrial deafness are syndromic disorders, affecting multiple organ systems. Kearns-Sayre syndrome is one example, causing progressive ophthalmoplegia, retinal degeneration, and heart block, in addition to hearing loss.3 Other examples include MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes), MERRF (myoclonic epilepsy with ragged red fibers) syndrome, and MIDD (maternally inherited diabetes and deafness).4 However, our case is an example of nonsyndromic mitochondrial deafness, without multi organ system involvement.

Inheritance patterns and pathogenicity of mitochondrial deafness are complicated, and numerous mutations in mitochondrial DNA have been implicated. Nonsyndromic mitochondrial hearing loss and deafness is thought to be caused by mitochondrial DNA mutations in the MT-RNR1 (encoding mitochondrial 12S ribosomal RNA) or MT-TS1 gene (encoding mitochondrial transfer RNA serine 1).5 Variants in MT-RNR1 are usually associated with predisposition to aminoglycoside toxicity and late onset sensorineural hearing loss, while variants in MT-TS1 area usually associated with childhood onset JUNE/JULY • JOURNAL MSMA

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hearing loss. Our case involves a mutation in the MT-TS1 gene.6 As demonstrated in the above case, cochlear implantation provides good speech and hearing outcomes in patients with mitochondrial deafness. Auditory detection levels for children with a cochlear implant are approximately 25dBHL, which is close to the normal hearing range and similar to adult results.2 For children with onset of deafness at less than one year of age, the age of implantation affects cochlear implant outcomes. Children implanted at or before 2 years of age are expected to have communication development similar to normal-hearing peers, easily understood speech, reduced language delay, and attendance at school with minimal support service.2 Children implanted at older ages are likely to have more speech and language delays.

In conclusion, there are numerous causes of congenital sensorineural hearing loss. Mitochondrial nonsyndromic deafness represents a very rare cause of hearing loss, and these patients are good cochlear implant candidates. Recognizing the various causes of congenital hearing loss and treating these patients early with amplification or cochlear implantation allows for development of speech and language in these children. n References

1. Glasscock ME, Shambaugh GE. Implantable Hearing Devices, in Surgery of the Ear, 4th ed., Glassock ME, Shambaugh GE (ed). Philadelphia, PA: W. B. Saunders Company; 1990: 571-577.

3. Horoupian D. Pathology of the Central Auditory Pathways and Cochlear Nerve, in Otologic Medicine and Surgery. New York, NY: Churchill Livingstone; 1988: 713734.

4. Shibata SB, Shearer AE, and Smith RJH. Genetic Sensorineural Hearing Loss, in: Cummings Otolaryngology Head & Neck Surgery, 5th ed. Philadelphia, PA: Mosby/ Elsevier; 2015: 2285-2300.

5. Kokotas H, Petersen M, Willems P. Mitochondrial deafness. Clin Genet.

2007;71(5):379-391. doi: 10.1111/j.1399-0004.2007 .00800.x 6. Pandya A. Nonsyndromic Hearing Loss and Deafness, Mitochondrial, in GeneReviews®, ed. internet, Adam MP, Ardinger HH, Pagon RA, et al (ed). Seattle, WA: University of Washington, Seattle; 1993- 2018. Accessed December 5, 2017. https://www. ncbi.nlm.nih.gov/books/NBK1422/

Author Information M-3 resident, University of Mississippi Medical Center, Jackson (Bounds). PGY IV, Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson (House). Professor, School of Medicine, Department of Otolaryngology and Communicative Sciences, The University of Mississippi Medical Center, Jackson (Carron).

Corresponding Author: Laura K. House, MD; Department of Otolaryngology and Communicative Sciences; The University of Mississippi Medical Center; 2500 North State St., Jackson, MS 39216.

2. Wackym PA, Tran A. Cochlear Implantation: Patient Evaluation and Device Selection, in Cummings Otolaryngology Head & Neck Surgery, 5th ed. Cummings CW, Flint PW (ed). Philadelphia, PA: Mosby/Elsevier; 2015: 2428-2443.

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The Hidden Repercussions of the Opioid Crisis in Mississippiâ&#x20AC;&#x2122;s Children: Neonatal Abstinence Syndrome/ Neonatal Opioid Withdrawal Syndrome LAUREN TUCKER, MD; TARA NATION, MSN, CPNP; RENATE SAVICH, MD; DOUGLAS TUCKER, MD; SUJITH RAMACHANDRAN, PHD; DANA LINDSAY, RN; CHAD BLACKSHEAR, MS; ROBERT D ANNETT, PHD Abstract Opioid use in the United States has risen sharply over the last decade, including use in pregnant women. As a result, the incidence of Neonatal Abstinence syndrome (NAS), also known as Neonatal Opioid Withdrawal Syndrome (NOWS), is increasing. NAS/NOWS is the withdrawal that an infant experiences after birth due to in utero exposure to opioids. NAS/NOWS causes a wide variety of signs and symptoms involving the central nervous system, autonomic nervous system and gastrointestinal tract. Infants with NAS/NOWS can be recognized by appropriate screening of infant and mother.

Management of NAS/NOWS includes non-pharmacologic and pharmacologic treatment interventions. Little information is available on the impact of NAS/NOWS on infants born in Mississippi. The aim of this article is to describe the diagnosis and management of NAS/ NOWS for Mississippi clinicians with the goal of increasing awareness and improving treatment.

Key Words: N eonatal Abstinence Syndrome (NAS), Neonatal Opioid Withdrawal Syndrome (NOWS), opioid, morphine, methadone, heroin, drug withdrawal Introduction Opioid use has risen sharply over the last decade. In the United States, opioid sales quadrupled from 1999 to 2010.1 In 2012, 255 million opioid prescriptions were dispensed, a rate of 81.3 prescriptions per 100 persons.2 Opioid abuse in pregnancy has increased over the same period. From 1998 to 2011, the prevalence of opioid abuse or dependence increased from 1.7 to 3.9 per 1000 delivery admissions among pregnant women.3 As a consequence, fetal exposure to opioids has increased as well. Newborns who are exposed to opioids in utero are at risk for developing withdrawal post-natally. Neonatal Abstinence Syndrome (NAS), also known as Neonatal Opioid Withdrawal Syndrome (NOWS), is the collection of withdrawal symptoms that occur with abrupt cessation at birth of illicit or prescribed opioid drugs used during pregnancy. From 2000-2012, the incidence of NAS/NOWS in the US increased almost 400%, from 1.2 to 5.8 per 1000 hospital births, costing the US an estimated $1.5 billion in 2012 alone.4,5 The aim of this article is to describe the diagnosis and management of NAS/NOWS for Mississippi clinicians with the goal of increasing awareness and improving treatment.

Ideally, women should be routinely screened for drug use during their pregnancy, and when opioid use is reported, referred to treatment

programs. Screening can involve several types of procedures including clinical interview and urine testing. In practice, broad spectrum screening for substance use (e.g., opioids, alcohol, cigarettes, illicit drugs) is strongly encouraged for pregnant women in Mississippi. For women reporting opioid use, monitoring during pregnancy is a critical part of the obstetrical care. State regulations surrounding opioid use in pregnancy can range from mandatory reporting and prosecution to defining opioid use as child abuse or merely encouraging testing. In Mississippi, there is no mandatory reporting of maternal opioid use,6 thus reassuring mothers that the primary concern is the health and well-being of their infant. This is essential to maintaining continuity of care during pregnancy. As these mothers approach delivery, ensuring optimal care of their infants needs to be reinforced.

In the sections that follow, information is provided on the clinical presentation of NAS/NOWS and a protocol for management that has been developed at the University of Mississippi Medical Center. While there is relatively little empirical evidence guiding the management of infants with NAS/NOWS, this protocol has been developed in a collaborative environment to provide a standard of care for infants and families targeting optimal outcomes.

Clinical Presentation Infants exposed to opioids can experience a wide range of signs and symptoms involving the central nervous system, autonomic nervous system, and gastrointestinal tract. These symptoms include extreme irritability, tremor, poor feeding, vomiting, diarrhea, temperature instability, sleep disturbances, hypertonia, and seizures (Table 1).7 Onset and severity of symptoms vary depending on multiple factors such as the type of drug used by mother, half-life of drug, timing of last dose, and duration of exposure, among others.8 Infants exposed to opioids with a short half-life (i.e. heroin) typically experience withdrawal symptoms within 3 days, whereas infants exposed to drugs with a longer half-life (i.e. methadone) can take up to 5-7 days.

Risk factors for more severe and prolonged withdrawal include term gestation, average birth weight, male sex, methadone use, tobacco use, and polysubstance abuse during pregnancy.8 Concomitant use of barbiturates or SSRIs can potentiate the effects of NAS/NOWS and worsen the withdrawal.

Diagnosis NAS/NOWS is a clinical diagnosis based on neonatal clinical findings.

When NAS/NOWS is suspected, infant urine and meconium

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Table 2: Modified Finnegan Scoring Toolaa

Table 2. Modified Finnegan Scoring Tool

SIGNS AND SYMPTOMS Increase muscle tone Excoriation Myoclonic jerks Generalized convulsions High-Pitched Cry Continuous high-pitched cry Sleeps less than 3 hours after feeding Sleeps less than 2 hours after feeding Sleeps less than 3 hours after feeding Hyperactive Moro Re�lex Markedly hyperactive Moro Re�lex Mild Tremors Disturbed Moderate-severe tremors disturbed Mild tremors undisturbed Moderately severe tremors undisturbed Sweating Yawning (Greater than 3-4 times/interval) Mottling Nasal Stuf�iness Sneezing (Greater than 3-4 times/interval) Nasal �laring Fever < 101F/38.3C Fever ≥ 101F/38.3C Respiratory Rate >60/min Respiratory Rate > 60/minute plus retraction Excessive Sucking Poor feeding Regurgitation Projectile vomiting Loose stools Watery Stools Total Score Central Nervous System Disturbances

Table 1. NAS/NOWS: Signs and Symptoms Neurologic Autonomic Gastrointestinal Excessive Irritability Fever Poor feeding High-pitched cry Yawning/Sneezing Excessive sucking Decreased sleep Tachypnea Vomiting Tremor Diaphoresis Diarrhea Increased Tone Nasal stuffiness Poor weight gain Seizures Mottling Dehydration

Treatment is comprised of two broad areas: non-pharmacologic interventions and pharmacologic interventions (Figure 1). While the Finnegan tool is employed for initiation, maintenance, and weaning of pharmacologic interventions, non-pharmacologic interventions should begin immediately after birth. Non-pharmacologic treatments include environmental, nutritional, and parental interventions. It is recommended that infants remain in a dark, quiet environment with limited stimulation and be cared for with gentle handling.11 Swaddling, skin-to-skin, massage, and music therapy can be beneficial as well.

Nutritionally, infants should have frequent on-demand feedings and be allowed to breastfeed when appropriate. Increased caloric content should be considered for infants with poor weight gain. Parents should be educated prenatally, if possible, and postnatally about NAS/NOWS and should be encouraged to actively participate in the care of their infant. Rooming-in with mother can decrease severity of symptoms.12 For more severe symptoms that are not controlled with nonpharmacologic measures, pharmacologic intervention is indicated.

Basic pharmacologic principles include administration of an opioid agonist with a subsequent scheduled taper once symptoms are well controlled. There is no consensus regarding optimal pharmacologic management of NAS/NOWS, but simply having a formal treatment

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Gastrointestinal Disturbances

Management Infants who are considered at risk for NAS/NOWS are monitored closely for signs and symptoms of withdrawal. There are several standardized systems for evaluation of withdrawal with the most widely used being the modified Finnegan assessment tool (Table 2).10 When there is a suspicion or indication of in utero opioid exposure, the assessment begins immediately after birth and continues every 3-4 hours until discharge. The Finnegan score is a representation of how the infant is doing at that moment, as well as the previous 3-4 hours since the last assessment. Optimal timing for assessment occurs after feeding. Infants should not be awakened to conduct this evaluation.

Use of the modified Finnegan tool requires training and practice among care providers to ensure reliability.

Metabolic/Vasomotor/ Respiratory Disturbances

toxicology testing with confirmation should be sent as soon as possible after birth, ideally with the first void or stool. The risk factors or indicators of NAS/NOWS include: maternal history of substance use or abuse during pregnancy, positive maternal urine drug screening during current or prior pregnancy, evidence of limited or no prenatal care, and other clinical indicators. Meconium drug screening is more sensitive than urine drug screening and can detect drug use from 20 weeks gestation to delivery.9 Urine drug screening can detect use in the past few days prior to delivery; however, urine drug screening results are more readily available in comparison to meconium. Thus, obtaining a combination of infant urine and meconium drug screening for the best results is recommended.

