February 2011 JMSMA

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February

VOL. LII

2011

No. 2


Save the Date for MSMA’s

143 Annual Session rd

May 19 – 22, 2011 Tupelo, Mississippi

Welcome Reception at HealthWorks, Tupelo’s new children’s health museum Meetings at BancorpSouth Conference Center

Accommodations at Tupelo’s Hilton Garden Inn CME and golf tournament at nearby Old Waverly Golf Course For a preliminary schedule of events or to register online, visit www.MSMAonline.com!

Questions? More information? Contact Becky Wells at 601-853-6733, Ext. 340 or BWells@MSMAonline.com.

President’s Reception at Tupelo Automobile Museum


Lucius M. Lampton, MD EDITOR D. Stanley Hartness, MD Richard D. deShazo, MD ASSOCIATE EDITORS Karen A. Evers MANAGING EDITOR PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD Leslie E. England, MD, Ex-Officio Myron W. Lockey, MD, Ex-Officio and the Editors THE ASSOCIATION Tim J. Alford, MD President Thomas E. Joiner, MD President-Elect J. Clay Hays, Jr., MD Secretary-Treasurer Lee Giffin, MD Speaker Geri Lee Weiland, MD Vice Speaker Charmain Kanosky Executive Director JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual). Periodicals postage paid at Jackson, MS and at additional mailing offices. CORRESPONDENCE: JOURNAL MSMA, Managing Editor, Karen A. Evers, P.O. Box 2548, Ridgeland, MS 39158-2548, Ph.: (601) 853-6733, Fax: (601)853-6746, www.MSMAonline.com. SUBSCRIPTION RATE: $83.00 per annum; $96.00 per annum for foreign subscriptions; $7.00 per copy, $10.00 per foreign copy, as available. ADVERTISING RATES: furnished on request. Cristen Hemmins, Hemmins Hall, Inc. Advertising, P.O. Box 1112, Oxford, Mississippi 38655, Ph: (662) 236-1700, Fax: (662) 236-7011, email: cristenh@watervalley.net POSTMASTER: send address changes to Journal of the Mississippi State Medical Association, P.O. Box 2548, Ridgeland, MS 391582548. The views expressed in this publication reflect the opinions of the authors and do not necessarily state the opinions or policies of the Mississippi State Medical Association. Copyright© 2011 Mississippi State Medical Association

FEBRUARY 2011 SCIENTIFIC ARTICLES

VOLUME 52

NUMBER 2

Autism and Vaccines: Search for Cause Amidst Controversy

35

Mississippi Medicine Up-to-Date: Medical Therapy for Systemic Lupus Erythematosus

39

Clinical Problem - Solving: A Pain in the Neck

44

Jericho Bell, MD; Omar Abdul-Rahman, MD and Susan Buttross, MD, FAAP

Jason K. Taylor, MD and Robert W. McMurray, MD

Sheree Carney Melton, MD

PRESIDENT’S PAGE

“Ain't Love Grand?”

48

Tim J. Alford, MD, MSMA President

EDITORIAL

Mississippi: How Did We Get to This Place?

54

Richard D. deShazo, MD, Associate Editor

SPECIAL ARTICLE

Introducing MPHP Medical Director Scott L. Hambleton, MD

58

Karen A. Evers, Managing Editor

RELATED ORGANIZATIONS

Mississippi State Department of Health

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DEPARTMENTS

Poetry and Medicine The Uncommon Thread Placement/Classified

62 64 64

ABOUT THE COVER:

WINTER SNOW SCENE AT CEDARS BY THE LAKE — MSMA Past President Randy Easterling, MD took this photograph of his horses after a snowstorm blanketed Mississippi February 12, 2010. Affectionately known as Sugar and Spice, the horses were given as an anniversary gift to his wife Janie. The horses roam the Easterling property, Cedars by the Lake, in Bovina, an unincorporated community located about seven miles east of Vicksburg in Warren County off Interstate 20. Dr. Easterling has been in the private practice of family medicine and addiction medicine in Vicksburg since 1987.❒ February

Official Publication of the MSMA Since 1959

VOL. LII

2011

No. 2

FEBRUARY 2011 JOURNAL MSMA

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JOURNAL MSMA FEBRUARY 2011


• SCIENTIFIC ARTICLES •

Autism and Vaccines: Search for Cause Amidst Controversy Jericho Bell, MD; Omar Abdul-Rahman, MD; Susan Buttross, MD, FAAP

I

NTRODUCTION

There is no doubt that the incidence of autism has increased. Prior to the 1980s autism was considered rare, occurring only 1 in every 2000 children. A 2006 study from the Centers for Disease Control and Prevention, however, reports an average prevalence of autism spectrum disorder to be 9 in 1000 children, or approximately 1 in 111.1 The increase may, in part, be due to broadened diagnostic criteria and increased awareness of the disorder. Nevertheless, the increase has been a steady one, and no one has been able to relate this increase to any single factor. There has been much discussion in the lay and scientific literature of possible causes. One major question has been “Do vaccines cause autism?” There have been two dominant theories over a vaccine-related cause for the increased incidence. The first was brought up in a widely publicized and controversial case series that suggested a link between the measles-mumps-rubella (MMR) vaccine and autism.2 The second postulated association is between autism and the vaccine preservative thimerosal. Many studies have investigated these concerns. This article will discuss these issues as well as what is known regarding possible causes of autism. AUTHOR INFORMATION: Dr. Bell is an assistant professor of internal medicine and instructor of pediatrics at the University of Mississippi Medical Center. Dr Abdul-Rahman, MD, is an associate professor of pediatrics and clinical geneticist at the University of Mississippi Medical Center with an interest in dysmorphology, craniofacial anomalies, and the genetic etiology of autism and other developmental disorders. Dr. Buttross, MD, FAAP, is a professor of pediatrics, assistant professor of child psychiatry and chief of the division of child development and behavioral pediatrics at the University of Mississippi Medical Center.

CORRESPONDING AUTHOR: Susan Buttross, MD, FAAP, 2500 North State Street, Jackson, MS 39216. REPRINTS should be addressed to Dr. Susan Buttross.

KEY WORDS:

AUTISM, VACCINES, IMMUNIZATIONS,

AUTISM SPECTRUM DISORDER, GENETICS, MEASLES-MUMPS-RUBELLA (MMR) VACCINE, THIMEROSAL

AUTISM AND MMR

The controversy surrounding an association between autism and the MMR vaccine originates from a 1998 case series.2 Twelve children were referred to a London pediatric gastroenterology unit for abdominal pain, diarrhea, and loss of acquired skills. Ultimately, nine were diagnosed with autism or an autism spectrum disorder (ASD). Through retrospective accounts by parents or physicians, onset of developmental problems in eight of the children was temporally associated with MMR vaccination. Additionally, nine children had terminal ileal lymphoid nodular hyperplasia per endoscopy. Authors hypothesized the MMR vaccine caused intestinal inflammation which altered intestinal barrier function and permitted the passage of gut-derived peptides. These peptides were posited to have an “opioid effect” on the brain, disrupting endogenous opioid regulation and thereby altering brain development.2 The implication of MMR being associated with autism came at a time when the medical community was already investigating a possible increase in the incidence of autism spectrum disorder. Ensuing studies regarding a possible association between MMR and autism will be discussed below. One United Kingdom study compared the incidence of autism before and after the 1988 introduction of the MMR vaccine.3 This population-based study showed a steady upward trend in the number of cases by year of birth. There was, however, no marked change in the trend after the introduction of the MMR vaccine. Additionally, age at diagnosis was no different in children vaccinated before or after 18 months of age or in unvaccinated children.

FEBRUARY 2011 JOURNAL MSMA

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A large retrospective cohort study was conducted of all children born in Denmark over seven years to compare the incidence of autism in vaccinated and unvaccinated children.4 Less than one percent of the 537,303 children in the cohort had autism or other ASD. Of all the children, 82% had received the MMR vaccine. The relative risk of autism and other ASD in the vaccinated group was 0.92 (95% confidence interval, 0.68 to 1.24) and 0.83 (95% confidence interval, 0.65 to 1.07), respectively. The study, therefore, did not support an association between MMR vaccination and autism or ASD. A United States population-based case-control study investigated a possible association between earlier age at first MMR vaccination and increased risk for autism. No such association was found.5 In a population-based study in Montreal the prevalence of ASD increased despite decreasing MMR immunization rates.6 Moreover, when a second MMR dose was added to the immunization schedule in 1996, no difference was seen in the rate of increasing prevalence. Similarly, in Yokohama, Japan, a total population study of 31,426 children showed a significant increase in the incidence of ASD in contrast to a concurrent significant decline in MMR vaccination rate.7 With the start of the MMR vaccination program in Finland in 1982, a countrywide surveillance system was established to monitor for serious adverse events.8 A retrospective study of 535,544 vaccinated children revealed no clustering of hospital admissions for autism related to MMR administration. Systematic reviews of the epidemiological evidence have failed to find support for any causal association between MMR vaccination and autism.9, 10, 11 In 2004 ten of the thirteen authors of the original report that first raised question of a link between autism or ASD and MMR vaccine issued a statement retracting that interpretation.12 The Lancet fully retracted the article in 2010.

AUTISM AND THIMEROSAL

Thimerosal is the other popularly scrutinized vaccine-related issue in the autism cause debate. Thimerosal is sodium ethyl mercury thiosalicylate, an organic compound that has been used as a preservative in several vaccines that are part of the routine vaccination schedule for children in the United States. There are differences in methyl mercury and ethyl mercury. Methyl mercury has a half-life of 50 days and is actively transported across the blood-brain barrier, whereas ethyl mercury’s half life is 7 days and ethyl mercury is not transported across the blood-brain barrier.13, 14, 15 The amount of ethyl mercury in vaccine doses ranges from <0.03 to 25 micrograms. Other than a hypersensitivity reaction, such a low dose has never been shown to be a risk to humans.16, 17 Still the American Academy of Pediatrics (AAP) and the United States Public Health Service (USPHS) issued a joint statement in 1999 recommending that thimerosal-containing vaccines be reduced or eliminated.18 This recommendation was made as a precautionary measure in response to a statement by the United States Food and Drug Ad-

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JOURNAL MSMA FEBRUARY 2011

ministration (FDA) saying that the total cumulative doses of ethyl mercury after multiple vaccinations could potentially exceed the Environmental Protection Agency guidelines for methyl mercury.16 In 2002, an advisory committee reported to the World Health Organization that there was no evidence of harm caused by the low levels of thimerosal in the vaccines and that continued use of thimerosal in vaccines was safe.19 The statements from the FDA and AAP/USPHS, however, led to ongoing concerns regarding a link between thimerosal and autism. Due to these concerns, there have been a number of epidemiologic studies completed to evaluate any possible link between thimerosal-containing vaccines and autism.20, 21, 22, 23 One such study compared the prevalence and incidence of autism in California, Sweden, and Denmark in children and the average exposure to thimerosal-containing vaccines in each location.24 The data from California examined populations-based data from the United States through immunization surveys and counts of children diagnosed with autism-like disorders seeking special education services. In Sweden and Denmark, national data on autism cases and national vaccination coverage levels were used. In all three regions the incidence and prevalence of autism spectrum disorders began to rise in 1985, and the rate of acceleration of diagnoses increased significantly in the early 1990s. However, in contrast to the United States, where the average thimerosal dose from vaccines increased through the 1990s, the doses in Sweden and Denmark, which were already low, decreased in the late 1980s. The authors concluded that the evidence was not consistent with the hypothesis that there was connection between thimerosal exposure in vaccines and autism. In another study completed in Denmark, the incidence of autism in children between the ages of 2 and 10 years was compared before and after thimerosal was no longer used in vaccines.25 Not only was there no trend toward an increase in autism during the time period that thimerosal was used, but when the thimerosal-containing vaccines were discontinued there was an increase in the incidence of autism. Study results out of Montreal and California were very similar to those of Denmark’s.17, 26 To date, no study has shown a decrease in the incidence of autism with the removal of thimerosal from vaccines. Even though a connection has not been shown between thimerosal and the increase in autism, thimerosal was removed from all routine childhood vaccines in 2001 with the exception of the influenza vaccine which is not a required vaccine for school entry. Since the removal, there has been a steady increase in the number of children diagnosed with autism.

