January 2014 JMSMA by Journal MSMA

January

VOL. LV

2014

No. 1

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 James A.Rish, MD President Claude Brunson, MD President-Elect Michael Mansour, MD Secretary-Treasurer R. 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 39158-2548. The views expressed in this publication reflect the opinions of the authors and do not necessarily state the opinions or policies of the Mississippi State Medical Association. Copyright© 2014 Mississippi State Medical Association.

Official Publication of the MSMA Since 1959

JANUARY 2014

VOLUME 55

NUMBER 1

Scientific Articles Palliative Care for the Terminal Heart Failure Patient

Walter L. Beard, MD; R. Craig Long, MD, PharmD; Stephen A. Geraci, MD

Top Ten Facts You Need to Know - About Obese Adults Admitted to Hospital

Dominique J. Pepper, MD; Michael Brewer, DO; Christian A. Koch, MD

Clinical Problem-Solving: Three Strikes and You’re Out

Cynthia Colson Garrett, MD

Special Article King David, Son of Jesse: The World’s First Parkinson’s Patient …Observations from November 2013

C. Randy Voyles, MD

President’s Page SGR – The Gift that Keeps on Giving

James A. Rish, MD

Related Organizations Mississippi State Department of Health

Departments From the Editor: The Coming Disaster of ICD-10

In Memoriam

About The Cover: Bottle Tree in an Herb Garden by William R. Locke, MD

Eudora Welty’s short story Livvie speaks of bottle trees: “Then coming around up the path from the deep cut of the Natchez Trace below was a line of bare crape-myrtle trees with every branch of them ending in a colored bottle, green or blue. There was no word that fell from Solomon’s lips to say what they were for, but Livvie knew that there could be a spell put in trees, and she was familiar from the time she was born with the way bottle trees kept evil spirits from coming into the house - by luring them inside the colored bottles, where they cannot get out again. Solomon had made the bottle trees with his own hands over the nine years, in labor amounting to about a tree a year, and without a sign that he had any uneasiness in his heart, for he took as much pride in his precautions against spirits coming in the house as he took in the house, and sometimes in the sun the bottle trees looked prettier than the house did...” Southern gardener Felder Rushing has made bottle trees popular locally. For more about the history of bottle trees visit his website: http://www.felderrushing.net/ HistoryofBottleTrees.htm Dr. Locke, a life-long resident of Starkville, is a co-founder of Starkville Clinic for Women, PA and is on staff at Oktibbeha County Hospital Regional Medical Center. He graduated from the University of Mississippi School of Medicine in 1979 and followed up with his OB/GYN residency in 1983. He has been in private practice for 28 years. r

January 2014 JOURNAL MSMA 1

From the Editor: The Coming Disaster of ICD-10

CD-10 was originally intended to debut in October 2013, like the “fumbled” health care exchanges. Imagine the disruption for medicine and healthcare across the country had both debuted at the same time! Fortunately, through the efforts of Mississippi’s AMA delegation (along with Alabama’s leadership), ICD-10 implementation was delayed a year. However, a year’s reprieve may be our only triumph against this looming disaster. AMA leadership clearly warns that physicians must ready themselves for the negative impact of ICD-10, which will force physicians and their offices to utilize about 68,000 outpatient diagnostic codes compared to the current 13,000 used under ICD-9. This expensive mandate will cause disruption of thousands of physician practices without any benefit for our patients, offering another example of the gargantuan appetite for data (not quality) by government and insurers. Experts say the new code set will affect not only claims submissions but also such processes as patient eligibility verification, pre-authorization for services, documentation of patient visits, and quality reporting. The cost for individual physician practices to adopt ICD-10 is estimated to be around

$83,000 for a small practice and as much as $2.7 million for a large group practice. The average physician practice will have to upgrade billing, claims processing, and electronic health record (EHR) software; revise coding tools and office forms; train staff; update fee schedules and payer Lucius M. Lampton, MD contracts; identify coverage changes; and finally, stockpile cash reserves or establish lines of credit to preserve cash flow. Beginning Oct. 1, 2014, services that are not coded (or wrongly coded) in ICD-10 will be rejected and go unpaid. All of this is going to happen to physicians’ practices for essentially no patient care benefit. It has been said that the art of medicine is simply the mastery of chaos. Wouldn’t it be nice if all we had to worry about was the chaos of disease, illness, and the health of our patients? The unnecessary chaos of ICD-10, as physicians face deadlines for EHR meaningful use and the ACA, is a dangerous distraction for our practices and our patients. Contact me at lukelampton@ cableone.net. —Lucius M. “Luke” Lampton, MD, Editor

