THE JOURNAL OF THE SOUTH DAKOTA STATE MEDICAL ASSOCIATION

Volume 70Number 8

August 2017

Volume 70 lNumber 8August 2017

The Journal of the South Dakota State Medical Association

ContentsPresident’s Comments339 Rational Health Care: Can it Happen? – Robert E. Van Demark, Jr., MD

Editorial341 Update on Medical School Accreditation – Keith Hansen, MD

The Journal342 Pharmacogenetics of PPIs: Lessons Learned – Chencheng Xie, MD;

Russell A. Wilke, MD, PhD

346 West Nile Review: 15 Years of Human Disease in South Dakota, 2002-2016 – Lon Kightlinger, MSPH, PhD

354 A Case of an Acute Myocardial Infarction Post Thrombolytic Treatment of Ischemic Stroke – A Management Dilemma – Kalyan Wagle, MD; Jimmy Yee, MD; Vishesh Kumar, MD; Amornpol Anuwatworn, MD; Tomasz Stys, MD; Adam Stys, MD; Christopher Stanton, MD

359 A Case of Incisional Endometrioma that Presented as an Abdominal Mass – Kelly Landeen, MS IV; Kristin Wempe, MD; Robert Miller, MD

363 Combined Melanocytic Nevus, Superficial Congenital and Deep Penetrating Types with Fibroepithelioma of Pinkus, Collision Tumor – A Case Report – Ashwyna Sunassee, MD; Amy M. Kerkvliet, MD; Ali D. Jassim, MD, PhD

366 Alkaptonuria: A Case Report With Diagnostic Challenge – Vasantha L. Gali, MD; Amy M. Kerkvliet, MD; Jacob M. Kusmak, MD, PharmD; Jana K. Elwood, PA

369 Laparoscopic Treatment of a Pyogenic Hepatic Abscess Caused by Transmural Duodenal Perforation of a Toothpick – Hassan Turaihi, MD; Jed Assam, MD; Justin Zanfes, MS IV; Thavam Thambi-Pillai, MD

Pharmacology Focus372 Differences in the Manifestation of Multiple Sclerosis in African American Patients

– Chamika Hawkins-Taylor, MHA, PhD

Extenuating Circumstances374 Data Sharing: Leading Data-Driven Population Health – Emily R. Griese, PhD;

Benson S. Hsu, MD, MBA, FAAP; David A. Pearce, PhD

Special Features376 Patient Education: Sports Injuries – Richard P. Holm, MD

377 Quality Focus: Encouraging and Communicating the Value of Immunization – Stephan D. Schroeder, MD

378 Board News – Margaret B. Hansen, PA-C, MPAS

380 SDSMA PAC Membership 2017

Member News381 For Your Benefit: Get Involved in the SDSMA

Legal Brief Highlight: Advanced Practice Nurses

Medical Students Hosting Third Annual Physician’s Cup Golf Tournament for Charity

382 AMA Delegate Report – 2017 Annual Meeting

383 Keep Your Information Up-to-Date: Log on Today

The Issue Is…CMS Raises Awareness of Chronic Care Management

Advertisers In This Issue384 Physician Directory

Office of Publication2600 W. 49th Street, Suite 200Sioux Falls, SD 57105605.336.1965Fax 605.274.3274www.sdsma.org

EditorKeith Hansen, MD

SDSMA PresidentRobert E. Van Demark, Jr., MD

Chief Executive OfficerBarbara A. Smith

SDSMA Vice PresidentMark East, MS

Staff Editor Elizabeth Reiss, MS–ereiss@sdsma.org, 605.336.1965

Advertising RepresentativeElizabeth Reiss, MS–ereiss@sdsma.org, 605.336.1965

South Dakota Medicine(ISSN 0038-3317)Published 12 times per year with one special issue by the South Dakota StateMedical Association.

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Cover photo by Robert Seidel, MD.

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339August 2017

President’s Comments

Rational Health Care: Can itHappen? By Rob e r t E . Van D ema r k , J r . , MD

SDSMA P r e s i d e n t

We have all been watching and waiting for sometype of movement on health care reform promised by the new administration. As of this

writing, the bill is being developed in the Senate. I recentlyread a thought-provoking essay on health care reformwritten by Dr. Joseph Zuckerman and Dr. Alex Jahangir.1Dr. Zuckerman is a past president of the AmericanAcademy of Orthopedic Surgeons and practices in NewYork City. The essay is entitled, “What’s Important:Rational Health-Care Reform.” I would like to share theirideas with you.

Over the past 100 years, attempts have been made by bothDemocrats and Republicans to develop some type of universal health coverage. Those attempts have includedsome common characteristics:1. Employer mandate;2. Individual mandate to share the risk of insurance;3. Cost sharing to provide individual responsibility;4. Defined benefits for “minimum” benefits;5. Subsidizing the poor for insurance coverage; and6. Employer tax deductibility for employee coverage.

The authors ask the question “whether health care is aright or a privilege.”

Entitlement or BenefitDrs. Zuckerman and Jahangir define an entitlement as “agovernment program that guarantees access to a benefitbased upon established rights or legislation.” SocialSecurity and Medicare are two examples of entitlementprograms. They ask the question “Is health care an entitlement or a benefit?” The authors feel that healthcare coverage in our country should be an entitlement forall, but it should be means-tested. There would be means-tested subsidies for the purchase of health coverage. Thiswould allow for a basic coverage package that could beexpanded by using your own resources.

For true health care reform, five important changes shouldbe done:1. Means Testing for MedicareCurrently, all Medicare patients receive the same benefits,regardless of their net worth. If means-testing was done,those with more financial resources would contributemore for their health care. This would also affect the overall cost curve of Medicare expenses.2. Increasing Individual Accountability for Good HealthHealthy lifestyle choices would be encouraged; patients

could be rewarded for not smoking, maintaining a normalweight and using preventive care options. This could beencouraged by lowering premiums or deductibles andlower co-insurance costs. Currently, many self-insuredcompanies do encourage this behavior. 3. Ensure that a Large Share of Insurance Revenue isSpent on Health CareThe Affordable Care Act (ACA) requires commercialinsurers to spend at least 80 percent of their premium revenues in clinical benefits for insured patient (“medicalloss ratio requirements”). This has translated into rebatesof $1 billion for policyholders in 2011 and 2012.4. Medical Liability ReformUnfortunately, the ACA did not address medical liability.The estimated yearly cost of defensive medicine in orthopedic surgery alone is $2 billion. In 2010, the annual cost of the U.S. medical liability system, includingdefensive medicine, was $55.6 billion. Medical liabilityreform would decrease the cost of care and practiceexpenses (the average liability premium for an orthopedicsurgeon is $34,920).5. Restructuring the Costs of Medical School EducationWe all know of the nationwide shortage of primary carephysicians. In 2014, medical school debt averaged$176,348 per graduate. This is one of the reasons that stu-dents don’t choose the lower paid primary care specialties.Without access to primary care providers, patients will usemore expensive sources of care (i.e., emergency depart-ments). One alternative would be free tuition for medicalstudents attending a U.S. medical school. Following completion of their training, the physicians would serve inan underserved area for a period of time. The averageannual tuition for medical school is $44,000. The yearlycost of tuition free education for 20,000 medical studentswould be less than $1 billion per year, which is less than0.2 percent of the 2014 annual Medicare outlay.

ConclusionUniversal coverage is both a moral and ethical approachin a country known for taking care of its citizens. Toaccomplish this, all key players in the health-care deliverysystem, including patients, will need to compromise andinnovate. Time will determine if this goal can be achieved.

REFERENCES1. Zuckerman JD, Jahangir AA. What’s important: rational health care reform.

J Bone and Joint Surg. 2017;99:613-5.

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341August 2017

Busy clinicians throughout South Dakota spend littletime thinking about their early years of medicaleducation and how their medical school prepared

them for practice. As one of those charged to ensure thatour medical school, the University of South DakotaSanford School of Medicine (SSOM), produces good doctors, I oversee the school’s maintenance of accreditation.This brief communication is an update on the school’supcoming LCME accreditation visit.

Why accreditation? The short answer is medical schoolsneed to be accredited in order for their graduates to enteraccredited residency programs, and the goal of accreditationis to ensure that the education provided by a medicalschool meets acceptable levels of quality.

What is accreditation? Medical schools in the U.S. andCanada are accredited by the Liaison Committee onMedical Education (LCME). The process of accreditationoccurs every eight years – more often for new schools orschools with quality issues. It begins with a year-long self-study, includes the writing of numerous documents,and ends with a site visit. Schools are measured against aset of 12 standards, each of which contains a list of elements. Wherever a deficiency is identified schools arecited for that element as “unsatisfactory” or “satisfactoryrequiring monitoring.” The site visit team writes up itsfindings in a report and submits it to the LCME, whichrenders the ultimate decision about accreditation or continuing accreditation for the school. SSOM has maintained full accreditation throughout its history.SSOM has maintained its accreditation due to the hardwork, enthusiasm, and dedication of our faculty members,both basic science and clinicians. Our faculty is a diversegroup of individuals throughout the state of South Dakotawho volunteer their busy time to educate our students.

Who does accreditation? The school site visits are done byan ad hoc team of independent peers who volunteer theirtime to come from similar roles at other schools. The decision-making LCME is similarly an appointed committee of medical school deans and associate deanswho meet three times yearly to review reports on schools.The late Dr. Robert Talley served and I am currently serving on this committee.

When is our accreditation? Our site visit is scheduled forSept. 24-28, 2017. Following a Sunday evening meetingwith Dean Mary Nettleman, the team will be visiting several of our campuses and sites over several days to meetwith faculty and students. The final decision will be rendered in February 2018.

Overall, this substantial process serves the school and itsstudents by assuring an excellent education program.

Editorial

Update on Medical SchoolAccreditation By J a n e t L i n d emann , MD , MBA

About the Author:Janet Lindemann, MD, MBA, Dean, Medical Student Education & FacultyAccreditation Lead, University of South Dakota Sanford School of Medicine; Chair,Liaison Committee on Medical Education.

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Pharmacogenetics of PPIs: Lessons Learned By Chencheng X i e , MD ; and Ru s s e l l A . Wi l k e , MD , PhD

IntroductionIn January 2017, South Dakota Medicine launched a seriesof monthly articles exploring the field of pharmacogenetics.In the first manuscript of this series, Drs. Larson andMiller reviewed the advantages and disadvantages ofCYP2C19 genotyping for patients taking clopidogrel.1

Because this same enzyme, CYP2C19, also metabolizesnearly 10 percent of all prescription medications, Drs. Petryand Hines recently followed with a manuscript discussingthe clinical impact of CYP2C19 gene variants on a secondclass of drugs, the SSRIs.2 This principle – that geneticvariation in one enzyme influences clinical outcome formore than one class of drugs – represents an importantprinciple in pharmacogenetics. CYP2C19 also metabolizesproton pump inhibitors (PPIs), one of the most widelyprescribed classes of medications in the entire world. Wetherefore now discuss the impact of CYP2C19 gene variants on three clinical outcomes for the PPIs: 1) H.Pylori eradication rates, 2) gastroesophageal refluxdisease, and 3) cancer risk.

LandscapeThe field of pharmacogenetics is rapidly advancing. Genesinfluencing drug response fall into two categories: pharma-codynamic (PD) genes and pharmacokinetic (PK) genes.While PD genes are known to influence a drug’s mechanism of action (encoding receptors, G-proteins, ionchannels, and other signal transduction proteins), PKgenes influence the tissue distribution of drugs and theirmetabolites (encoding proteins like uptake transporters,efflux transporters, and drug metabolizing enzymes).3 Overthe past decade, genetic variation in the cytochromesP450 (CYP enzymes) has been shown to alter clinical outcome for a variety of commonly used drugs.

Four CYP enzymes are responsible for the hepatic oxidation of the large majority of prescription drugs:CYP2C9 metabolizes 15-20 percent of all prescriptiondrugs, CYP2C19 metabolizes 5-10 percent of all prescriptiondrugs, CYP2D6 metabolizes approximately 25 percent of

all prescription drugs, and CYP3A4 metabolizes approxi-mately 40 percent of all prescription drugs.3 Because genevariants are relatively common for the first three of theseenzymes (CYP2C9, CYP2C19, and CYP2D6), SouthDakota Medicine has regularly reviewed the impact ofgenetic variability in these enzymes on a number of important prescription drugs throughout the year. Forexample, Drs. Larson and Miller reviewed the clinicalimpact of genetic variability in CYP2C19 on outcomesrelated to the use of clopidogrel in January.1

The CYP2C19 gene encodes an enzyme that activatesclopidogrel in vivo, and loss of function places patients atrisk for therapeutic failure. Because CYP2C19 gene variants are quite common in the general population, thisdrug-gene relationship is clinically actionable.4,5 Althougheach patient inherits two copies of CYP2C19 (one fromtheir mother, and one from their father), a single abnormal copy of the CYP2C19 gene is enough to lead totherapeutic failure for clopidogrel. Patients with oneabnormal copy of the CYP2C19 gene have a threefoldincrease in risk for coronary artery stent thrombosis onclopidogrel after PCI (compared to patients with two normal copies of CYP2C19 given the same medication).6

This drug-gene interaction (DGI) is consistent with our current knowledge about drug-drug interaction (DDI).When patients on copidogrel are given another CYP2C19substrate (e.g., a proton pump inhibitor), even a modestreduction in the enzymatic bioactivation of clopidogrel isassociated with a measurable increase in risk for majoradverse cardiovascular events [O.R.=1.42, 95 percent C.I.1.30-1.55].7 Interestingly, this effect size is greater for some CYP2C19 substrates (omeprazole) than others(rabeprazole).7

GI OutcomesAlthough the frequency of CYP2C19 gene variants variesby geographic race, loss of function variants are fairly common in all populations tested to date: nearly one infive patients of European ancestry has an abnormal copy

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of the CYP2C19 gene, as do one in four patients ofAfrican ancestry and one in three patients of Asian ancestry.8 Because these gene variants are so common, andbecause CYP2C19 metabolizes nearly 10 percent of allprescription drugs, medical centers in South Dakota havestarted deploying automated decision support for somedrugs metabolized by CYP2C19.9,10 While published guidelines are available for antiplatelet agents5, no suchguideline exists for the proton pump inhibitors (PPIs). YetPPIs are among the most commonly prescribed drugsmetabolized by this enzyme.