SCORE 2 1 3 5 2 3 1 2 3 2 3 1 2 3 4 1 1 1 1 1 2 1 2 1 2 1 2 2 3 2 3

The modified Finnegan scoring tool is used as a guide for medication initiation, maintenance, and weaning. Infant with suspected NAS/NOWS are scored based on the above signs and symptoms every 3-4 hours until discharge. The scores for each sign or symptom are added together to determine a total score. 3 consecutive scores >8 or 2 consecutive scores >12 are considered abnormal.

Adapted from Finnegan L, Connaughton J, Kron R, Emich J. Neonatal abstinence syndrome: Assessment and management. Addict Dis. 1975;2:141–158 a

protocol with strict weaning guidelines, regardless of initial treatment agent, decreases length of stay and duration of therapy.13 Morphine is considered by most as the first-line agent. If an infant has three consecutive Finnegan scores greater than or equal to 8 or two consecutive scores greater than or equal to 12 despite adequate nonpharmacologic measures, then pharmacologic intervention is initiated with morphine.8 Dosages of morphine are escalated until scores stabilize. If the maximum allowable dose of morphine is reached without improvement in scores, then second-line agents are added such as clonidine or phenobarbital. Once scores are stabilized for 2448 hours, weaning can begin. Morphine should be weaned by 10% stabilizing dose every 24-48 hours until discontinued.

If the infant remains asymptomatic after birth or symptoms are well controlled with non-pharmacologic measures and Finnegan scores

FigureFigure 1. Algorithm for Pharmacologic Treatment Treatment of NAS/NOWS 1. Algorithm for Pharmacologic of NAS/NOWS

Screen Infants to assess risk for Neonatal Abstinence Syndrome (NAS) Infant Identified as at Risk for NAS

Environmental Measures

Skin Care

Swaddle, low noise, dim light, Encourage skin to skin, avoid waking and overheating

Prophylactic barrier cream, monitor for breakdown and treat as indicated

No

NAS Scoring with M-FS

Parental Support

Nutrition

Communicate regularly with family, Provide Parent Guide

Encourage Breastfeeding, Feed on Demand, Frequent small feeds, May need higher calorie formula/BM

Scoring: Begin within 2 hrs of life Every 3-4 hours 2 consecutive scores ≥ 12 Or 3 consecutive scores ≥ 8

Yes

Observation Monitor scores every 3-4 hrs Consider Substance Half-Life

Pharmacologic Intervention Required Start with PO Morphine 0.05mg/kg/dose q3-4 hrs Next score ≤ 8

Short Half-Life Monitor 72 hours If NAS Scores <8, Discharge Home with appropriate follow up.

Long Half-Life Monitor 5-7 days If NAS Scores <8, Discharge Home with appropriate follow up.

• Maintain current dose • Monitor NAS scores q3-4 hours • Escalate as needed • If scores < 8 for 24-48 hours, begin wean

WEANING PROTOCOL: • Morphine: o Once scores < 8 for 24-48 hours, wean by 10% stabilizing dose q24-48 hours • If scores increase after wean, increase back to last effective dose.

• After scores stable for 48 hours, begin wean again o Discontinue Morphine once scores are < 8 for 24-48 hours on 0.02mg/kg/dose o If scores < 8 for 48 hours after discontinuation of morphine, discharge home with appropriate follow up • Morphine + Clonidine: o Wean Morphine first as noted above. o Once morphine is down to 0.05 mg/kg/dose, decrease Clonidine by 25% daily until discontinued. Then resume Morphine wean.

Next score > 8 Escalate: o 9-12: Increase dose by 0.02mg/kg/dose o 13-16: Increase dose by 0.04 mg/kg/dose o 17-20: Increase dose by 0.06 mg/kg/dose • Increase dose q3hrs until scores stabilize • Max Dose: 0.2 mg/dose • If requires > 1mg/kg/day add Clonidine: 0.5-1 µg/kg q 3-6 h • Once NAS scores < 8 for 24-48 hours, begin wean

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remains low, discharge can be considered with close follow up. Infants with exposure to opioids with short half-lives, can be discharged after close monitoring for a minimum of 72 hours, whereas infants with exposure to opioids with long half-lives should be monitored for a full 5-7 days prior to discharge. For infants who require pharmacologic intervention, discharge is considered once all medications are weaned with subsequent stable scores and appropriate follow up is arranged.

Average length of stay for these infants is approximately 20 days.14 For all infants managed on the current protocol, followup is essential.

Our NICU followup clinic includes a multi-disciplinary team of pediatricians/neonatologists, nurses, registered dietitians, an early interventionist, and a neurodevelopmentalist. With uncertainty regarding outcomes for infants with opioid exposure, monitoring through their second birthday appears indicated to ensure a healthy baby.

Conclusions The incidence of NAS/NOWS has increased nationally in association with increased opioid use and abuse. While Mississippi has one of the highest opioid prescribing rates in the country, the true incidence of NAS/NOWS in Mississippi is not known. Increasing awareness and assisting in diagnosis and treatment is the goal of this article. Work is currently underway to better determine the morbidity characteristics in Mississippi, and efforts are being made to increase awareness and develop standardized management protocols. It is unclear whether routine screening of mother and infant would increase recognition of NAS/NOWS and improve care in Mississippi, and the long term developmental outcomes of NAS/NOWS are also unknown. The opioid crisis has claimed countless lives and headlines while earning the distinction of the health crisis of our generation. We cannot forget that the effect on our most vulnerable victims of the crisis remains relatively unknown. Hopefully, by raising awareness and improving treatment, we can help offset the impact of NAS/NOWS in our state. n References

1. Ko JY, Wolicki S, Barfield WD, et al. CDC Grand Rounds: Public Health Strategies to Prevent Neonatal Abstinence Syndrome. MMWR Morb Mortal Wkly Rep. 2017;66:242-245. DOI: http://dx.doi.org/10.15585/mmwr. mm6609a2.

2. Opioid Overdose. Centers for Disease Control and Prevention, 31 July 2017. https://www.cdc.gov/drugoverdose/maps/rxrate-maps.html.

3. Maeda A, Bateman BT, Clancy CR, Creanga AA, Leffert LR; Opioid abuse and dependence during pregnancy: temporal trends and obstetrical outcomes.

Anesthesiology. 2014;121:1158–65.

4. Patrick SW, Davis MM, Lehman CU, Cooper WO; Increasing Incidence and Geographic Distribution of Neonatal Abstinence Syndrome: United States 2009-2012. J Perinatol. 2015; 35(8):650-655.

5. Patrick SW, Schumacher RE, Benneyworth BD, et al. Neonatal Abstinence Syndrome and Associated Health Care Expenditures: United States, 2000-2009.

JAMA. 2012; 307(18):1934-40.

6. Miranda L, Dixon V, Reyes C. How States Handle Drug Use During Pregnancy.

ProPublica. 30 September 2015. https://projects.propublica.org/graphics/ maternity-drug-policies-by-state.

7. Hudak ML, Tan RC; Committee on Drugs; Committee on Fetus and Newborn; American Academy of Pediatrics. Neonatal Drug Withdrawal. Pediatrics.

2012;129:540-560.

8. Kocherlakota P. Neonatal Abstinence Syndrome. Pediatrics. 2014;134:547-561.

9. Cotton SW. Drug testing in the neonate. Clin Lab Med. 2012;32(3):344-348.

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10. Finnegan L, Connaughton J, Kron R, Emich J. Neonatal abstinence syndrome: Assessment and management. Addict Dis. 1975;2:141–158.

11. Grossman MR, Berkwitt AK, Osborn RR, et al. An Initiative to Improve the Quality of Care of Infants with Neonatal Abstinence Syndrome. Pediatrics.

2017;139:1-8.

12. Hunseler C, Bruckle M, Roth B, Kribs A. Neonatal opiate withdrawal and rooming in: A retrospective analysis of a single center experience. Klin Padiatr.

2013;225(5)247-251.

13. Hall ES, Wexelblatt SL, Crowley M, et al. A Multicenter Cohort Study of Treatments and Hospital Outcomes in Neonatal Abstinence Syndrome.

Pediatrics. 2014;134:527-534.

14. Patrick SW, Schumacher RE, Horbar JD, et al. Improving Care for Neonatal Abstinence Syndrome. Pediatrics. 2016;137:1-8.

Author Information Assistant Professor of Pediatrics, Center (Tucker). Certified Pediatric Nurse Practitioner (Nation). Professor of Pediatrics (Savich).

Assistant Professor of Anesthesiology (Tucker). Assistant Professor of Pharmacy Administration (Ramachandran). Research Nurse (Lindsay). Biostatistician (Blackshear). Professor of Pediatrics (Annett). All in the Department of Pediatrics, University of Mississippi Medical Center, Jackson. Conflicts/Disclosures: None.

Corresponding Author: Lauren Tucker, MD, University of Mississippi Medical Center, Division of Neonatology, 2500 N State Street, Jackson, MS 39216. Office: 601-984-4421 (lctucker@umc. edu).

S C I E N C E

O F

M E D I C I N E

Malignant Solitary Fibrous Tumors of the Nasal Cavity ERIC TILLOTSON, MD; MARIA F. GONZALEZ, MD Abstract Background - Solitary fibrous tumors (SFT) are uncommon mesenchymal neoplasms that were first described in the pleura but now are often diagnosed in extra-pleural sites. These tumors rarely occur in the head and neck, including the nasal cavity, with extremely rare cases displaying malignant features.

Methods - A 59-year-old female presented with sinus symptoms. A subsequent computed tomography scan revealed a heterogeneously enhancing mass lesion centered in the left nasal cavity prompting a craniotomy.

left nasal cavity with destruction of the nasal septum, nasal turbinates, and involvement of bilateral ethmoid sinuses (Figure 1A).

Figure 1A. A computed tomography scan showing a large heterogeneously enhancing mass lesion (red arrow) centered in the left nasal cavity with destruction of the nasal septum, nasal turbinates, and involvement of bilateral ethmoid sinuses.

Results - Histological examination revealed a spindle cell tumor with pleomorphism, and abundant mitoses. The immunoprofile is consistent with a SFT. The tumor invaded the orbital roof, and sphenoid margin.

Conclusion - Malignant SFT are extremely rare in the nasal cavity with only two cases reported. This paper reports one such case in a female patient with demonstration of the malignant behavior that can be a characteristic of these tumors with significant differences in the presentation and morphologic findings.

Key Words: fibrous, malignant, nasal, STAT6 Introduction Solitary fibrous tumors (SFT) are uncommon mesenchymal neoplasms that were first described in the pleura but now are diagnosed more commonly in extra-pleural sites. These spindle-cell tumors rarely occur in the head and neck including the nasal and paranasal sinuses. Thirty-nine cases of SFT involving the paranasal sinuses had been reported up to 2015.1 However, only two cases of malignant SFT (M-SFT) have been described to date. In 2007, a case of M-SFT invading into the skull base was described as the first case with such a presentation.2 In many cases, the behavior of these tumors is difficult to predict based on histological examination despite the proposition of several criteria to indicate malignancy, the most reliable of which being mitotic activity. Herein we describe a case of M-SFT with invasion into the bones of the skull and discuss relevant clinical and diagnostic considerations.

Materials and Methods Case Report A 59-year-old female with a 40-pack-year smoking history presented in November 2016 with sinus congestion and related symptoms. At that time she was diagnosed with a sinus infection with swelling of the left eye. Her symptoms persisted for several months, and a computed tomography (CT) scan was performed revealing a well-circumscribed, lobular large heterogeneously enhancing mass lesion centered in the

Figure 1B. This gross examination image of the specimen shows that the tumor had a white lobulated appearance and was well-circumscribed.

Six months later, she underwent debulking of the nasal tumor and biopsy at an outside hospital. The slides showed a pleomorphic spindle cell tumor with 20 mitotic figures in 10 high power fields (HPFs). The tumor was positive for signal transducer and activator of transcription 6 (STAT-6) while it was negative for melanocytic markers, cytokeratins, desmin, myogenin, and chromogranin. The morphology and this immunoprofile support the diagnosis of a malignant solitary fibrous tumor.