Journal Editorial Advisory Board Myron W. Lockey, MD Chair, JMSMA Editorial Advisory Board Journal MSMA Editor Emeritus, Madison Timothy J. Alford, MD Family Physician, Kosciusko Medical Clinic Michael Artigues, MD Pediatrician, McComb Children’s Clinic Diane K. Beebe, MD Professor and Chair, Department of Family Medicine, University of MS Medical Center, Jackson Claude D. Brunson, MD Senior Advisor to the Vice Chancellor for External Affairs, University of Mississippi Medical Center, Jackson Jeffrey D. Carron, MD Associate Professor, Department of Otolaryngology & Communicative Sciences, University of Mississippi Medical Center, Jackson Gordon (Mike) Castleberry, MD Urologist, Starkville Urology Clinic Mary Currier, MD, MPH State Health Officer Mississippi State Department of Health, Jackson

Bradford J. Dye, III, MD Ear Nose & Throat Consultants, Oxford Daniel P. Edney, MD Executive Committee Member, National Disaster Life Support Education Consortium, Internist, The Street Clinic, Vicksburg

2 JOURNAL MSMA January 2014

Paul “Hal” Moore Jr., MD Radiologist Singing River Radiology Group, Pascagoula

Owen B. Evans, MD Professor of Pediatrics and Neurology University of Mississippi Medical Center, Jackson

Jason G. Murphy, MD Surgeon Surgical Clinic Associates, Jackson

Maxie L. Gordon, MD Assistant Professor, Department of Psychiatry and Human Behavior, Director of the Adult Inpatient Psychiatry Unit and Medical Student Education, University of Mississippi Medical Center, Jackson

Ann Myers, MD Rheumatologist Mississippi Arthritis Clinic, Jackson

Scott Hambleton, MD Medical Director Mississippi Professionals Health Program, Ridgeland John Edward Hill, MD Family Physician, North Mississippi Medical Center Tupelo W. Mark Horne, MD Internist, Jefferson Medical Associates, Laurel Brett C. Lampton, MD Internist/Hospitalist, Baptist Memorial Hospital, Oxford

Philip L. Levin, MD President, Gulf Coast Writers Association Emergency Medicine Physician, Gulfport William Lineaweaver, MD Sharon Douglas, MD Editor, Annals of Plastic Surgery Professor of Medicine and Associate Dean for VA Medical Director Education, University of Mississippi School of Medicine, JMS Burn and Reconstruction Center, Jackson Associate Chief of Staff for Education and Ethics, G.V. Montgomery VA Medical Center, Jackson Michael D. Maples, MD Vice Preisdent, Chief of Medicial Operations Baptist Health Systems, Jackson Thomas E. Dobbs, MD, MPH State Epidemiologist Mississippi State Department of Health, Hattiesburg

Alan R. Moore, MD Clinical Neurophysiologist Muscle and Nerve, Jackson

Darden H. North, MD Obstetrician/Gynecologist Jackson Health Care-Women, Flowood Jimmy L. Stewart, Jr., MD Program Director, Combined Internal Medicine/ Pediatrics Residency Program, Associate Professor of Medicine and Pediatrics University of Mississippi Medical Center, Jackson Samuel Calvin Thigpen, MD Hematology-Oncology Fellow, Department of Medicine University of Mississippi Medical Center, Jackson Thad F. Waites, MD Clinical Cardiologist, Hattiesburg Clinic W. Lamar Weems, MD Urologist, Jackson Chris E. Wiggins, MD Orthopaedic Surgeon Bienville Orthopaedic Specialists, Pascagoula John E. Wilkaitis, MD Chief Medical Officer Brentwood Behavioral Healthcare, Flowood

Medical Assurance Company of Mississippi

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For over 30 years, Mississippi physicians have looked to Medical Assurance Company of Mississippi for their professional liability needs. Today, MACM is an integral part of the health care community providing a legacy of services to our insureds. A dedicated staff and physician involvement at every level guarantees that the interests of our policyholders remain the top priority. This, combined with the many years of loyalty and support from our insureds, is what allows us to be the carrier of choice in Mississippi. Call on us to assist with your professional liability needs.