It is clear that CYP2C19 loss of function variants are associated with PPI efficacy in the context of mucosalulcers within A) the esophagus, B) the stomach, and C)the duodenum. It is also clear that CYP2C19 genotypeinfluences H. Pylori eradication rates based on biopsyand/or breath test. A seminal study published two decadesago by Furuta and colleagues11 showed that H. Pylorieradication rates on combination therapy with omeprazoleand amoxicillin were strongly influenced by CYP2C19genotype (29 percent cure rate in patients with two functional copies of the gene, 60 percent cure rate inpatients with one loss of function copy, and 100 percentcure rate in patients with two loss of function copies).Paradoxically, for this class of drugs, CYP2C19 loss offunction is actually associated with better clinical outcome,because patients who metabolize PPIs poorly have highercirculating levels of these drugs and greater gastric acidsuppression.

Although CYP2C19 metabolizes all drugs within thisclass, the impact of CYP2C19 genotype varies becauseeach PPI is metabolized to a greater or lesser degree byother CYP enzymes as well (e.g., CYP3A4).Correspondingly, CYP2C19 genotype appears to impactoutcome for omeprazole and lansoprazole more stronglythan it impacts outcome for esomeprazole or rabeprazole.12

Nonetheless, a CYP2C19 genotype effect can still beobserved in patients taking esomeprazole. In 2015, Saitoand colleagues reported that H. Pylori eradication rates ontriple therapy (esomeprazole plus amoxicillin and clar-ithromycin) were also influenced by CYP2C19 genotype(52 percent cure rate in patients with two functionalcopies of the gene, 72 percent cure rate in patients withone loss of function copy, and 85 percent cure rate inpatients with two loss of function copies).13 Interestingly,H. Pylori eradication rates were still statistically higherwhen patients with one loss of function copy and two lossof function copies were grouped together.13 This drug-gene

relationship may therefore be actionable in carriers (i.e.,even in heterozygotes).

As noted, the impact of CYP2C19 on PPI efficacy is notlimited to H. pylori eradication and mucosal ulcers in thestomach and the duodenum. CYP2C19 genotype alsoinfluences the degree to which PPIs can attenuate clinicalsigns and symptoms attributable to gastroesophageal refluxdisease (GERD). In a large meta-analysis,14 investigatorsin Japan recently observed a CYP2C19 genotype effect onthe resolution of reflux esophagitis and non-erosive refluxdisease – across 15 separate study populations – despitepatients being exposed to different doses of different PPIs.Extensive metabolizers (patients with two functionalcopies of CYP2C19) have a higher risk of being refractoryto PPI therapy than poor metabolizers [O.R. = 1.66, 95%CI. 1.02-2.66].14 While the impact of CYP2C19 genotypeon the healing rate for Barrett’s esophagus remains lessclear, emerging data show an association betweenCYP2C19 genotype and risk of esophageal cancer.15

Given the importance of this class of drugs, and theweight of the evidence, it is surprising that a gene-baseddosing guideline has not yet been published for the PPIs.While genetic differences in CYP2C19 activity varyaccording to race, these gene variants are found in all pop-ulations. Genetic information is therefore now includedon the drug label (i.e., within the package insert) for allPPIs. The U.S. Food and Drug Administration (FDA)guidance for omeprazole is shown in the box.

Future OutlookThe FDA currently requires genetic information in thelabels (package inserts) for almost 200 prescription med-ications. The Clinical Pharmacogenetics ImplementationConsortium (CPIC) publishes guidelines to help clinicians

Box 1. FDA Label Guidance Based on Genotype

“The systemic exposure to omeprazole varies with a patient’smetabolism status: poor metabolizers > intermediate metabolizers> extensive metabolizers.”

[Poor metabolizer = 2 abnormal copies of CYP2C19]

[Intermediate metabolizer = 1 abnormal copy]

[Extensive metabolizer = 0 abnormal copies]

“Approximately 3% of Caucasians and 15 to 20% of Asians areCYP2C19 poor metabolizers [2 abnormal copies of CYP2C19]. In a pharmacokinetic study of single 20 mg omeprazole dose, theAUC of omeprazole in Asian subjects was approximately four-fold of that in Caucasians.”

U.S. FDA. Table of pharmacogenomic biomarkers in drug labeling.www.fda.gov/Drugs/ScienceResearch/ResearchAreas/Pharmacogenetics/ucm083378.htm.

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use genetic information to dose dozens of medications.

Several of these guidelines outline decision support for clinicians to act on CYP2C19 gene variants in the contextof antiplatelet agents or antidepressants. However, they donot specify when patients should be genotyped, and theydo not provide decision support for additional drugsmetabolized by this enzyme, like the PPIs. Because genevariants in CYP2C19 are very common in the generalpopulation, and because they clearly impact clinical out-come for the PPIs, efforts are needed to deploy automatedbest practice advisories (BPAs) for this important class ofdrugs.

Key unanswered questions include the following: Shouldwe use genotype to select which PPI (omeprazole isimpacted more than rabeprazole)? Or should we simplyuse genotype to adjust the dose? Prospective longitudinalstudies are also needed to quantify the magnitude of eventreduction (e.g., Barrett’s esophagus, and cancer) whengene-based drug dosing is utilized.

Acknowledgments: The authors would like to thank Toni LeVasseur for assistance with the preparation of this manuscript, and Wenjie Jessie Lu, PhD,for helpful comments regarding FDA label changes.

This work was funded by National Institutes of Health (1U01HG007253)and through a generous gift from T. Denny Sanford that created Imagenetics(merging Internal Medicine and Genetics).

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Don’t forget to send in your favorite scenic photo for

South Dakota Medicine front cover consideration. Send photos to ereiss@sdsma.org.

REFERENCES1. Larson EA and Miller NJ. Point-counterpoint: CYP2C19 genotyping for clopidogrel.

South Dakota Medicine. 2017;70(1):13-5.2. Petry N and Hines L. Point-counterpoint: Gene-based prescribing for SSRIs. South

Dakota Medicine. 2017;70(6):246-8. 3. Wilke RA, Reif DM, Moore JH. Combinatorial pharmacogenetics. Nature Reviews

Drug Discovery. 2005;4(11): 911-8. 4. Scott SA, Sangkuhl K, Gardner EE, Stein CM, Hulot JS, Johnson JA, et al. Clinical

Pharmacogenetics Implementation Consortium guidelines for cytochrome P450-2C19 (CYP2C19) genotype and clopidogrel therapy. Clinical Pharmacology andTherapeutic. 2011;90(2): 328-32.

5. Scott SA, Sangkuhl K, Stein CM, Hulot JS, Mega JL, Roden DM, et al. ClinicalPharmacogenetics Implementation Consortium guidelines for CYP2C19 genotypeand clopidogrel therapy: 2013 update. Clinical Pharmacology and Therapeutics.2013;94(3):317-23.

6. Mega JL, Close SL, Wiviott SD, Shen L, Hockett RD, Brandt JT, et al. CytochromeP-450 polymorphisms and response to clopidogrel. New England Journal ofMedicine. 2009;360(4):354-62.

7. Niu, Q, Wang Z, Zhang Y, Wang J, Zhang P, Wang C, Yin X, Hou Y. Combinationuse of clopidogrel and proton pump inhibitors increases major adverse cardiovas-cular events in patients with coronary artery disease: a meta-analysis. Journal ofCardiovascular Pharmacology and Therapeutics. 2017;22(2):142-52.

8. Man M, Farmen M, Dumaual C, Teng CH, Moser B, Irie S, Noh GJ, Njau R, CloseS, Wise S, Hockett R. Genetic variation in metabolizing enzyme and transportergenes: comprehensive assessment in 3 major East Asian subpopulations withcomparison to Caucasians and Africans. Journal of Clinical Pharmacology.2010;50(8):929-40.

9. Weitzel KW, Elsey AR, Langaee TY, Burkley B, Nessl DR, Obeng AO, Staley BJ,Dong HJ, Allan RW, Liu JF, Cooper-Dehoff RM, Anderson RD, Conlon M, Clare-Salzler MJ, Nelson DR, Johnson JA. Clinical pharmacogenetics implementation:approaches, successes and challenges. American Journal of Medical Genetics (C)Seminars in Medical Genetics. 2014;166C(1):56-67.

10. Oberg V, Hines L, Differding J, Fisher M, Wilke RA. Navigating pleiotropy in precision medicine: pharmacogenes from trauma to behavioral health.Pharmacogenomics. 2016;17(5):499-505.

11. Furuta T, Ohashi K, Kamata T, Takashima M, Kosuge K, Kawasaki T, Hanai H,Kubota T, Ishizaki T, Kaneko E. Effect of genetic differences in omeprazole metabolism on cure rates for Helicobacter pylori infection and peptic ulcer. Annals of Internal Medicine. 1998;129(12):1027-30.

12. Kuo CH, Lu CY, Shih HY, Liu CJ, Wu MC, Hu HM, Hsu WH, et al. CYP2C19 polymorphism influences Helicobacter pylori eradication. World Journal ofGastroenterology. 2014;20(43):16029-36.

13. Saito Y, Serizawa H, Kato Y, Nakano M, Nakamura M, Saito H, Suzuki H, Kanai T.First-line eradication for Helicobacter pylori-positive gastritis by esomeprazole-based triple therapy is influenced by CYP2C19 genotype. World Journal ofGastroenterology. 2015;21(48): 13548-54.

14. Ichikawa H, Sugimoto M, Sugimoto K, Andoh A, Furuta T. Rapid metabolizer genotype of CYP2C19 is a risk factor of being refractory to proton pump inhibitortherapy for reflux esophagitis. Journal of Gastroenterology and Hepatology.2016;31(4):716-26.

15. Wang H, Song K, Chen Z, Yu Y. Poor metabolizers at the cytochrome P450 2C19locus are at increased risk of developing cancer in Asian populations. PublicLibrary of Science PLoS One. 2013;8(8):e73126.

About the Authors:Chencheng Xie, MD, Department of Internal Medicine, University of South Dakota Sanford School of Medicine.Russell A. Wilke, MD, PhD, Department of Internal Medicine, University of South Dakota Sanford School of Medicine.

In 2002 an African arbovirus emerged in South Dakota.During the subsequent 15 years, 2,359 South Dakotanshave been reported with West Nile disease, including

745 hospitalized and 38 deaths. There have also been 206donated blood units discarded due to contamination withWest Nile virus (WNV) in South Dakota. Assumedly,tens of thousands of other unreported South Dakotanshave also been infected.

WNV is a mosquito-borne flavivirus first described inUganda, East Africa, in 1937.1 Sixty-two years later thevirus was first detected in the Western Hemisphere duringthe summer of 1999 in New York.2 During the next threeyears, WNV swarmed across North America, reachingSouth Dakota in 2002. South Dakota’s first WNV detection was in a Brown County crow on July 22, 2002,followed by a human case onset on July 23, 2002. SouthDakota’s first WNV death was the following year in July2003. By 2006 WNV had spread to all contiguous 48United States and four Canadian provinces. WNV is nowenzootic in most of temperate North America and isexpected to persist as a public health threat to SouthDakota into the foreseeable future.

The primary vector of WNV in South Dakota is the night-biting Culex tarsalis mosquito.3 Although birds are the primary reservoir of WNV, humans are among the incidental mammalian hosts. Human infection is generally

asymptomatic or mild, with approximately 20 percent ofhuman WNV infections provoking acute self-limitedfebrile illness (non-neuroinvasive) characterized by fever,headache, fatigue and myalgia, and less than 1 percent ofpatients developing more severe neuroinvasive disease(NID) syndromes including meningitis, encephalitis andacute flaccid paralysis or poliomyelitis.4 Long-term seque-lae include cognitive lapses, functional difficulties andneurologic dysfunction.5 Approximately 9 percent ofWNV-NID cases are fatal. WNV neuroinvasive and non-neuroinvasive cases are mandatory reportable diseaseevents in South Dakota and the U.S.

Since 1999 there have been 45,975 human WNV diseasecases and 2,005 WNV-associated deaths reported in theU.S. (Table 1). In South Dakota 2,359 human WNV disease cases, including 509 WNV-NID cases and 38WNV-associated deaths, have been reported since 2002when the virus was first detected in the state. The peakepidemic year in South Dakota was 2003 when 1,039human WNV cases and 14 deaths were reported, accountingfor 44 percent of all cases and 37 percent of South Dakotadeaths historically. The fewest WNV cases were reportedin 2011 (n=2).

South Dakota has experienced a disproportionate WNVmorbidity and mortality burden with 0.3 percent of theU.S.’ population, but 2.1 percent of the WNV neuroinvasive

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West Nile Review: 15 Years of Human Disease inSouth Dakota, 2002-2016 By Lon K i gh t l i n g e r, MSPH , PhD

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AbstractDuring the past 15 years, 2002-2016, West Nile virus (WNV) has emerged in South Dakota resulting in 509neuroinvasive disease (NID) cases, 745 hospitalizations and 38 deaths. Culex tarsalis is the state’s primary mosquito vector. South Dakota’s average annual incidence of WNV-NID and death rate are the highest of anystate in the U.S. WNV cases have been reported from all counties in the state. All age groups have been infectedwith cases peaking in the 40-44 year age group, but deaths peaking in cases 70 years and older. Although SouthDakota’s WNV season lasts six months, May-October, the first week of August has been the peak week of WNVdisease onsets. West Nile is now enzootic in South Dakota. Every citizen, local mosquito control programs, medical and public health infrastructures must continue to prevent and respond to annual WNV outbreaks, andprepare for the next arboviral disease to emerge.

cases and 1.9 percent of deaths. The annualized incidencefor WNV-NID in the U.S. has been 0.4 cases per 100,000population per year (Table 2). Upper Great Plains stateshave had the highest average annual incidence of WNV-NID. The five highest WNV-NID incidence statesinclude South Dakota 3.1, North Dakota 2.6, Nebraska1.8, Wyoming 1.6 and Colorado 1.3 cases per 100,000population per year. The high rate of WNV-NID is graph-ically evident in the national incidence map showingcounty-level incidence (Figure 1).6 The dark swath of highincidence counties runs from north Texas up the GreatPlains concentrating in the Dakotas and Nebraska. Theannualized incidence for total WNV cases (neuroinvasiveand non-neuroinvasive) also ranks South Dakota with thehighest incidence in the country, 15.1 cases per 100,000population per year, and the other above-mentioned statesalso ranking as top incidence states. The overall nationalWNV death rate (non-annualized) was 0.62 deaths per100,000 population from 1999 to 2016. South Dakota hashad the highest WNV death rate with 3.93 deaths per100,000 during those years. Other states with high WNV

death rates again include our neighboring states Nebraska,Wyoming and North Dakota.