GENETICS OF AUTISM

Among the autism spectrum disorders, autism is the most studied entity, and evidence for genetic etiologies continues to be gathered. For example, it is well-known that the recurrence risk for siblings of affected individuals is significantly higher than the general population.24 In addition, twin studies have


shown that concordance rates for monozygotic twins are far greater than similar rates for dizygotic twins.25 Finally, a number of susceptibility loci identified in familial cases of autism have been identified. Approximately 90-95% of autism is idiopathic in nature with the remainder believed to be due to a number of different etiologies including environmental agents such as in utero rubella infections, chromosomal abnormalities, and single gene disorders such as tuberous sclerosis complex and Fragile X syndrome. As the sophistication of genetic testing improves, an increasing number of etiologies are expected to be identified in idiopathic autism. The routine evaluation and management of children with autism and ASD involve a multi-disciplinary approach. Consultations from neurologists, behavioral/developmental pediatricians, physical and occupational therapists are frequently sought. Recently, due to the identification of heritable and genetic etiologies, clinical geneticists are increasingly called upon to assist in the diagnostic evaluation of autistic children. A number of studies over the last decade identifying a multitude of genetic etiologies have been published with recommendations regarding cytogenetic and molecular testing, primarily for individuals with autism. However, a recent study demonstrated that children who have developmental delay with autistic features, but not meeting the absolute criteria for autism, receive a similar benefit from genetic testing.26 The most common genetic abnormality detected in children with autism is a chromosomal imbalance. Some of the typical abnormalities detected include deletions on chromosomes 16 and 22 as well as duplications on chromosome 15, but numerous other chromosome abnormalities have been detected. Studies have shown that the overall detection rate for chromosome abnormalities in children with autism has been relatively low at around 5%.24, 25, 26, 27 However, most of the studies performed to date utilized the high-resolution karyotype. Recent advances in chromosomal evaluation strategies including genomic microarray analysis are expected to increase the yield of chromosomal aberrations detected in children with autism. Most genetic practices are currently using microarray technology routinely in children who present with autism or autistic features. Single-gene disorders such as Fragile X syndrome (FMR1 gene) and tuberous sclerosis complex (TSC1 and TSC2 genes) are also seen at rates of 1-2% in children with autism.24, 25, 26, 27 Additional genes that have been discovered recently include SHANK3, NLGN3, NLGN4, SLC6A8, FOXP2, and CNTNAP2, all of which play critical roles in neuronal synaptic formation that can give rise to developmental language disorders and autism.28 Testing for individual genes can be costly and is usually deemed necessary only when the family history suggests an X-linked or autosomal dominant form of speech/language disorder and/or autism. However, screening for Fragile X syndrome utilizing molecular testing of the FMR1 gene is routinely recommended.

Metabolic disorders are relatively uncommon in children with autism as metabolic testing usually has yields of less than 1%. However, some conditions such as creatine deficiency, adenylosuccinase deficiency, and mitochondrial disorders have recently gained attention as important conditions to consider.29 Creatine deficiency is unique in that replacement of creatine can reverse the symptoms in affected patients with certain subtypes of the disorder. Mitochondrial disorders may be ameliorated through the use of certain cofactors such as carnitine, coenzyme Q10, and vitamin B complex, though the literature supporting these vitamin cocktails is tenuous at this time. One recent case of a child with a mitochondrial disorder who regressed following immunizations highlights the importance of routine screening for metabolic conditions. Although immunizations have been excluded as increasing the risk of autism, studies in rare conditions such as mitochondrial disease are needed to determine the risk-benefit ratio for this unique subgroup of the population. Finally, metabolic disorders frequently carry a recurrence risk of 25% for future pregnancies, which is much greater than the 5-7% recurrence risk for families who have children with idiopathic autism. Many centers utilize a combination of urine testing for creatine, guanidinoacetate, purines, pyrimidines, and organic acids to screen for most metabolic disorders that can present with autism or autistic-like features, particularly with comorbidities such as seizures. In summary, a thorough medical evaluation, including ruling out possible genetic or metabolic causes, may help families know more about the risk of recurrence.

CONCLUSION

The question of vaccines causing autism has been thoroughly investigated over the last decade. The Institute of Medicine has published multiple Immunization Safety Reviews during this period. The most recent review once again concluded that the evidence does not support a causal relationship between thimerosal-containing vaccines or the MMR vaccine and autism.11 A great deal remains unknown, and research is ongoing for possible causes of autism. We are hopeful that environmental and genetic studies will provide answers so that new cases can be prevented. It is also our hope that the weight of evidence that has been amassed throughout the international scientific community will empower providers to confer reassurance to their patients that vaccines are not causally linked to autism.

REFERENCES 1.

2. 3.

Rice C. Prevalence of autism spectrum disorders: Autism and Developmental Disabilities Monitoring Network, United States, 2006. MMWR Surveillance Summaries. 58, 1-20. 12-10-2009. 5-6-2010.

Wakefield A, Murch S, Anthony A et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet. 1998;351:637-642.

Taylor B, Miller E, Farrington C et al. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet. 1999;353:2026-2029.

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4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Madsen K, Hviid A, Vestergaard M et al. A population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med. 2002;347:1477-1482.

DeStefano F, Bhasin T, Thompson W, Yeargin-Allsopp M, Boyle C. Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta. Pediatrics. 2004;113:259-266.

Fombonne E, Zakarian R, Bennett A, Meng L, McLean-Heywood D. Pervasive developmental disorders in Montreal, Quebec, Canada: prevalence and links with immunizations. Pediatrics. 2006;118:E139-E150. Honda H, Shimizu Y, Rutter M. No effect of MMR withdrawal on the incidence of autism: a total population study. J Child Psychol Psychiatry. 2005;46:572-579.

Makela A, Nuorti J, Peltola H. Neurologic disorders after measlesmumps-rubella vaccination. Pediatrics. 2002;110: 957-963. Stratton K, Wilson C, McCormick ME. Measles-Mumps-Rubella Vaccine and Autism. Washington, DC: National Acadamy Press; 2001.

Wilson K, Mills E, Ross C, McGowan J, Jadad A. Association of autistic spectrum disorder and the measles, mumps, and rubella vaccine: a systematic review of current epidemiological evidence. Arch Pediatr Adolesc Med. 2003;157:628-634. Immunization safety review: vaccines and autism. Washington, DC: National Acadamies Press; 2004.

Murch S, Anthony A, Casson D et al. Retraction of an interpretation. Lancet. 2004;363:750. Magos, L. Review on the toxicity of ethylmercury, including its presence as a preservative in biological and pharmaceutical products. J Appl Toxicol. 2001;21:1.

Pichichero, ME, Gentile, A, Giglio, N, et al. Mercury levels in newborns and infants after receipt of thimerosal-containing vaccines. Pediatrics. 2008;121:e208. Kerper, LE, Ballatori, N, Clarkson, TW. Methylmercury transport across the blood-brain barrier by an amino acid carrier. Am J Physiol. 1992;262:R761. Thimerosal in Vaccines. www.fda.gov/BiologicsBloodVac cines/SafetyAvailability/VaccineSafety/UCM096228.

Celebrity Roast of

Steve Holland

Mississippi House of Representatives

17. 18. 19. 20. 21. 22. 23. 24. 25 26. 27. 28. 29.

Clements, CJ, Ball, LK, Ball, R, Pratt, RD. Thiomersal in Vaccines: is removal warranted. Drug Saf. 2001; 4:567.

Joint statement of the American Academy of Pediatrics (AAP) and the United States Public Health Service (USPHS). Pediatrics. 1999;104:568. Vaccines and biologicals. Recommendations from the Strategic Advisory Group of Experts. Wkly Epidemiol Rec. 2002;77:305

Fombonne, E, Zakarian, R, Bennett A, et al. Pervasive developmental disorders in Montreal, Quebec, Canada: prevalence and links with immunizations. Pediatrics. 2006;118: E139.

Stehr-Green, P, Tull, P, Stellfeld, M, et al. Safety of thimerosal-containing vaccines: a two-phased study of computerized health maintenance organization databases. Pediatrics. 2003;112:1039.

Madsen, KM, Lauritsen, MB, Pedersen, CB, et al. Thimerosal and the occurrence of autism: negative ecological evidence from Danish population-based data. Pediatrics. 2003;112:604.

Schechter, R, Grether, JK. Continuing increases in autism reported to California’s developmental services system: mercury in retrograde. Arch Gen Psychiatry. 2009;65:19.

Ritvo E, Jorde LB, Mason-Brothers A et al. The UCLA-University of Utah epidemiological survey of autism: recurrenece risk estimates and genetic counseling. Am J Psych. 1989;146:194-199.

Baily A, Le Couteur A, Gottesman I et al. Autism as a strongly genetic disorder: evidence from a British twin study. Psychol Med. 1995;25:6377.

Abdul-Rahman OA, Hudgins L. The diagnostic utility of a genetics evaluation in children with pervasive developmental disorders. Genet Med. 2006;8:50-54.

Chudley A, Gutierrez E, Jocelyn LJ, Chodirker BN. Outcomes of genetic evaluation in children with pervasive developmental disorder. Dev Behav Pediatr. 1998;19:321-325.

Vernes SC, Newbury DF, Abrahams BS et al. A functional genetic link between distinct developmental language disorders. N Engl J Med. 2008;359:2337-2345. Newmeyer A, deGrauw T, Clark J, Chuck G, Salomons G. Screening of male patients with autism spectrum disorder for creatine trasporter deficiency. Neuropediatrics 2007;38:310-312.