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Working with Young Physicians January 2014 JOURNAL MSMA 3

• Scientific Articles • Palliative Care for the Terminal Heart Failure Patient Walter L. Beard, MD; R. Craig Long, MD, PharmD; Stephen A. Geraci, MD [This month’s article in the End-of-Life care series, “Palliative Care for the Terminal Heart Failure Patient,” is another useful and welcome submission. Although general concepts of palliative care have been discussed in the first 5 articles in this series, there are unique features to many clinical situations where they are to be applied. If you did not have an opportunity to read the “Concepts in End-of-Life Care” and POLST articles published in previous issues (J Miss Med Assoc. 2012;53(11), 2013;54(3) and 2013;54(10)), you may choose to do that after reading this paper. It is always a challenge to help patients navigate end-of-life pathways, especially when persistent dyspnea and fatigue are present from heart failure or obstructive lung disease. The editors wish to thank the authors of this series for their excellent papers and the tool sets they have provided practicing physicians to help our patients at this point in their lives. We have articles on end-of-life care in children coming in future issues of the journal. These articles have taught us that dying is best when experienced as a part of life, rather than the end of life.] —Richard deShazo, MD; Associate Editor

bstract

Heart failure is a chronic disease afflicting millions of patients worldwide. Advances in treatment have allowed sufferers to enjoy overall prolonged survival and enhanced quality of life. Yet, a consequence of these therapeutic successes is that more patients survive to end-stage disease, with severe symptoms, poor quality of life, and no options available to prolong their survival reasonably. End-stage heart failure patients require a comprehensive palliative approach to care during their final months, with treatment goals focusing on symptom relief. Often, specific heart failure therapies can further this cause and should be administered when appropriate to alleviate specific symptoms, while other general palliative measures should also be considered as with other terminal patients. End-of-life palliative strategies must conform to accepted principles of ethical care. Constant communication with patients and families is essential to achieve best treatment goals for this growing segment of the population. Author Affiliations: Resident physician in the Department of Internal Medicine at the University of Mississippi Medical Center, Jackson, Mississippi; (Dr. Beard); Assistant Professor of Medicine, Division of Cardiovascular Diseases, Advanced Heart Failure Service, at the University of Mississippi Medical Center (Dr. Long); Professor and Chair, Department of Medicine, at the Quillen College of Medicine, East Tennessee State University. He previously served as Professor and Vice Chairman for the Department of Medicine at the University of Mississippi Medical Center (Dr. Geraci). Corresponding Author: Walter L. Beard, MD, Department of Internal Medicine, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216. Telephone: (601)984-5601. Fax: (601)984-6601 (wbeard@umc.edu). Disclosure: No funding from any source was used in the preparation of this manuscript. This manuscript has not been published previously, and is not under consideration for publication by any other journal. All authors attest that they have no real or apparent financial or scientific conflicts of interest related in any way to the content of this manuscript; that they meet accepted criteria for authorship; and have approved the final version of this paper.

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Key Words: Congestive heart failure, treatment, palliation, ethics Introduction Heart failure is a chronic condition affecting over 5.8 million people1 with an attendant annual economic burden of $34 billion in the United States.2 The increasing prevalence of risk factors for developing heart failure—including hypertension, coronary artery disease, obesity, and diabetes—along with a progressively aging population, has increased the incidence of heart failure; the lifetime risk for a 40-year-old is now approximately 20%.1 Heart failure is a common diagnosis resulting in adult hospital admission3, and individuals with end-stage heart failure (New York Heart Association functional Class IV, American Heart Association Stage D) have their highest rates of hospital admission and readmission as they approach end-of -life.4,5 Chronic heart failure overall has a predicted mortality exceeding that of many malignancies, with a median survival of six months for Class IV patients.6,7 Guideline-based medical therapy improves symptoms in chronic heart failure; in addition, to cardiac resynchronization therapy for some and implantable cardiac defibrillators for others also reduce mortality.8 Yet despite optimal treatment employing these advancements, many patients are not candidates for destination therapy (transplantation, ventricular assist devices) and suffer progressive and eventually terminal heart failure. In these patients when no additional life-sustaining therapy is available or reasonable, treatment goals shift to focus on reducing symptoms and maintaining a maximal quality of life during their final months. Contrasting with diseases which the public commonly associates with a fatal outcome (e.g., cancer, AIDS, dementia), palliative, non-life-prolonging treatment is rarely sought or anticipated by most heart failure patients until the latest stages of their disease.9 Similarly, physicians are less likely to discuss a palliative terminal treatment strategy for heart failure patients as they

are for other terminal diseases, despite expert recommendations for such an approach.8 As a result, fewer heart failure patients enter hospice care or into a treatment plan that excludes mortality reduction as a goal. However, palliative end-of-life care meets ethical principles of practice, and terminal heart failure patients are no less deserving of this compassionate, symptomabating strategy than are patients with other terminal diseases. Accepted guidelines exist to determine which patients would qualify for terminal palliative care,8,10-12 and the decision process should involve specialists in cardiac disease or heart failure specifically. These considerations are far beyond the scope of this discussion. However, the primary care physician or other generalist will often assume the role of principal health care provider for these patients, making an understanding of appropriate available options essential to comprehensive, ethical palliation. Traditional palliative care at end-of-life focuses upon medications and other therapies to relieve pain, nausea, and anxiety while concurrently excluding any testing, procedures or treatments which would fail to do so (but are used to prolong survival in patients with less advanced disease). Yet, the chronic heart failure patient may have symptoms which can be relieved significantly with drugs and other therapies used in patients with earlier stage disease. Debate often arises when a given treatment could also potentially prolong survival or when an intervention might further reduce survival.