Human WNV cases have been reported in all 66 SouthDakota counties and in at least 320 communities over the15 years (Figure 2 and Table 3). Counties with the highestincidence of WNV illness include Marshall 74.5 cases per100,000 per year, Sanborn 67.9, Potter 63, Sully 58.3 andPerkins 58.1; whereas counties with the most cases reported are among the state’s most populated counties,Brown 292 cases, Pennington 197, Minnehaha 150,Hughes 87 and Davison 85 cases. Counties with the lowest WNV annualized incidence include Union 8.8,Yankton 8.3, Lincoln 7.4, Minnehaha 5.9 and Custer 5.7cases per 100,000 population per year.

People of all races, sexes and ages have been infected andsickened by WNV in South Dakota. South Dakota maleshave been disproportionately affected by WNV with 56percent of the 2,359 WNV cases having been male and 44percent female. Race stratification shows WNV diseaserates at 90.5 percent White, 8 percent American Indian,

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Table 1. West Nile virus human cases, United States and South Dakota, 1999-2016:** WNV Neuroinvasive cases (NID), NID rate,* WNV non-NID cases, WNV-associated deaths and viremic blood donors.

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0.4 percent other race, and 1.1 percentunknown race, which is proportionately similarto the state’s population race percentages. Theelderly are at highest risk of developing WNV-NID disease. The median age of South DakotaWNV-NID cases was 52 years, while the WNVnon-neuroinvasive case median age was 44years, and the death median age was 80 years.Both case numbers and incidence peaked in the40-44 year age group (Figure 3). However, 24percent of NID cases and 85 percent of deathswere among individuals 70 years of age andolder.

The WNV human disease season runs fromMay to October in South Dakota (Figure 4).The peak week of illness onset has been duringthe second week of August; however, if the2003 WNV epidemic cases are removed, theremaining year’s cases peak during the firstweek of August. The most case onsets during asingle week were during the second week ofAugust during the 2003 epidemic with 213cases. During the other years the most caseonsets were during the first week of August2012 (n=49). Ninety percent of SouthDakota’s human WNV cases occurred duringthe nine-week period from the second week ofJuly through the second week of September.South Dakota’s six-month WNV season startswith 0.4 percent of patient illness onsets duringthe month of May, 2.0 percent in June, 19.7percent in July, 59.8 percent in August, 17.4percent in September and 0.7 percent of illnessonsets during October. Since the infectiousmosquito bite occurs two days to two weeksprior to onset of disease symptoms, mosquitocontrol and bite prevention should take placebefore and during the peak disease onset periods.

Over the past 15 years, human WNV infectionhas caused extensive disease and death inSouth Dakota and is likely to threaten the public’s health into the future. South Dakotahealth care providers should be alert forpatients with WNV neuroinvasive and non-neuroinvasive symptoms, use appropriate laboratory testing, and report cases to theSouth Dakota Department of Health. No

Table 2. West Nile virus neuroinvasive disease (NID), total cases, deathsand rates reported to CDC, 1999-2015 (rates calculated with 2010 census).

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Table 3. Human WNV cases and annualized incidence (cases per 100,000 population per year) in South Dakota counties, 2002-2016.

Figure 1. Average annual incidence of West Nile virus neuroinvasive disease reported to CDC by county, 1999-2015.

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WNV vaccine is available. City, tribal and county officialsshould assure appropriate mosquito control for their communities, and all citizens should protect themselvesand their families from mosquito bites.7 The unpredictedemergence of WNV in South Dakota demonstrates thatan exotic, tropical virus can become enzootic in a temperate

Great Plains state. We must stand prepared to detect andcombat other mosquito and tick transmitted diseases, suchas Zika, St. Louis encephalitis and Ross River fever, bymaintaining local mosquito control competence, insectsurveillance, climate monitoring and laboratory testingcapacity.

Figure 2. Distribution of human West Nile cases, South Dakota 2002-2016. Each dot represents one case

randomly distributed within counties.

Figure 3. West Nile human cases and deaths by five-year age groups, South Dakota 2002-2016.

Figure 4. West Nile human cases by week of WNV season, South Dakota 2002-2016.

REFERENCES

1. Smithburn KC, Hughes TP, Burke AW, Paul JH. A neurotropic virus Isolated fromthe blood of a native of Uganda. American Journal of Tropical Medicine.1940;20:471-2.

2. CDC. Outbreak of West Nile-like viral encephalitis – New York, 1999. MMWR. 1October 2016; 48:845-8.

3. Hildreth MB, Hoffman R, Carlson C, Beyer R, Rounds A, Gotland R, Wulf C,Schaeffer J, McKenzie M, Weyrich L, Kightlinger L. West Nile virus surveillance inmosquitoes from South Dakota during the 2003 through 2005 transmission sea-sons. National Conference on West Nile Virus in the United States, San Francisco,CA February 23-24, 2006.

4. Hayes E, Sejvar J, Zaki S, Lanciotti R, Bode A, Campbell G. Virology, pathology,and clinical manifestations of West Nile virus disease. Emerging InfectiousDiseases. 2005;11:1174-9.

5. Sejvar J. Clinical manifestations and outcomes of West Nile virus infection.Viruses. 2014;6:606-23.

6. CDC. Retrieved from www.cdc.gov/westnile/resources/pdfs/data/7-wnv-neuro-incidence-by-county-map_1999-2015_07072016.pdf.

7. CDC. 2013. West Nile virus in the United States: guidelines for surveillance, pre-vention, and control, 4th revision. Retrieved fromwww.cdc.gov/westnile/resources/pdfs/wnvguidelines.pdf.

About the Author:Lon Kightlinger, MSPH, PhD, State Epidemiologist, South Dakota Department of Health

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A Case of an Acute Myocardial Infarction PostThrombolytic Treatment of Ischemic Stroke –A Management Dilemma By Ka l y an Wag l e , MD ; J immy Ye e , MD ; Vi s h e sh Kuma r, MD ;

Amo rnpo l Anuwa two rn , MD ; Toma s z S t y s , MD ; Adam S t y s , MD ; and Ch r i s t o phe r S t an t on , MD

AbstractAcute ischemic stroke and myocardial infarction are emergency clinical events that require prompt intervention. Concurrent occurrence of both events magnifies the complexity of the clinical management. We present a case of a patient who presented with acute ischemic stroke, complicated by acute myocardialinfarction shortly after thrombolytic was administered. This case highlights the importance of individualizationof management especially in complex cases where there are no clear specific guidelines to follow.

IntroductionConcurrent incidence of acute ischemic stroke and acutemyocardial infarction are relatively common.Approximately 9 percent of patients presenting with acuteischemic stroke have a myocardial infarction at the sametime or within a few days following the event.1

Atherosclerosis is a global phenomenon affecting majorarterial system including cerebral vascular system, coronaryarteries, and carotid arteries. Simultaneous occurrence ofischemic stroke and myocardial infarction are inherentlylinked by the same pathogenesis of atherosclerosis.However, presentation of acute myocardial infarction postthrombolytic treatment of an acute ischemic stroke is anuncommon presentation as thrombolytic treatment is oneof the management modalities in the treatment of acutemyocardial infarction when timely percutaneous coronaryintervention is not feasible. This manuscript will highlightthe importance of individualization of care in an atypicalpresentation. Taking into account current guidelines ofacute coronary syndrome and acute ischemic stroke, ourgoals were to determine the clinical course of action thatwill give our patient the best chance of favorable clinicaloutcome in the absence of specific guidelines.

Case PresentationA 68-year-old male with a past medical history of uncontrolled diabetes, hypertension, and obesity presented

to the emergency department with sudden onset of slurredspeech and right facial droop. The initial diagnosis was anacute ischemic stroke. Computed tomography (CT) of thehead and CT angiography of the head and neck did notreveal any intracranial hemorrhage. Tissue plasminogenactivator (TPA) was administered as the window of presentation was within the allotted 4.5 hours since theonset of symptoms. Dysarthria improved slightly there-after, but persisted. The patient was admitted to the neurology critical care unit for further observation.Electrocardiogram (EKG) repeated two hours after theonset of thrombolytic therapy revealed 1 mm ST elevationin the inferior leads (II, III, aVF). This was a new findingcompared to baseline, suggestive of acute early infarction(Figure 1). The patient was asymptomatic without anyprior history of cardiac disease and did not have any cardiac complaints of chest pain or chest pressure. Initialtroponin at the time of admission was within normal limits. Subsequent troponin was 0.03 ng/mL (normal isless than 0.02 ng/mL) three hours later, and 0.10 ng/mLsix hours later. Echocardiography (ECHO) revealedreduced left ventricular ejection fraction of 40-45 percentwith a large area of apical akinesis suggestive of stress cardiomyopathy (Figure 2). Due to the lack of cardiacsymptoms and presentation of acute ischemic stroke withthrombolytic therapy administered, the decision was totreat conservatively without early invasive angiography

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given the high likelihood of stress cardiomyopathy.Antiplatelet and anticoagulant therapies were held due torecently administered thrombolytic therapy and concernof possible hemorrhagic transformation of acute ischemicstroke. Troponin continued to trend upwards andincreased to 2.09 ng/mL approximately since hours since

initial presentation. The patient continued to remainasymptomatic from a cardiac perspective. Repeat EKGafter eight hours showed resolution of the inferior ST elevation. Magnetic resonance imaging (MRI) of thebrain revealed a 2.5 cm acute infarct in the left frontalparietal region.

Figure 1. A) Baseline EKG prior to thrombolytic revealing Q waves in the inferior leads suggesting prior inferior infarct. B) EKG approximately two hours after thrombolytic revealing acute ST elevation in inferior leads (II, III, aVF) with minimal

reciprocal changes.

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After discussion with the neurology team, they felt that itwas permissible to start intravenous heparin drip 24 hourspost thrombolytic administration. At this time, thepatient was being treated for non ST-elevation myocardialinfarction (NSTEMI). In addition to intravenous heparin,a full dose aspirin was given, but clopidogrel was held dueto a possibility that the patient may need coronary artery

bypass surgery and the patient being considered a high riskfor intra-cerebral hemorrhage. Troponin peaked at 12.73ng/mL on the third day since admission, and the decisionwas to proceed with coronary angiography to evaluate forcoronary artery disease. Coronary angiography showed athrombotic total occlusion of the postero-lateral branch ofthe left circumflex artery. There was a chronic total

Figure 2. A) End diastole. B) End systole revealing apical lateral, apical and apical septum akinesis.

Figure 3. A) Dominant left circumflex supplying left posterolateral branch with an abrupt thrombotic occlusion (star). The left anterior descending (LAD) artery is chronically occluded. B) Right coronary arteriogram revealing non dominant right

coronary artery with distal 100 percent occlusion and right to left collaterals supplying the LAD artery.

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occlusion of the proximal left anterior descending artery,99 percent occlusion of mid right coronary artery with 100percent occlusion of the distal right coronary artery, whichappeared to be chronically occluded. Balloon angioplastywas performed on the posterolateral branch of the left circumflex with suboptimal result. A coronary stent wasnot placed due to the small caliber of the vessel andextremely small distal runoff disease. Cardiac thallium viability scan showed myocardial infarction in the mid,apical, apex and inferior region involving the septum thathad minimal or no viability. Cardiothoracic surgery wasconsulted for possible coronary artery bypass surgery forhis coronary artery disease. Due to undetected viability onthe cardiac thallium viability test, the patient was deemedto be a poor surgical candidate for coronary artery bypasssurgery at this time. The patient had significant improve-ment in neurological deficit and was discharged home instable condition and on optimal medical therapy (betablockers, statins, angiotensin converting enzymeinhibitor, and aspirin). Clopidogrel was started one monthlater as outpatient due to concerns of intracranial bleeding.The patient continues to do well from a cardiac perspective during his one month follow up after discharge, and no further plan for revascularization wasindicated.

DiscussionThe occurrence of two major vascular events simultaneously,(i.e., acute ischemic stroke and acute myocardial infarction)carries a worse prognosis than with either alone.Treatment modality of one entity could be a relative contraindication for the other. The line of treatment isusually guided by the severity of either events and to theindividualized judgment of the physician. Our patient presented with acute symptoms of stroke, and thrombolyticwas administered appropriately. Unfortunately, he developed an acute myocardial infarction manifesting asinferior ST elevation on EKG despite being asymptomaticfrom a cardiac perspective. In the setting of synchronousevents, both must be addressed simultaneously, as treatingmyocardial infarction with percutaneous coronary inter-vention would delay potential thrombolytic therapy foracute stroke and may result in significant neurologicalimpairment.2

Acute myocardial infarction or prior myocardial infarctionin the presence of a large akinetic segment of myocardiumwith or without left ventricular thrombus itself is animportant cardio-embolic phenomenon that can lead tostroke. The risk of cerebral vascular accident is highest the

first five days after a myocardial infarction.3

Approximately 50 percent of cerebral vascular accidentoccurring in the first month after a myocardial infarctionare preceded by a large anterior wall infarct.3 Our patient’sinitial EKG showed inferior Q waves indicating that hehad inferior infarct in the past. This was corroborated bythe coronary angiogram finding of chronic total occlusionof the left anterior descending artery and distal right coronary artery. ECHO revealed apical akinesis and midventricular hypokinesis, which increases his risk of leftventricular thrombus formation and stroke due to stagnationof blood flow in the left ventricle. Acute myocardialinfarction within the previous three months is considereda relative contraindication for therapy with thrombolyticaccording to the American Heart Association/AmericanStroke Association stroke guidelines.4,5 In one study, however, that duration can be shortened to seven weeks asit takes the myocardium approximately seven weeks torecover from a myocardial infarction.4,5 The reason is dueto increased risk of cardiac rupture, secondary to break-down of the existing fibrin clot within the necroticmyocardium and/or degradation of collagen. It is reason-able to assume that our patient had a silent myocardialinfarction in the past. Since it is unclear timeframe ofwhen it occurred, thrombolytic administration could havebeen detrimental to the patient if he had myocardialinfarction within the last three months.