She presented to our institution with bilateral nasal congestion, frontal headaches, left-sided facial numbness, left-sided blurred vision, watery eye, rhinorrhea, hyposmia, intermittent bilateral ear congestion, and 25-pound weight loss since November. She underwent craniotomy with cranialization of the frontal sinus and opening of the orbital cavity for resection of the anterior skull base tumor in July 2017. Grossly, the tumor had a tan-white and hemorrhagic appearance, measured 7.5 cm in the greatest dimension, and was well-circumscribed. Serial sections revealed a tan-pink firm parenchyma with hemorrhagic areas (Figure 1B).

Results and Discussion Histological examination of the specimen revealed a hypercellular spindle cell tumor with patternless pattern, thick bands of collagen and branching vessels (Figure 1C-1E). Multiple foci of pleomorphic cells with hyperchromatic nuclei and numerous mitoses (16 per 10 HPFs) were identified (Figure 1D-1E). No necrosis was seen.

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Figure 1C. This representative section of the tumor identified in the submucosa of the nasal cavity shows spindled and hyperchromatic tumor cells. (Hematoxylin and Eosin, 100X). Inset: High power magnification demonstrates the pleomorphic and hyperchromatic tumor cells (red arrows).

(Hematoxylin and Eosin, 400X) Figure 1D. This high magnification photomicrograph of the tumor shows 4 mitoses in one high power field. The red circles mark the numerous mitotic figures. (Hematoxylin and Eosin, 400X) Figure 1E. This low magnification image of the tumor shows the characteristic “patternless” pattern of growth, “staghorn” capillaries (red arrow) and collagen fibers. (Hematoxylin and Eosin, 40X)

Microscopically, the tumor involved the orbital roof and sphenoid margins. The tumor was positive for STAT6 (Figure 1F), cluster of differentiation 34 (CD34) (Figure 1G), B-cell lymphoma 2 (BCL2) (Figure 1H) and CD-99 (Figure 1I) while it was negative for SRY-related HMG-box-10 (SOX10), soluble in a 100% saturated

ammonium sulfate solution protein (S100), desmin, smooth muscle actin, and pancytokeratin. The morphology and this immunoprofile support the diagnosis of a malignant solitary fibrous tumor. The patient was scheduled for postoperative radiation for positive margins but was postponed because of necrosis in her flap.

Figure 1F. The tumor cells show strong and diffuse staining for STAT6. (STAT6 immunohistochemistry stain, 400X) Figure 1G. The tumor cells also show strong and diffuse positivity for CD34. (CD34 immunohistochemistry stain, 400X) Figure 1H. Weak but diffuse staining of the tumor cells for BCL2 is demonstrated. (BCL2 immunohistochemistry stain, 400X) Figure 1I. Diffuse expression of the tumor cells for CD99 is demonstrated. (CD99 immunohistochemistry stain, 400X)

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Discussion 4,7,8 1. Differential Diagnosis of SolitaryofFibrous TumorBenignTumorand Borderline lesions.

Solitary fibrous tumor de- Table Table 1. Differential Diagnosis Solitary Fibrous Benign and Borderline lesions..4,7,8 scribes a histologic specSolitary NeurofibroSchwannoma Leiomyoma Dermatofibroma trum of fibroblastic mesFibrous ma enchymal neoplasms that tumor rarely metastasize.1 These Frequency <0.1% NIA NIA Rare NIA tumors, originally described Sex NP NP NP NP NP Adults 5th decade 50 Y NIA Varies with type in the pleura, now are seen Age more commonly in exHaphazard; Unencapsula- Alternating Intersecting Infiltrative; fascicular tra-pleural locations. The Microscopy Patternless ted cellular & fascicles most common extrathopattern hypocellular racic SFTs reported in the areas (Antoni A literature include the larynx, & B) Bland Undulating, Wavy and Oval to Tapering to plump; hypopharynx, parapharyn- Nuclei cytology; pointy tapered elongate small nucleoli geal space, tongue, orbit, no/rare without atypia paranasal sinuses and nasal mitoses cavity.2 To the best of our Cytoplasm Minimal Thin Elongated Eosinophilic Indistinct knowledge only 2 cases of processes fibrillary malignant SFT in the nasal Immunostain + cavity have been reported, STAT6 none of them in female pa+ + + tients.3-4 One case reported CD34 + + BCL2 in 2007 by Zeitler describes + + S100 a 70 year old man with a past GFAP + medical history of hyper- SOX10 + + tension, asthma, and chron- NFP + + ic obstructive pulmonary DESMIN + +/disease was presented with SMA + +/slowly progressive left-sid- CALDESMON + ed nasal obstruction symp- BetaCATENIN + toms with associated facial EMA + capsule swelling. Magnetic reso- VIMENTIN + nance imaging (MRI) and Molecular; NAB2Biallelic Loss of merlin AGLM :loss of APC (in FAP).

STAT6 inactivation expression 22q11.2 B-catenin (85% CT of the paranasal sinuses Genetic of NF1 gene ;amplify sporadic cases) demonstrated a mass in the mutation (17q11.2) cation of Xq left nasal cavity extending in NFT1 into the inferomedial ex- Prognosis Usually not Very good Recurrence low Excellent Good traconal space of the left aggressive orbit and into the ipsilateral Treatment S S S S S +/- R/C NIA: no information available; NP: no predilection, Y: years.S: surgery, R: radiotherapy, C: chemotherapy. maxillary sinus. The tumor TNIA: no information available; NP: no predilection, Y: years.S: surgery, R: radiotherapy, C: chemotherapy. STAT6: STAT6: Signal transducer and activator of transcription 6; CD34: Cluster of differentiation 34; BCL2: B-cell lymphoma 2; S100 also extended through the Signal transducer and activator of transcription CD34: Cluster differentiation 34; BCL2: lymphoma S100: soluble in a 100% saturated ammonium sulfate6;solution protein;of GFAP: glial fibrillary acidicB-cell protein, SOX10:2;SRY-related cribriform plate with intra- soluble in a 100% saturated ammonium sulfateSMA: solution protein; GFAP: glialEMA: fibrillary acidic protein, SOX10: SRY-related HMG-box 10; NFP: neurofilament protein; Smooth muscle actin; epithelial membrane antigen cranial enhancement in the HMG-box 10; NFP: neurofilament protein; SMA: Smooth muscle actin; EMA: epithelial membrane antigen left subfrontal region. Biopsy of this mass revealed a spindle-cell neoplasm with atypical features and immunoreactivity for The second case reported by Papadakis in 2013 involved a 53-yearCD34 and bcl-2, confirming the diagnosis of SFT. A left-sided anterior old man presenting with recurrent epistaxis and nasal obstruction. craniotomy was performed and revealed a subfrontal skull base defect His past medical history included hypertension. A CT scan revealed around the cribriform plate. The tumor removed en bloc, following a large mass filling the left nasal cavity and maxillary sinus with bony preoperative embolization of the left internal maxillary artery. Patho- remodeling. Endoscopic medial maxillectomy with anterior and logic examination revealed a 6.5 x 4.2 x 2.5 centimeter M-SFT with a posterior ethmoidectomy was performed. Pathological examination high mitotic rate (> 10 mitoses/10 HPFs), focal bizarre giant cells, and revealed a spindle-cell neoplasm with atypical features including osseous involvement of the inferior turbinate. All surgical margins were necrosis and > 4 mitoses per 10 HPFs. Immunohistochemistry studies negative. Immunohistochemistry showed reactivity with vimentin, showed positivity for CD34, bcl-2, and vimentin. Stains for CD99 and CD34, bcl-2, and CD99. Stains for desmin, S-100, and human chori- actin were reportedly negative. The patient was discharged two days onic gonadotropin were negative. The patient was scheduled to receive after surgery without adjuvant radiotherapy or chemotherapy. Close external beam radiation therapy following surgery; however, he was di- follow up with endoscopy monthly and CT after 10 months reportedly agnosed with adenocarcinoma of the colon 5 weeks after his craniofa- did not reveal any recurrent or residual disease at the time the report cial resection. Unfortunately, he died of postoperative complications was written.4 following a radical colectomy.3 JUNE/JULY â&#x20AC;˘ JOURNAL MSMA

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In our case the clinical pre4,7,8 2. Differential Diagnosis for Solitaryfor Fibrous TumorMalignancies.

Table 2. Differential Diagnosis Solitary Fibrous TumorMalignancies.4,7,8 sentation was similar. Un- Table like the other two patients M-SFT MPNST SS LMS FS that have been reported with Frequency <0.1% NIA NIA NIA <3% of all M-SFT of the nasal cavity, nonepithelial our patient was a female with tumors a strong smoking history Sex NP NP M:F 1.2:1 NP NP (sporadic) (40-pack-year) and showed Adults 5th decade 3/4th Adults 55 Y significant weight loss. We Age decade also identified differences in HaphaMyxoid & Sheets or Fascicular Fascicular Microscopy the histologic examination. zard; cellular fascicles; Herring In our case, pleomorphism Patternareas; herringbone and mitoses were frequently less perivascu- bone Pattern; lar cuffs seen throughout the entire Ropey specimen and no necrosis collagen was identified. Unlike the Short Elongated; Mono and Cigar Moderate Nuclei other two cases of M-SFT, spindle tapered; Biphasic; shaped; atypia; our case lacks necrosis. cells; buckled; varying variable tapering; Immunoreactivity for STAT6 supported the morphologic suspicion of SFT. Although pleomorphism and frequent mitoses were present, no necrosis was identified in our case. The lack of necrosis in our case is notable as necrosis is a common feature of M-SFTs; however, it is not necessary for the diagnosis.

SFT accounts for less than (<) 0.1% of all sinonasal neoplasms, usually affecting adults with no gender predilection.1 Solitary fibrous tumors and M-SFT of the nasal cavity present with unilateral nasal mass, rhinorrhea, epistaxis and exophthalmos.1-4 The clinical presentation varies based on tumor location.

Cytoplasm Immunostain STAT-6 CD34 CD31 BCL2 S100 GFAP SOX10 NFP DESMIN CALDESMON SMA BetaCATENIN EMA VIMENTIN CK TLE1 Other stains Molecular

mitoses > 4/10 HPF

wavy

nuclear morphology

atypia; mytoses

elongated

Minimal

Scant; amphophilic

Scant; indistinct

Eosinophilic; fibrillary

Scant

+ + + + -

+/+ + + -

+

-/+

+/-

+ -/+ + +/+

Loss of NF1 on 17q11 and TP53 on 17q13 S +/- R/C

T(X;18) (p11;q11) SS18-SSX

NAB2STAT6

-

+

+ + + -/+ + -/+ -

Complex

UPS 3rd most common sarcoma in sinonasal tract NIA 6th decade Storiform; fascicular; haphazard

Spindle and pleomorphic cells

Amphophiliceosinophilic -/+ -

-

+/+ Reticulin Complex

+ Complex

S S +/- R/C S+/-R S+/-R S+/-R Radiologically, SFTs present Treatment M-SFT: malignant solitary fibrous tumor, MPNST: malignant peripheral nerve sheath tumor, SS: synovial sarcoma, as highly vascular soft-tissue LMS: leiomyosarcoma, FS: fibrosarcoma, UPS: undifferentiated pleomorphic sarcoma; NIA: no information available; tumors, sometimes seen NP: no predilection, F: female; M: male, Y: years; STAT6: Signal transducer and activator of transcription CD34: LMS: with prominent collateral M-SFT: malignant solitary fibrous tumor, MPNST: malignant peripheral nerve sheath tumor, SS: synovial 6; sarcoma, Cluster of differentiation 34; CD31: Cluster of differentiation 31; BCL2: B-cell lymphoma 2; S100: soluble in a 100% NP: no feeding vessels which can be leiomyosarcoma, FS: fibrosarcoma, UPS: undifferentiated pleomorphic sarcoma; NIA: no information available; saturated ammonium sulfate solution protein; GFAP: glial fibrillary acidic protein, SOX10: SRY-related HMG-box 10; of predilection, F: female; M: male, Y: years; STAT6: Signal transducer and activator of transcription 6; CD34: Cluster a helpful diagnostic feature differentiation 34; CD31: differentiation 31; BCL2: lymphoma 2; S100: soluble in a 100% saturated neurofilament protein;Cluster SMA: of Smooth muscle actin; EMA: B-cell epithelial membrane antigen; CK: cytokeratin; TLE1: ammoni when present. A visible fatty NFP: sulfate solutionenhancer protein; GFAP: glial fibrillaryR:acidic protein, SOX10: SRY-related HMG-box 10; NFP: neurofilament protein transducing-like protein 1; S: surgery, radiotherapy, C: chemotherapy. component is often identi- SMA: Smooth muscle actin; EMA: epithelial membrane antigen; CK: cytokeratin; TLE1: transducing-like enhancer protein 1 fied. These findings should surgery, R: radiotherapy, C: chemotherapy. alert the radiologist to the possible diagnosis of SFT. However, the appearance. Tumor histology varies. Classic fibrous pleural SFTs are findings are not specific and the differential includes high-grade sarco- more hypocellular with thin-walled, branching capillaries always present and sometimes prominent. In cellular SFTs, collagen fibers are mas and a metastatic lesion.5 scant or absent, and tumors are composed of solid nests of neoplastic The histologic appearance and immunoprofile are the same regardless cells with very prominent branching and anastomosing "staghorn" capthe location of the tumor. Histologically, SFTs are spindle cell neo- illaries. Tumor cells may not show the spindled morphology in cellular plasms that grow in a “patternless” pattern or with a vague storiform SFT, becoming more ovoid to round. Mitoses and necrosis are vari300 VOL. 59 • NO. 6/7 • 2018

able. Four mitotic figures/10 HPFs is the historical cutoff in the literature for SFT.6 According to the World Health Organization (WHO), patient age older than 55 years, tumor size greater than 15 cm, necrosis, and more than 4 mitoses per 10 HPFs probably suggest more aggressive behavior.1 Differential diagnosis in cases of SFT and M-SFT can be vast with many benign and malignant histologic mimickers. Cytomorphology, immunoprofile and cytogenetic findings are essential to correctly diagnose these entities. (Tables 1-3).