Ethical Principles of Healthcare

All care delivered to patients should adhere to the four basic principles of medical ethics: autonomy, non-maleficence, beneficence, and justice.13 Palliative strategies for terminal heart failure patients must adhere to these principles. Autonomy. Defined as self-determination, this principle states that patients with appropriate mental capacity must be allowed to make informed decisions and choices about their medical care. Physicians must provide patients with their expert opinion and supporting data regarding their disease process, prognosis, and expected clinical course, and treatment options at a level of complexity understandable by the patient, without influence of the provider’s personal values into the process. Autonomy also assures the right of patients to delegate decision-making authority to a surrogate in the event they should no longer possess the cognitive ability to exercise informed decision-making. The choice to adopt a palliative strategy must be agreed to by the competent patient or designated surrogate, as should each step or modification in the specifics of therapy. Non-maleficence. Physicians pledge to this principle of “do no harm” in the Hippocratic Oath. When life-sustaining interventions can no longer be expected to provide additional acceptable life quality, or particularly if they add to patient discomfort and suffering, instituting or continuing such treatments, in fact, violates the principle of non-maleficence. Conversely, providing treatments which produce meaningful symptom relief but secondarily could either prolong or shorten survival are fully consistent with non-maleficence. Several available treatments for heart failure symptoms have the

potential for not being mortality-neutral but nonetheless would not be excluded when adhering to this principle. The potential effects on life expectancy must be discussed with patients who must decide whether or not to accept such therapy. Beneficence. This is the principle that all actions taken by a physician should ultimately benefit the patient. In the nonterminal patient, beneficence usually includes offering treatments which prolong survival should the patient wish to accept any associated negative consequences (e.g., side effects, cost, inconvenience, discomfort). With the same caveats, symptom relief is always considered beneficial to patients but is most often placed secondary to improving survival. It is in the setting when mortality reduction is no longer a realistically achievable goal that symptom reduction becomes the primary achievable benefit of health care. When institution of a given intervention, or exclusion of an intervention, results in disparate effects (i.e., relieving symptoms while potentially shortening lifespan), careful discussion with the patient/surrogate is crucial, as the relative importance of these disparate effects must be assigned based upon the patient’s, rather than the provider’s, value set. Justice. Justice is the principle of fair and equitable provision of health care resources to patients as indicated for their condition, independent of other (e.g., financial, social) considerations. This concept is key in developing palliative care strategies; specifically, all symptom-relieving treatments should be made available for patient consideration. Conversely, treatments such as internal cardiac defibrillators, which provide no symptom relief, could be withheld (or deactivated if previously implanted) in patients with a very limited life expectancy and no reasonable expectation of benefit to avoid repeated and usually ineffective discharges in a dying patient.14 Excluding or discontinuing treatments which do not meet the primary goal of palliation is fully consistent with the principle of justice.8

General Treatment Options for Heart Failure

Pharmacotherapy with agents from several different drug classes remains the cornerstone of treatment for most patients with heart failure.8 Some medications provide both mortality and symptom reduction, while others reduce symptoms with variable effects on heart failure-associated survival. Similarly, nonpharmacologic interventions such as device therapy may reduce mortality in some heart failure patients while having no effect on symptoms, and are not appropriate choices in the terminal patient. Drug classes that decrease both mortality and symptoms include angiotensin converting enzyme inhibitors (ACEI),15,16 angiotensin receptor blockers (ARB)17, beta adrenergic receptor blockers (BB),18,19 mineralocorticoid (aldosterone) receptor antagonists (MCA),20,21 and the vasodilator combination isosorbide dinitrate/hydralazine.22,23 Other agents reduce symptoms without a clear, consistent effect on survival (e.g., digoxin, diuretics, opioids, nitroglycerin analogs, sodium nitroprusside), while a few (e.g., positive inotropic agents)8,24,25 may significantly reduce symptoms but potentially shorten remaining lifespan. Non-pharmacologic treatment options such

January 2014 JOURNAL MSMA 5

as cardiac resynchronization therapy (CRT) and left ventricular assist devices (LVAD)26 may reduce both symptoms and mortality, while others (e.g., renal replacement therapy) reduce symptoms but at significant comfort and financial cost without a clear effect on survival. Still others (e.g., implantable cardiac defibrillators) are devoid of symptomatic benefit and entail significant financial cost. Table 1 summarizes pharmacologic treatment options, highlighting expected symptomatic benefits, most common adverse consequences, and other relevant features. Table 2 provides a similar summary of nonpharmacologic options to be considered in this population.