Benefiting the

Mississippi Academy of Family Physicians Foundation King Edward Hotel Roasters Jackson, MS

Saturday, February 26, 2011 Reception 6:30 pm Roast 7:00 pm Black tie optional

Hotel Reservations 601-353-5464 $99 Double Rate

Governor Haley Barbour Dr. David Cole Randy Easterling, M.D. Bobby Harrison Bucky Murphy Marshall Ramsey

Tickets are $125 Individual; $200 Couple $500 Reserved Table of Five $1,000 Reserved Table of Ten

To order tickets, inquire about sponsorship opportunities or for more information, please contact Julie Humphreys at 601-853-3302 or julie@msafp.org. 38

JOURNAL MSMA FEBRUARY 2011


• MISSISSIPPI MEDICINE UP-TO-DATE •

A

Medical Therapy for Systemic Lupus Erythematosus Jason K. Taylor, MD and Robert W. McMurray, MD

BSTRACT:

The many clinical manifestations of systemic lupus erythematosus (SLE) result in the involvement of many specialties of medicine in its treatment. An understanding of the indications, potential side-effects, and toxicity monitoring required of common agents used as medical therapy in SLE disease management is important for all providers who care for lupus patients. Pharmacological therapy is based on the type and severity of clinical manifestation and involves four primary classes of drugs: non-steroidal antiinflammatory drugs, antimalarials, corticosteroids, and immunosuppressives/cytoxics.

KEYWORDS:

INTRODUCTION

SYSTEMIC LUPUS ERYTHEMATOSUS, MANAGEMENT, THERAPY, REVIEW

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease primarily managed by rheumatologists. However, since there is a shortage of rheumatologists, primary care physicians and specialists other than rheumatologists are often the first to encounter these patients. A general understanding of the clinical and laboratory manifestations of SLE for disease recognition is important for all physicians for appropriate referral. Moreover, SLE patients are treated with drugs which require regular toxicity monitoring. In this paper, AUTHOR INFORMATION: Dr. Taylor and Dr. McMurray, Department of Medicine, University of Mississippi School of Medicine, Jackson; Medical Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson.

CORRESPONDING AUTHOR: Jason K. Taylor, MD, Divison of Rheumatology, University of Mississippi Medical Center, 2500 N. State St. Jackson, MS 39216. Ph: 601-984-5540 (office) Fax: 601984-5535. Email: jktaylor@medicine.umsmed.edu

CONFLICT OF INTEREST DISCLOSURES: No funding sources were involved in the preparation of this manuscript. All authors attest to no conflict of interest for the subject matter discussed in this manuscript. All authors actively participated in the writing of this manuscript.

we provide a brief review of medical therapy for outpatient management of SLE with recommendations for appropriate drug toxicity monitoring.

DIAGNOSIS AND CLINICAL MANIFESTATIONS

SLE is predominantly a disease of women with a female:male ratio of 8:1. Peak incidence occurs during the reproductive years. Approximately 1 in 2000 individuals in the general population is affected with prevalence varying due to race, ethnicity, and socioeconomic status.1,2 For instance, lupus is 3 times more common in African-American women than Caucasian women, and African-Americans frequently have more severe disease. Though definitive epidemiological information for Mississippi is lacking, this proves to be important statistical data for a state such as Mississippi which has a large AfricanAmerican population. An exact etiology for SLE remains unknown, but a variety of genetic, environmental, hormonal, and immunologic components are known to play a role. There is disease clustering within families and a high concordance rate among monozygotic twins. Examples of environmental influences on SLE development include infectious microbes causing immune dysregulation leading to autoimmunity and disease initiation and exposure to ultraviolet (UV) radiation causing inflammation and tissue damage.1 Sex hormones and fertility also affect disease pathogenesis.2 ANA (anti-nuclear antibody) production is the key immunologic disturbance seen in SLE. The clinical manifestations of SLE are diverse in presentation and severity and include both non-organ-threatening and organ-threatening disease. The American College of Rheumatology (ACR) has designated 11 classification criteria for SLE which encompass most of the major clinical and laboratory features of the disease (Table I). These classification criteria have been designed for studies and are not required for diagnosis. Non-organ threatening disease manifestations include rash, arthritis, pleuritis, and pericarditis and non-specific constitutional features such as fatigue, fever, and weight loss. Major organ-threatening SLE disease includes proliferative glomerulonephritis, pneumonitis, diffuse alveolar hemorrhage, my-

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• SCIENTIFIC •

ocarditis, cerebritis, transverse myelitis, severe autoimmune hemolytic anemia, and thrombocytopenia.

PHARMACOLOGIC TREATMENT

Primary care physicians are frequently involved in the management and monitoring of SLE patients in collaboration with specialists such as rheumatologists, dermatologists, neurologists, and obstetrician/gynecologists. Core tasks for the primary care physician are not only to recognize major organ disease but also to have a general understanding of the clinical indications, mechanism of action, dosing, common side-effects, and toxicity monitoring required of the primary pharmaceutical agents used to treat mild, stable, or severe SLE. This understanding is even more important in a complex disease such as SLE in which many of the clinical manifestations may be confused with the potential adverse events of the drugs used to treat the disease. Standard pharmacological therapy for active lupus include four classes of drugs: non-steroidal anti-inflammatory (NSAIDs) drugs, antimalarials, corticosteroids, and immunosuppressive/cytotoxic agents used alone or in combination. The choice of SLE medical therapy is dependent on both the extent and severity of disease and the specific organs involved. Mild disease manifestations such as arthritis, serositis, and rash may be managed with nonsteroidal anti-inflammatory agents, low dose corticosteroids, and local measures such as topical steroid creams, and ointments. Organ-threatening disease requires high dose corticosteroids and immunosuppressive therapy. (Table 2)

NSAIDS

NSAIDS are important first line drugs for the treatment of constitutional features such as fever and headache, musculoskeletal symptoms such as arthritis and myalgias and mild serositis such as pericarditis and pleuritis. These agents provide both analgesic and anti-inflammatory effects by inhibiting prostaglandins, thus treating pain, inflammation, and pyrexia. A multitude of NSAIDs are now commercially available with varying dosing requirements. In general, analgesic effects are reached at low or moderate doses while higher doses are associated with greater anti-inflammatory effects. The more common potential adverse events are gastrointestinal bleeding, hepatitis, and renal impairment. Rarely, aseptic meningitis may develop, most commonly in association with ibuprofen use. Important in the management of SLE patients is that active lupus may mimic the adverse effects of NSAIDs on the kidneys and liver. New or acute renal failure or a decline in previous chronic kidney disease renal function may be due to SLE effects on the kidneys or NSAID use itself. Liver enzyme abnormalities secondary to NSAIDs may be confused with autoimmune hepatitis.3,4 In cases considered to be an adverse drug effect, typically the NSAID is stopped and SLE disease activity is assessed by measurement of anti-DNA and complement levels.

ANTIMALARIALS

Antimalarial agents are some of the most commonly prescribed medications for SLE. They are frequently used to treat non-life threatening manifestations of SLE such as constitutional and musculoskeletal, serosal, and cutaneous disease. In addi-

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tion, antimalarials may have long-term protective effects in preventing future flares.3 These drugs exert their immunomodulatory effects by increasing intracytoplasmic pH which alters the assembly of class II MHC molecules, thus decreasing antigen processing and presentation by macrophages and dendritic cells.4 Hydroxychloroquine is the most commonly used antimalarial in the U.S., the least toxic, and is generally initiated at a dose of 400 mg daily. Beneficial effects of antimalarials include improvement in lipid profiles and prophylaxis against thromboembolic events.4 Antimalarial agents are typically welltolerated with mild side effects which may include gastric upset, headache, myalgia, or rash. Though rare, most worrisome for antimalarial use is the risk of ophthalmologic toxicity. Retinopathy may occur from drug pigment deposition on the retina. Current recommendations are for an ophthalmologic evaluation to include visual acuity, slit-lamp, fundoscopic, and visual fieldtesting at baseline and every 6-24 months thereafter dependent on comorbid conditions.3,4

effective for synovitis. Low- to medium dose oral corticosteroids (prednisone 5 mg to 30 mg) may be used treat constitutional symptoms and systemic disease manifestations of arthritis, cutaneous disease, and serositis. Higher dose oral preparations (12 mg/kg/day) and bolus methylprednisolone (500-1000 mg) for 3-5 consecutive days may be required to treat organ-threatening disease.3,4 Long-term corticosteroid therapy may be associated with many potential side effects. Toxicities may include hypertension, weight gain, myopathy, osteonecrosis, hyperlipidemia, striae, hyperglycemia, glaucoma, peptic ulcer disease, osteoporosis, and increased susceptibility to infections.3 Short-term use of higher doses may cause electrolyte imbalances or psychosis. These potential toxicities warrant dose tapering and reduction once control of disease activity is achieved and steroid-sparing/cytotoxic agents are initiated. Many SLE patients will require maintenance therapy with low dose corticosteroids or steroid-sparing agents to prevent disease recurrence.

Corticosteroids used alone or in combination with other agents are important in the acute and chronic management of a variety of clinical manifestations of SLE. Corticosteroids have rapid onset and possess potent anti-inflammatory and immunosuppressive properties. Multiple mechanisms of action exist including inhibition of prostaglandins and leukotrienes, decreasing circulating lymphocytes, and modulation of cytokine production. Multiple corticosteroid preparations may be used to treat different SLE disease manifestations. Topical or intralesional steroids (e.g. triamcinolone) may be used for cutaneous lesions. Intra-articular corticosteroids (e.g. methylprednisolone) may be

Moderate-to-severe SLE, characterized by involvement of major organs or extensive involvement of nonmajor organs, or failure of response to corticosteroids or inability to taper corticosteroids may dictate use of immunosuppressive/cytotoxic agents. Treatment goals are to first suppress autoimmune disease activity into remission with intensive immunosuppressive therapy. This is followed by an extended period of less intensive maintenance therapy with less potentially toxic agents to prevent recurrent SLE flares.5 Table 3 lists recommended monitoring for commonly used immunosuppressive and cytotoxic agents used as medical therapy for SLE.

CORTICOSTEROIDS

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IMMUNOSUPPRESSIVES/CYTOTOXICS


• SCIENTIFIC •

Azathioprine Azathioprine is a purine antagonist antimetabolite that interferes with DNA synthesis and is used most commonly as a steroid-sparing agent in SLE patients. Starting dose is 1 mg/kg/day (50-100 mg) with a typical maintenance dose of 2-3 mg/kg/day (150-300 mg). Adverse effects may include gastrointestinal disturbance (nausea, vomiting, or diarrhea) and dose related bone marrow effects (thrombocytopenia and leukopenia), but these are rare. Complete blood counts and liver enzymes should be monitored at initiation and every 2 to 4 months 3-5 thereafter on a practical basis.

Mycophenolate Mofetil Mycophenolate mofetil inhibits the purine synthesis salvage pathway thus blocking proliferation of lymphocytes specificially. Myocophenolate mofetil has shown promise in the treatment of SLE nephritis in addition to cutaneous disease, refractory thrombocytopenia, and pulmonary hemorrhage.3,5 Most patients are started on 500 mg/day and titrated up to a maintenance dose of 1500 mg to 3000 mg/day. Common side effects include nausea, diarrhea, and leukopenia.2 Baseline blood counts and liver enzymes at start and every 3 months are recommended laboratory monitoring.5

Cyclosporine Cylcosporine works by inhibiting the production of the proinflammatory T- cell cytokine Il-2. There is supportive evidence for its use in the treatment of membranous nephritis. Cyclosporine dosages range from 2.5 mg to 5 mg/kg/day. Side effects may include hypertension, gum hypertrophy, hypertrichosis, and mild elevations in serum creatinine. Among recommended laboratory monitoring is a serum creatinine every 2 weeks until dose is stable, then monthly thereafter.2-3,5

Cyclophosphamide Cyclophosphamide is the primary cytotoxic drug used to treat severe SLE disease. Beyond its more notable use to treat nephritis, cyclophosphamide may also be employed to treat severe cytopenias and neurologic pulmonary SLE. Cyclophosphamide can be dosed orally, but intermittent pulse intravenous therapy exhibits better toxicity profiles. Nausea and vomiting are occasional side effects which can be ameliorated with the addition of appropriate anti-emetic agents. Other effects may include a dose-dependent leukopenia with continued intravenous use and increased risk of infections, especially herpes zoster which should be treated immediately with antivirals. Ovarian failure (increased risk in older women at start of treatment and higher cumulative dose), azoospermia, hemorrhagic cystitis, and transitional squamous cell carcinoma are other potential adverse effects.2,5 Ovarian failure rate may be reduced by concomitant use of oral contraceptives.