Our patient had increased risk of atherosclerosis relatedvascular complications, (i.e., stroke, myocardial infarc-tion, peripheral vascular disease) secondary to his uncon-trolled diabetes mellitus. Vascular insult in one territoryincreases systemic inflammation, sympathetic responseand instability of the vulnerable atherosclerotic plaque inother vascular territories resulting in increased tendencyfor thrombosis.6 This may also explain the increased inci-dence of acute stroke following myocardial infarction orvice versa. In one study, it was found that patients withsignificant carotid artery disease who underwent coronaryangiogram had an approximately 47 percent chance of sig-nificant coronary artery disease.7 This supports the prac-tice of a thorough cardiovascular evaluation in patientspresenting with cerebral vascular accident, in order toreduce future risks of myocardial infarction.1

Stress cardiomyopathy, also known as broken heart syn-drome, or Takotsubo cardiomyopathy, is associated withtransient regional systolic dysfunction of the left ventricleinvolving territories of more than one epicardial vessels.Typically, there is dyskinesis, akinesis or hypokinesis of

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mid and apical segments of the left ventricle, similar toour patient’s imaging. In the absence of chest pain and inthe presence of a new stressor (recent stroke), our patientwas thought to have stress cardiomyopathy induced STchanges and troponin elevation; however, coronaryangiography proved this diagnosis wrong. Stress cardiomy-opathy occurs in approximately 1-2 percent of patientspresenting with troponin positive suspected acute coro-nary syndrome (ACS) or suspected ST elevation myocar-dial infarction (STEMI).8 In one study, stress cardiomy-opathy was associated with troponin elevation as high as15 ng/ml.9 If troponin elevation is markedly elevated,stress cardiomyopathy is less likely, and consideration ofacute coronary syndrome should be in the primary differ-ential.9

Common complications of thrombolytic administrationare hemorrhage, anaphylaxis, or arterial re-occlusion. Oneof the plausible explanations in our case could be disrup-tion of intra-cardiac thrombus and coronary embolismafter use of thrombolytic therapy, leading to myocardialinfarction in view of wall motion abnormality seen on

ECHO. There have been few cases reported of intra-car-diac thrombus dislodgement after administration ofthrombolytic.10.11 If this were the case, a visible apicalthrombus may not be visualized due to dislodgement.

ConclusionSimultaneous occurrence of major vascular events such asmyocardial infarction, acute ischemic stroke creates amanagement dilemma. In the absence of definitive guide-lines, the treatment will have to be individualized. A mul-tispecialty approach is the best scenario that will givepatients their best chance of recovery that likely will leadto improved prognosis. While treating one vascular event,one should always keep in mind the possibility of anothervascular bed event. In patients who present with an acuteischemic stroke, we recommend a thorough cardiovascularevaluation in order to reduce or prevent future cardiovas-cular events.

Acknowledgements: The authors would like to acknowledge James Higgins,Alex Pham, Terezia Petraskova and Dr. Shenjing Li for their contributions tothis paper.

REFERENCES1. Rolak L, Rokey R. The patient with concomitant stroke and myocardial infarction:

clinical features. In: Coronary and Cerebral Vascular Disease: A Practical Guide toManagement of Patients with Atherosclerotic Vascular Disease of the Heart andBrain. Futura. 1990:117-37.

2. Omar HR, Mangar D, Camporesi EM. Simultaneous thrombosis of 2 vascular territories: is thrombolytic therapy a better option?. Am J Emerg Med.2013;31(9):1412-13.

3. Mooe T, Eriksson P, Stegmayr B. Ischemic stroke after acute myocardial infarction: a population-based study. Stroke. 1997;28(4):762-7.

4. Maciel R, Palma R, Sousa P, Ferreira F, Nzwalo H. Acute stroke with concomitantacute myocardial infarction: will you thrombolyse?. J Stroke. 2015;17(1):84-6.

5. De Silva DA, Manzano JJ, Chang HM, Wong MC. Reconsidering recent myocar-dial infarction as a contraindication for IV stroke thrombolysis. Neurology.2011;76(21):1838-40.

6. Suarez JI. Acute myocardial infarction, ischemic stroke, sympathetic stress, andinflammation: birds of a feather. Stroke. 2006;37(10):2449-50.

7. Hertzer NR, Young JR, Beven EG, et al. Coronary angiography in 506 patients with extracranial cerebrovascular disease. Arch Intern Med. 1985;145(5):849-52.

8. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest. 2007;132(3):809-16.

About the Authors:Kalyan Wagle, MD, Resident Physician, Department of Medicine, Queens HospitalCenter, Icahn School of Medicine at Mount Sinai.Jimmy Yee, MD, Cardiovascular Fellow, Department of Cardiovascular Disease,University of South Dakota Sanford School of Medicine.Vishesh Kumar. MD, Cardiovascular Fellow, Department of Cardiovascular Disease,University of South Dakota Sanford School of Medicine. Amornpol Anuwatworn, MD, Cardiovascular Fellow, Department of CardiovascularDisease, University of South Dakota Sanford School of Medicine.Tomasz Stys, MD, Associate Professor of Medicine, Department of CardiovascularDisease, University of South Dakota Sanford School of Medicine. Adam Stys, MD, Professor of Medicine, Department of Cardiovascular Disease,University of South Dakota Sanford School of Medicine. Christopher Stanton, MD, Associate Professor of Medicine, Department ofCardiovascular Disease, University of South Dakota Sanford School of Medicine.

Please note: Due to limited space, we are unable to list all references. You may contact South Dakota Medicine at 605.336.1965 for a complete listing.

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A Case of Incisional Endometrioma that Presented as an Abdominal MassBy K e l l y L a n d e en , MS1V; K r i s t i n Wempe , MD ; a n d Rob e r t M i l l e r , MD

IntroductionIncisional endometriosis is a rare complication of abdomino-pelvic surgeries, particularly obstetrical surgeries, in premenopausal women. 1,2 Although not fatal, the associatedsymptoms can cause severe pain and discomfort, and proper identification and treatment is necessary.3

Case PresentationA 45-year-old gravida 4, para 4 female presented for surgical evaluation of an abdominal wall mass in the leftinguinal area. She reported having the mass for approxi-mately three years, with increasing pain and discomfortover the previous 12 months. She denied further symptomsor changes in mass size during this time. She described nocyclic changes in her discomfort or the mass itself.Surgical history included a low transverse caesarean section with tubal ligation in 2011 and a total laparoscopichysterectomy in 2015 with trocar incisions in the leftlower quadrant, suprapubic region, and the umbilicus.

Upon physical examination, a firm lesion was palpated inthe left groin superior to the inguinal ligament. It waslocated at the lateral aspect of the low transverse incisionfrom the patient’s prior caesarean. The mass was solid withno fluctuance, and there was no warmth or erythema.Mild tenderness was noted. The lesion was not freelymobile nor firmly fixed. No skin changes or palpableadenopathy were noted. The physical exam did not helpto narrow down the differential diagnosis in this patient.

Differential diagnoses of an abdominal wall mass includedesmoid tumor, lipoma, hematoma, injection granuloma,suture granuloma, abdominal wall hernia, abscess,endometriosis, metastatic disease, lymphoma, sarcomas,and mesenchymal tumors.2

Abdominal imaging completed prior to this patient’sappointment included an ultrasound and computerizedtomography (CT) scan. Abdominal ultrasound demon-strated a left lower quadrant subcutaneous hypoechogenicmass measuring 2 x 1.6 cm with irregular borders, and a 7mm surrounding hyperechogenic area extending to theskin (Figure 1).

AbstractAlthough endometriosis is a common condition in women of reproductive age, the incidence of endometriomain prior surgical incision sites is rare.We present a case of an abdominal wall mass in a female patient with a history of obstetrical surgery. The mass was visualized with ultrasound and computerized tomography, removedby wide excision, and identified via frozen section. This case demonstrates the importance of a thorough surgical and obstetrical history in any woman who presents with an abdominal wall mass.

Figure 1. Left lower quadrant abdominal ultrasound. Arrowspoint to irregular borders of 2 x 1.6 cm hypoechogenic mass.

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Figure 2. Transverse abdominal CT demonstrating a 2.2 x 1.7 x 2.7 cm subcutaneous soft tissue density (arrow) found in left lower quadrant.

Figure 3. Microscopic view of pathology specimen. Endometrial glands (arrow) surrounded by fibroadipose tissue of the abdominal wall.

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REFERENCES1. Cramer DW, Missmer SA. The epidemiology of endometriosis. Ann N Y Acad Sci.

2002 Mar; 955:11-22.2. Stein L, Elsayes KM, Wagner-Bartak N. Subcutaneous abdominal wall masses:

radiological reasoning. AJR Am J Roentgenol. 2012 Feb; 198(2):W146-51.3. Akbulut S, et al. Scar endometriosis in the abdominal wall: A predictable condition

for experienced surgeons. Acta Chir Belg. 2010 May-June; 110(3)303-7.4. Buck Louis GM, ENDO Study Working Group, et al. Incidence of endometriosis by

study population and diagnostic method: the ENDO study. Fertil Steril. 2011 Aug;96(2):360-5.

5. Macer M and Taylor S. Endometriosis and infertility: a review of the pathogenesisand treatment of endometriosis-associated infertility. Obstet Gynecol Clin NorthAm. 2012 Dec; 39(4):535-49.

6. Erel S, et al. Recurrence of scar endometriosis due to misdiagnosis as incisionalhernia at first operation: case report. Am J Case Rpts. 2008 Mar; 9:136-9.

7. Al-Jabri K. Endometriosis at Caesarian section scar. Oman Med J. 2009 Oct;24(4);294-5.

About the Authors:Kelly Landeen, MS IV, University of South Dakota Sanford School of Medicine Classof 2018.Kristin Wempe, MD, General Surgery Resident, Grand Rapids Medical EducationPartners; University of South Dakota Sanford School of Medicine Class of 2017.Robert Miller, MD, General Surgeon, Rapid City Medical Center; Clinical AssistantProfessor, Department of Surgery, University of South Dakota Sanford School ofMedicine.

Abdominal CT scan revealed an ill defined 2.2 x 1.7 x 2.7cm subcutaneous soft tissue density of the left lower quad-rant abdominal wall (Figure 2). Margins were somewhatindistinct with some stranding in the adjacent adipose.

The patient underwent excision of the abdominal wallmass. Intra-operatively, she was found to have a darklypigmented soft tissue mass that adhered to and includedthe anterior rectus sheath. The mass and surrounding fascia were excised completely and sent to pathology forfrozen section. Pathology reported a central firm grittygrey pink to tan purple nodular tissue with greatest margins 3.5 x 2.2 x 2 cm (Figure 3). Intraoperative frozensections and final pathology were consistent with benignendometriosis. No malignancy was identified. The fasciawas repaired primarily without mesh, and closed with non-absorbable monofilament suture. Postoperative recoverywas uneventful.

DiscussionEndometriosis is the presence of hormone-responsiveextrauterine endometrial tissue, and can manifest as anendometrioma, a well-circumscribed mass of endometrialtissue. It is common in the female population, with variedprevalence depending on age, reproductive history, andgynecologic history. Approximately 50 percent ofteenagers with intractable dysmenorrhea haveendometriosis.1 It is also found in asymptomatic women,with a 4 percent incidence in asymptomatic patientsundergoing tubal ligation, and an estimated prevalence of11 percent in the general, undiagnosed population.1,4

The pathogenesis of endometriosis has been exploredextensively, with various existing theories including outflow obstruction, retrograde menstruation, endometrialmetaplasia, or immune dysfunction. Common symptomsassociated with endometriosis include dysmenorrhea,cyclic pain, and infertility. It is unclear if there is a causalmechanism to these symptoms due to their multifactorialnature and to the unclear pathogenesis of this condition.5

The incidence of endometriosis in the abdominal wall isfar less common than traditional endometriosis.Approximately 0.1 percent of women undergoing caesare-an section or other obstetric surgery will developendometriosis in surgical scars due to inadvertent directimplantation of endometrial tissue at the time of surgery.In a retrograde study of 15 patients with abdominal wallendometriosis, symptoms included a palpable and/or painfulmass, similar to the patient presented in this case study. 3

The recurrence of incisional endometrioma is rare but canoccur if misdiagnosed at the first operation, where it is typically mistaken for an incisional hernia.6 This misdiag-nosis is most often a result of the scarce cases ofendometriomas encountered by general surgeons.

Incisional endometriomas are best diagnosed with thorough gynecological history and imaging of the mass,typically by ultrasound and CT or magnetic resonanceimaging. Wide surgical excision is the most effective treatment; medical management with progestin, oral contraceptives, and gonadotropin agonists are less effective and only provide partial symptomatic relief.7

ConclusionThorough gynecologic history taking is necessary forrecognition of incisional endometriosis. For correct identification and treatment, it is important that generalsurgeons and primary care providers, in addition to obstetricians, be aware of this condition. Although theincidence is rare, it is important to consider incisionalendometrioma in any female with an abdominal wall massand a history of obstetrical surgery.

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Case ReportA 21-year-old white male presented to the dermatologyclinic for evaluation of moles. The specific lesions of concern included nevi that were raised, growing, itchyand painful at times. He had a history of significant actinicdamage with blistering, peeling sunburns and chronic sunexposure. Examination revealed at least 60 pigmentedmacules and papules scattered over the trunk and extrem-ities, which were generally symmetric, with homogenouscolor and regular borders. The lesions of specific noteincluded lesions of the right axilla, right midline, rightproximal lower leg, left mid lower leg and left lumbar back(Figure 1) which were described as brown papules withslightly irregular shape, color variation and irregular borders.

On microscopic examination, two of the lesions werefound to be compound nevi. Two other lesions were calleddysplastic nevi with moderate atypia. The left lumbarlesion showed a proliferation of melanocytes with two sep-arate cellular components, and an epithelial proliferation(Figure 2). In the central part of the lesion, there weremelanocytes with abundant, pale cytoplasm, “dusty”appearing melanin and moderately enlarged nuclei,arranged as small nests, with many interposed

melanophages and fibrotic stroma (Figure 3). Around andbeneath them, were nests, cords and strands of plump,oval to small round melanocytes that matured withdescent from the junction, and were positioned adjacentto small vessels and epithelial adnexal structures in thesuperficial reticular dermis (Figure 4). Above themelanocytic proliferation, was a proliferation of epithelialcells in which there were lace-like interconnecting strandsof squamous keratinocytes and nests of basaloid cells, withintervening fibrocyte-rich stroma (Figure 5).

Combined Melanocytic Nevus, SuperficialCongenital and Deep Penetrating Types withFibroepithelioma of Pinkus, Collision Tumor – A Case ReportBy A shwyn a S un a s s e e , MD ; Amy M . K e r k v l i e t , MD ; a n d

A l i D . J a s s im , MD , PhD

AbstractWe present a case of collision tumor composed of a combined melanocytic nevus with superficial congenital anddeep penetrating components and a fibroepithelioma of Pinkus on the left lumbar back of a 21-year-old male.He presented to the dermatologist for evaluation of numerous moles, and the lesion in question was describedas a brown variegated papule with slightly irregular shape and irregular borders. This case is being reported as itis very unusual to see a fibroepithelioma of Pinkus in conjunction with a melanocytic lesion.