8 Table3.3 Common CommonImmunohistochemical Immunohistochemical Markers.

Overview of the markers in this article.8 Table Markers.

Overview of the markers discusseddiscussed in this article.

ANTIBODIES TO: STAT6 (Signal Transducer and Activator of Transcription 6) CD34 (Cluster of differentiation 34) Bcl-2 (B-cell lymphoma 2)

EXPRESSED BY: Solitary fibrous tumor, and rarely in well-differentiated/dedifferentiated liposarcomas, unclassified sarcomas, and desmoid tumors, among others.

Benign and malignant vascular tumors, solitary fibrous tumor, epithelioid sarcoma, dermatofibrosarcoma protuberans, gastrointestinal stromal tumors.

Synovial sarcoma, solitary fibrous tumor, other spindle cell tumors Melanoma, benign and malignant peripheral nerve sheath tumors, cartilaginous S-100 (solubility in 100% protein) tumors, normal adipose tissue, Langerhans cells, many others GFAP (Glial fibrillary acidic Gliomas, some schwannomas protein) SOX10 (SRY-related HMG-box Melanomas of all subtypes, clear cell sarcomas, neurofibromas, schwannomas, 10) and malignant peripheral nerve sheath tumors NFP (Neurofilament protein) Neural and neuroblastic tumors Desmin Benign and malignant smooth and skeletal muscle tumors Benign and malignant smooth and skeletal muscle tumors, myofibroblastic SMA (Smooth muscle actin) tumors and pseudotumors.

H-Caldesmon Leiomyosarcoma Myogenin, MyoD1 (Myogenic Rhabdomyosarcoma nuclear regulatory proteins) Fibromatoses, and rarely in solitary fibrous tumors, synovial sarcomas, Beta-catenin endometrial stromal sarcomas, clear cell sarcoma, osteosarcoma, and liposarcoma.

EMA (Epithelial membrane Carcinomas, epithelioid sarcoma, synovial sarcoma, perineurioma, meningioma, antigen) anaplastic large cell lymphoma Vimentin Sarcomas, melanoma, lymphoma, some carcinomas HMB-45 (Human metastatic Melanoma, PEComa, clear cell sarcoma, melanotic schwannoma melanoma 45) Carcinomas, epithelioid sarcoma, synovial sarcoma, some angiosarcomas and Cytokeratins leiomyosarcomas, mesothelioma, rhabdoid tumor CD31(Cluster of differentiation Benign and malignant vascular tumors 31) ERG (ETS-related gene) Benign and malignant vascular tumors TLE1 (transducing-like enhancer Synovial sarcoma, and rarely in malignant peripheral nerve sheath tumors, protein 1) solitary fibrous tumor, rhabdomyosarcoma,

Immunohistochemistry is an important tool in differentiating SFTs from histologic mimics. Solitary fibrous tumors express CD34 (90% of cases) and CD99 (70%), especially the fibrous forms. A smaller subset of tumors is positive for epithelial membrane antigen (30%), smooth muscle actin (20%), and BCL-2 (30%).

Transducing-like enhancer protein 1 (TLE1) is weakly positive in occasional cases, whereas mucin 4 (MUC4) is negative. Very rare cases show focal staining for S100 protein or desmin, and tumors are virtually always negative for cytokeratins.7,8 Molecular studies have identified a NAB2-STAT6 fusion in SFT which results in strong nuclear signal in STAT6 immunohistochemistry in these tumors.9 In a recently published study strong nuclear STAT6 was expressed in 285 of 2,021 mesenchymal tumors evaluated, including 206 of 240 SFTs, 49 of 408 well-differentiated/dedifferentiated liposarcomas, 8 of 65 unclassified sarcomas, and 14 of 184 desmoid tumors, among others. The STAT6 expression in SFTs in this study was predominately limited to the nucleus. Complete absence of STAT6 was most common in pleomorphic liposarcoma (60%) and alveolar soft part sarcoma (72%). In this study STAT6 immunohistochemistry displayed 97% sensitivity for SFTs.10 Prognostic indicators in SFT have been somewhat unreliable in studies to date, but do predict outcome to some extent. In one larger study, a 3-tiered model stratified patients by overall risk of metastasis (low, moderate, or high) based on age (less than 55 vs greater than (≥) 55),

tumor size (<5, 5-9, 10-14, or ≥15 cm), and mitotic figures (0, 1–3, or ≥4). Necrosis was excluded due to the difficulty in reliably discerning tumor necrosis from necrosis secondary to treatment or infarct-type necrosis. No patients in the low-risk group developed metastasis or died of disease over a median follow-up of 50 months. The 10-year metastasis-free rates in moderate and high-risk groups were 64 and 0%, respectively. The 10-year disease-specific survival rates in moderate and high-risk groups were 93 and 0%, respectively.6 Surgical resection is the treatment of choice with radiotherapy in cases of positive surgical margins.4 Local recurrence is common when tumors arise in difficult-to-access sites (orbit, nasal sinuses) and where complete, en-bloc resection is challenging.

All patients who present with symptoms and signs of sinusitis with evidence of abnormalities of the eye require radiologic imaging to exclude infection, tumor, or undisclosed trauma to the organ. In this case, physical examination and radiologic evaluation reveal a rare case of malignancy delineated by histopathologic evaluation with invasive potential which requires close follow-up due to its risk of recurrence, metastasis, and death. n

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References

1. El-Naggar AK, Chan JK, Grandis JR, et al. WHO Classification of head and neck tumors (4th edition). IARC: Lyon; 2017.

2. Minami K, Kuba K, Matsumura S, et al. Solitary Fibrous Tumors of the Nasal and Paranasal Sinuses. Nihon Jibiinkoka Gakkai Kaiho. 2015; 118(7):875-81.

3. Zeitler D, Kanowitz S, Har-El G. Malignant solitary fibrous tumor of the nasal cavity. Skull Base. 2007; 17: 239–246.

4. Papadakis I, Koudounarakis E, Haniotis V, et al. Atypical solitary fibrous tumor of the nose and maxillary sinus. Head Neck. 2013; 35: E77–E79.

5. Wignall O, Moskovic E, Thway K, et al. Solitary Fibrous Tumors of the Soft Tissues: Review of the Imaging and Clinical Features With Histopathologic Correlation. Am J Roentgenol. AJR 2010; 195:W55–W62.

6. Demicco E, Park M, Araujo D, et al. Solitary fibrous tumor: a clinicopathological study of 110 cases and proposed risk assessment model. Modern Pathology.

2012; 25(9):1298-306.

7. ImmunoQuery | Get it Right, Right Now. ImmunoQuery | Get it Right, Right Now. https://app.immunoquery.com/view/panel/dx?dxgroups=796.

Accessed August 10, 2017.

8. Goldblum JR, Folpe AL, Weiss S, eds. Enzinger & Weiss’s Soft tissue tumors.

Philadelphia, PA: Elsevier Saunders; 2014.

9. Schweizer L, Koelsche C, Sahm F, et al. Meningeal hemangiopericytoma and solitary fibrous tumors carry the NAB2-STAT6 fusion and can be diagnosed by nuclear expression of STAT6 protein. Acta Neuropathol. 2013; 25(5):651-8.

10. Demicco E, Harms P, Patel R, et al. Extensive Survey of STAT6 Expression in a Large Series of Mesenchymal Tumors. Am J Clin Pathol. 2015; 143(5): 672-682.

Author Information Anatomic and Clinical Pathology resident, post graduate year 2, University of Mississippi Medical Center (Tillotson). Assistant Professor, Department of Pathology, University of Mississippi Medical Center (Gonzalez).

Corresponding Author: Maria F. Gonzalez, MD, Assistant Professor, Department of Pathology, University of Mississippi Medical Center. 2500 N. State St. Jackson, MS 39216. Ph: (601) 984-1876 mfgonzalez@umc.edu.

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We Are Back on Track WILLIAM GRANTHAM, MD

T

he fact that you are reading this column tells you something important—the Journal MSMA is back on track. Writing, editing and publishing a journal like this one is a monumentally complex task.

I want to personally commend the volunteer physician editors and our staff managing editor for going to extraordinary lengths to increase the scientific content and enhance the physical design of our Journal. Editor Dr. Luke Lampton and associate editors Drs. Stanley Hartness and Richard deShazo work closely with our staff managing editor Karen Evers. The volumes produced in 2018 have increased in heft and value to the membership.

Likewise, members of the Journal Editorial Advisory Board have volunteered to review more manuscripts than ever before. The Committee on Publications chaired by Dr. Dwalia South monitors the entire effort and annually makes recommendations to the Board of Trustees on ways to improve the Journal. One such recent suggestion is to move from twelve issues to ten combining June with July and November with December. You will still receive a backdated 2017 issue with an index to volume 57, and 2018 issues are on time. I’m particularly pleased to have the Journal on track so we can better notify you of socioeconomic events and endeavors that are time-sensitive.

You may also notice that the advertising in the Journal is increasing. We have an exceptionally talented marketing director at MSMA. Jill Gordon joined our staff late last year and in six months has tripled the advertising revenue generated by our journal. It costs about $180,000 a year to produce a high quality Journal like ours. Roughly half of that is printing and postage costs and the other half covers staff salaries/benefits and office overhead costs.

Advertising last year brought in $32,000. In 2018, we will likely see advertising hit the $100,000 mark for the first time ever as Jill continues to bring in new advertisers.

Moving forward, we must maintain the high standards set by the editors. At the same time, we must be nimble

William M. Grantham, MD MSMA President 2017-2018 and increase opportunities to use technology. The Board of Trustees has asked the Committee on Publications to take MSMA to that next level with a searchable, digital, online iteration to supplement – not replace – the printed Journal. I know the printed word still works best for many, yet I believe that it is essential that our MSMA pivot to also be relevant and accessible to younger physicians who rely almost exclusively on electronic information. This is the next crucial step we must take to keep our Journal vibrant. It’s an exciting road ahead. n

William M. Grantham, MD MSMA President 2017-2018

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Electronic Medical Records: It Takes a Forest!

STANLEY HARTNESS, MD

I

t was billed as the greatest thing since the proverbial loaf of sliced bread.

The Health Information Technology for Economic and Clinical Health (HITECH) Act of 2009 signed into law as part of the “stimulus package” represents the largest U.S. initiative to date designed to encourage widespread use of electronic medical records. However, when I retired from Kosciusko Medical Clinic at the end of 2009, the hand across my forehead was the swipe heard ‘round the world—I had dodged the Electronic Medical Records (EMR) bullet!

Alas, my reprieve was short lived. On relocating to Jackson and signing on in time with two different clinic systems, I had to learn not one but two different EMR systems. Talk about too much sugar for a nickel!

One of the shortfalls of EMR that struck me early on was the temptation to espouse the “copy and paste” syndrome as opposed to recording original observations. Although our patients probably weren’t aware of our entries, they were painfully aware that their visits had suddenly become less personal.