OTHER AGENTS

Methotrexate promotes its immunosuppressive and antiinflammatory effects by functioning as an antimetabolite that inhibits dehydrofolate reductase and promotes adenosine release. Methotrexate is FDA approved for the treatment of rheumatoid arthritis but is primarily used as a steroid-sparing agent for articular and cutaneous SLE manifestations. Initial doses are 7.510 mg/wk and may be increased at monthly intervals up to 20 mg/wk. Common adverse effects include oral ulcers, nausea, vomiting, diarrhea, fatigue, and liver enzyme elevations. Blood counts and liver enzymes should be monitored every 1-3 months.3,5 Rituximab, an anti-CD20 chimeric murine/human monoclonal antibody, reduces B cells. Rituximab has been used in SLE disease refractory to conventional therapy with cyclophosphamide. Treatment regimens are variable, and more studies are needed to better determine its role in SLE treatment and how to monitor patients appropriately for toxicity. Common adverse effects include infusion reactions, allergy, angioedema, headache, nausea, leukopenia, and urticaria.5

SUMMARY

Advances in the pharmacologic treatment of SLE have led to significant improvements in mortality and morbidity. Key to the management of this complex disease with variable clinical manifestations is an understanding of the common agents used to quiet active autoimmunity. Armed with a knowledge of the indications, side-effects, and appropriate drug toxicity monitoring of these medicines, primary care physicians can more effectively collaborate with specialists in SLE disease management.

REFERENCES 1.

2. 3. 4.

5.

Pisetsky DS. Systemic lupus erythematosus. A. Epidemiology, pathology, and pathogenesis. In: Klippel JH, Crofford LJ, Stone JH, Weyand CM, editors. Primer on the rheumatic diseases. 12th ed. Atlanta: Arthritis Foundation; 2001: 329-334. McMurray RW. Nonstandard and adjunctive medical therapies for systemic lupus erythematosus. Arthritis care and research. 2001; 45:86-100.

Manzi, S. Systemic lupus erythematosus. C. Treatment. In: Klippel JH, Crofford LJ, Stone JH, Weyand CM, editors. Primer on the rheumatic diseases. 12th ed. Atlanta: Arthritis Foundation; 2001:329-334.

Aranow C, Ginzler EM. Systemic lupus erythematosus: Treatment of constitutional symptoms, skin, joint, serositis, cardiopulmonary, hematologic and central nervous system manifestations. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, editors. Practical Rheumatology. 3rd ed. Mosby; 2004:439-448. Tassiulas IO, Boumpas DT. Clinical features and treatment of systemic lupus erythematosus. In: Firestein GS, Budd RC, Harris ED, McInnes IB, Ruddy S, Sergent JS, editors. Kelley’s Textbook of Rheumatology. 8th ed. Philadelphia, PA: W.B. Saunders; 2009:1263-1300.

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• CLINICAL PROBLEM-SOLVING •

Presented and edited by the Department of Family Medicine, University of Mississippi Medical Center, Diane K. Beebe, MD, Chair

A

A Pain in the Neck Sheree Carney Melton, MD

71-year-old African–American female presented to the emergency department (ED) with a 2 day history of fever and nausea but without vomiting. She also complained of urinary frequency and new-onset urge incontinence. She denied any abdominal pain or changes in her bowel habits. She denied any sick contacts. The patient’s medical history included hypertension, type 2 diabetes, hyperlipidemia, osteoarthritis and a history of ductal carcinoma in situ in her right breast with lumpectomy 5 years ago without history of recurrence. She was taking medications for her hypertension, diabetes and hypercholesterolemia. She did not smoke or drink. The patient had a temperature of 100.4°F, a heart rate of 104 beats per minute and a normal blood pressure. She was noted to be in some distress, looking as if she did not feel good. She had shallow breathing though her respiratory rate was normal. However, she was alert and responded appropriately to questions. The remainder of her exam was benign including her abdominal exam. A urinalysis showed 3+ leukocyte esterase, 30-49 white blood cells (WBC) per high power field (hpf) (reference 2-5 WBC/hpf) and trace bacteria/hpf. In a 71-year-old female with symptoms of fever, urinary complaints and new-onset incontinence, I would think of a urinary tract infection. This is common in the elderly as well as in 1 people with a history of diabetes mellitus. This patient is also complaining of nausea but without any gastrointestinal symptoms. This further suggests that the patient’s symptoms may be due to a urinary tract infection. Diabetes-related hyperglycemia may also cause nausea and urinary frequency, but this is most commonly seen without fever unless an infection is present. A blood glucose determination was not performed at this initial presentation. The patient’s symptoms of nausea and fever ac1 companied by pyuria suggest that she has pyelonephritis. The AUTHOR INFORMATION: Dr. Melton is in private practice with Central Mississippi Health Services. She was a third year resident in the Department of Family Medicine at the University of Mississippi Medical Center in Jackson. CORRESPONDING AUTHOR: Sheree Carney Melton MD, 1134 Winter St., Jackson, MS 39204. Email: smeltonmd@comcast.net.

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JOURNAL MSMA FEBRUARY 2011

decision to be made is whether to treat the patient as an inpatient or outpatient. Patients with mild pyelonephritis can be treated 1 with an oral fluoroquinolone for 7 days. However, trimethoprim-sulfamethoxazole (Bactrim) double strength can be used as well. In this patient, except for fever, her vital signs are all within normal limits. In addition, she is not vomiting and, therefore, should be able to tolerate oral medicines. I will discharge her home and treat her as an outpatient with oral antibiotics. I would also prescribe medication to manage her nausea. I would follow her in clinic in one week to reassess her symptoms and instruct her to return to ER or clinic if her symptoms worsen or do not improve. The patient was discharged home with a prescription for ciprofloxacin (Cipro) and promethazine (Phenergan). She returned to the ED the next day with the same complaints. However, this time she also complained of neck and back pain. Her temperature was 102.7° F, her pulse was 100 beats per minute and her blood pressure was normal. She was in mild distress. Her neck was supple with full range of motion. She had no tenderness to palpation along her spine. Her neurological, pulmonary and cardiac exams were normal. She had an elevated glucose of 208 mg/dL. Her complete metabolic profile was otherwise within normal limits. She had a WBC of 9.5 k/uL. Urinalysis showed 2+ leukocyte esterase, 15-19 wbc/hpf and trace bacteria. The patient now presents with fever, neck and back pain. The symptoms of fever and back pain are again consistent with the diagnosis of pyelonephritis. The patient can still be treated as an outpatient because she is able to take oral medicines. Also, her vital signs are stable (except fever) and do not make one worry about sepsis. Her symptoms of neck pain accompanied by fever could suggest meningitis. However, given her normal physical exam as well as an abnormal urinalysis, I would still diagnose this patient with a urinary tract infection. If she does not improve, a lumbar puncture will be warranted. The patient was treated with intravenous levofloxacin (Levaquin) in the ER, although the oral form is just as efficacious, and discharged. She was instructed to continue the ciprofloxacin as previously prescribed and to keep her follow up appointment. However, the patient presented to the


same ED the next day. She was accompanied by her family who stated that the patient was confused and also had poor appetite, weakness and nausea with vomiting. There were no complaints of headache, chest pain or shortness of breath. She had a temperature of 103.1° F and was alert but oriented only to person and place. Her other vital signs were normal as was her physical exam including her neck exam which was supple with full range of motion. Her WBC was elevated at 14.1 K/uL with 72.9 % segmented neutrophils and 18.7% lymphocytes; the remainder of her complete blood count was normal. Complete metabolic profile was within normal limits except for an elevated glucose of 192 mg/dL. Her C-reactive protein (CRP) was elevated at 2.4 mg/dL (reference < .05 mg/dL) and erythrocyte sedimentation rate (ESR) was elevated at 57 mm/h (reference 0-30 mm/h). Head computed tomography (CT) was negative for infarction and lesions. A chest radiograph was also negative for any acute processes. The patient is most likely having some type of inflammatory process demonstrated by her elevated ESR and CRP. In addition, she has fever, tachycardia and a leukocytosis. Unfortunately, these acute phase reactants (ESR and CRP) are not very specific. They reflect the presence and intensity of inflammation.2 I am worried that the patient has some infectious process with systemic or central nervous system (CNS) involvement given her new mental status changes. I will order a blood culture and urine culture though her urine culture may be sterile since the patient has been taking antibiotics. The patient was admitted to the hospital with the diagnosis of fever and altered mental status thought to be caused by her urinary tract infection. She was prescribed ceftriaxone (Rocephin) with the plan to tailor therapy after her urine culture returned. By the next morning, the patient’s mental status was close to baseline. She remained afebrile. Her WBC decreased to 11.4 k/uL. Her urine culture showed no growth. She was still weak so she was kept in the hospital for a physical therapy evaluation. On hospital day 2, the patient complained of shortness of breath and was wheezing. Her temperature was 100° F, and her other vital signs were normal. She denied any pain. On physical exam, she had decreased air movement and mild edema of her upper and lower extremities. It was decided to perform a lumbar puncture (LP) given the patient’s continued low grade fever to evaluate her change in status. Cerebrospinal fluid analysis (CSF) showed a WBC of 27/microL (reference 0-5 WBC/microL): 4% were polymorphonuclear lymphocytes and 71% were lymphocytes. Glucose and protein were normal. The patient’s CSF analysis was sent for bacterial, fungal and AFB smear. Her gram stain and meningitis panel were negative. The patient initially improved greatly after receiving intravenous antibiotics. This may indicate that her disease process was caused by a bacterial pathogen that was susceptible to ceftriaxone. No urine culture was taken during her first presenta-