Figure 1. Pigmented papular left lumbar back skin lesion.

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The left lumbar lesion as described had three distinctparts; fibroepithelioma of Pinkus, conventional nevus andan atypical nodular nevocellular proliferation versus bluenevus versus proliferating center in a congenital nevus.MART-1 highlighted the melanocytic proliferation; however, no pagetoid pattern was seen. MIB-1 (Ki-67)showed increased proliferative index. HMB-45 showedfocal staining at the superficial part of the melanocyticproliferation; however, the deeper part did not stain,though the small atypical nodule of melanocytic prolifer-ation showed HMB-45 positivity. The p16 stain showedpositive staining within the melanocytes including thefocal atypical nodular proliferation.

DiscussionFibroepithelioma of Pinkus (FeP) is a rare subtype of basalcell carcinoma (BCC) that may clinically mimic a varietyof benign skin tumors.1 It was first described in 1953 byHermann Pinkus2 as a premalignant fibroepithelial tumor.More recently, FeP has been described to more closelyresemble a trichoblastoma than BCC.3 Another school ofthought is that FeP is not premalignant, but a malignantneoplasm made up of trichoblasts whose fenestrated designmakes it distinctive among the various morphologicaltypes of basal cell carcinoma.4 FeP manifests clinically as asolitary, and sometimes multiple flesh-colored or slightlybrown-gray, well-demarcated plaque.5-6 It is typically foundon the trunk with a predilection for the lumbosacral area.It is most commonly seen in persons aged 40-60 years with a slight female predilection.7 The differential diagnoses include dermal melanocytic nevus, pedunculatedfibroma, acrochordon, and seborrheic keratosis.1

Histopathologically, FeP is characterized by tumor islands

Figure 2. Hematoxylin and eosin stained section of skin showing a melanocytic proliferation (horizontal arrow),

and an epithelial proliferation (vertical arrow)

Figure 3. Melanocytes with abundant pale cytoplasm, melanin pigment, moderately enlarged nuclei

Figure 4. Melanocytes showing maturation with depth

Figure 5. Fibroepithelioma of Pinkus (FeP) component consisting of lace-like interconnecting strands of

keratinocytes and nests of basaloid cells

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and anastomosing strands of basaloid, usually palisading atthe periphery, surrounding a fibrous stroma.8 These featuresare thought to be created by tumor strands spreading downeccrine ducts.9 Congenital melanocytic nevi histopatho-logically show cords, strands, nests, and single units ofmelanocytes spreading between collagen bundles in thedermis and may have deep components.10 The final diagnosis of this case was of a combined melanocyticnevus, with superficial congenital and deep penetratingnevus components. The FeP and deep penetrating nevus-like component appeared fully excised with thearea of congenital nevus extending to the margin. Thedeep penetrating nevus-like component had small andmonomorphous nuclei, with retention of p16 staining,and relatively low proliferation rate, which were reassuringfindings. Complete excision is adequate treatment of FeP,and due to its non-aggressive clinical behavior, it has agood prognosis.11 Despite a rare documented case report ofa metastatic basal cell carcinoma with FeP features, nospecial follow-up is recommended in most cases.12 Thismakes a very interesting and atypical case as collisionbetween FeP and melanocytic proliferation has not beenpreviously documented.

REFERENCES1. Reggiani C, Zalaudek I, Piana S et al. Fibroepithelioma of Pinkus: case reports of

the literature. Dermatology. 2013;226:207-11.2. Zalaudek I, Ferrara G, Broganelli P et al. Dermoscopy of fibroepithelioma of Pinkus.

Arch Dermatol. 2006;142(10):1318-22.3. Bowen AR, Leboit PE. Fibroepithelioma of Pinkus is a fenestrated trichoblastoma.

Am J Dermatopathol. 2005;27:147-54.4.Gutte RM. Fibroepithelioma of Pinkus: a distinctive variant of trichoblastic carcino-

ma. Indian J Dermatol Venereol Leprol. 2013;79:725.5. Barr RJ, Herten RJ, Stone OJ. Multiple premalignant fibroepitheliomas of Pinkus: a

case report and review of the literature. Cutis. 1978 Mar;21(3):335-7.6. Lang PG, Maize J et al. Basal cell carcinoma. Cancer of the Skin. Philadelphia, PA.

Elsevier Saunders 2005;101-33.7. Su MW, Fromer E, Fung MA: Fibroepithelioma of Pinkus. Dermatol Online J. 2006

Sep 8;12(5)2.8. Longo C, Soyer HP, Pepe P et al. In vivo confocal microscopic pattern of fibroepithe-

lioma of Pinkus. Arch Dermatol. 2012;148:556.9. Stern JB, Haupt HM, Smith RR. Fibroepithelioma of Pinkus: eccrine duct spread of

basal cell carcinoma. Am J Dermatopathol. 1994;16585-7. 10. Magana M, Sanchez-Romero E, Magana P et al. Congenital melanocytic nevus:

two histopathological forms. Am J Dermatopathol. 2015 Jan;37(1):31-7.11. Cohen PR, Tschen JA. Fibroepithelioma of Pinkus presenting as a sessile thigh

nodule. Skinmed. 2003;2:385-7. 12. Colvett KT, Wilson FC, Stanton RA. Atypical presentation of metastatic basal cell

carcinoma. South Med J. 2004;97:305-7.

About the Authors:Ashwyna Sunassee, MD, Pathology Chief Resident, PGY-4 and Clinical Instructor,Pathology, University of South Dakota Sanford School of Medicine.Amy M. Kerkvliet, MD, Staff Pathologist, Sanford Pathology, Sioux Falls, South Dakota.Ali D. Jassim, MD, PhD, Staff Pathologist, Sanford Pathology, Sioux Falls, South Dakota.

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Alkaptonuria: A Case Report With Diagnostic Challenge By Va s an th a L . Ga l i , MD ; Amy M . Ke r kv l i e t , MD ;

J a c ob M . Ku smak , MD , Pha rmD ; and J an a K . E lwood , PA

AbstractAlkaptonuria is a rare autosomal recessive metabolic disorder caused by deficiency of homogentisic acid (HGA)oxidase, the only enzyme capable of catabolizing HGA. Deficiency of this enzyme leads to excess HGA whichdeposits in the connective tissue. We present a case of a 64-year-old woman who was referred to the dermatology clinic for a full body mole check and skin cancer screening. Clinically she had blue/gray pigmentation of the external ear and sclera. Also she had a domed papule on the left cheek with punctate graypigmentation which was biopsied. Histopathological examination showed a benign dermal nevus and nonpolarizable, yellow-brown, irregular shaped fibers. Subsequent organic acid screen showed markedly elevated urinary HGA, diagnostic of alkaptonuria. On specific inquiry, the patient revealed she had a history ofbilateral Achilles tendon rupture, black urine, arthritis, and external ear discoloration for many years. The pigmented material was then considered to be HGA deposition within the dermal collagen fibers. However,without the appropriate clinical data and confirmatory lab findings, the pigmented fragments on skin biopsy represent a diagnostic challenge. Measures like low protein diet and ascorbic acid supplementation will slowdown the disease progression and potential complications later in life; however, there is no definitive treatmentfor the disease. We emphasize the prompt recognition of the clinical signs and symptoms as well as the importance of the microscopic findings.

Introduction

Alkaptonuria is a rare autosomal recessive inherited metabolic disorder caused by mutation of thehomogentisic acid oxidase (HGD) gene which codes forthe homogentisate oxidase enzyme.1 This enzyme helps inbreakdown of the amino acids phenylalanine and tyrosine,which are important building blocks of proteins. As aresult, a substance called homogentisic acid (HGA) accumulates in the body. Excess HGA and related compounds are deposited in connective tissues and causedarkening of the cartilage and skin. When excreted in theurine, oxidation of HGA turns urine black over time.1

The presence of any of these findings should prompt confirmatory biochemical testing.

Case Summary

A 64-year-old woman was referred to the dermatologyclinic for a full body mole check. On clinical examination

the lesions of concern were a 5 mm flesh-colored papulewith gray punctate pigmentation on the left cheek, and a7 mm erythematous palpable scale on left lower leg suspicious for actinic keratosis. It was also noted that shehad bluish discoloration of her sclera and in the ears forseveral years. Past medical history consisted of arthritis oflarger joints (primarily in the right hip and bilateralknees), diffuse myalgias, bilateral Achilles tendon rupture,and status post lumpectomy for stage I invasive ductal car-cinoma of the breast, with no active disease.Histopathological examination of the left cheek lesionshowed a benign dermal nevus and non-polarizable, yellow-brown, irregular shaped fibers (Figures 1 and 2).Subsequent organic acid screen showed urinary HGA of5940 mmol/mol creatinine; reference values: <11, diagnosticof alkaptonuria. The pigmented material in the biopsy wasthen considered to be HGA deposition within the dermalcollagen fibers. Subsequent genetic testing confirmed that

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she has mutations in both copies of HGD gene and bothof her children are carriers.

Cardiology evaluation revealed premature coronary calcifications and mild aortic valve sclerosis without significant stenosis. She continues to have stable to slightlyworsening arthritis and is followed by orthopedics and cardiology. She is not taking any medication for the alkaptonuria and no medication is proven to stop the progression of the disease.

DiscussionAlkaptonuria is a rare inborn error of phenylalanine andtyrosine metabolism. It has an estimated incidence of onein 250,000 to one in 1 million live births in the U.S.2 Adeficiency of the hepatic enzyme HGD leads toaccumulation of HGA.1Oxidized HGA imparts darkeningof the body fluids, especially urine, which is the onlypathognomonic sign present at birth. Gradual depositionof the oxidized HGA in connective tissue leads to pig-mentation of skin (ochronosis), sclerae, and cartilage. Thepigmentation typically appears after the third decade oflife.3 Other manifestations include musculoskeletal pain,tendon rupture, and degenerative arthropathies. Rare presentations include premature coronary calcifications orcalcific valvular disease of the heart secondary to the deposition of HGA. Diagnosis of alkaptonuria primarilydepends on thorough clinical evaluation and is confirmedby elevated urinary HGA levels.

Medications such as quinolones have been reported tocause cutaneous hyperpigmentation that appears similaron histologic examination. Urine HGA levels, in conjunction with the clinical history, would help in arriving at a correct diagnosis.5,6

To date, no curative treatment is available. Dietary management of protein intake and vitamin C supplemen-

Figure 1. Photomicrograph demonstrating nests of nevus cells that extend to the deep margin of the specimen (hematoxylin-eosin, original magnification 40x).

Figure 2. Higher-power view photomicrograph depicting irregular shaped amber-colored refractive fibers (red arrow)admixed with nevus cells (red star) (hematoxylin-eosin,

original magnification 400x).

Figure 3. Simplified diagram of phenylalanine metabolic pathway. A) 4-hydroxyphenylpyruvic acid dioxygenase (enzyme targeted in alkaptonuria management), B)

Homogentisate oxidase (deficient enzyme in alkaptonuria).

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tation have both been advocated as measures to decreaseformation of HGA; however, this has not been systemati-cally proven to alter the underlying metabolic defect.7

National Institute of Health trials have reported that theexperimental drug nitisinone, a 4-hydroxyphenylpyruvatedioxygenase enzyme inhibitor (Figure 3), has shown toreduce HGA production as much as 95 percent.8 Theseresults suggest that early treatment with nitisinone mayprove beneficial in young patients who have not yetdeveloped joint or cardiac complications. In the eventthat this therapy proves useful, it makes the timeliness ofdiagnosis even more critical.

Our patient demonstrated the typical alkaptonuria triad:ochronotic dermal pigmentation, severe degenerativearthritis, and darkening of urine upon oxidation. Despitethese clear signs, a diagnosis of alkaptonuria was notestablished until a dermatology consultation was obtainedfor a skin lesion. Indeed, literature searches reveal thechallenges in diagnosing alkaptonuria due to itsmultisystem involvement.9,10 Rare cases like these emphasize how crucial it is to take a detailed history,

review the patient’s entire medical record and maintainopen communication with our fellow consultants.

Conclusions and Relevance This case is presented for its rarity, and because of possibletreatment advances, our article emphasizes theimportance of early diagnosis.

Journal

REFERENCES1. Zatkova A, Sedlackova T, Radvansky J, et al. Identification of 11 novel homogenti-

sate 1,2 dioxygenase variants in alkaptonuria patients and establishment of anovel LOVD-based HGD mutation database. JIMD Rep. 2012;4:55-65.

2. Wendy JI, William AG. Alkaptonuria GeneReviews - NCBI Bookshelf [Internet].Last Update: 2013 Aug 22.

3. Groseanu L, Marinescu R, Laptoiun D et al. A late and difficult diagnosis ofochronosis. J Med Life. 2010 Oct-Dec; 3(4):437-43.

About the Authors:Vasantha L. Gali, MD, Department of Pathology, University of South Dakota SanfordSchool of Medicine.Amy M. Kerkvliet, MD, Department of Pathology, University of South Dakota SanfordSchool of Medicine.Jacob M. Kusmak, MD, Pharm D, Department of Dermatology, University of SouthDakota Sanford School of Medicine.Jana K. Elwood, PA, Department of Dermatology, University of South Dakota SanfordSchool of Medicine.

Please note: Due to limited space, we are unable to list all references. You may contact South Dakota Medicine at 605.336.1965 for a complete listing.

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Laparoscopic Treatment of a Pyogenic HepaticAbscess Caused by Transmural Duodenal Perforationof a ToothpickBy Ha s s a n Tu r a i h i , MD ; J e d A s s am , MD ; J u s t i n Z an f e s , MS IV; a n d

Th a v am Th amb i - P i l l a i , MD

AbstractThe development of pyogenic hepatic abscess resulting from perforation of the gastrointestinal tract is a rarepathologic finding. It is a condition that can be fatal making early detection and subsequent removal of theinciting foreign body critical to avoid more deleterious sequela. Yet, its initial presentation tends to be nonspecific and typically is only discovered once surgical investigation into the cause of persisting abscess formation is performed. In this study, laparoscopic treatment of a 52-year-old male with a non-resolving hepatic abscess due to transmural gastrointestinal perforation of a toothpick is presented. Although a rare finding, reports of foreign body induced hepatic abscess have recently increased in the world literature, allowing some preliminary efforts in proposing diagnostic characterization. Yet, more case studies will berequired to permit validation of these findings making continued reporting of this pathologic process critical.