Along with confidentiality and security issues (not to mention computer server crashes), one of the major drawbacks has been that different EMR systems simply can’t or don’t communicate with each other. This reminds me of the Republicans and Democrats in Washington, D.C.! Case-in-point: as the collaborating physician for the Premier Medical Clinic of Carthage, I recently had occasion to see a patient in follow-up who had been diagnosed with pneumonia several days earlier in a Jackson hospital ER. Naturally her records had to be faxed. Of the 33 pages I received for that single ER visit, fully 22 of them dealt with her BMI and recommended diet and exercise regimens!

Along with this communication shortfall, considering the reams of paper expended to print out patient diagnoses and descriptions of their illnesses to satisfy EMR meaningful use requirements, the rainforests are probably disappearing at a rate that even National Geographic has underestimated!

No doubt, EMRs are here to stay. And while they were ostensibly created for ease and patient safety, ear-piercing wailing and fingernail-on-chalkboard gnashing of teeth usually accompany any system update or (heaven forbid!) adoption of a totally new system. It’s enough to make us long for the days of paper charts when clinic notes were more personal and could be recorded in less than 33 pages. Hopefully the Mississippi Forestry Commission is already on top of this. n

Stanley Hartness, MD; Jackson JMSMA Associate Editor

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E D I T O R I A L

To Cut or Not To Cut: Is Waiting the Best Solution to Many of Medicine's Problems?

BRITT CROSS, DO

I was working a shift the other night in the emergency department when I received a text message from a friend. Apparently after a failed high-five attempt, he had somehow caught his ring on the window of a school bus and twisted his ring finger. This caused some swelling of his finger that prevented him from removing his wedding ring. Matters only worsened after several failed removal attempts resulted in some skin damage of the finger around the ring which limited further removal attempts. It was at this point when he reached out asking for advice. I told him to stop by the ER and I would take a look.

Upon arrival, his finger was indeed swollen around the proximal interphalangeal joint. I tried pulling and twisting the ring with a little soapy water, but this was hindered by the skin damage both around and just distal to the ring. My friend asked my advice as to what I would normally do in this situation. I considered a few other options, but ultimately cutting the ring seemed like the simplest and quickest option. He then posed this question to me: “Why can’t we just wait and see what happens?”

The question made me sit back and wonder the same thing. Working in an emergency department, the expectation has always seemed to be that problems should be solved right away.

Patients present in the middle of the night expecting quick answers to chronic problems. A followup patient in the ER usually means a bad outcome or failed treatment. Certainly, a problem with an obvious solution must be resolved immediately. But in some cases, what’s the rush?

The incident had occurred 12 hours prior, and no obvious ischemia or strangulation symptoms to the finger had occurred yet. The ring still felt fairly loose at the base of the finger. The suspected sprained finger showed no signs of fracture. “I could just watch it and return if it starts to become painful or changes in color or sensation. We could then just cut off the ring at that time.”

So we decided to wait. Over the next few days, the swelling began to subside, and the skin healed slightly. On day 5, the patient was able to remove the ring with gentle traction and maneuvering.

He never had any symptoms of worsening pain or circulation issues, and both he and his grateful wife were pleased that he was able to keep his wedding ring intact.

Sometimes it’s a simple patient encounter that reminds us to take a step back and examine how we approach some facet of our treatment plans. Just because a problem can be solved instantly doesn’t mean it’s always the best way. The ER environment encourages speed and efficiency as well as instant results. In this case, allowing the body a little time to heal itself turned out to be the best solution. n

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Schneider’s approach makes medical sense, MBML restrictive regulations not patient-centered Dear JMSMA Editor, I am writing regarding Dr. Jennifer Schneider’s excellent article (Schneider J. A patient-centered approach to the opioid overdose crisis.

J Miss Med Assoc. 2018;59(5)292.). Importantly, using evidence-based literature, she supports a more patient-centered approach to opioid prescribing rather than restrictive actions by local/state government or licensure boards. The vast majority of patients take prescription opioids or other Schedule II drugs for valid medical reasons; they also have an improved quality of life and are much more functional than they would be without such medications. Dr. Schneider confirms that most patients who take opioids on a chronic basis are not addicted but rather have physical dependence and, therefore, are not at risk for overdose.

Recently, the Mississippi Board of Licensure passed what probably rank as the most stringent regulations in the country governing opioid prescriptions. I’m afraid three things will happen in response to this imprudent action. First, the number of opioid and Schedule II prescriptions will diminish greatly (it has already fallen in the past two years as good physicians fear punitive Board actions). Secondly, patients taking opioids chronically will use illicit drugs (from which they will die) to cope with the pain and anxiety, and certainly they will have a reduced quality of life. Lastly, I am afraid that such restrictive prescribing will also move toward other drugs in the non-opioid categories as “Big Brother” seeks to protect the population from itself. For example, loperamide (an anti-diarrhea medication) and gabapentin (an analgesic for peripheral neuropathy) have been targeted despite no evidence that they are being abused. All of this will not help the problem one bit in my estimation.

Doctors and their patients are the only ones that can accurately decide what medications are needed. In summary, it is never a good idea for government or state boards to attempt to solve a problem by restrictive means (think “Prohibition,” “The War on Drugs,” “The Wall”) as it never works. n

—John C. Morrison, MD Jackson

Mississippi Dental Board reviews “regs” for office-based general anesthesia, puts qualifications and best practices under scope Dear JMSMA Editor, The Mississippi Board of Dental Examiners is currently reviewing regulations regarding the administration of intravenous sedation/deep sedation/ and general anesthesia in dental offices. These regulations pertain to all dental practices, including oral surgeons, pediatric dentists, and general dentists, among others.

I am writing this letter to the Journal of the Mississippi State Medical Association because the issues involve medical anesthesiologists and the safe administration of general anesthesia in an office setting.

Below is a summary of a letter I sent to the Dental Board regarding these issues after lengthy consultations with my pediatric dental colleagues.

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Important concerns I have are the following:

1. QUALIFICATIONS OF ANESTHESIOLOGISTS

“Dental anesthesiologists”, medical anesthesiologists, and oral surgeons each have specific standards and requirements. Certified Registered Nurse Anesthetists, or CRNAs should not be used as the sole qualified provider in the event of an emergency.

2. TRANSFER AGREEMENTS

Ambulatory Surgical Centers (ASC) are required to have a transfer agreement to a nearby hospital in the case of an emergency.

A dental office providing general anesthesia/deep sedation should have the same requirements. Reliance on calling “911” in an emergency will not provide patients with the highest level of care.

3. MEDICAL EQUIPMENT AND MEDICATIONS

Any general dentist office performing deep sedation and/or general anesthesia should be equipped with standard airway and medical equipment, medications, intravenous access, and backup generators. My letter to the Dental Board lists equipment and specific medications in more detail, yet it is still not an exhaustive list.

4. DANTROLENE

Dantrolene is a drug used specifically for the treatment of malignant hyperthermia, a genetic disorder often triggered by certain anesthetic agents. Unfortunately, there is no other medication that will specifically treat this disorder, which is often discovered in children undergoing general anesthesia. My letter to the Dental Board discusses best practices for reconstituting, stocking, and administering this drug.

5. POST-ANESTHESIA RECOVERY UNIT (PAR)

Post-anesthesia care units (PACU) must meet certain equipment, medication, and monitoring standards, as well as meeting staffing standards (must be staffed by qualified RNs). Any notion that these patients can be monitored or discharged by anyone other than the anesthesiologist or qualified PACU nurse is fraught with danger. The patient cannot be “recovered” by office personnel.

6. PRE-ANESTHETIC EVALUATION

Many studies by the American Society of Anesthesiologists demonstrate that a pre-anesthetic evaluation, in person or over the phone, will allow the safer administration of anesthesia. They should be performed by medical personnel trained in obtaining an adequate medical history.

7. CONTROLLED SUBSTANCES

I suggest that controlled substances be authorized to the practitioner who performs the procedure, and that the medications not be “brought in” by itinerant anesthesiologists.

8. INSPECTIONS

As the Mississippi Board of Health has no authority to inspect any office operatories, the Board of Dental Examiners must have a qualified staff to insure safety and compliance with its regulations regarding office-based anesthesia. This will require a staff of knowledgeable inspectors to perform these inspections, probably every other year.

9. OCCUPATIONAL REVIEW COMMISSION AND RESTRAINT OF TRADE

The use of “restraint of trade” filing actions against the Dental Board by both itinerant and medical anesthesiologists is a possibility, but one that I believe the Dental Board can cooperate with the Medical Board to solve this potential problem.

10. COST SAVINGS FROM DENTAL OFFICE ANESTHIA FOR PEDIATRIC PATIENTS

Many proponents of dental office anesthesia for pediatric patients have touted the alleged “cost savings” to both insurance companies, patients, and, especially, Medicaid. My letter to the Dental Board discusses some perhaps unintended complications from this assumption.

11. MALPRACTICE INSURANCE

In order to protect the public, dentists performing deep sedation/general anesthesia in their office practices should be required by the Dental Board to carry an adequate amount of malpractice insurance to cover the potential loss of life due to malpractice/ malfeasance.

The Dental Board will next meet at 8 a.m. on Friday, July 27, 2018. I will be on the agenda. I ask all interested parties to appear to discuss these issues with the Board, especially my dental, pediatric and anesthesiology colleagues. n

—Heddy-Dale Matthias, MD Madison

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Express your opinion in the JMSMA through a letter to the editor or guest editorial. The Journal MSMA welcomes letters to the editor. Letters for publication should be less than 300 words. Guest editorials or comments may be longer, with an average of 600 words. All letters are subject to editing for length and clarity. If you are writing in response to a particular article, please mention the headline and issue date in your letter. Also, include your contact information. While we do not publish street addresses, e-mail addresses, or telephone numbers, we do verify authorship, as well as clarify ambiguities, to protect our letter writers.

You can submit your letter via email to KEvers@ MSMAonline.com or mail it to the Journal office at MSMA headquarters: P.O. Box 2548, Ridgeland, MS 39158-2548.

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C O M M E N T A R Y

NPs and Elderly Care: We Can Do Better

I

n the ongoing conversation regarding nurse practitioners (NPs) and scope of practice, one group of patients is often left out— the elderly. While national nursing groups are pushing for NPs to be recognized as equal to physicians, it’s the most vulnerable patients who would suffer the most from a heedless expansion of scope. The elderly as a group tend to be more susceptible to infections, falls, Katherine Pannel, DO and medication side effects.

But they also can be hurt more by the misdiagnosis of an undertrained midlevel provider.

Some policy makers advocate for this expansion without full knowledge of what it means. Many see physician shortages in areas like rural Mississippi and want to patch the need with independent NPs. But this solution isn’t an apples-to-apples comparison and it shoves aside the legitimate concerns centered around the disparity of training between physicians and NPs. For Dr. Katherine Pannel, a geriatric psychiatrist practicing in North Mississippi, allowing unsupervised NPs to practice on her patient cohort is frightening.

“Not on my watch,” Dr. Pannel said. “I work with NPs and I trust them to do their job. But being a physician isn’t the job of an NP. My patients can be exceptionally sensitive to changes in medication and treatment.” “Plus,” she said, “the underlying causes are often extremely hard to diagnose. Training and experience make all the difference in the world when it comes to helping the geriatric psychiatric patient.”

Reimbursement is another issue for elderly patients. Medicare is a volatile system and many physicians don’t accept it as payment.

Would midlevel providers be any different? Here again, Dr. Pannel and other physicians see an issue. “The underserved deserve the same level of care as everyone else,” she said. “The underserved have payment issues, and that’s not going to change if an NP is attempting to provide the treatment.”

There’s also research indicating that seniors prefer to be treated by a physician rather than an NP. A survey done in 2014 by Baselice &

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Associates shows that preference for a physician over an NP increases with age. In fact, 75% of those surveyed who were 65 or older strongly prefer a physician. And 71% aged 55 to 64 felt the same way.

So, while the population continues to age, the systems —in place and proposed— struggle to meet their needs. Mississippi is graduating record numbers of new physicians from the medical schools. Now, Mississippi really needs more residency training slots. The Office of Physician Workforce is facilitating the growth of new residency training programs, but that is a slow, deliberate process. Meanwhile, the need is outpacing resources for the foreseeable future and tensions in the system will continue.“I absolutely love my patients,” Dr. Pannel said. “And I refuse to see any one of them become part of a cautionary tale about NP misdiagnosis. We can do better.

Mississippians shouldn’t have to expect diminished care in their twilight years when many need care the most.”

Policy and advocacy that make it possible to give the elderly the best care possible will become more important as the number of seniors rises. This means Mississippi has some serious questions to answer about how to address geriatric needs without diminishing standards of treatment and care.