tion prior to antibiotic therapy; therefore, negative urine cultures here are not reliable. The patient’s LP results are abnormal. She has an elevated cell count which is present in both bacterial and viral CNS infections. In bacterial CNS infections, the WBC is usually >1000/microL and has a predominance of poly3 morphonuclear lymphocytes. In viral CNS infections, the WBC is usually <250/microL with a predominance of lymphocytes.3 This patient’s CSF pattern suggests a probable viral infection. More diagnostic studies are needed to determine the cause of infection. The CSF should be sent for bacterial and fungal culture, and PCR testing should be done for the most common viral pathogens that cause CNS infections.4 The patient should also have serological studies done for the arboviruses.5 Detection of IgM antibodies in serum can diagnose some causes of encephalitis. The patient should be treated empirically because we do not have a clear cause for her symptoms and because she has an abnormal CSF profile.6 She is already taking antibiotics that should cover bacterial infections. HSV-1 coverage with acyclovir (Zovirax) should also be initiated as soon as possible because of the high rate of morbidity and mortality associated with HSV infection.7 On hospital day 3, the patient began to complain of severe left upper extremity pain that she rated as 10 out of 10 on a pain scale. She also refused to move her left arm. The patient’s vital signs were normal. Her left arm and hand were tender to touch. Uric acid and an anti-nuclear antibody panel were normal. ESR was elevated at >100mm/h. CRP was elevated at 34.7 mg/dL. A CT of her left arm indicated some edema in her forearm region but no discrete focal fluid collection was noted. The patient has complained of musculoskeletal pain for several days and has had several rheumatologic tests to evaluate her symptoms. Her negative anti-nuclear antibody panel is not suggestive of lupus. Her normal uric acid does not indicate that her left arm pain and edema are due to gout. The ESR and CRP are significantly higher than they were previously. This suggests that a systemic inflammatory response has intensified.2 However, given her negative autoimmune test as well as the fact that she has monoarticular joint pain, I am not convinced that her CNS infection and her left arm pain are related. On hospital day 4, the patient’s mental status declined, and she was responsive only to touch of her left upper extremity. Her temperature was 103.1° F, and her blood pressure was 194/103 mm Hg. She was also noted to be tachypneic, tachycardic and using her accessory muscles to breathe. She had an elevated WBC of 17.8 k/uL. Cardiac biomarkers were normal. CT chest with angiogram showed no pulmonary embolus. An arterial blood gas was normal. She was transferred to the intensive care unit. Infectious disease and neurology were consulted. A repeat LP was performed. Included in the analysis were CSF IgM for West Nile Virus; CSF polymerase chain reaction (PCR) was also performed for HSV 1 and 2 DNA. Serological tests for HSV1, Varicella, Western Equine, St. Louis encephalitis and

FEBRUARY 2011 JOURNAL MSMA

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• SCIENTIFIC •

West Nile were also drawn. In addition, a rickettsial panel was obtained. She was prescribed doxycycline (Vibramycin), meropenem (Merrem), vancomycin (Vancocin) and acyclovir. She was also prescribed methylprednisolone (SoluMedrol). Head CT was unchanged from the previous study. The patient’s condition has worsened as her fever has returned and her mental status has changed. I am concerned that she has become encephalopathic. Encephalitis is defined as the presence of an inflammatory process of the brain in association with clinical evidence of neurologic dysfunction.6 Her elevated blood pressure is not consistent with the diagnosis of sepsis. However, because it is extremely elevated in the presence of altered mental status, transfer to the intensive care unit is appropriate. She will be given multiple antibiotics and an antiviral to cover infections that commonly cause encephalitis. On day 5, the patient was more responsive but still febrile. Her CSF findings were significant for a cell count of 36/microL with 93% lymphocytes. MRI of brain showed chronic small vessel disease. Her CSF culture showed no growth. On hospital day 6 and 7, the patient’s mental status improved to baseline. She complained of neck pain, however. She was afebrile for 24 hours. Her second CSF profile is still consistent with a viral cause of her encephalitis. She also had a MRI of brain which is more sensitive and specific than CT of the brain in the evaluation of a patient with suspected encephalitis.6 However; the findings may be normal and remain normal throughout the illness. There are MRI patterns that can aid in identifying the cause of encephalitis. For instance, in patients with herpes simplex encephalitis, edema and hemorrhage in the temporal lobes can be present. In this patient’s case, her relatively normal MRI does not eliminate encephalitis. However, the patient’s cognitive function is now improving while taking antibiotics and antiviral medications. The patient should continue her current medication regimen until serology returns negative.7 The patient remained in the hospital receiving antibiotics and antiviral therapy for several more days while her serological studies were pending. Her mental status improved, and she remained afebrile. On hospital day 10, her CSF viral encephalitis titer and serology returned positive for West Nile virus. She was discharged that same afternoon. The patient was seen for follow up one month later. Her mental status was at baseline. She still complained of weakness but was feeling better overall. The patient has tested positive for West Nile virus. Most patients with West Nile virus only present with a febrile illness and flu-like symptoms; they may improve without treatment. However, a small proportion of patient’s will present with neuroinvasive disease. In the neuroinvasive manifestation of the virus, patients can present with encephalitis, meningitis, flaccid paralysis or a mixed pattern.8

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There is no treatment for West Nile, so her improvement on antibiotics is coincidental. In addition, I do not know what caused her symptoms of left upper extremity pain and edema; however, I am confident that it is unrelated to her West Nile infection. Our patient’s advanced age is her most important risk factor for severe neurologic disease.10 During 2004-2008, 5,868 cases of neuroinvasive disease in the United States were reported. Nine percent of all of those cases were fatal, and the case-fatality ratio increased with age with the highest percentage being in those over the age of 60.10

KEY WORDS: WEST NILE VIRUS, CNS INFECTIONS, REFERENCES

1.

ALTERED MENTAL STATUS LIST

Naber KG, Bergman B, Bishop MC, Bjerklund-Johansen TE, et al. EAU guidelines for the management of urinary and male genital tract infections. Eur Urol. 2001;40:576-588.

2.

Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. New Engl J Med. 1999;340(6):448-454.

3.

Spanos A, Harrell FE, Durack DT. Differential diagnosis of acute meningitis. An analysis of the predictive value of initial observations. JAMA. 1989;17;262(19):2700-2707.

4.

Whitley RJ, Gnann JW. Viral encephalitis: familiar infections and emerging pathogens. Lancet 2002;359(9305):507-513.

5.

Whitley RJ. Viral encephalitis. 1990;323(4):242-250.

6.

New

Engl

J

Med.

Tunkel AR, Glaser CA, Bloch KC, Sejvar JJ, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2008; 47(3):303-327.

7.

Hjalmarsson A, Blomqvist P, Skoldenberg B. Herpes simplex encephalitis in Sweden, 1990-2001: incidence, morbidity, and mortality. Clin Infect Dis. 2007;45(7):875-880.

8.

Davis LE, DeBiasi R, Goade DE, Haaland KY, et al. West Nile virus neuroinvasive disease. Ann Neurol. 2006;60(3):286-300.

9. 10.

Sejvar JJ, Haddad MB, Tierney BC, at el. Neurologic manifestations and outcome of West Nile virus infection. JAMA 2003;290 (4):511-515.

Lindsey NP, Staples JE, Lehman JA, Fischer M. Surveillance for human West Nile virus disease-United States, 1999-2008. Morb Mortal Wkly Rep Surveill Summ. 2010; 59:1-17.

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FEBRUARY 2011 JOURNAL MSMA

47


• PRESIDENT’S PAGE •

I

“Ain’t Love Grand?”

planned to write about nurse practitioners seeking independent practice within the state of Mississippi, but the death on Christmas Eve of Marcia Llewellyn Meek Wasson, a remarkable patient and friend, compelled me to do otherwise. By the time that this writing makes its way to print, her husband, Reverend Alton Lockett Wasson Sr. will have turned 100 on January 1, 2011, arriving at the century mark on 1-111! Theirs is an exemplary story of the power of the caregiver.

Reverend Wasson is not your average 100-year-old! Having retired four times from the United Methodist Church, he was called back into service following each retirement, ultimately serving over 15 charges and 31 churches. At the age of 95 he dislocated his shoulder, arm-wrestling with his son Alton, Jr. Only two years ago, charged with the TIM J. ALFORD, MD specific task of issuing the benediction at a wedding, he rose to the lectern and 2010-11 MSMA PRESIDENT exuberantly proclaimed “Ain’t Love Grand?!” He often joked that his goal was to beat all of his fourteen siblings in the age category. This would not be an easy task as it seems all had favorable genetics for longevity. His wonderful perspective on life and death brought him to the following statement as he scattered the cremated remains of one older brother into the family farm creek, “I’ve thrown you into the creek many times, but this time I won’t be pulling you out.”

His dear wife, Marcia, had been his partner in ministry and focused her infinite love and attention on her own children and those of their congregations. She had once put it to me, “You’ve got to make sure he makes it to 100.” Also in her 90s and his wife for 72 years, she gladly assumed the role of primary care giver. I have known and cared for many elderly couples in my 30 years of practice but have never witnessed two individuals more devoted to one another. Marcia was one whose youthful outlook, quick wit and boundless energy did not correspond to her chronological age. Last year when her only grandchild, Sage, brought their beloved great-granddaughter, Sophia, for her first visit, Marcia laid down on the wood floor in the front bedroom and held Sophia’s hand as the baby napped on the quilt pallet. I rarely saw her without her trademark colored cloth tied into her hair. She was always good for authentic stories and last Christmas entertained our family on her “blow-harp” (harmonica), giving a performance of Christmas favorites. continued on page 51

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President's Page continued from page 48 Marcia enthusiastically bought into the quest of helping Alton reach the 100 mark. I concede that she had everything to do with Alton reaching the century mark though she humbly deferred the credit to others. Indeed, the importance of care giving has been under recognized and undervalued economically and historically. Her calls to my home would begin unintroduced on her end with, “He’s too pale.” (Bleeding gastric ulcer) or, “He just choked on his breakfast.” (Esophageal stricture) or, “He just fainted.” (Sick sinus syndrome, pacemaker placed at age 98 in 2008.) Such calls were always followed with a home visit to begin sorting things out.

Stepping back in time amidst an abundance of cobalt blue bottles, Depression glass and ceramic figurines, their living room and kitchen merged into one room with staple goods displayed with other kitchen essentials in an orderly and most practical manner. It was here they shared daily devotionals and prayed with one another at an old heart pine table built by their late son, Lonnie. Alton would read scriptures from a pocket-sized New Testament that I am sure he could not see but must have committed to memory.

If I have given the impression that they were home bound, they were not. Up until as recently as this past fall, they staffed the Helping Hands Ministry Thrift Store and attended two services at First United Methodist Church each week. For years, they served as volunteers at the Natchez Trace Visitor’s Center just off the Trace here in Kosciusko and were known to invite wayward travelers home for a hot meal. This service to others “charged their batteries” as they liked to say. They had slowed down a bit in recent months and spent the majority of their time in their simple home reading and relating tales from their shared past. On one of my home visits elicited by Marcia on behalf of Alton, I noticed that Marcia had herself experienced a fall and was extremely pale, fatigued, and complained of night sweats. As in the case of so many primary care-givers, this was taking a physical and emotional toll on Marcia. Roles were reversing. Colleague Bobby Graham, MD confirmed my worst fears that this presentation represented the classic triad of Chronic Lymphocytic Leukemia but was able to get a few more months of function out of her 93-year-old bone marrow. She eventually succumbed to complications of her immunocompromised state and died on Christmas Eve 2010 following a one-week siege in the Baptist SICU.

Alton Wasson, Jr., her son and former Yale chaplain, would later explain that his father was present at the bedside when Marcia drew her last breath. Both Senior and Junior Altons and daughter Marcia Elaine spoke with gratitude for the patience and kindness of her physicians, especially the neurologist who helped them navigate the final moments of her life. They were touched by nurses and other members of the team as well who showed respect and compassion to the end.