BackgroundThe majority of ingested foreign bodies pass unremarkablythrough the gastrointestinal tract, with less than 1 percentof patients experiencing perforation.1 The development ofpyogenic hepatic abscess (PHA) secondary to perforationof a foreign body through the gastrointestinal tract is evenmore unusual. Recently there has been an increase in thenumber of these cases reported.2

PHA is a condition that can be fatal, making early detection and subsequent removal of any inciting foreignbody critical to avoiding more deleterious sequela.3 Initialpresentation tends to be non-specific, including symptomssuch as fever, vomiting, anorexia, and weight loss there-fore requiring a high index of clinical suspicion, as thesepatients can pose a challenging diagnostic evaluation.4 Inthis case we present the laparoscopic treatment of a 52-year-old male with a non-resolving hepatic abscess due totransmural gastrointestinal perforation of a toothpick.

CaseA 52-year-old male presented to the emergency departmentwith a two week history of worsening abdominal pain,localizing to the right upper quadrant (RUQ). Associatedsymptoms included fevers, headaches, chills, night sweats,and diminished appetite. The patient’s past medical history

was significant for two recent emergency department visits for more generalized complaints of diffuse abdominalpain, nausea, and diarrhea. There was no prior history ofliver biopsy or surgery and no history of recent travel ortrauma. The patient had a 27-pack year smoking history.Physical examination revealed notable tenderness of theepigastrium, no abdominal distention or organomegalywere appreciated, and there was no evidence of jaundice.Laboratory studies demonstrated an elevated WBC count(15.9 K/�L, Ref: 4-11 �L), CRP (85.5 mg/L Ref: < 3.0mg/L), and lipase (114 U/L Ref: 20-100 U/L). A CEA andCA 19-9 as well as AST, ALT, and bilirubin were all within normal limits. Stool culture for clostridium difficilewas negative.

Imaging studies included an abdominal ultrasound of theright upper quadrant which showed evidence of a linearechogenic opacity approximately 5 cm in the left mediallobe of the liver (Figure 1). A CT scan with oral and intravenous contrast demonstrated an ovoid hepaticlesion 6.1 x 2.4 x 2.7cm (Figure 2) notable for a centralarea of linear hypodensity (Figure 3). Magnetic resonanceimaging (MRI) further defined the lesion as a non-enhancing central lobular T2 hyperintensity with a thickrim of hyperenhancing tissue suggestive for a reactiveabscess surrounding a foreign body.

The patient was referred to interventional radiology (IR)for percutaneous drainage of the abscess and drain place-ment. A collection of 5 cc of purulent fluid was draineddemonstrating negative results on gram staining and noculture growth. Upon completion of an unremarkablethree day hospital stay the patient was discharged on acourse of amoxicillin-clavulanate and oxycodone-acetaminophen. During his three week follow-up, bloodwork revealed a normal WBC count with no evidence ofanemia, unfortunately the patient continued to suffer frompersistent right upper quadrant pain. A CT of theabdomen and pelvis performed both with and withoutcontrast revealed a persistent 5.7 x 2.4 cm area of mixeddensity with adjacent duodenal inflammatory changes andevidence of a linear hyperintensity extending from the leftmedial lobe of the liver through to the adjacent descendingduodenal segment.

The patient was scheduled for diagnostic laparoscopy.

Laparoscopy revealed an extensive amount of adhesions inthe upper abdomen consequential to the combination of aretained foreign body, liver abscess, and previous IRdrainage (Image 1). Laparoscopic lysis of adhesions wasperformed, along with the adherent duodenum being carefully peeled away from the liver using sharp and bluntdissection. Resulting ingress revealed the presence of atoothpick extending from the second part of the duodenuminto the left medial segment of the liver (Images 2 and 3).The toothpick was removed and an intraoperative ultra-sound identified no further drainable abscess. Repair ofthe duodenal perforation was performed, cholecystectomywas also undertaken in a standard fashion due to interfer-ence of the gallbladder with duodenal repair through itsinvolvement in the inflamed tissue (Image 4). Goodhemostasis was achieved using a fibrin sealant.

Patient had an uneventful postoperative course, he wasdischarged home on a two week regimen of amoxicillin-

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Figure 1. Ultrasound revealing linear opacity.

Image 1. Extensive inflammation and adhesions noted in the right upper quadrant involving the liver, gallbladder

and duodenum.

Figure 2. CT with contrast shows abscess and duodenal inflammation.

Figure 3. CT without contrast clearly shows foreign body.

Image 3

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clavulonate. At two weeks follow up, the patient wasallowed to return to normal activity without restrictions.

DiscussionForeign body induced PHA from gastrointestinal perforationis a rare event.1,3,7 Fish bones, toothpicks, and chickenbones represent the most commonly ingested objects causing such pathology.1,5 The most frequent sites of perforation with resulting liver abscess are the duodenumand stomach.3,7 For all gastrointestinal perforations by aforeign body, the ileocecal and rectosigmoid region arenoted as being more susceptible.1,6 While foreign bodiesare becoming more recognized as a prominent cause ofnon-resolving hepatic abscesses, an absence of definitivediagnostic characteristics makes early detection and treatment of this pathology a complex challenge.1,4 A preliminary effort in elucidating diagnostic criteria hasbeen performed by Leggieri et al. who have proposed analgorithm to evaluate PHA for the presence of a foreignbody.2

Commonly, initial patient history is non-specific in identifying PHA from a foreign body, as the symptoms areoften generalized with signs of abscess formation delayedweeks or months after the inciting event.1,5 For imagingstudies, ultrasound and CT are the most sensitive and preferred for initial screening.3,7 Yet, given the diverse sizeand composition characteristics of inciting foreign bodiesreports on imaging efficacy has been variable betweenstudies.2,7 As a result, definitive diagnosis is often madethrough surgical exploration.6

The current recommended and definitive treatment for aforeign body induced hepatic abscess is laparoscopicremoval of the foreign body with ensuing abscess drainageand perforation repair as applicable.1,5 Other methods thathave been successfully employed range from radiological-guided percutaneous extraction to hepatic lobe resection.3,4,7

Endoscopic retrieval has also been described in instanceswhere the foreign body’s migration is caught in earlier

stages prior to mucosal healing.3,6

Although a rare finding, the reporting of foreign bodyinduced hepatic abscesses has recently increased in theworld literature. The majority of these cases tend to befound in studies from Eastern nations, with the pathologymore unlikely in Western nations.7 At this time therehave been no studies identified by the authors that havesought to evaluate possible causes for this disparity.Preliminary efforts have been made to develop a diagnosticcharacterization for a foreign body induced PHA.2 Yet, theability to more broadly apply this information will requiresubstantially more cases that will be only be attainablethrough continued reporting of this rare process.

REFERENCES1. Santos SA, Alberto SC, Cruz E, Pires E, Figueira T, Coimbra E, Estevez J, Oliveira

M, Novais L, Deus JR. Hepatic abscess induced by foreign body: case report andliterature review. World J Gastroenterol. 2007;13:1466-70.

About the Authors:Hassan Turaihi, MD, Department of Surgery, University of South Dakota SanfordSchool of Medicine.Jed Assam, MD, University of South Dakota Sanford School of Medicine.Justin Zanfes MS IV, University of South Dakota Sanford School of Medicine.Thavam Thambi-Pillai, MD, Associate Professor of Surgery, University of SouthDakota Sanford School of Medicine.

Please note: Due to limited space, we are unable to list all references. You may contact South Dakota Medicine at 605.336.1965 for a complete listing.

Image 4. Critical view of safety demonstrated during cholecystectomy.

Image 2 and 3: Toothpick embedded in the liver parenchyma resulting in abscess cavity.

Image 2

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Pharmacology Focus

IntroductionMultiple sclerosis (MS) is a disease of the central nervoussystem that is characterized by deteriorating myelin orgray matter (GM) loss, evidenced by spots or lesions onthe brain, as illustrated by magnetic resonance imaging(MRI). Although each case is unique, certain symptomscommonly appear in affected patients. Early characteriza-tions include double vision, extreme fatigue, memory lossand temporary numbness or tingling in the lower extremities.1

The ways in which MS disability manifests vary signifi-cantly. Some are stricken by vision impairment, perma-nent loss of limb function and are confined to a wheel-chair. Others suffer tremendous fatigue and memory loss.A vast array of treatments are available to amelioratesymptoms and slow progression of the disease, whosedetection and diagnosis hinges on diagnostic criteria firstdescribed by Poser and colleagues in 1983.1 First diagnosedin the late 1800s, MS diagnosis and treatment guidelineshave been available only for the last 50 years.

Of the over 400,000 sufferers in the U.S., MS is most commonly diagnosed in White American patients andoften female. Further, early studies of African Americanand White American veterans had suggested that MSoccurrence in African American patients was small;owing such low incidence to factors such as African ancestry, genetic factors, and socioeconomic predictorswhich are yet to be uncovered.2 One population study byLanger-Gould, however, contradicts the idea of rates ofMS between White Americans and African Americans aslow as two to one, respectively.3 In this study of 496 MSpatients with just over 21 percent of those identifying asAfrican American patients, a higher incidence of MS wasfound among African American patients. 3 This study wasthe first of its kind and began to challenge the long heldbelief that MS is a rare disease for African Americans,domestic or abroad.

Differences in occurrence and progression of MS betweenAfrican American and White American patients was firstacknowledged in the 1970s.4 It has long been debatedwhether the differences in MS outcomes for AfricanAmerican and White American patients represent clinical differences. Research still questioning the notion,suggests that African American patients have not beenstudied enough to draw such conclusions. To the contrary,studies supporting the idea claim greater gray matterdegeneration in a broader portion of the brain as definingproof of a clinical difference among the two racial groups.2

In this article, the overall variations in disease profile forAfrican Americans with MS – symptoms, severity andtherapeutic outcomes – are highlighted in an attempt toshed light on this disparity and encourage more focusedstudies on African Americans suffering with MS.

MS Prevalence and Symptom Profile for the African American PatientAfrican Americans have a lower overall prevalence of MSthan White American patients.2,5 However, the precisepopulation of African American patients with MS isunknown. It is debated whether affected, AfricanAmerican patients are more likely to receive a diagnosis atan older age or younger age.2,6,7 Nevertheless, AfricanAmericans are known to experience more severe disability,are more prone to a secondary progressive MS diagnosis(the last and most debilitating stage of MS), have a diag-nosis of transverse myelitis, suffer decreased motor function,and suffer optic nerve damage.2,6 These differences are suspected to be due to both genetic and socio-culturalinfluences. Socioeconomic status, later diagnosis, samplingbias and genetic predisposition are all likely culprits forthe more aggressive symptoms and exacerbations inAfrican American patients.3 Whatever the individualmanifestations of the disease, advances in treatment promote greater quality of life for all patients. Still, treatment differences between African American andWhite American MS patients persist and encourage more

Differences in the Manifestation of Multiple Sclerosis inAfrican American Patients By Ch am i k a Hawk i n s -Ta y l o r, MHA , PhD

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Pharmacology Focus

research focused on this underserved population.8,9 Theliterature also suggests that in later stages of MS, AfricanAmerican patients may go untreated as symptoms occurand worsen.8

Differences in the manifestation of MS symptoms areunderstood to a limited extent between AfricanAmericans and White Americans. One study of amatched sample of early stage, MS patients, 54 AfricanAmerican and 54 White American, investigated the differences in both cortical thickness and thalamic volume.10 Global, cortical thickness was significantly lowered in African American patients as well as temporallobe atrophy.10 This research was among the earliest toreport differences in gray matter as a result of the MS disease process. Further evidence suggests that relapsesoccur more frequently and for longer instances amongAfrican American patients.8 African-Americans tend toexperience worse post relapse recoveries, faster transitionfrom relapsing – transitioning to secondary-progressiveMS and more rapid accumulation of ambulatory disabilitycompared with White Americans.8 These patients suggestlower health-related quality of life as a result of moresevere physical symptoms and express diminishing abilityto perform daily activities.11

Treatment Response DifferencesMS treatments are far more advanced in their ability toslow the disease process and address symptoms. Stillpatient responses to treatment vary widely by race,although more study is needed. In general, AfricanAmerican patients have shown poorer therapeuticresponses to conventionally disease modifying therapiescompared with White American patients. A study comparing treatment response differences in AfricanAmerican and White American patients found thatAfrican American patients experienced greater disabilityover a shorter period of time, suggesting that conventionaltherapies, namely interferons, glatiramer acetate andnatalizumab had a lesser therapeutic effect in AfricanAmerican patients than in White American patients.8 Anearlier study by Cree and colleagues showed that AfricanAmericans treated with interferon beta 1a (Avonex orRebif) had more exacerbated conditions after six-monthand 12-month treatment response measures. AfricanAmerican patients also had an increased number oflesions following the two treatment timeframes.12

Dimethyl fumarate (DMF) is among treatments demonstrating positive outcomes in African Americanpatients.13

ConclusionProgress in the understanding and treatment of MS isapparent in the general population but less so amongAfrican American patients. Of the studies reviewed forthis article, all but one purported to include a representa-tive sample of African American patients (AfricanAmericans in the U.S. population represent just under 14percent, according to U.S. Census reports). However, ofthese, six studies included less than 100 AfricanAmericans and two were based on a retrospective analysisof data from the same large study. No study was a report ofa randomized, clinical trial. Such evidence supports theneed for more population-based studies with an increasingnumber of African American subjects to understand thephysiology of the disease progression and also to uncoverthe true differences in clinical manifestations and treatmentresponses. Taking these positive steps works toward alleviating negative disparities and enhancing the under-standing and management of MS in African Americanpatients.

REFERENCES1. Poser CM, Paty DW, Scheinberg L, et al. New diagnostic criteria for multiple scle-

rosis: guidelines for research protocols. Ann Neurol. 1983;13(3):227-31.2. Cree BA, Khan O, Bourdette D, et al. Clinical characteristics of African Americans

vs Caucasian Americans with multiple sclerosis. Neurology. 2004;63(11):2039-45.3. Langer-Gould A, Brara SM, Beaber BE, Zhang JL. Incidence of multiple sclerosis

in multiple racial and ethnic groups. Neurology. 2013;80(19):1734-9.4. Huere´r AF: Comments on the natural history of multiple sclerosis in Mississippi

blacks and whites. Univ Mich Med Center J. 1976;42:120-35. Ventura RE, Antezana AO, Bacon T, Kister I. Hispanic Americans and African

Americans with multiple sclerosis have more severe disease course thanCaucasian Americans. Mult Scler. 2016:1352458516679894.