Palliative Treatment

Even when all agree that mortality reduction is no longer the primary or even a significant consideration, developing a palliative strategy can be challenging. Definition of an acceptable quality of life varies greatly among individuals and includes a host of values and preferences, while specifics of a patient’s medical condition will determine whether a given goal is achievable; this fact precludes a “one size fits all” approach. Adverse consequences, attendant to all available interventions to some degree, necessitate cost-benefit decisions and frequent re-assessment when side effects occur. Cost, in this process, includes not only financial considerations but also consumption of time, energy, family resources, discomfort, complications, additional loss of functionality, and emotional distress. Relief of dyspnea, maintenance of sufficient strength and endurance (i.e., fatigue reduction) to permit some pleasurable activities and a degree of independence, pain relief, assurance of sufficient cognitive function for comfortable interaction with others, and relief of nausea are common and reasonable goals for most patients. Depression is quite frequent among patients with terminal disease, and depressed heart failure patients often benefit from directed interventions.10-12,27-29 Dyspnea Dyspnea is a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.30 It is one of the most common complaints among patients with advanced disease. Dyspnea in heart failure patients is most often due to pulmonary venous congestion, although poor oxygen delivery (due to severely reduced cardiac output and/or anemia) will also produce the sensation of dyspnea. It is important to note that dyspnea as defined here is distinctly different from pain with breathing, with the latter symptom addressed as pain relief (see below). Loop diuretics decrease pulmonary venous pressure and hydrostatic edema through both venodilation (intravenous formulations) and intravascular volume reduction (all routes of administration); combinations of diuretics from different classes can be used in refractory volume overload. Organic nitrates similarly reduce pulmonary and systemic venous pressures, and relieve venous congestive symptoms, and can be used as

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Table 1. Pharmacologic Therapy for Heart Failure Symptom Reduction Table 1. Pharmacologic Therapy for Heart Failure Symptom Reduction Therapy (drug)

Supplemental Oxygen (Nasal cannula, high flow oxygen ) Angiotensin Converting Enzyme Inhibitors

Typical Dose Range

Varies depending modality

Actions to Improve Symptoms Increase oxygen saturation

Dyspnea

++++

Low Edema Side Effects Output (For the Palliative Patient)

Enalapril Vasodilate thus Cough (2.5-20 mg decreasing both AngioBID) preload and edema Captopril afterload Hypotension (25-50 mg TID) Promote sodium +++ ++ ++ Ramipril and water (5 mg BID) excretion Trandolapril (4 mg daily) Angiotensin Valsartan Receptor (40-160 mg Blockers BID) Candesartan (4-32 mg daily) Beta Blockers Carvedilol Blocks Bradycardia, (6.25-25 mg sympathetic tone Hypotension BID) delivered to heart BronchoMetoprolol ++ ++ +/- spasm Succinate (Chronic) (Chronic) Worsening of (12.5-200 mg HF daily) Bisoprolol (1.25-10 mg daily) Loop Diuretics Furosemide Promote sodium Hypotension (20-600 mg and water Ototoxicity daily) excretion. Bumetanide ++++ +/++++ (0.5-10 mg daily) Torsemide (10-200 mg daily) Ethacrynic acid (25-400 mg daily) MineraloSpironoPromote sodium Gynecocorticoid lactone and water mastia Inhibitors (25-50 mg excretion in distal +++ +/+++ daily) segment of Eplerenone nephron (25-50 mg daily) Organic Isosorbide Decrease preload, Hypotension Nitrates Dinitrate afterload, and wall Headache 20-40 mg stress via TID venodilation +++ +/-

Hydralazine

Dobutamine

Milrinone

Digoxin

Morphine

Nitroglycerin Transdermal patches 0.1 – 0.4 mg/hr 37.5-100 mg Arterial TID Vasodilation

2-20 mcg/kg/min IV 0.375-0.75 mcg/kg/min IV

Increase cardiac inotropy, lusitropy (relaxation) and cardiac output Improves inotropy and cardiac output

0.125-0.5 mg Increases inotropy daily Increases vagal activity to heart

Varies Titrate to effect

Decrease sensation of dyspnea Venodilation

+++

++++

+/-

Tachycardia Headache Lupus-like Syndrome Flushing Nausea Tachycardia Arrhythmia Hypotension Ventricular Arrhythmia Hypotension Headache Nausea Bradyarrhythmia