As I write this on Christmas night, a new year looms and along with it a busy legislative agenda so busy that the goodness of our profession will run the risk of giving way to the politics of the moment. This Christmas there is no sound of the harmonica in our home, and we miss Marcia. But there is a new bright star lit by the example of a good and decent person who got it right, finding true joy in devotion to others through her sacrificial caregiving. I continue to discover that the essential ingredient of compassion in our medical practices is found in the goodness of those we are called to help.

REFERENCES

Quill, Timothy, E. Dying and Decision-Making – Evolution of End of Life Option, N Engl J Med. 2004;350(20),20292032. Latham PH, Posner J. Caring for Persons with Dementia. American Stroke Association, 2006

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• MSDH • Mississippi Reportable Disease Statistics

November 2010

* Totals include reports from Department of Corrections and those not reported from a specific district. ** Address unknown for 2 cases.

For the most current MMR figures, visit the Mississippi State Department of Health web site: www.HealthyMS.com

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Not actual size

UMHC recognized for achievement in cardiac care among “America’s Best Hospitals” – u.s. news & world report

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• EDITORIAL •

Mississippi: How Did We Get to This Place? DISCOVERY PROCESS

Richard D. deShazo, MD, Associate Editor

It’s another day at work, and most of the patients on the medical service are obese, diabetic and hypertensive souls suffering complications of the metabolic syndrome. The wheelchairs are now all double-wide, and the new ambulances are capable of transporting “patients up to 800 pounds.” The kids in daycare and beyond never lose their baby fat, and we have a developing epidemic of type 2 diabetes in adolescents. Only a third of our young people meet health and fitness criteria to serve in the military. Over the last several months, I have spent time traveling, listening, and reading to better understand Mississippi’s obesity epidemic. If I have it wrong, please let me know.

POVERTY, LIMITED CHOICES AND POOR HEALTH

Mississippi is disproportionally challenged health-wise. The burden of diabetes, hypertension, stroke, osteoarthritis and cancer, driven by obesity, continues to increase. Twenty-two percent of Mississippi youth in the 10-17 year old age group are obese, and one-third of Mississippians will have diabetes by 2015. The economic effects of this epidemic are equally daunting. For instance, beyond the personal and social costs, the cost of providing Medicaid benefits to obese children averages $6,730 as compared to $2,446 per year for non-obese children. Of children born in 2000, 40 percent of African Americans and 27 percent of Caucasians in the U.S. will have diabetes. If there is not a sea-change, Mississippi’s perpetual worst-case scenario health status will perpetuate our worst-case scenario economic status. How can we address our poverty problem with a work force of obese, chronically ill workers whose life expectancy will be less than that of their parents? Our physician-to-patient ratio is at the same rank order as our health status. How can we produce or attract enough health professionals to care for a chronically ill population of this size? The mixture of poverty, limited choices and poor health is a substrate that could unravel the already porous social fabric of our state.

WHAT ARE THE ORIGINS OF THIS PROBLEM?

My opinions, for the most part, have come from conversations with Mississippi physicians and historians. I am still learning. Mississippi’s history and Mississippi's health are intertwined and, to a great degree, related to the geography of the state. We are actually five “states” joined together by serendipity. The coastal areas with their French Catholic heritage have had economies sustained by military installations, ship building, a fishing industry and access to the commerce of New Orleans and Mobile economies adequate to support a fee-for-service health-care system. People who can pay market rates for healthcare can get it. North Mississippi has proximity to Memphis. A previously flourishing furniture industry and the momentum provided by the Ole Miss campus in Oxford and the Mississippi State campus in Starkville have sustained fee-for-service healthcare in population centers. Likewise, central Mississippi has the financial continuity of state government, and the Pine Belt has the lumber and railroad industries to provide economic sustenance for a retail health system. The rural areas outside of the larger cities in these four areas, however, have languished with low-wage jobs and challenged public schools. And most of Mississippi is rural and outside metropolitan areas. Distance, poverty, and discrimination have limited access to our healthcare system, and under-education has fostered health illiteracy. The majority of the working poor access healthcare episodically and only after symptoms or emergencies develop. The Delta has been and continues to be a special case. The importation of slaves by the French before Mississippi’s statehood addicted the developing agrarian economy—creeping north from Louisiana to Natchez and beyond—to cheap labor. Although Mississippi’s alluvial plain provided the opportunity for extraordinary agricultural productivity, the wealth produced was never widely distributed. Social infrastructure for the care of the poor (black and white) failed to develop because of racial tensions, many of which were driven out of the interest to minimize labor costs. Before the Civil War, African Americans as slaves had more access to healthcare than poor whites. After the War, this majority of poor blacks and whites had little access to healthcare and, when offered, it was often second-class. When the uninsured working poor did seek care, they were often “full-pay” and wound up with higher healthcare costs than the insured and garnished wages. Outmigration from the Delta began in Reconstruction when there were more than 500,000 African Americans there. 1 It was further stimulated by the Great Flood of 1927 and continues to the present.2 Those Mississippians, black and white, who have been so fortunate as to receive an education or a skill are quick to leave. Now the store fronts in Delta towns that previously housed successful merchants are empty or occupied by health and home hospice agencies, medical supply shops and an occasional pharmacy. Care for patients with chronic disease is the only growth industry.

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VENTRICULAR TACHYCARDIA IN MISSISSIPPI

• EDITORIAL •

Economies based on agriculture are innately fragile. With automation of farming, there are now more farm personnel than jobs and many of those pay little more than subsistence wages. The unpredictability of the farm cycle and military contracts and the resulting variation in expendable income that supports the lumber and furniture interests have resulted in a financial history that, when grafted, resembles ventricular tachycardia on an ECG. That economy continues to perpetuate tensions among poor, under-educated and under-skilled blacks, whites and now Latin groups competing for limited opportunities. Most agree that today’s health disparities are perpetuated by economic issues more so than racism.

ATTEMPTS TO PROVIDE ACCESS TO HEALTHCARE

Politics in Mississippi has typically pitted whites against blacks and haves against have-nots. But there have been noble attempts to address the healthcare needs of those who cannot pay for traditional fee-for-service health care in Mississippi. The first was the charity hospital system which grew out of the old maritime hospital in Natchez to five hospitals with varying degrees of quality. The last of these hospitals closed in the 1980s. The development of federally qualified health centers (FQHC) and rural health centers was closely linked to Mississippi through the first rural FQHC in Mound Bayou. Although the beginning of this movement was opposed by our society (detailed in The Good Doctors by John Dittmer3), there are now more than 20 of these clinics in the state. The ability of FQHC clinics to care for the under-insured and uninsured is a major component of the Health Care Reform Package of 2010 through which 11 billion new dollars will be invested. As they expand to meet the need, mid-level practitioners could be the only providers available to staff them in Mississippi.

THE COUP DE GRAS

Add to this mixture of poverty, health disparities, health work force shortages and fragile economy the advent of refined sugar which first came to the state in the post-Civil War period. More recently, highly processed, easily accessible, inexpensive food products with habit forming mixtures of sugar, salt and fat have taken us to the next level.4 The many “food deserts” in Mississippi, areas that lack supermarkets with fresh food, encourage a reliance on highly processed, habit-forming foods available in convenience stores and fast-food restaurants. There is a disproportional density of these businesses in centers of poverty. Financially challenged public schools have used federal school breakfast and lunch programs as a source of operating capital while serving similar, cheap, fried and processed foods. At the same time, physical education and health education programs have been minimized or discontinued.

NOW WHAT?

To be sure, Mississippi is the epi-center of the national obesity epidemic. Although this is a national problem, the effects on our state are multiplied. We are headed to a state composed of obese, aging, chronically ill, diabetic, and unemployable citizens. The approach to the problem has to be bottom-up rather than top-down. Healthy choices cannot be mandated in a democracy, but they should at least be available. Changing unhealthy behaviors in adults is a daunting task. Fostering healthy behaviors in children is less so. In many Mississippi families, children are the most literate family members and serve to transfer information retrograde to their parents. The Mississippi Healthy Schools Act which requires exercise and education on health and wellness in public schools and is supported by individual school health councils is a landmark piece of legislation. This Act mandates 150 minutes per week of physical education and activity plus 45 minutes per week of health education in K-8 as well as higher nutrition standards5 (for instance, school cafeteria changes to 1% milk and whole wheat bread products). Unfortunately, no financial support for implementation came with the legislation. Implementation of similar programs in Arkansas has shown that it is possible to stem the tide of childhood obesity. It has also been shown that unless changes occur in the elementary years, obesity persists into adulthood. Unfortunately, our public schools are struggling to implement the Healthy Student’s Curriculum. The reasons are many: the potential loss of revenue from going beyond the minimum federal requirements of the breakfast and lunch programs, a curriculum already packed with other mandates, and lack of external support for health education. We have made a start.6 The external support piece is where we physicians have leverage.

WHO WILL LEAD?

Physicians in Mississippi have a unique opportunity and a duty to lead in the implementation of the Mississippi Healthy Schools Program in every public school in the state. The future of our state depends on it. Principals and school superintendents will require support and encouragement in the implementation of this program. Each of us can insist that the mandated school health councils are actually formed in all of our schools in our areas of the state. We can encourage employees, patients, civic clubs and church members to support and participate in these councils. We can also encourage our institutions of higher learning to deploy

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the army of pre-professional and professional students enrolled in health professions training in our state institutions to assist in this process through the service-learning experiences encouraged by accrediting agencies.

WHAT NEXT?

Who can better lead and who are better prepared to do so? Should addressing the obesity epidemic not be a primary goal of our medical society? There are many things we can do (Table). For more information about the Mississippi Healthy Schools Program, www.healthyschoolsms.org. ❒ Some Things Mississippi Physicians Can Do to Address Obesity in Our Communities

Make sure mandated local and district health councils are in place and serve on them. Visit classrooms and assist with delivery of Health Student's Curriculum. Meet your district school nurse and support EPSDT programs Share information on state school health policy with parents and patients. Partner with physical education teachers to conduct fitness testing in schools. Lead local health fairs.

REFERENCES

1.

Wilkerson I. The Warmth of Other Sons. The Epic Story of America’s Great Migration. Random House, New York City, NY, 2010.

2.

Barry, JM. Rising Tide: The Great Mississippi Flood of 1927 and How It Changed America. Simon & Schuster; 1st Touchstone ed. 1998.

4.

Kessler DA. The End of Overeating ? Control of the Insatiable American Appetite. Rodale Inc., New York City, NY, 2009.

3.

5.

6.

Dittmer J. The Good Doctors. Simon and Schuster, New York City, 2010.

Mississippi Office of Healthy Schools. www.healthyschoolsms.org. Accessed December 17, 2010.

Year One. Mississippi Center for Health Policy, Jackson, Mississippi, 2010.

Feel the Burn Exercise at a moderate intensity to get the most benefit from your workout. A light sweat, faster breathing and some strain in your muscles are all good indicators you’re exercising effectively. If you have a health condition or any other physical barrier, it’s a good idea to talk to your doctor before you begin. be healthy. exercise.

www.bcbsms.com Blue Cross & Blue Shield of Mississippi, A Mutual Insurance Company, is an independent licensee of the Blue Cross and Blue Shield Association. ® Registered Marks of the Blue Cross and Blue Shield Association, an Association of Independent Blue Cross and Blue Shield Plans.