6. Kaufman MD, Johnson SK, Moyer D, Bivens J, Norton HJ. Multiple sclerosis:severity and progression rate in African Americans compared with whites. Am J Phys Med Rehabil. 2003;82(8):582-90.

7. Cree BA, Reich DE, Khan O, et al. Modification of multiple sclerosis phenotypes byAfrican Ancestry at HLA. Arch Neurol. 2009;66(2):226-33.

8. Weinstock-Guttman B, Jacobs LD, Brownscheidle CM, et al. Multiple sclerosischaracteristics in African American patients in the New York State MultipleSclerosis Consortium. Mult Scler. 2003;9(3):293-8.

9. Klineova S, Nicholas J, Walker A. Response to disease modifying therapies inAfrican Americans with multiple sclerosis. Ethn Dis. 2012;22(2):221-5.

10. Al-Kawaz M, Monohan E, Morris E, et al. Differential impact of multiple sclerosison cortical and deep gray matter structures in African Americans and CaucasianAmericans. J Neuroimaging. 2017;27(3):333-8.

11. Buchanan RJ, Huang C, Chakravorty BJ. Health-related quality of life amongAfrican Americans with multiple sclerosis. Ethn Dis. 2011;21(3):377-84.

12. Cree BA, Al-Sabbagh A, Bennett R, Goodin D. Response to interferon beta-1atreatment in African American multiple sclerosis patients. Arch Neurol.2005;62(11):1681-3.

13. Zhovtis Ryerson L, Green R, Confident G, et al. Efficacy and tolerability of dimethylfumarate in White-, African- and Hispanic- Americans with multiple sclerosis.Ther Adv Neurol Disord. 2016;9(6):454-61.

About the Author:Chamika Hawkins-Taylor, MHA, PhD, Assistant Professor, College of Pharmacy,South Dakota State University.

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E x t e n u a t i n g C i r c u m s t a n c e s :

Data Sharing: Leading Data-Driven Population HealthBy Em i l y R . G r i e s e , P hD ; B en s on S . H s u , MD , MBA , FAAP ; a n d

D a v i d A . P e a r c e , P hD

Healthcare systems able to effectively leveragetheir data in the application of advanced analyticsare uniquely positioned to innovate the way they

provide health care. Health care data, however, is oftenhighly unstructured, requiring a unique skillset to manageand analyze it for innovative application. This becomes abarrier as well-trained data scientists are often difficult torecruit and to date haven’t had a direct pipeline for theirexpertise within the health care sector. Fortunately, theupper Midwest is uniquely positioned at an intersection ofacademic institutions with nationally recognized data programs, opening the door for collaboration withresearchers leading their fields in advanced analytics.Thus, programs such as the Sanford Data Collaborative, afirst of its kind data sharing initiative that places real-life,timely health care data in the hands of leading researcherswith the ultimate goal of driving health care delivery to transform community health, are well positioned for success.

The success and growth of data sharing initiatives like thishinge on expertise found both internal and external to aninstitution. Internally, appropriate legal provisions andreview processes are of utmost importance prior to datadistribution to ensure the highest level of patient privacy.Infrastructure must be in place to protect the release of alldatasets including an ironclad data usage agreement withprovisions to safeguard data transfers and use. Externally,public expertise should be sought in the creation of a privacy board, or a body designed to review projects withthe privacy of the community in mind.

Partnering with external academic institutions who havean existing structure to uphold research integrity (forinstance, through institutional review boards) is furthercrucial to providing the necessary foundation for successfuldata sharing. The Sanford Data Collaborative looked tofoster lasting partnerships across regional academic institutions and sought guidance from academic leaders to

serve on an advisory board and help identify populationhealth topics that would be beneficial to researchers andcommunities alike. By further serving on an advisoryboard, academic leaders have the ability to provide crucialexpertise on the potential impact of data sharing for theirinstitutions as well as for their communities and region.Additionally, direct meetings with academic researchersprovide an opportunity to discuss project ideas and available data elements. These meetings also presented anopportunity to reiterate the need for truly multidisciplinaryteams that can bring diverse expertise (i.e., data science,pharmacy, nursing, business, health informatics, etc.) bothin advanced data analytics but also in translating itsimpact for innovative healthcare delivery. As such, teamswith multidisciplinary expertise willing to identify novelapproaches to population-level data sets are most likely tobe successful as a data sharing partner.

Equally important to building collaborative relationshipsexternally is the need to build a collaborative internalinfrastructure. For the Sanford Data Collaborative, keyleadership from across the enterprise, spanning research,data analytics, health plan, and health care delivery, werebrought together to identify priorities and to create aprocess that could push past research for research sake andwork to translate innovative advanced analytics solutionsinto clinical application and ultimately positive communityhealth impact. As such, along with an analytics phasethere is a need to move towards validation (see Figure 1),where researchers have the opportunity to confirm findingswithin a healthcare system, providing evidence for futurestudies and data to further pioneer improvements inhealth care delivery.

It is evident that data sharing with the appropriate structures in place can bring healthcare systems to theforefront of health care innovation. Advanced analyticmodeling focused on predictive risk stratification, chronicdisease management, diagnostic testing strategies, or

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technology utilization, for example, has the potential tosharpen data-driven provider practices, applying algorithmsthat can offer increasingly robust evidence upon whichcare decisions can be made – more precisely and efficiently.The ability to predict and prescribe health care at the population level through the application of existing bigdata further opens a new door for health care delivery andits impact on community health outcomes. As such, success for the Sanford Data Collaborative is in bringingtogether multidisciplinary teams of researchers and clinicians to leverage population-based data, driving anintegrated vision to further understand and impact of thelarger healthcare environment within our communities.

About the Authors:Emily R. Griese, PhD, Assistant Scientist, Center for Health Outcomes and PreventionResearch, Sanford Research, Sioux Falls, South Dakota; Assistant Professor,University of South Dakota Sanford School of Medicine.Benson S. Hsu, MD, MBA, FAAP, Medical Director, Pediatric AirMed Flight Program,Sanford Children’s Hospital; Pediatric Critical Care Physician, The Miller PediatricCritical Care Unit, Sanford Children’s Hospital; Secondary Assistant Scientist,Children’s Health Research Center, Sanford Research, Sioux Falls, South Dakota;Associate Professor, Department of Pediatrics, University of South Dakota SanfordSchool of Medicine.David A. Pearce, PhD, Executive Vice President, Innovation and Research, SanfordHealth; Senior Scientist, Childrens Health Research Center, Sioux Falls, South Dakota;Professor, Department of Pediatrics, University of South Dakota Sanford School ofMedicine.

Figure 1. Data Collaborative Phases

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As a gung-ho football guard for the De SmetBulldogs back in the ‘60s, I had the “do or die”mentality for my team. That type of attitude can

make winning teams, but can also can be a formula forserious injury. Now, as a physician with over 32 years ofexperience, I have a better understanding of how whilesome sports activities can be helpful, others can beextremely harmful.

Let us look at concussions, for example, or really any typeof head injuries that often occur in football or other contact sports. These players need to avoid further headtrauma for a defined period of time or it can cause permanent brain damage. They must also avoid repeatedhead injury, as that can also lead to serious long-term con-sequences. The 2015 film Concussion, starring Will Smith,is based on a true story and highlights the dangerous resultsof repeated head injuries in professional football players.

However, it is not just head injuries that can cause seriousor permanent damage. In wrestling or dance, athletes areunder pressure to “make weight”, often taking extrememeasures to do so. This results in the promotion of malnutrition and even life-threatening eating disorderslike anorexia and bulimia. Problems can also arise fromtrauma to young immature bones, like knee injuries in soccer players and ankle injuries in basketball players.Also, running around outside on a hot day can bring onproblems from overheating and under hydrating. Therecan be wounds to the psyche of little leaguers being pressured by over-competitive parents; head and backinjuries from dropped cheerleaders; neck trauma fromgymnastics; and any kind of injury from the worst of allinjury makers: college rodeo.

This is not to deny all the good that comes from learninghow great it is to be in condition, or the value that comes

from friendships and camaraderie associated with teamsports. Hey, ask me anytime about the fabulous footballteam DeSmet had in ‘66, and you will know how important that was to me. With proper training, coaching,and a healthy respect for the dangers of any sport, mostinjuries can be avoided. Also, correctly identifying,addressing, and treating injuries that do occur can significantly reduce the risk of permanent disabilities laterin life.

I believe the emphasis in sports should be to start childrenon a lifetime plan of exercise, taken with every safety precaution, so that sports and good health can be enjoyedthroughout their life.

P a t i e n t E d u c a t i o n :

Dr. Rick Holm wrote this Prairie Doc Perspective for “On Call, “ a weekly program where medical professionals discuss health concerns for the general public.“On Call “ is produced by the Healing Words Foundation in association with the South Dakota State University Journalism Department. “On Call “ airs Thursdays on

South Dakota Public Broadcasting-Television at 7 p.m. Central, 6 p.m. Mountain. Visit us at OnCallTelevision.com.

Sports Injuries By R i c h a r d P. Ho lm , MD

Special Features

The decision-making process for adult immunizationcan be complex in how it affects both providersand patients. Multiple social, psychologic and

economic factors influence vaccination rates and the goalto improve those numbers. While the value of vaccinationhas evidence-based support, the spectrum of vaccine decision-making covers a broad range of factors. Cost,available access, health literacy and social media all play arole in delivering vaccine in a timely and efficient manner.

From their initial inception to the present, vaccines havealways raised a safety and effectiveness concern. Thoughnot perfectly safe or completely effective, data is clear thattheir public health benefit is very strong and overwhelm-ingly safe. For patients who are hesitant or against vaccines, there are numerous communication strategies tohelp educate and motivate them to receive vaccination.

Providers, regardless of their specialty or location, shouldstrongly recommend and encourage immunization. Mostimportant is the direct influence of the provider to remindthe patient to keep updated on vaccinations. This shouldinclude all levels of clinic staff from the front desk toadministration. If appropriate, the use of posters, flyers andinformation sheets along with social media can remindand incentivize patients to obtain the needed vaccines.Clinic work flow and electronic medical records need toremind and emphasize updated vaccination status. Often,nurses and medical assistants are leading efforts to makesure immunization status is timely.

Collaborating with pharmacies in reference to vaccineadministration is another tool to improve rates and assistwith efficient payment of herpes zoster vaccine. Othersources to utilize include the State Department of Health,county and public health nurses, home health agenciesand neighboring physician offices. Multiple professionalassociations and advocacy groups along with the Centersfor Disease Control and Prevention (CDC) can provide

resources and advice while also acknowledging and celebrating success in reaching immunization goals.

Immunization Information System (IIS) is a database tohelp clinical systems communicate with one anotherregarding patient immunization status. This registry allowsproviders to partner in delivering appropriate and timelyimmunizations by providing comprehensive and up-to-date vaccination records to all health care facilities. Also,the Medicare Quality Payment Program (QPP) has initiatives that allow providers to use immunization registry reporting as a tool to achieve quality paymentmeasures.

FluFIT is another program that promotes vaccination bycombining yearly influenza vaccine with fecal immuno-chemical tests (FIT) for colorectal cancer. Providing twoimportant health maintenance elements as a bundle is anefficient use of patient time. The impact of underservedand minority populations as well as diminished patienthealth literacy can lower rates and require ongoing effortsto encourage health maintenance including immunization.

The Great Plains QIN is working with providers andpatients to increase immunization rates for influenza,pneumonia and herpes zoster. The challenge of infectiousdisease prevention lies in increasing the percentagereceiving timely administration of these extremely impor-tant agents.

Please contact me at Stephan.schroeder@area-a.hcqis.orgor Katy Burket, RN, at katy.burket@area-a.hcqis.org forfurther information on tools and technical assistance forincreasing immunizations.

377August 2017

Special Features

“Quality Focus “ is a monthly feature sponsored by SDFMC, South Dakota’s Quality Improvement Organization. For more information about the SDFMC, visit their website at www.sdfmc.org.

Q u a l i t y F o c u s :

Encouraging and Communicating the Value of ImmunizationBy S t e ph an S ch r o e d e r, MD , CMQ , CMD

Med i c a l D i r e c t o r, S o u t h D a k o t a F o und a t i o n f o r Med i c a l C a r e

This material was prepared the Great Plains Quality Innovation Network, the Medicare Quality Improvement Organization for Kansas, Nebraska, North Dakota and South Dakota, under contractwith the Centers for Medicare & Medicaid Services (CMS), an agency of the U.S. Department of Health and Human Services. The contents presented do not necessarily reflect CMS policy.11S0W-GPQIN-SD-F1-232/0817

SOURCES1. Poland CM, Bronson EK, The need for multidisciplinary perspective on vaccine

hesitancy. Vaccine. 2015 Jan 3; 33(2):277-9.

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What is a confidential monitoring program?When an applicant or a licensee has been determined byan evaluation to be impaired in a manner where the individual demonstrates the inability to practice in theirhealth-related profession with reasonable skill and safetydue to mental health issues, physical issues, or substanceuse related disorders (alcohol or drug abuse, dependency,or addiction), the applicant or licensee is enrolled in a confidential monitoring program. The confidential monitoring program is an agreement between the participant (applicant or licensee) and the BMOE staffreview panel to defer any recommendation for disciplineon a license as long as the participant can be monitored to ensure their ability to safely practice. See the flowchartgraphic for the process.

Medical Board Monitoring Program (MBMP)

What is the purpose of the BMOE staff review panel?The review panel administers the program for the individual. The participant’s case stays at the staff level and does not go to the full BMOE unless the participant isunable to comply with the MBMP. The review panel consists of the BMOE executive director and one BMOEboard member who will, in effect, “be considered one ofthe staff” in order to make the recommendation as towhether the individual is eligible for the MBMP.

What are the eligibility requirements for the MBMP?The MBMP monitors impaired healthcare providers. Thepotential participant will have undergone an evaluationthat demonstrates their inability to practice in one’shealth-related profession with reasonable skill and safetydue to mental health issues, physical issues, or substanceuse related disorders (alcohol or drug abuse, dependency,or addiction).

Do I need to enroll in the MBMP if I already participatein a monitoring program administered by my employment or other entity? You can continue in your current monitoring programwithout enrolling in the MBMP. However, you must reportyour participation in any and all monitoring/wellness programs, other than the MBMP, on or before you submityour annual license renewal application. You also need tobe aware that the MBMP is the only state BMOE approvedconfidentially protected program for South Dakotalicensees.