Sedation Respiratory Depression

from anemia or hypoxemia; respiratory muscle fatigue from chronic tachypnea; anorexia and malnutrition; sleeplessness from sleep apnea, orthopnea, paroxysmal Therapy Actions Dyspnea Low Edema Side Effects/ nocturnal dyspnea, periodic apnea, and depression; deOutput Considerations pression itself; and heart failure complications includCardiac Improves Expensive Resynchronization cardiac output ++++ ++++ ++ Implantation ing uremia and hepatic dysfunction. Since advanced Therapy and decreases Invasive heart failure does not protect against other concurend-diastolic procedure pressures rent illnesses, common conditions such as infection Renal Improves Hypotension Replacement hypervolemia ++++ +/++++ Time consuming and inflammation should also be excluded or treated. Therapy Fatigue is best addressed by identifying the most (Ultrafiltration) Non-Invasive Improves May be likely primary mechanism in a given patient and exPositive Pressure oxygenation ++++ +/+/uncomfortable Ventilation and ventilation Possible worsen panding the scope of intervention when other palliative HF efforts are insufficient. When issues similar to those Aspiration if vomiting or causing dyspnea are paramount, treatments discussed altered mental status above should be considered initially. Although BB and ACEi/ARB can improve functional status in most heart failure patients, those in the terminal stages have likely exhausted the benefits of these treatments and may oral, sublingual or transdermal preparations; care must be exdevelop additional symptoms from adverse effects such as ercised to maintain sufficient nitrate-free intervals to avoid the hypotension, renal dysfunction or bradycardia which necesrapid development of vascular resistance (tachyphylaxis), howsitate dose reduction or discontinuation. Continuous infusion ever. Naturally-occurring opioid narcotics (morphine) produce of positive inotropes may produce a dramatic short-term bensystemic venodilation through a histamine agonist effect, while efit, though patients receiving dobutamine (but not milrinone) all opioid agonists (including synthetic agents) reduce the senwill develop tachyphylaxis with continuous infusions over sation of dyspnea through central (CNS) effects. Opioids carry days-weeks. Respiratory support with noninvasive ventilathe acknowledged effects on cognition and perception and, as tion can lower the proportion of the (reduced) cardiac output a result, should not be used in lieu of other treatments which consumed by respiratory muscles and improve overall energy do not depress level of consciousness. Augmentation of cardiac levels. Erythrocyte transfusion (taking caution to avoid voloutput with arterial vasodilators (hydralazine, nitroprusside) ume overload) or erythropoietin analog administration can be or positive inotropic agents (dobutamine, milrinone) and comconsidered when anemia is severe and contributing to fatigue. bined vasodilators (ACEi, ARB) may also improve dyspnea whether due to venous congestion or inadequate cardiac output. Systemic Edema Renal replacement therapy (RRT), specifically ultrafiltration, Right heart failure is often profound in end-stage pacan be considered for patients with refractory volume overload tients. The resulting systemic venous hypertension results in despite less invasive treatments. Though mechanical circulaboth dependent hydrostatic edema (legs, abdominal organs) tory support devices are very effective at improving forward and hypo-oncotic edema (from hepatic congestion/reduced output and reducing venous pressure, these are used only in protein synthesis, gut edema with protein malabsorption, and highly selected patients and not considered palliative options serum protein dilution secondary to salt and water overload). due to their invasive nature, cost, and potential myriad of side Pleural effusions and ascites are also consequences in many effects including thromboembolism. patients. Manifestations of intestinal edema include abdomiSupplemental oxygen should always be considered as a nal pain, nausea, poor appetite, compromised gastrointestipalliative option. Positive airway pressure therapy (continunal absorption of nutrients and subsequent lean muscle loss. ous positive airway pressure [CPAP]), bi-level positive airway Although venodilating agents may limit further hydrostatpressure [BiPAP]), and noninvasive ventilation can be considic edema development, most carry the side effect of primarily ered when other options fail. In patients with pleural effusions causing edema independent of venous pressure. Two approaches or ascites, the symptomatic benefits of therapeutic thoracentesis can be tried here, with volume removal being the focus of both. or paracentesis are usually transient unless other factors (sysDiuretics and RRT are obvious modalities and are typically intemic venous hypertension, hypoalbuminemia) can be correctstituted first. However, promotion of improved cardiac output ed. Nesiritide has not been shown to affect mortality or reduce 31 through inotropic support will, via improved renal perfusion, dyspnea significantly. secondarily lower total body salt and water and has the benefit of Fatigue resulting in fewer electrolyte abnormalities than does high-dose The mechanism of fatigue in heart failure is often multidiuretic therapy. Leg elevation, compressive stockings, and refactorial; contributors include reduced oxygen transport to stricted intake of salt and fluids may also help, but late-stage pamuscles and peripheral organs; reduced arterial oxygen content tients are usually already employing these strategies maximally. Table 2. Non-Pharmacologic Therapy for Heart Failure Table 2. Non-Pharmacologic Therapy For Heart Failure Symptom Reduction Symptom Reduction