“The national groups insist that NPs will flood into underserved areas if given autonomy,” Dr. Pannel concluded. “But how likely is that, really?” — MSMA n

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Mississippi Medical Political Action Committee

2018 I.V. LEAGUE PLATINUM WILLIAM M.GRANTHAM, MD J. CLAY HAYS, JR., MD DEBBIE JOINER THOMAS E. JOINER, MD DEREK MARSHALL, MD LORI MARSHALL, MD

ANONYMOUS JOSEPH D. AUSTIN, MD JANIE EASTERLING S. RANDY EASTERLING, MD HUGH A. GAMBLE, II, MD

KAMLESH H. PAREKH, MD JAMES M. RISER, MD ROWLAND ROBERSON, MD ANN ROBERSON, MD NEIL B. SLOAN, MD

GOLD DOUGLAS R. BACON, MD SUSHMA CHOWDHARY, MD YASHWANT CHOWDHARY, MD THOMAS E. DOBBS, MD

DANIEL P. EDNEY, MD F. HENRY FLAUTT, JR., MD SCOTT L. HAMBLETON, MD MICHAEL G. KANOSKY, MD MICHAEL MANSOUR, MD

GREGORY A. PATINO, MD MEREDITH TRAVELSTEAD,MD BRIAN K. TSANG, MD ANGELA B. WINGFIELD, MD

SILVER J. STEPHEN BEAM, MD JOHN W BETHEA, JR., MD CLAUDE D. BRUNSON, MD JENNIFER J. BRYAN, MD THOMAS J. COBB, MD RENIA RUSH DOTSON, MD J. EDWARD HILL, MD W. MARK HORNE, MD

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J. ANN REA, MD MERRELL ROGERS SOMPRASONG SONGCHAROEN, MD SUTHIN SONGCHAROEN, MD J. MARTIN TUCKER, MD THAD F. WAITES, MD JOHN ADAMS WEBSTER,III,MD CHRISTOPHER H.WYATT,MD

BRONZE TIM J. ALFORD, MD CHRISTOPHER ANDERSON,MD JAMES M. BROCK, JR., MD FREDA BUSH, MD H.CLARK ETHRIDGE,JR.,MD JAN T. GOFF, MD MAXIE L. GORDON, MD

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g{tÇ~ çÉâ? àÉÉ To the 2018 members of the Mississippi Medical Political Action Committee

AUDIE M. ADAMS, MD JAMES G. ADAMS, MD OLUFEMI O. ADELEYE, MD JONATHAN R. ADKINS, MD CAROL FRANKS AKIN, MD R. L. ALEXANDER, III, MD KATHERINE PIGOTT ALEXIS, MD TIM J. ALFORD, MD SALEEM A. ALI, MD CYNTHIA E. ALLEN, MD RUSSELL ELBEY ALLMAN, JR., MD JEFF D. ALMAND, MD STEPHEN T. AMANN, MD CHRISTOPHER D. ANDERSON, MD BRIAN T. ANTHONY, MD ADELO E. AQUINO, MD MICHAEL ARTIGUES, MD PATRICIA ARTIGUES WILLIAM C. ASHFORD, MD JOSEPH D. AUSTIN, MD PETE T. AVARA, III, MD JOHN B. AVERETTE, MD DOUGLAS R. BACON, MD JOHN D. BAILEY, MD STEPHEN W. BAKER, MD ZACHARY K BALDWIN, MD TAYLOR M. BANAHAN, MD J. RUSSELL BARNES, MD KENNETH R. BARRAZA, MD AUSTIN M. BARRETT, MD ERICA H. BASS, MD JOHN MICHAEL BATEN, MD BRYAN N. BATSON, MD BRADLEY R. BAUGH, MD SCOTT EDWARD PATRICK BAYMILLER, MD VICTOR T. BAZZONE, MD TIMOTHY BEACHAM, MD J. STEPHEN BEAM, MD THOMAS BASS BEASLEY, MD JAMES R. BECKHAM, MD DONALD W. BENEFIELD, MD ALLISON DERRICK BENNETT, MD BARRY D. BERTOLET, MD JOHN W BETHEA, JR., MD LENORA BIGLER STEVEN A. BIGLER, MD W. MORGAN BILLINGTON, JR., DO DON J. BLACKWOOD, MD MARK E. BLACKWOOD, MD EARL J. BLANCHARD, JR., MD KEVIN PAUL BLANCHARD, MD BENJAMIN D. BLOSSOM, MD PATRICK L. BOLER, MD

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RACHEL C. GARNER, MD THOMAS C. GARROTT, MD BRYAN GASPARD, MD R. LEE GIFFIN, MD HILTON L. GILLESPIE, JR., MD J. BARRY GILLESPIE, MD LAURIE GILLESPIE JAMES GILMORE, MD WALTER E. GIPSON, IV, MD RODERICK C. GIVENS, MD CHERYL L. GLADNEY, MD CHRISTINA C. GLOVER, MD E. CHAD GNAM, III, MD PARVESH K. GOEL, MD JAN T. GOFF, MD RICHARD A. GOLDBERG, DO JESSICA EILEEN GORDON, DO KYLE F. GORDON, MD LLOYD J. GORDON, III, MD MAXIE L. GORDON, MD CAROLYN GORTON MARY KATHERINE GORTON S. CARLTON GORTON, II, MD W. MACK GORTON, MD MICHAEL C. GRAEBER, MD JACOB MARTIN GRAHAM, MD WILLIAM M. GRANTHAM, MD JAMES REED GREEN, JR., MD BRADLEY N. GREENHAW, MD RAYMOND F. GRENFELL, III, MD JOSHUA G. GRIFFIN, MD MEREDITH GRIFFIN, MD D. FRANK GUEDON, MD SHY GUEDON DARYL P. GUEST, MD DEGAIL J. HADLEY, DO KENNETH A. HAHN, MD ADRIENNE HAIDAR AHMAD A. HAIDAR, MD ALLISON HAILMAN-DOYLE, DO W. C. HAIRE, JR., DO BETHANY R. HAIRSTON, MD JOHN C. HALBROOK, III, MD J. MACK HALTOM, III, MD SCOTT L. HAMBLETON, MD GEORGE M. HAMMITT, III, MD KAREN EMILY HAND, MD BURNETT HANSON, MD LILLIE HANSON R. HOUSTON HARDIN, MD ERIC D. HARDING, MD CHERYL HARDY, PHD CAROL D. HARRIS, MD WM. KEITH HARRIS, MD DONNIS K. HARRISON, MD SCOTT E. HARRISON, MD PHIL HARTNESS BETH HARTNESS D. STANLEY HARTNESS, MD JOHN F. HASSELL, MD ARLIN HATFIELD, MD LANDALL C. HATHORN, MD J. CLAY HAYS, JR., MD J. EDWARD HILL, MD JEAN HILL JULIAN B. HILL, JR., MD, FACP RYAN CARL HILL, MD

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BRENDA P. HINES, MD KENNETH L. HINES, MD RANDALL S. HINES, MD ROB HINES BENJAMIN K. HINTON, MD E. RHETTSON HOBGOOD, MD CHIP D. HOLBROOK, MD JOHN G. HOLLAND, MD MAUREEN S. HOLLAND, MD JOHN J. HOLLISTER, MD EDWARD H. HOLMES, MD JAMES W. HOLMES, MD RICHARD E. HOLMES, SR., MD W. MARK HORNE, MD JASON HOSEY, MD JEFFREY C. HOUIN, JR., MD JAMES R. HOUSE, III, MD A. ARCHIE HOWARD, JR., MD CRAIG HOWARD, MD WILLIAM P. HOWARD, MD G. ELI HOWELL, II, MD ANTOINETTE M. HUBBLE, MD JEFFREY L. HUDSON, MD ROGER LEE HUEY, MD VERNON THOMAS HUGHES, JR., DO M. GLENN HUNT, MD NOEL K. HUNT, MD CHRISTIN COLLIER HURT, MD CAMERON S. HUXFORD, MD JERRY D. HYER, MD ORHAN ILERCIL, MD DAVID H. IRWIN, JR., MD KRIS IVANCIC PAUL D. JACKSON, MD W. DOTIE JACKSON, MD HOLLYE R. JOHNSON, MD JAMES C. JOHNSON, JR., MD JEFF N. JOHNSON, MD JOHN JEFFREY JOHNSON, MD KURT D. JOHNSON, MD DEBBIE JOINER THOMAS E. JOINER, MD STEPHEN CRAIG JONES, MD CLARENCE ALLEN JUSTICE, MD AZAD KABIR, MD MICHAEL G. KANOSKY, MD YEKATERINA KARPITSKAYA, MD KENT L. KEBERT, MD MARK J. KELLUM, MD RICHARD A. KELLY, MD CHARLES A. KERGOSIEN, MD P. BENJAMIN KERR, MD PAVEL L. KHIMENKO, MD MARY ANN KING, DO THOMAS E. KING, III, MD KENT A. KIRCHNER, MD JIMMY LAMAR KITTRELL, JR., MD FRANK G. KOE, MD ROD GEOFFREY KRENTEL, MD JANUS J. KULPA, MD RENATA KULPA PAMELA R. LACY, MD PAMELA A LAMBERT STEPHEN C. LAMBERT, MD BRETT C. LAMPTON, MD LOUISE LYELL LAMPTON JOHN A. LANCON, MD

CHARLES LANEY, MD JEFFREY T. LASETER, MD VIRAL LATHIA, MD CARLOS LATORRE, MD JOHN F. LAURENZO, MD PENNY J. LAWIN, MD ERIC D. LAWSON, MD A. KEITH LAY, JR., MD CLIFTON T. LEATHERBURY, MD CHRISTOPHER J. LEBRUN, MD JOHN P. LEE, MD HENRY T. LEIS, MD PHILIP LEVIN, MD MATTHEW W. LEWIS, MD W. MARK LEWIS, MD JAY J. LIBYS, MD HAL T. LIDDELL, MD ERIC E. LINDSTROM, MD NANCY LINDSTROM C. KENNETH LIPPINCOTT, MD NELSON K. LITTLE, MD STEVEN B. LIVERMAN, MD WILLIAM R. LOCKE, MD ANDREA F. LOGAN, MD T. BRUCE LONGEST, JR., MD R. H. LOPEZ-SANTINI, MD CHESTER C. LOTT, MD FRANK A. LOVELL, MD RODNEY N. LOVITT, MD KURRE T. LUBER, MD AUBREY B. LUCAS, MD SHERI LUEBRECHT, MD EVA MAGIROS, MD RAYMOND JOHN MAGUIRE, MD JOHN H. MALLETT, MD PRESLEY D. MALLETT, MD KAREN MALTBY, MD J. MICHAEL MANNING, MD MICHAEL MANSOUR, MD DANETT MAPLES, MD DON E. MARASCALCO, MD WILLIAM L. MARCY, MD TYLER G. MARKS, MD DEREK E. MARSHALL, MD LORI H. MARSHALL, MD ANDREW A. MARTIN, MD IRVIN L. MARTIN, III, MD N. SHARON MARTIN, MD J. LAWRENCE MASON, JR., MD PAUL G. MATHERNE, MD TAYLOR MATHIS, MD ARTHUR M. MATTHEWS, JR., MD WANDA MATTHEWS CHRIS L. MAULDIN, MD WILLIAM H. MCCLATCHY, MD W. DAVID MCCLENDON, JR., MD FRED J. MCDONNELL, MD HAMILTON M. MCGEE, MD DAVID G. MCHENRY, MD DAVID L. MCKELLAR, MD EVERETT C. MCKIBBEN, MD GERALD MCKINNEY, MD, FACS ROBERT H. MCKINNEY, MD SHAWN A. MCKINNEY, MD, FACS JOHN R. MCPHERSON, MD J THOMAS MCREYNOLDS, MD ROBERT KERSEY MEHRLE, MD