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A

• SPECIAL ARTICLE • Introducing MPHP Medical Director Scott L. Hambleton, MD Karen A. Evers, Managing Editor

sk Scott L. Hambleton, MD how he’s doing and he’s likely to reply, “Living the dream!” As the newly appointed medical director of the Mississippi Professionals Health Program (MPHP), he’s doing what he is passionate about: being able to intervene on behalf of Mississippi physicians and offering them solutions for their problems. A Tennessee native, Dr. Hambleton officially took helm of MPHP in November having practiced addiction medicine, primarily at Pine Grove Behavioral Health. His passion for working with other professionals with impairment issues stems from his own experience. He voluntarily discloses he was married in 1995 and divorced ten years later as a direct result of addiction. More importantly, his recovery journey is what leads him to obsess over loving what he does. “The primary reason that I am alive is because of my participation in the Physician Health Programs in Tennessee, North Carolina and Mississippi,” he divulged. “The long term program of recovery mandated by these Physician Health Programs literally saved my life. I can say, unequivocally, that I could not have gotten sober without their help. My involvement with these programs and their medical directors inspired me to do the things that were necessary to recover from active addiction and reenter the field of Scott L. Hambleton, MD medicine as a productive and stable physician. The more I learned about treatment and recovery, the more passionate I became,” he said emphatically. Eventually, he decided to complete an addiction medicine fellowship and work in the field full-time. “My involvement with recovering professionals while working in treatment was extremely gratifying. Participating in the transformation of the lives of these men and women, from chaos and unmanageability to stability and productivity was truly rewarding. Families and friendships were healed and seemingly hopeless situations were often completely reversed,” he said. Dr. Hambleton graduated from the University of Tennessee at Chattanooga in 1987, worked for a few years and then went to medical school at the University of Tennessee in Memphis. After graduating in 1994, he began the accelerated family practice residency at the University of Tennessee in Knoxville which he completed in 1996. In 2006, he began an addiction medicine fellowship sponsored by the University of Florida at Pine Grove Behavioral Health. His experience with addicted patients began in his family practice residency, private practice, and emergency medicine. After a fellowship in addiction medicine, he served as the medical director of various programs at Pine Grove Behavioral Health in Hattiesburg, including the Women’s Center and Gentle Path Programs which provide residential treatment to females with substance use disorders and eating disorders and treatment for males and females with sexual addiction. He was also closely involved with the Pine Grove Next Step Program which treats men with substance use disorders and the Pine Grove Professional Enhancement Program treating professionals with disruptive behavior or other personality issues which cause difficulty in the workplace. “These are truly world class, nationally respected programs which provided me with a solid foundation and treatment perspective for working with these individuals,” he said. “Professionals require a higher caliber of treatment for many reasons. The aftercare planning and licensure related issues are often very complex. Additionally, the cognitive distortion and denial systems that accompany addiction in professionals, and physicians in particular, can be very complicated and difficult to treat.” “I feel that my experience with initial treatment at the earliest stages of recovery will provide me with a solid foundation for the monitoring and intervention of participants in the Mississippi Professionals Health Program,” he added. When asked what should be done about the stigma associated with recovering professionals, Dr. Hambleton said, “Unfortunately the stigma does exist, although it is much less than it used to be. I think that education of physicians and other health care providers should be dramatically increased. The competition for time in medical school and residency programs is

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often very intense, and unfortunately most physicians report that they feel unprepared to treat addicted patients because of lack of adequate training.” Consider the following: • As many as 20 percent of the patients in a typical family medicine practice will have a substance use disorder. •

As many as 50 percent of patients in a psychiatric practice will have an addictive disorder. The yearly cost of addiction in the United States exceeds $600 billion.

Dr. Hambleton went on to say, “A patient in the midst of active addiction can be very unpleasant and may require much time. Manipulative and dishonest behaviors often manifest themselves. Many practices are extremely busy, so addicted patients can be overlooked. Not surprisingly, by some reports, less that five percent of referrals for patients with addiction to residential treatment come from physicians.” “Addicted patients behave in a predictable way, and the behavior of the addicted professional is also predictable, as is the course of untreated addiction. Recovery in the addicted professional is also predictable and well documented. I believe that as understanding of addiction as a brain disease increases in physicians and other health care providers, the stigma of addiction will decrease. Ironically, although over 90 percent of the physicians in the MPHP will return to stable and productive medical practices at the end of a 5-year recovery contract, much confusion and stigma about addiction persist. Education is the answer, and I hope that Mississippi physicians will lead the way,” he explained. Dr. Hambleton would like to use the influence of the MPHP and his position as medical director to provide education about three subjects for which he has great enthusiasm. He outlines: “1) Education of physicians, health care providers and the public, in general about addiction as a brain disease. I believe the stigma of addiction will decrease in direct proportion to the increase in understanding of addiction as a brain disease. 2) The epidemic of prescription drug abuse. I believe this epidemic exists primarily because of lack of understanding of addiction by the providers as well as the public. Ultimately, although it is painful to admit, the prescriptions originate from the physician or other prescriber! 3) Recovery in the impaired professionals’ family. I have tremendous compassion for addicted patients and their family, specifically for the families in the midst of an active addiction. Their behavior will often ravage the lives of the people he or she encounters. Remarkably, these behaviors are easily predictable, and the resultant consequences are often the only thing that will cause the individual to accept help! Education of the public, the health care providers, and the families of the professionals we monitor, will be extremely important. Recognition of behaviors and facilitating intervention rather than abandoning the addicted patient or worse, enabling the active addiction must be an integral part of the necessary education. The MPHP is an ideal way to promote this type of awareness.”

EDUCATION

Profile

• Addiction Medicine Fellowship: University of Florida at Pine Grove Behavioral Health, Hattiesburg, November 2007. • Residency: University of Tennessee Medical Center at Knoxville, Accelerated Family Practice Residency, October 1996. • Medical School: University of Tennessee, Center for Health Sciences, Memphis 1994. • University of Tennessee at Chattanooga, B.A. Chemistry, 1987.

BOARD CERTIFICATION

• American Society of Addiction Medicine 2008. • American Board of Family Practice 1998; recertification 2008.

PROFESSIONAL MEMBERSHIPS • • • • •

American Society of Addiction Medicine American Association of Family Practice Mississippi State Medical Association American Medical Association Treasurer, Mississippi Society of Addiction Medicine: 2009 - present

EMPLOYMENT

• Emergency Medicine and Urgent Care: Southeastern Emergency Physicians, July 1995 June 2000; Kings Mountain Hospital, Kings Mountain, NC, June 2000 - February 2002. Pinnacle Healthcare, Shelby, NC, January 2003 March 2004. • Addiction Medicine Fellowship: Pine Grove Behavioral Health, November 2006 - November 2007. • Addiction Medicine: Pine Grove Behavioral Health, Attending Physician at A and D/ Dual Diagnosis Unit, November 2007 - March 2008 • Addiction Medicine: The Oxford Centre, Medical Director, March 2008 - November 2008. • Addiction Medicine: Pine Grove Behavioral Health, March 2009 - December 2010. Attending Physician at A and D/Dual Diagnosis Unit; Medical Director Women’s Center: March 2009 - July 2010; Medical Director Gentle Path July 2009 present. Other duties included direct supervision of six family nurse practitioners on staff at Pine Grove.

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When asked what issues related to MPHP concern him Dr. Hambleton replied, “I am concerned about protecting the integrity of the program and shielding it from any outside influences which could diminish its effectiveness. Protecting the confidentiality of the MPHP participants as well as making sound recommendations for intervention and ongoing monitoring will be my primary concerns. I would like the MPHP to continue using the Federation of State Physician Health Programs’ model of abstinence-based recovery. I would like to accomplish this with as much transparency as possible while maintaining the confidentiality of our participants.� “Remarkably, over 96 percent of recovering physicians respond to abstinence based treatment. Less than three to four percent are unable to recover and return safely to practicing medicine. Those statistics are unbelievably successful. Although I have much compassion and concern for the small percent who are unable to return to practice, I refuse to do anything which might jeopardize the integrity of the MPHP. I believe this type of conservative approach will best facilitate the continued great success we have had in Mississippi,� Dr. Hambleton said. As an addictionologist, one more matter important to MSMA members Dr. Hambleton feels strongly about is prescription drug abuse. “Physicians and other prescribers are ultimately the source of the medication that is being abused!� He explained, “There are many reasons for the crisis; however, I believe that providers’ increased understanding of addiction as a brain disease could be one of the easiest ways to help control the problem. The key point is that it is possible to provide excellent, compassionate care for our patients while using a conservative, thoughtful approach when prescribing medications with the potential for abuse. I think the worst-case scenario for us (MSMA) would be to not address this issue internally now, resulting in forced legislative changes later.� Another underlying cause of the prescription drug abuse problem relates to improper boundaries between the physician and patient. “Many physicians have difficulty setting limits with their patients, and saying ‘no’ can be very uncomfortable at times. Boundary courses can be very helpful for clarification and education, and Medical Boards routinely require physicians to attend these courses. I hope MSMA members will examine this issue and actively participate in the search for and implementation of solutions,� he said. In closing Dr. Hambleton remarked, “When I was Scott L. Hambleton, MD offered the position as medical director of the Mississippi Professionals Health Program, I considered the opportunity What I enjoy most about being a doctor: I love being to be the dream of my life. I consider myself to be able to intervene on behalf of my patients and offer exceedingly blessed. I am truly, ‘Living the dream!’�� solutions for their problems. I like to watch them get better!

You’re most likely to see me around: Lake Caroline or the Ross Barnett Reservoir. On the weekends I love to: Watch football and the History Channel, putt around the yard or go fishing. I also like to bird hunt. Sports teams I root for are: The Tennessee Volunteers or the Colts! If I’m watching a movie or listening to music, it’s probably: Anything except rap.

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• POETRY AND MEDICINE •

[This month, we print a poem by John D. McEachin, MD, a Meridian pediatrician. This poem, written recently, offers up a proverbial “pearl” of wisdom for the doc in the ditch when faced with anothers doc’s wife wanting to treat off the shelf! The prolific Dr. McEachin holds a special place at the Journal as our unofficial poet laureate. For more of Dr. McEachin’s poetry, see past JMSMAs and look for more in coming months. Any physician is invited to submit poems for publication in the journal, attention: Dr. Lampton or email him at lukelampton@cableone.net.]—ED.

“Pediatric Pearl No. 1” Doctor’s wife calls you just after church is out. “Joe has fever, sore throat, cough! Strep throat, no doubt? He’s got aching and headache; he’s also hoarse! Joe needs meds; and I’ve got samples here, of course! “Just tell me what to start; these are what I’ve got! Z-Pak, Cefzil, Amoxil! Which ‘hits the spot’? Rob will always treat our son with one of these. He’s fishing today— so which one, if you please.”

I swallow hard, for this case will not be fun! Doctor’s wife— loaded gun— I mean a “shotgun.” She’s not about to conceive what is coming! And it is for sure not “Dixie” I’m humming! “Sue, it’s not likely Joe’s problem is strep throat, So here’s a suggestion I would like to float. Let’s use supportive care; sit on it tonight. If Joe’s alert and drinking, he’ll be alright!