January 2014 JOURNAL MSMA 7

Pain

Alleviating pain is unarguably one of the most important aspects to palliative care, and pain is a common complaint in advanced heart failure.28 Identifying specific pain-inducing processes will allow for effective palliation for many, but not all, patients suffering pain. Anginal pain is common in heart failure (as coronary artery disease is common among heart failure patients). Anti-anginal agents including nitrates, BB, calcium channel blockers, and ranolazine can all be effective, alone or in combination, though symptomatic hypotension may limit options. Whenever possible, anti-anginal drugs that also are used to treat heart failure (e.g., carvedilol, metoprolol) or are believed not to exacerbate heart failure (amlodipine) are preferred. At times, patients with debilitating class IIIB or IV symptoms (angina with minimal activity or at rest) can and should be considered for catheter-based therapy (percutaneous intervention) limited to culprit lesions and guided by imaging when necessary. A second source of pain is systemic venous hypertension, producing splanchnic organ congestion; approaches which reduce systemic edema (see above) are best in this setting, though hypotension or other symptomatic side effects again may be limiting. Whether from angina, systemic congestion, or other sources, pain can be treated in heart failure patients as in patients with other terminal diseases. Opioid agonists and non-narcotic analgesics (excluding non-steroidal anti-inflammatory drugs which can hasten decompensation) can be used with common oral and, if needed, topical or injectable formulations, titrated to individual needs. Pretreatment prior to activities known to initiate/worsen pain in a given patient reduces total amount of drug needed and therefore side effects. Maintenance analgesic administration (long-acting or continuous infusion) supplemented with short-acting agents is a typical effective approach. Patients should be warned of the expected side effects, including respiratory and cognitive depression; laxatives should be prescribed to patients receiving daily opioid therapy.32 Depression magnifies the intensity of most symptoms (particularly pain), and should be screened for and treated when present (see below). Cognitive Impairment The ability to meaningfully interact with family and friends, health care providers, and others is an initial goal of most palliative regimens. In advanced heart failure, cognitive dysfunction can arise from several mechanisms, with inadequate oxygen delivery to the brain (reduced cerebral perfusion flow, pressure, or arterial oxygen content) most commonly seen. Efforts to increase cardiac output via afterload reduction (arterial vasodilators) or improved myocardial contractility (intravenous inotropic therapy) may be the most effective initial strategy, though both can critically reduce perfusion pressure, limiting net benefit. Correction of anemia and hypoxemia (see above) can also improve cognitive function when these are contributory. As with other symptoms, depression must be considered in any patient experiencing unpleasant/inappropriate mental function.

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Nausea Nausea may originate from ileus, bowel edema or ischemia, or drug side effects. In addition to addressing these cause-specific mechanisms (including reducing or eliminating non-essential medications), anti-emetics believed comparatively safe in heart failure patients include metoclopramide, antihistamines (e.g., meclizine, diphenhydramine) and selective 5HT3 antagonists (e.g., ondansetron, granisetron). In general, phenothiazines are avoided due to risk of symptomatic hypotension and anticholinergic side effects.33 Depression Individuals with heart failure are more likely to develop depression compared to the general population. Non-pharmacologic therapy (including psychotherapy and cognitive behavioral therapy)34 can be tried, but antidepressant drugs are often required. Disease-drug and drug-drug interactions resulting in prolonged half-lives and higher average serum concentrations in these patients often require dose reductions. In general, serotonin reuptake inhibitors such as citalopram or duloxetine are often tried first, but newer serotonin norepinephrine reuptake inhibitors may also be considered. Drugs with higher risk of interactions (e.g., fluoxetine) or anticholinergic side effects (tricyclic antidepressants) are less commonly employed. Principles of Treatment Selections Some principles are obvious in creating a palliative strategy, but no “usual” or “standard” approach can exist for these complex patients or the complicated decisions being made for their care. Treatment selection should be aimed at limiting patient stress and cost where possible. Oral and topical medications are preferable to parenteral drugs for patients who can swallow and have reliable gastrointestinal function, eliminating the need to maintain intravenous access. Oxygen at rates deliverable with a concentrator (rather than requiring tank use) reduces patient/family inconvenience and cost. Continuous infusion medications and patient-controlled analgesics will allow more autonomy than intermittent dosing delivered by a health care professional. Drugs which more specifically address a particular symptom with fewer potential adverse symptoms are preferred over others (for example, diuretics and oxygen rather than morphine for dyspnea), provided they deliver the desired benefits. Issues for further consideration With the focus in the terminal palliation patient being solely on alleviatiing symptoms, the list of goal-related side effects requiring treatment adjustment is far smaller than for patients for whom prolonged survival is paramount. Most agree that in this population, diagnostic testing (e.g., for electrolytes) should be excluded, and discussions with patients and families should assure their understanding of potential sequelae of this strategy. When a given palliative intervention produces additional or worsened symptoms, regimen adjustments are warranted. Many treatments for dyspnea, edema, and reduced cardiac