COURTNEY MEREDITH, MD KATHLEEN A. MESSENGER, MD CARLA METTETAL CARY N. METTETAL, DO KAY E. MIDLER, DO MARC JEFFREY MIHALKO, MD SHELI MILAM, MD WM. HUGHES MILAM, MD DEREK MILES, MD JOHNNY F. MILES, JR., MD SONYA MITCHELL MILES, MD REGINA C. MILLS, MD BLANE A. MIRE, MD ELIZABETH W. MITCHELL, MD LARKIN H. MITCHELL, MD HANNA M. MITIAS, MD EMAD HASHIM MOHAMED, MD SARFRAZ M. MOLVI, MD JAMES M. MONROE, DO MICHAEL W. MONTESI, MD DAVID L. MOODY, MD VICKI MOODY ALAN R. MOORE, MD JEFFREY A. MORRIS, MD C. TROY MORRISSETTE, MD LOUIS JEFF MOSES, MD JAMES A. MOSS, JR., MD JONATHAN BARRY MULLINS, MD STEVEN M. MURPHEY, MD JASON G. MURPHY, MD ANDREW J. MYRICK, JR., MD ROBIN D. NATIONS, MD CHARLES L. NAUSE, JR., DO JOHN C. NEILL, MD SCOTT E. NELSON, MD VIRGINIA C. NELSON, DO HEATHER NEWLON, MD JEFFREY DEAN NOBLIN, MD LUTHER B. OAKES, MD W. THOMAS OAKES, JR., MD W. GARRETT OGG, MD Y. GRACE OH, MD EUGENE K. O'HEA, MD TUNDE OLUTADE, MD JAMES W. O'MARA, JR., MD MANUEL L. ONG, JR., MD MATT L. OSWALT, MD STEPHEN K. OTEY, MD MARY ELLIS PACE, MD REBECCA C. PACE, MD GINGER PACE-HERNDON, MD LEENA PANDE, MD VICTOR G. PANG, MD RICHARD STEPHEN PANNEL, DO JOHN F. PAPPAS, MD KAMLESH H. PAREKH, MD BILLY D. PARSONS, MD PRAVINCHANDRA P. PATEL, MD GREGORY A. PATINO, MD BRANDY R. PATTERSON, MD GREGORY O. PATTON, MD MICHAEL F. PAYMENT, MD JASON A. PAYNE, MD ERIC J. PEARSON, MD REBECCA PEARSON RICHARD A. PECUNIA, MD SAMUEL H. PEEPLES, MD

DENISE E. PHILLIPS, MD DOUGLAS C. PHILLIPS, MD EDWARD K. PHILLIPS, MD JOHN O. PHILLIPS, MD, PHD EMILE PICARELLA, MD TREVOR R. PICKERING, MD SONDRA PINSON TERRY W. PINSON, MD VINCENT J. PISCIOTTA, MD TRACY BLAIR PITTMAN, MD TERRY C. PITTS, DO DAVID A. POMIERSKI, MD MARTIN M. POMPHREY, MD RADHA PRASAD CHARLES K. PRINGLE, JR., MD THOMAS GLENN PUCKETT, MD JEANETTE PULLEN, MD JOE S. PULLIAM, MD JANI L. PURVIS, MD TIMOTHY M. QUINN, MD MILTON R. RAINES, MD RICHARD DOUGLAS RAINEY, MD J. RANDALL RAMSEY, MD ARUN R. RAO, MD BEVERLY RAY MARK A. RAY, MD EDITH SMITH RAYFORD, MD, MBA J. ANN REA, MD DAVID L. REEVES, MD D BRIAN REMLEY, MD WILLIAM L. RENO, III, MD DAVID S. REYNOLDS, MD J. MATTHEW RHINEWALT, MD CHARLES DAVID RICHARDSON, MD DAVID R. RICHARDSON, MD HARRY LEE RICHARDSON, JR., MD SHARON RICHARDSON HEATHER RIFKIN ANGELA MARIE RILEY, MD JAMES M. RISER, MD JAMES A. RISH, MD ANN CHANCELLOR ROBERSON, MD ROWLAND M. ROBERSON, MD ANDREA ROBERTS JAMES E. ROBERTS, JR., MD JESS CLIFTON ROBERTS, MD A. U. ROBERTSON, MD MERRELL ROGERS MALCOLM MOUNGER SAWERS ROLAND, MD ELIZABETH R. ROSE, MD APRIL MICHELLE ROSS, MD DIANE ELLEN ROSS, MD RANDOLPH J. ROSS, MD R. SCOTT RUNNELS, JR., MD RUDOLPH S. RUNNELS, SR., MD E LANE RUSHING, MD RICHARD L. RUSSELL, MD

BRADLEY C. SAMS, MD STUART F. SAMSON, MD ANDREA SANDERS H. JAY SANDERS, IV, MD VANESSA L. SANDIFER, MD BEN F. SANFORD, JR., MD BHARAT H. SANGANI, MD DAVID N. SAWYER, MD PAT H. SCANLON, JR., MD TIFFANY ANN SCARFF, MD AMANDA R. SCHIEFER, MD ROBIN H. SCHWARTZ, MD M. SHANE SCOTT, DO BEN W. SEALE, MD JEFFREY K. SEALE, MD, FACOG BRADLEY N. SECREST, MD FIDEL FABIAN SENDRA, MD MANOJKUMAR P. SHAH, MD MISTY T. SHARP, MD WALTER R. SHELTON, MD CHESTER DUANE SHERMER, MD TIMOTHY D. SHUMAKER, MD EDWARD J. SHUMSKI, JR., MD XIAOHONG SI, MD KATHRYN LAURA SIGURNJAK, MD KEITH M. SIMNICHT, MD LAUREN STEELE SIMPSON, MD SHANE M. SIMS, MD JAMIE D. SISK, MD J. WOODY SISTRUNK, MD B. TODD SITZMAN, MD, MPH ROBERT L. SKINNER, DO JACOB SKIWSKI, MD VICTORIA SKIWSKI NEIL B. SLOAN, MD WAYNE A. SLOCUM, MD BARBARA D SMITH JASON V. SMITH, MD P. BRENT SMITH, MD ROBERT B. SMITH, MD STEVEN P. SMITH, MD THOMAS B. SMITH, MD ADAM SMITHERMAN LIZ SMITHERMAN SOMPRASONG SONGCHAROEN, MD SUTHIN SONGCHAROEN, MD C. DALLAS SORRELL, MD DAVID L. SPENCER, SR., MD JAMES W. STEPHENS, MD MICHAEL EDWARD STEUER, MD CARL W. STEVENS, II, MD STEVEN W. STOGNER, MD BETH STONE JAMES E. STONE, JR., MD R. HARPER STONE, MD W. ROSS STONE, MD LEIGH ANNE STRONG, MD MARK H. STRONG, MD, FACC

KENNETH W. STUBBS, MD PAIGE SUARES R. NEAL SUARES, JR., MD ITALO SUBBARAO, DO SABRA SULLIVAN, MD,PHD WM DAVID SULLIVAN, MD JEFFREY T. SUMMERS, MD PAUL J. TALBOT, MD JIAHUAI TAN, MD AREMMIA D. TANIOUS, MD J. DEAN TANNER, MD CRYSTAL L. TATE, MD PAMI JO TAYLOR, MD WILLIAM G. THAGGARD, MD ABHASH C. THAKUR, MD GREGORY THALKEN, MD HAROLD R. THOMAS, JR., MD KENNETH R. THOMAS, MD ALLEN HALE THOMPSON, MD WILL P. THOMPSON, MD GEORGE M. THURBER, MD ROBERT C. TIBBS, III, MD C. RANDOLPH TILLMAN, MD GREGORY A. TIMBERLAKE, MD ANCEL C. TIPTON, JR., MD RAYMOND E. TIPTON, JR., MD MEREDITH M. TRAVELSTEAD, MD JENNIFER G. TRIHOULIS, MD BRIAN K. TSANG, MD STACEY TSANG J. MARTIN TUCKER, MD JOEL A. TUCKER, MD SAM C. TUMMINELLO, MD JOHN TURBA, MD LEE HARRIS TURK, MD D. MICHAEL TURNER, JR., MD HELEN R. TURNER, MD JO ANNE ELEANOR JOHNSON TURNER, MD KRISTEN Y. TURNER, MD SHERRY DENISE TURNER, DO CHARLES C. UPTON, JR., MD TIMOTHY G. USEY, MD GEORGE KARL VAN OSTEN, III, MD LIZZETTE VAN OSTEN GREGORY A. VANCE, MD JOHN P.F.H. VANDERLOO, MD MATTHEW A. VANLANDINGHAM, MD PAUL D. VANLANDINGHAM, MD KARTHIK V. PRASAD, MD ROBERT D. VOLLER, JR., MD DAVID I. WADDELL, MD FRANK C. WADE, JR., MD STANLEY A. WADE, JR., MD TERRY WADE THAD F. WAITES, MD SUE DUDLEY WALKER, MD RICHARD E. WALLER, MD

WILLIAM L. WALLER, MD DAVID L. WALT, MD GEORGE L. H. WARD, MD JAMES E. WARRINGTON, MD PAUL W. WARRINGTON, MD ERIC D. WASHINGTON, MD JAMES R. WATSON, MD D. ERIC WEBB, MD MARK C. WEBB, MD JOHN ADAMS WEBSTER, III, MD RICHARD E. WEDDLE, MD GERI LEE WEILAND, MD ROGER D. WEINER, MD THOMAS E. WELDON, MD JEREMY B. WELLS, MD PEGGY J. WELLS, MD RALPH P. WELLS, MD WILLIE LEE WELLS, MD MATTHEW B. WESSON, MD FLAVIA WEST-HUDDLESTON, MD KIM WESTMORELAND TERRY A. WESTMORELAND, MD RAUN WETZEL, MD ANNE BROWN WHITEHURST, MD JOHN ELGIN WILKAITIS, MD, MBA BRIAN L. WILKINSON, MD BARRY W. WILLBRANDT, MD A. TERREL WILLIAMS, MD J. BARTON WILLIAMS, MD ROGER A. WILLIAMS, MD DIANE WILLIAMSON KAREN WILLIAMSON STONEY WILLIAMSON, MD TODD DAVID WILLIAMSON, DO JAMES P. WILSON, MD WOODIE JEFF WILSON, JR., MD B. PEARSON WINDHAM, MD ANGELA B. WINGFIELD, MD MICHAEL H. WINKELMANN, MD JOHN E. WITCHER, MD DANIEL A. WITTERSHEIM, MD DUKE J. WOOD, DO KATHLEEN WOOD PATRICK BRIAN WOOD, MD JAMES W. WOODALL, JR., MD JAMES S. WOODARD, MD ANNA WOODSON, MD JAMES WOOTTON, III, MD CHRISTOPHER H. WYATT, MD BEN W. YARBROUGH, MD RYAN A. YATES, MD DOUGLAS L. YEAGER, MD WILLIAM E. YOE, MD JAMES A. YORK, MD D. RUSSELL YOUNG, MD RONALD A. YOUNG, MD

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318 VOL. 59 • NO. 6/7 • 2018

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I M A G E S

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ASHINGTON COUNTY GENERAL HOSPITAL, 1958 – Owned and operated by Washington County, Washington County General Hospital was one of the state’s first Hill-Burton facilities, with construction beginning in 1950 after funding was provided by the Mississippi Commission on Hospital Care. The hospital construction movement in the state, most especially the state’s embrace of the Hill-Burton Act (the Hospital Survey and Construction Act of 1946), would become the most forceful agent of racial transformation in the state, and hospitals became the first public places integrated. Despite the strong support of Southern white politicians (Hill was an Alabama Senator), facilities receiving Hill-Burton funding were not allowed to discriminate on the basis of race, color, national origin, or creed, although separate but equal facilities in the same hospital were allowed until 1963 when the U. S. Supreme Court finally struck down this aspect in Simkins v. Cone, which ended racial segregation at Mississippi and the nation’s hospitals. Vestiges of racism in hospital staffs would remain for a period, but the medical community largely ended segregation and discrimination within its hospital walls by the mid 1960s due to these significant financial incentives and requirements to receive federal monies. “The General” would open in 1953. The famous architect N. W. Overstreet and Associates, well-known for many medical facilities of the period including Whitfield, designed the structure. This postcard image, postmarked in 1958, expressed on its back that this facility was “thoroughly modern, handsome, commodious, beautifully equipped, and has a capacity of 200 beds, plus 35 bassinets.” The hospital also advertised loudly in that era of segregation that it “accommodates all races and creeds, without discrimination.” This hospital replaced the other hospitals, most especially King’s Daughters, which closed when “The General” opened. The facility is now known as Delta Regional Medical Center. If you have an old or even somewhat recent photograph or image which would be of interest to Mississippi physicians, please send it to me at lukelampton@cableone.net or by snail mail to the Journal. n

Lucius M. “Luke” Lampton, MD; JMSMA Editor

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Backing into the Future [This month, we print a delightful poem by John D. McEachin, MD, FAAP, a Meridian pediatrician and the Journal’s unofficial poet laureate. Written in 2008, this insightful poem, at this time of commencements, contemplates the future and ancient interpretations of it. Dr. McEachin writes: “In the spring, as we gather at graduation exercises of the various scholastic levels, I am often reminded that ‘commencement’ in its purest interpretation is a ‘beginning,’ and the future is approached by different routes. The ancient Hebrew philosophy of time, events, and the future is a mindset that continues today — even with geopolitical — and medical implications. As you read this little poem, you will note the influence of the ancient East, as well as the darkness of left and goodness of right. Left (North) becomes ‘sinister’ in the Latin Vulgate translation of the Bible. Examples of right (South, good): ‘Right hand of God......Goats on the Left, and Sheep on the Right.’ Right is always good in any translation of the Scriptures. Of medical and mental health significance, regardless of its origin, left was frowned upon for centuries as evil, sinister. Children with left-handed inclinations were often subjected to harsh mental and physical punishments if conversions were not forthcoming. Ophthalmology carries the stigma, if you will, in the designation of: left eye, OS-Sinister; right eye, ODDexter. (Both eyes, OU-Uterque—for completion sake!!) I suppose it’s a miracle that the ‘vena amoris’ (vein of love) continues even today in many cultures as the vein housed in the left hand’s fourth finger –the wedding ring finger!! Tradition has this vein connecting directly to the heart!!” For more of Dr. McEachin’s poetry, see past JMSMAs. Any physician is invited to submit poems for publication in the journal, attention: Dr. Lampton or email him at LukeLampton@cableone.net.]— Ed.