I am licensed in another state and am enrolled in thatstate’s monitoring program. Now I am also licensed inSouth Dakota where I currently practice. Do I have toenroll in the MBMP, and how do I keep my previousmonitoring program informed that I am in compliance?Yes, you do need enroll in the MBMP as it is the only stateBMOE approved monitoring program. The MBMP will thencontact your previous monitoring program and sendreports regarding your compliance.

Do the BMOE members know who is in the MBMP?The MBMP participation list is only known to designatedBMOE staff and the BMOE investigative review panel. TheBMOE members do not know who is in the MBMP exceptfor the one board member who is assigned to the BMOE

The South Dakota Board of Medical and Osteopathic Examiners (BMOE) staff submits a column to South Dakota Medicineto inform South Dakota licensed physicians and other licensees about various topics of interest that come to the BMOE.Recently there has been a change in vendors for the health professionals’ assistance program. As a result, those individualswho were being monitored by the previous vendor have been transferred to the BMOE staff administered Medical BoardMonitoring Program (MBMP). This month’s column will point out resources available to individuals who wish to participatein a confidential monitoring program as well as answer some of the frequently asked questions (FAQ) regarding the functioning of a confidential monitoring program. There will be no diminution or changes in services with the MBMP.

379August 2017

investigative review panel. All monitoring will remain confidential to the BMOE board members as long as theparticipant is compliant and doing well in the monitoringprogram.

Does the public know who is in the MBMP?An individual’s participation in the MBMP is confidential tothe public as long as the participant is in compliance withprogram requirements. The public does not have access to information that would identify participants in the program, except in rare cases where the BMOE staff filesformal disciplinary charges against a participant whichmay include noncompliance with an MBMP contract.

Who administers the MBMP?The MBMP is administered by BMOE staff and the established review panel pursuant to authority granted by administrative rules promulgated by the BMOE.

What happens when a licensee or applicant self-reports?The MBMP monitors participants struggling with impairmentissues related to substance abuse, mental health issues, orphysical disability, and is not a disciplinary program. TheMBMP considers a licensee’s or applicant’s self-report to bea positive first step toward bringing a potentially harmfulsituation under control before their professional reputationis damaged.

The MBMP will gather information and make referrals forevaluation as needed. The MBMP then works with thelicensee or applicant to put the required supports in placeto ensure the participant is able to continue to practicesafely. The majority of individuals participating in the program are actively practicing.

Who evaluates the potential participants?Potential participants are evaluated depending upon thecase history of each individual. Some individuals may self-report or apply to the MBMP after having beeninvolved in the judicial system; for example, a DUI or otherincident where evaluations are already available. In othercases, there may be questions as to whether a diagnosisindicative of impairment exists. That individual would bereferred to the appropriate evaluator or evaluation teamprior to entering the confidential MBMP.

Who treats the participants?Once a determination of impairment is made and the participant enters the MBMP, the participant chooses a

medical and support team. The MBMP participant is anactive participant with their medical and support team. As determined by the previously mentioned evaluationrecommendations, this team is comprised of a monitoringphysician or other healthcare provider; a monitoring therapist, psychologist, or counselor; a work-site monitor,and an aftercare monitor. The medical and support teamwill be approved by the MBMP.

Is it a good idea to have the licensing board administerthe program?The BMOE has a legal obligation and mission to ensuresafe medical practice for the protection of the public whoseek professional medical services within the State. TheBMOE has promulgated administrative rules that provide a transparent process for the investigation and regulationof medical practice while providing due process rights toapplicants and licensees. While the process is transparent,participation remains confidential. Healthcare facilitieshave immunity when reporting employees to the BMOEstaff.

Who is the contact person?For the convenience of the licensee or applicant, one person on the BMOE staff is designated for contact purposes. Separate and dedicated phones, both mobileand land-line with a toll-free phone number option, areavailable. A separate and dedicated email is also accessible.A separate and dedicated website is being developed.Please contact:Randi SterlingMedical Board Monitoring Program (MBMP)Phone: 605-367-7700| Toll free: 888-340-4371| Cell: 605-400-4542Email: mbmp@state.sd.us

Who answers general questions?Any general questions should be directed to the BMOEexecutive director, Margaret Hansen.

SummaryThe BMOE has a long history of monitoring its licensees.The BMOE has agreements in place with the monitoringcompanies, Affinity eHealth and Soberlink to serve theMBMP. The BMOE is continuing to research other regionaland national monitoring programs including protocols,processes, budgets, and program services, to identify bestpractices.

Board News is a monthly feature sponsored by the South Dakota Board of Medical and Osteopathic Examiners. For more information, contact the Board at SDBMOE@state.sd.us or write to SDBMOE, 101 N. Main Avenue, Suite 301, Sioux Falls, SD 57104.

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House Club $300+(Physician and Spouse)

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E. Paul Amundson, MD

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House Club $300+(Physician and Spouse) Member $175+ Member $175+Chairman’s Club

$1,000+(Physician and Spouse)

Membership 2017

Your SDSMA PAC membership is very important in order to elect

political candidates who understand the practice of organized medicinein South Dakota. To donate toSDSMA PAC, please visit

www.sdsma.org.

BENEFITFor Your Benefit:

Thank you for your membership in theSDSMA. As a member, you have severaldirect opportunities to become moreinvolved in the important work of theSDSMA:

• Doctor of the Day – serve as thephysician for the South Dakota StateLegislature for one day during session;

• Physician lobbyist – serve as a volunteer lobbyist during the legislativesession;

• SDSMA PAC – help friends of medicine become elected officials andlawmakers;

• SDSMA committees and task forces –serve the organization and yourself;

• SDSMA appointments to state boards,committees and commissions – theSDSMA is asked to nominate and recommend physicians to fill positionsto numerous vacancies every year;

• Membership sections for medical students and residents – we needleaders at each stage of a physician’scareer; and

• Districts and specialty societies – forlocal involvement.

If you’d like to get involved, give us a callat 605.336.1965 or visit www.sdsma.orgfor more information.

Get Involved in the SDSMA

“For Your Benefit” is the SDSMA’s monthly update on programs and services available to members.

Member NewsVisit www.sdsma.org for the latest news and information.

381August 2017

In 2017, the South Dakota legislature granted certified nurse practitioners (CNP) andcertified nurse midwives (CNM) the authority to provide certain direct patient careservices independently, provided they have completed 1,040 hours of patient careunder the collaboration of a physician, certified nurse practitioner, or certified nursemidwife.

The CNP and CNM’s direct patient care practice must be within their personal abilitiesand skills. SDSMA advises that the collaboration should also be consistent with thenature of the physician’s practice and area of expertise. Collaborating physicians mayexpose themselves to potential liability for the acts or omissions of the collaboratingprofessional; therefore, care should be taken to provide appropriate collaboration andto provide for appropriate insurance coverage.

More information is available in the SDSMA legal brief Advanced Practice Nurses:Scope of Practice and Collaboration Requirements at www.sdsma.org. Through theSDSMA Center for Physician Resources, the SDSMA has developed more than 50legal briefs that are available to members. In addition, the Center develops and delivers programs for members in the areas of practice management, leadership andhealth and wellness.

Legal Brief Highlight: Advanced Practice Nurses

The first-year American Medical Association representatives at the University of SouthDakota Sanford School of Medicine have announced the third annual Physician’s CupGolf Tournament. The tournament will be held on Aug. 12 at Prairie Green Golf Coursein Sioux Falls. All proceeds will benefit LifeScape, which provides education, care, andmedical services for adults and children with mental and/or physical disabilities.

The tournament will be a four person scramble with a shotgun start at 10 a.m.Registration is $100 per participate, which includes a golf towel, two drinks and ameal following the round. To register, call Michael Blankespoor at 712.470.6819 oremail usdssom.ama@gmail.com.

Medical Students Hosting Third Annual Physician’s Cup Golf Tournamentfor Charity

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Member News

Members of the South Dakota State Medical Association (SDSMA) and the SDSMA Medical Student Section attended the AmericanMedical Association (AMA) Annual Meeting in Chicago in June with hundreds of others from across the country. The gathering was filledwith activities and policy debate that will help shape the future of health care in the nation. Some policies adopted by the AMA House of

Delegates (HOD) include the following:

The Health Threat of Psychoactive SubstancesNew psychoactive substances (NPS) are quickly emerging, transient and difficult to track. While some coordinated public health responses have been used to combat NPS outbreaks, most strategies and solutions remain disconnected, lacking necessary informationand data sharing capability. With the eruption of both illicit and synthetic drugs, as well as a lack of regulation, physicians are also searching for further education to aid in treating patients. Delegates voted to support multifaceted, multiagency approaches to combat NPS.Delegates also supported increased NPS surveillance and early warning systems for more actionable information that can quickly aid lawenforcement, public health officials, emergency physicians and vulnerable populations in mitigating the growing NPS problem.

Pain Care and Opioid-Use DisorderWhile reversing the opioid epidemic remains a vital focus, AMA delegates adopted resolutions to seek strategies and education to help themillions who live with chronic pain. Chronic pain affects 100 million Americans. With such a high burden on the American public, the HODtook actions aimed at improving pain care while expanding access to buprenorphine for patients with opioid-use disorder and encouragingthe safe storage and disposal of controlled substances.

Veterans’ Access to CareThe AMA will continue working with the U.S. Department of Veterans Affairs (VA) to provide quality of care to veterans and advocate newfunding for the Veterans Choice Program (VCP). The HOD also adopted new policy that includes encouraging the VA to continue developing and enhancing alternative pathways for veterans to seek care outside the VA system if it cannot provide them with adequateor timely care, supporting the consolidation of VA community care programs, and making the VCP permanent.

Support for Transgender PatientsThe HOD adopted policies in an attempt to enhance care for the thousands of Americans who identify as transgender, as well as for manyothers who do not identify with one particular gender. Delegates directed the AMA to work with other appropriate organizations to “informand educate the medical community and the public on the medical spectrum of gender identity.” The authors of the adopted resolutionwrote that gender is “incompletely understood as a binary selection” because gender, gender identity, sexual orientation, and genotypicand phenotypic sex are not always aligned. The HOD also adopted policy opposing any efforts that would prevent a transgender personfrom “accessing basic human services and public facilities in line with one’s gender identity.”

Access to Care for Refugees and Detained Immigrants Delegates adopted a series of resolutions that affirmed the AMA’s commitment to patients’ health and well-being, regardless of their immigration status. They also voted to support a ban on law-enforcement officials’ use of information contained in patient medical recordsas part of immigration enforcement actions against people living in the U.S. illegally. The new policy reinforces the AMA’s longtime opposition to any federal legislation requiring physicians to establish the immigration status of their patients or collect and report dataregarding an individual patient’s legal resident status. The HOD took several other actions touching on the health and well-being of refugeepatients and patients held in immigration detention facilities. One such action focuses on supporting programs to promote education aboutavailable low-cost health care plans to refugees. This policy is part of AMA delegates’ efforts to increase access to health care for immigrants, who are at higher risk for chronic health and mental health conditions.

Mitigating Sexual Exploitation and Sex Trafficking of MinorsThe resolution adopted requests that AMA advocate for the development of laws and policies that utilize a public health framework toaddress the commercial sexual exploitation and sex trafficking of minors by promoting care and services for victims instead of arrest andprosecution. Testimony was in unanimous support of the resolution. Some delegates spoke of their professional experience in working withsurvivors of human trafficking, and relayed the trauma experienced by these survivors. Others discussed the need to address human trafficking as an important goal of public health.

Promoting the AMA Model Medical Staff Code of Conduct and its Application to Employed PhysiciansDelegates adopted a resolution that requests that the AMA actively educate state and specialty medical societies about the AMA Medical

AMA Delegate Report – 2017 Annual Meeting

ISSUEThe Issue Is...

383August 2017

“The Issue Is” is the SDSMA’s monthly update on key policy issues ofimportance to physicians.

Member News

The Centers for Medicare and Medicaid Services (CMS) has introduced Connected Care, a public education campaign toraise awareness of the benefits of chronic care managementservices for Medicare beneficiaries living with multiple chronic conditions and to provide health care professionalswith support to implement chronic care management.

Learn more about the Connected Care campaign by visitinggo.cms.gov/CCM, which has additional resources, including webinars and campaign toolkits for health professionals and partners.

Staff Code of Conduct and promote its use. In addition, the resolution requests that the AMA advocate for employed physicians to be afforded the same right of review as non-employed physicians in accusations where conduct is characterized as “disruptive, intimidatingor inappropriate.” The resolution received unanimous support. Testimony focused on the distinction between employed and non-employedphysicians, and how the rights of both categories of physicians should be treated equally with respect to medical staff privileges. TheReference Committee heard lengthy testimony about the distinction between contract rights and medical privilege credentialing, and howthe credentialing of medical staff should remain separate from the rights employed physicians obtain/lose through employment contracts.

Efforts to Improve Access to Diabetes Self-Management Training ServicesThis resolution asks that the AMA actively support regulatory and legislative actions that will mitigate barriers to diabetes self-management training utilization; and support outreach efforts to foster increased reliance on diabetes self-management training by physician practices in order to improve the quality of diabetes care.

Native American Medical School EnrollmentA resolution concerning the declining Native American medical school enrollment asks that the AMA partner with key stakeholders to studywhy enrollment is declining in spite of an overall substantial increase in medical school enrollment. The reference committee heard testimony on the need for increased diversity of the physician workforce.

Physician and Medial Staff Member Bill of RightsDelegates adopted a series of fundamental medical staff rights and responsibilities based on existing AMA policy. New language affirmsthat the AMA recognizes the right of medical staff to determine which non-physician health care professionals may be members of themedical staff.

Respectfully submitted,

Mary S. Carpenter, MD Robert L. Allison, MDSDSMA Delegate to the AMA SDSMA Alternate Delegate to the AMA

Keep Your Information Up-to-Date: Log on Today

CMS Raises Awareness ofChronic Care Management

In order for the SDSMA office to provide members with timelyinformation, it is important that members regularly review theircontact information on file with the SDSMA. Have you changedpractice locations? Is your email correct? Is your mail going to theright place?

All SDSMA members have an existing online profile. Visitwww.sdsma.org and log into your secure online account. Next,access your profile by clicking the “Update my Profile” link at thetop of the page.

Please take a few minutes to review your profile and make anynecessary updates. Updating your secure account keeps yourinformation up to date and notifies the SDSMA of any changes soyou are accurately listed in the member directory and ensures thatyour membership materials, emails and renewal notices are sent tothe appropriate mailing and email addresses.

Do you have a new photo? Updated photos can be uploaded toyour user account or emailed to membership@sdsma.org.

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