“Oh, by the way, strep throat rarely coughs at all. His symptoms are viral, but thanks for the call. Ring back with any change— now don’t hesitate! No samples for now— no need to medicate!”

“I can’t believe this! Heavens and saints above!” “ Knew you’d understand, Sue! Please give Joe my love!!!” —John D. McEachin, MD Meridian 62

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Knowing ng Our Insureds ureds FEBRUARY 2011 JOURNAL MSMA

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• THE UNCOMMON THREAD • Envy

R. Scott Anderson, MD

T

he conversation had seemed harmless enough at the time, as harmless as any conversation at a VA psychiatric hospital ever got anyway. They’d come in last night before they went home and gave Mr. Thomas the bad news. His lungs were failing. A lifetime of three packs of cigarettes a day had taken their toll, and he’d be spending the rest of his days on a ventilator trying to keep his oxygen level up and his CO2 down.

“How come he’s going on that there breathing machine first?” Bibb Kless fired from the next bed.

“Mr. Kless, we’re only talking to Mr. Thomas. You stay on your side of the curtain and keep quiet. We’re done talking to you,” Benny said in a serious doctor voice.

“I got the same thing he got…the empazema, and he’s a whole lot younger than me.”

“Mr. Kless, your blood gasses are fine. You don’t need a ventilator.” “You ain’t checked ‘em since I got in this place.”

“They were fine then and they’re fine now, so you get back over there on your side of the curtain and hush up.”

Mr. Thomas hadn’t said much. The truth was he just didn’t have the wind to say anything at all. It took all of his energy just to lay there. So that’s what he did, just laid there quietly as they trached him, but the two doctors could see old Bibb watching them through the slit in the curtains and hear him muttering under his breath….“I smoked more cigarettes before I got out of the Navy than that sissy bastard smoked in his whole life. What a nut job”…and here sat that damned nut job in the morning light with the stem of the ventilator hose between his lips, his leathery old cheeks puffin’ in and out, and there laid Mr. Taylor as still and dead and blue as a rock. ❒ R. Scott Anderson, MD, a radiation oncologist, is medical director of the Anderson Regional Cancer Center in Meridian and past vice chair of the MSMA Board of Trustees. Additionally, he is an accomplished oil-painter and dabbles in the motion-picture industry as a screen-writer, helping form P-32, an entertainment funding entity.

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Haǀe zŽu ŽŶƐidered a LiĨe SeƩlemeŶƚ &Žr zŽur Kld LiĨe /ŶƐuraŶcĞ WŽlicLJ? tŚĂƚ ŝƐ Ă >ŝĨĞ ^ĞƩůĞŵĞŶƚ͍ ůŝĨĞ ƐĞƩůĞŵĞŶƚ ŝƐ ƚŚĞ ƐĂůĞ ŽĨ ĂŶ ĞdžŝƐƟŶŐ ůŝĨĞ ŝŶƐƵƌĂŶĐĞ ƉŽůŝĐLJ ŽŶ ƚŚe ƐĞĐŽŶĚaƌLJ ŵĂƌŬĞƚ ƚŽ Ă ƚŚiƌĚ ƉĂƌƚLJ ŝŶǀĞƐƚŽƌ͘

tŚŽ Žƌ tŚĂƚ DĂLJ YƵĂůŝĨLJ͍ 9 /Ĩ ƚŚĞ ƉĞƌƐŽŶ ŝŶƐƵƌĞd ďLJ ƚŚĞ ƉŽůŝĐLJ ŝƐ ĂŐĞ ϳϬ Žƌ ŽůĚĞƌ 9 /Ĩ ƚŚĞ ƉĞƌƐŽŶ ŝŶƐƵƌĞd ŚĂƐ ĂŶLJ ŵĂũŽƌ ŵĞĚŝĐĂů ĐŽŶĚŝƟŽŶƐ 9 /Ĩ ƚŚĞ ƉŽůŝĐLJ ŚĂƐ Ă ĚeĂƚŚ ďeŶĞĮƚ ŽĨ ΨϮϱϬ͕Ϭ0Ϭ Žƌ ŵŽƌĞ 9 WŽůŝĐŝĞƐ ŝŶĐůƵĚŝŶŐ͕ ďƵƚ ŶŽƚ lŝŵŝƚĞĚ ƚŽ͕ ƵŶŝǀĞƌƐaů ůŝĨĞ͕ ƚĞƌŵ ŝŶƐƵƌĂŶĐĞ͕ ǀĂƌŝĂďůĞ ůŝĨe ŝŶƐƵƌĂŶĐĞ Žƌ ǁŚŽůĞ ůŝĨĞ ŝŶƐƵƌĂŶce 9 /Ĩ ĂŶLJ ĐĂƐŚ ǀĂůƵĞ ĞdžŝƐƚƐ ŝŶ ƚŚĞ ƉŽůŝĐLJ͕ ƚŚĞ ĂŵŽƵŶƚ ŝƐ ƌĞůĂƟǀĞlLJ ƐŵĂůů

&Žƌ DŽƌĞ /ŶĨŽƌŵĂƟŽŶ ŽŶ >ŝĨĞ ^ĞƩůĞŵĞŶƚƐ͕ ĐŽŶƚĂcƚ͗ ,͘ >ĂƌƌLJ &ŽƌƚĞŶďĞƌƌLJ͕ W ͕ >h͕ Ś& džĞĐƵƟǀĞ WůĂŶŶŝŶŐ 'ƌŽƵƉ͕ W 1640 Lelia Drive, Suite 220 PO Box 16566 Jackson, MS 39216 ;ϲϬϭͿ ϵϴϮͲϯϬϬϬ

tŚLJ hƐĞ Ă >ŝĨĞ ^ĞƩůĞŵĞŶƚ͍ 9 dĞƌŵ lŝĨĞ iŶƐƵƌĂŶĐĞ ƉŽůŝĐLJ ǁŝůů ĞdžƉŝƌĞ 9 KůĚ ƉŽůŝĐLJ ƚŚĂƚ iƐ ŶŽ ůŽŶŐĞr ŶĞĞĚĞĚ Žƌ ƉƌĞŵŝƵŵƐ ĐĂŶŶŽƚ ďĞ ƉĂŝĚ 9 ƉŽůŝĐLJ ƚŚĂƚ ǁĂƐ ƉƵƌĐŚĂƐeĚ ĨŽƌ Ă ďƵƐŝŶĞƐƐ ďƵLJ/ƐĞůů ĂŶĚ ŝƐ ŶŽ ůŽŶŐĞƌ ŶĞĞĚĞĚ 9 ƉŽůŝĐLJ ǁĂƐ ƉƵrĐŚĂƐĞĚ ĨŽƌ Ă bƵƐŝŶĞƐƐ ƚŚĂƚ ŚĂƐ ďĞĞŶ ƐŽůĚ Žƌ ŝƐ ŶŽƚ Ŷeeded 9 dŚĞƌĞ ŵĂLJ ďĞ Ă ďĞƩeƌ ƉŽůŝĐLJ ĂǀĂiůĂďůĞ Ăƚ Ă ůŽǁĞƌ ĐŽƐƚ

9 ƐƚĂƚĞ ǀĂůƵĞ ŚĂƐ ĐŚĂŶŐĞĚ ĂŶd ƚŚĞ ƉŽůŝĐLJ ŝƐ ŶŽ ůŽŶŐĞƌ ŶĞĞded

^ĞĐƵƌŝƟĞƐ KīĞƌĞĚ dŚƌŽƵŐŚ sĂůDĂƌŬ ^ĞĐƵƌiƟĞƐ͕ /ŶĐ͘ DĞŵďĞƌ &/ER ͕ ^/W /ŶǀĞƐƚŵĞŶƚ ĚǀiƐŽƌLJ ^ĞrǀŝĐĞƐ KīĞƌeĚ dŚƌŽƵŐŚ sĂůDĂƌŬ dǀŝƐĞƌƐ͕ /ŶĐ͘ Ă ^ ZĞŐŝƐƚĞrĞĚ /ŶǀĞƐƚŵĞŶƚ ĚǀŝƐŽƌ ϭϯϬ ^ƉƌŝŶŐƐŝĚĞ DƌŝǀĞ͕ ^ƵŝƚĞ ϯϬϬ ŬƌŽŶ͕ KŚŝŽ ϰϰϯϯϯ-ϮϰϯϭΎ ϭͲϴϬ0-765-5201 džĞĐƵƟǀĞ WůĂŶŶŝŶŐ 'ƌŽƵƉ ŝƐ Ă ƐĞƉaƌĂƚĞ ĞŶƟƚLJ ĨƌŽŵ sĂlDĂƌŬ ^ĞĐƵƌŝƟĞƐ͕ /ŶĐ͘ ĂŶĚ sĂůDĂƌŬ dǀŝƐĞƌƐ͕ /ŶĐ͘ In a lifĞ ƐĞƩůement agreement, the current life insurance policy owner transfers the ownership ĂŶĚ ďĞŶĞĮĐŝĂrLJ ĚĞƐŝŐŶĂƟons to a third party, who receives the death proceeds at the passing of the insured. As a result, this buyer has Ă ĮŶĂŶĐŝĂl interest in the seller’s death. When an individual decides to sell their policy, he or she must provide complete access to his or her medical history, and other personal inforŵĂƟŽŶ͕ ƚhat mĂLJ Ăīect his or her life expectĂŶĐLJ͘ dŚŝƐ ŝŶĨŽƌŵĂƟon is requested during the ŝŶŝƟĂl ĂƉƉůŝĐĂƟŽŶ for a life ƐĞƩůĞŵĞŶƚ͘ Ōer the coŵƉůĞƟŽŶ ŽĨ ƚhe sale, there may be an ongoinŐ ŽďůŝŐĂƟŽŶ to disclose siŵŝůĂƌ ĂŶĚ ĂĚĚŝƟonal inforŵĂƟŽŶ Ăƚ Ă ůater date. ůŝĨĞ ƐĞƩlement may aīect the seller’s eligibility for certain public assistance programs, such as Medicaid, and there may be tax consequences. Individuals should discuss ƚŚĞ ƚĂdžĂƟŽŶ of the proceeds received with their tax advisor. ValMark SecƵƌŝƟĞƐ considers Ă ůŝĨĞ ƐĞƩůĞŵĞŶƚ Ă ƐecuritLJ ƚƌĂŶƐĂĐƟŽn. ValMark and its registered represĞŶƚĂƟǀĞƐ ĂĐƚ ĂƐ brokers on the transacƟŽŶ ĂŶĚ ŵĂLJ receive a fee from the purchaser. A life seƩůĞŵĞŶƚ tƌĂŶƐĂĐƟon may require an extended period oĨ ƟŵĞ ƚo complete. Due to complexity of tŚĞ ƚƌĂŶƐĂĐƟon, fees and costs incurred witŚ ƚŚĞ ůŝĨĞ ƐĞƩlement tranƐĂĐƟŽŶ ŵĂLJ ďe ƐƵďƐƚĂŶƟally higher than otheƌ ƐĞĐƵƌŝƟes.


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