In the ancient Hebrew world The future was never ahead; Rather, always facing the East, It was backed into instead.

Backing into the unknown, while Facing historical antiquity Is a worthy template for today If we contemplate its gravity.

East represented antiquity, and Time and distance were as one; Well-defined in Biblical times, “Qedem,” East, housed the rising sun.

God alone knows our future So, our arm must reach behind; He will take our hand and lead us On the journey He has in mind!

Thus, South was always to the right And was designated “Yemen,” Just as Rachel’s son of the South Was Joseph’s sibling, Benjamin.

– John D. McEachin, MD Meridian

“Smo-al” was North and to the left Of one who faced the East; “Olam” represented a distance afar, Hidden beyond the West, at least!

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* Dr. Dennis Kinlaw, former President of Asbury College, Wilmore, Kentucky, gave a lecture on this material about 25 years ago. I have never forgotten the cultural and religious implications of this treatise. The Hebrew terms used may on some occasions be phonetic.

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Walking With the Black Dog DWALIA S. SOUTH, MD MSMA PAST PRESIDENT AND COMMITTEE ON PUBLICATIONS CHAIR

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omorrow I shall be leaving 62 behind and with that leaving, hopefully, will soon abandon the trail of tears wrought by my most recent annus horribilis.

Sixty-two is often a milestone year. A worker can begin to collect his Social Security at this age if so desired.

My first husband, Chard, was ecstatic at turning 62 to file for his benefits. I suggested that he wait three years so that he could draw the full amount. His comment, “Hell, I’m drawing it now; I’ll never see 65!” This statement proved prophetic. On July 3 of his 62nd year, his first Social Security check was direct deposited into the bank. The following day was, of course, a holiday, and on the morning of July 5, without warning, he died of a massive heart attack.

On my own 62nd birthday last year, I paused to remember my husband’s premature death and that particular annus horribilis. A few short days after this anniversary there soon unfolded a chain of events that have rocked my world both personally and professionally. Now, mind you, as a cancer survivor, it takes quite a bit of torque to pull the rug from under me. After crossing that dread chasm, life takes on new priorities and perspectives. While events of this past year don’t compare to losing a husband or being diagnosed with cancer, the angst it has caused ranks pretty high on the list of slings and arrows of outrageous fortune.

South

Where to start? The point of this missive is to convey a hint of the cruel and unnecessary pain of the heart and soul inflicted by the past twelve months. After careful consideration, I feel the information from my first draft is too explicit at this juncture to divulge in its entirety. So I will amend and compact this and perhaps end with some information that may prove helpful to physician readers should similar incidents befall them. Luke Lampton and I both agree that a book should be written about our mutual hellacious experiences of this past year as we have “walked with the black dog of depression.”

For the past 22 years, I have been an employed physician practicing Family Medicine in a Federally Qualified Health Center in rural northeast Mississippi. Our administration requires me and the other physicians in our 7 clinic system to precept 10 Family Nurse Practitioners who also practice in these 7 small towns. Although we have no influence on the hiring process, all of us are required to sign the protocols of every FNP they employ.

A couple of years ago the clinic administrator hired an NP who had had some problems with the Nursing Board and was only able to work under the constant oversight of a physician. I was assigned to be her preceptor.

In a concise and very inadequate nutshell, this nurse experienced some technical difficulty when it was discovered that she had written some very appropriate controlled prescriptions for approximately 60 patients before it was realized that her DEA certificate was inactive! Every one of those prescriptions was honored and her DEA authority unquestioned by at least 7 dispensing pharmacies in our area. The medicines were consumed by the patients, and their metabolites were flowing toward the Gulf of Mexico almost 2 years before her actions were ever called into question.

Our credentialing department and all the local pharmacies had written evidence that her DEA license was active until February 28, 2017.

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When this very bright and clinically adept NP suddenly realized that having written those controlled prescriptions in 2015 without my cosignature would likely prevent her from getting her unrestricted license back, both she and our administration begged me to intervene on her behalf. In retrospect, her response should have been to inform the Board of Nursing (BON) and the DEA about the misguided signing of the prescriptions and to throw herself on their mercy (if indeed either of those organizations possesses that quality). Instead, the requested option was to have me review the charts and to belatedly cosign my name below hers on the original prescriptions. Pharmacists sent original scripts back to my office for review and signature at her request.

I protested loudly that this would not do any good as the prescriptions were already on the PMP web site in her name, that history could not be rewritten, but fool that I am, I complied with the request. I co-signed those prescriptions written for our mutual patients after reviewing the charts with every employee in our clinic witnessing the event and also under the watchful eye of our recording security cameras. I did not then appreciate how that attempt to retroactively give my blessing to the actions of a trusted colleague constituted prescription “fraud and diversion” or in any way harmed our patients.

But, as we all know, no good deed seems to go unpunished these days.

As with most modern day primary care physicians, I have grown quite numb to giving my tacit approval to long ago events by signing my name to them. I scrawl my signature literally hundreds of times a day to documents attesting remote actions and prior treatments carried out on behalf of my patients by other health care providers (home health, nursing home, hospice, physical therapy, etc.). At that time and in this situation, I quite wrongly assumed that co-signing her prescriptions (which I was informed was my duty as her preceptor) would not be perceived any differently. After all, I had already been doing exactly that on her behalf for well over a year!

A Board of Nursing (BON) investigator and a DEA agent came to our clinic on May 9, 2017, to investigate our Nurse Practitioner and spent the entire afternoon in a merry chase. I continued to see patients and sometime after 5:00 pm, as they readied to leave our clinic, the DEA agent very cordially asked me to prepare a written statement about the situation and informed me that ‘they’ would be back in about one week to pick it up.

Congratulations to our physicians in the Class of 2018 Physician Leadership Academy.

Leaders for a healthier Mississippi.

LaToya Mason, MD Anesthesiology Shawn McKinney, MD Breast Surgery Tamara Glenn, MD Psychiatry Resident Michelle Owens, MD Obstetrics/Gynecology

But on the very next day, Wednesday, May 10, that same DEA agent contacted me and told me that because ‘they’ had a conflicting “big important meeting” coming up the next week that they would need to return the following day to pick up my statement. Fool that I am, and not realizing that ‘they’ would then be coming after me, I hurriedly prepared a written synopsis of what had occurred with our NP. I only learned months later that the NP had conveyed to the investigators that it was “Dr. South’s idea” to belatedly co-sign below her name on the prescriptions.

On the afternoon of Thursday, May 11, I blocked out time on my clinic schedule to meet with the DEA investigators. I should never have agreed to this meeting without the presence of counsel. How

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could I have been so naïve? They read my statement, scratched their heads a bit, and then informed me that our NP would be arrested and taken to jail in a few days. They told me she would be charged with ‘fraud and diversion’ and informed me that if I wished to avoid similar circumstances, publicity, federal charges, censure by the MSBML, and potentially years of legal wrangling, that I could very quietly simply surrender my DEA license for a one year period and all would be well. Remarks were made that I was being given preferential treatment because of my long years of past service to my profession, our state and because of my “clean record” throughout 37 years of medical practice.

I was blindsided and in complete shock that day. Fool that I am, I went to my file cabinet, retrieved my DEA certificate and surrendered it to them. In retrospect, I should have politely refused to meet with them or to do or sign anything without first consulting with a lawyer.

The following week our NP actually was arrested as promised. Immediately the new head of the Mississippi Bureau of Narcotics (MBN) and some top DEA folks held a news conference in Jackson announcing their actions of the prior week and shook their fingers at all prescribing healthcare providers across the state with threats that they would soon be coming after “all you drug pushers disguised in white coats.” This, in fact, was the “big important meeting” for which I provided the grist for their mill and became a trophy on their wall!

Then on Wednesday, May 17, their vitriol was spewed out to the general public via television, radio, and newspapers about their trophy witch hunt. A mug shot photo of our NP was published, with a horrible photo of me immediately adjacent to it, giving the distinct but false impression to viewers that I had also been arrested for criminal activities. (For the life of me I could not imagine where they obtained this awful scowling headshot to publish, no one had taken my picture! I later realized that they had used an image from my concealed firearms permit, something which I have carried since I was Tippah County Coroner many years ago.)

It is the understatement of the year to say that I was mortified by this misguided public humiliation and maltreatment. Only then did we turn for legal representation to clarify things, but the public cannot un-hear or un-see what has been so malignantly portrayed to them.

Giving up my DEA certificate for one year was the wrong thing to do. It has caused my patients to suffer, has cost both me and our clinic system significant income, and has required multiple days away from work to come to Jackson to clarify this before the Medical Licensure Board. I was forced to give up my practice taking care of my nursing home patients, and to resign as medical director of a Hospice due to the inability to care fully for the aged infirm and dying patients. I have only recently been informed that it was not kosher for me to precept any Practitioner in our office who DOES have controlled prescriptive authority. If one of my patients requires prescription medication for pain, anxiety, insomnia,

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testosterone replacement therapy or even pseudo-ephedrine for sinuses, I have to explain with embarrassment that I do not have privileges to write these meds and that I would have to ask a nurse practitioner to examine the patient and treat them appropriately as they deem fit. I have had to daily face the appearance of being a sanctioned criminal who is no longer a full-fledged physician. I have had to explain this deficit not only to patients but also to credentialing hospitals, third party payers, malpractice carriers and insurance companies repeatedly for the past year.

This crippling edict has proved to be the gift that just keeps on giving!

Thus, in the fall of 2017, I was required to come before the Executive Committee of the Medical Licensure Board to explain my situation. I was informed that this was necessary because of all the negative statewide publicity. After having served for several years on that same board, I know that the MSBML is almost totally complaint driven. Therefore, someone somewhere wanted my actions called into question. Their final judgment was that signing those prescriptions belatedly was “ill-advised” and no punitive action by the Board (other than great stress and expense) was incurred.

Briefly updating, on May 1, 2018, I filled out the form applying for a new DEA certificate as instructed and paid them another $731. So I guess I will sit back on my bull’s-eyed hindquarters and wait for this to materialize. (At the time of this revision, it has now been 13 and ½ months since I gave up my DEA certificate, and I seem to be no closer to being made a “whole physician” once again.)

I have been walking closely tailed by the ‘Black Dog’ called Depression for a year now. I am more than a little bitter about this whole messy “War on Opiates” which has ultimately become a “War on Physicians” and the suspiciously perfect storms to which Dr. Lampton and I have both been subjected. This “annus horribilis” has only been endured through God’s mercy, and the love and kindness of true friends, colleagues and that of my family which continues to grow by leaps and bounds.

Because the whole story is not yet complete, and you, dear reader, can only process so much at one sitting, the resolution and summary of the lessons learned are “to be continued…” in a future issue of this Journal MSMA. It is painful to reveal all these things to you, but it is my hope in doing so that my brothers and sisters in the field of medicine may benefit from it.

“We are troubled on every side, yet not distressed; we are perplexed, but not in despair; Persecuted, but not forsaken; cast down, but not destroyed.” 2 Corinthians 4:8-9 n

Dwalia S. South, MD Ripley

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