output may lower systemic blood pressure, particularly when used in combination; marginal blood pressure is very common among terminal heart failure patients independent of medication effects. Narcotic analgesics also carry this risk, as do anti-anginal drugs, vasodilating positive inotropic agents, and sedatives/ hypnotics. Progressive symptomatic azotemia can be tolerable for many patients, while requiring medication adjustment in others. Invasive interventions (such as refractory class IV angina requiring percutaneous coronary intervention, or extreme volume overload requiring hemofiltration) may be justified in some settings but necessitate some discomfort, risk of debilitating complications, consumption of precious time and energy, and potential financial costs to the patient. A team approach with regular communication and personalization/modification of regimens is the best available strategy in these complex situations.

References

Conclusion The epidemic of heart failure is a product of both failures and successes of modern medicine. Overall, a growing number of patients will die from heart failure despite best medical efforts. A thoughtful, principle-based approach to provide heart failure patients with the best possible quality of life during their final days is as important as evidence-based care earlier in the disease course. Those providing such care should be supported with the best information available to achieve this worthwhile end.

5. Nohria A, Tsang SW, Fang JC, et al. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. J Am Coll Cardiol. 2003 41(10):1797-1804.

1. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics-2012 update: A report from the American Heart Association. Circulation. 2012;125:e2-e220. 2. Heidenriech PA, Trogdon JG, Khavjou OA, Butler J, Dracup K, Ezekowitz MD, et al. Forecasting the future of cardiovascular disease in the United States: A policy statement from the American Heart Association. Circulation. 2011;123(8):933-44. 3. Fonarow GC, Abraham WT, Albert NM, Stough WG, Gheorghiade M, Greenberg BH, O’Connor CM, Nunez E, Yancy CW, Young JB. Day of admission and clinical outcomes for patients hospitalized for heart failure: Findings from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF). Circulation Heart Fail. 2008;1(1):50-57. 4. Chaudhry SI, McAvay G, Chen S, Whitson H, Newman AB, Krumholz HM, Gill TM. Risk factors for hospital admission among older persons with newly diagnosed heart hailure. J Am Coll Cardiol. 2013;61(6):635-642.

6. Stewart S, MacIntyre K, Hole DJ, Capewell S, McMurray J. More ‘malignant’ than cancer? Five year survival following a first admission for heart failure. Eur J Heart Fail. 2001;3:315-322. 7. Askoxylakis V, Thieke C, Pleger ST, et al. Long-term survival of cancer patients compared to heart failure and stroke: A systematic review. BMC Cancer. 2010;10:105.

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January 2014 JOURNAL MSMA 9

Jessup MJ, Abraham WT, Casey DE, et al. 2009 Focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 119(14):1977–2016. Bakitas M, Macmartin M, Trzepkowski K, et al. Palliative care consultations for heart failure patients: How many, when and why? J Cardiac Fail. 2013;19(3):193-201.

10. Adler ED, Goldfinger JZ, Kalman J, et al. Palliative care in the treatment of advance heart failure. Circulation. 2009;120:2597-2606. 11. Goodlin SJ. Palliative care in congestive heart failure. J Am Coll Cardiol. 2009;54(5):386-396. 12. Goodlin S.J., Hauptman PJ, Arnold R, et al. Consensus statement: palliative and supportive care in advanced heart failure. J Cardiac Failure. 2004;10:200-209. 13. Beauchamp TL, Childress JF. Principles of Biomedical Ethics. 2009. New York: Oxford University Press. 99-280. 14. Lampart R, Hayes DL, Annas GJ, et al: HRS expert consensus statement on the management of cardiovascular implantable electronic devices in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm. 2010;7:1008-26. 15. Garg R, Yusuf S. Overview of randomized trials of angiotensinconverting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials. JAMA. 1995;273:1450-1456.

Med. 2001;345(20):1435-43. 27. Wilson J, McMillan S. Symptoms experienced by heart failure patients in hospice care. J Hospice and Palliative Nursing. 2013;15(1):13-21. 28. Goodlin SJ, Wingate S, Albert NM, et al. Investigating pain in heart failure patients: the pain assessment, incidence, and nature in heart failure (pain-hf) study. J Card Fail. 2012;18:776-783. 29. Bekelman DB, Havranek EP, Bekcer DM, et al. Symptoms, depression, and quality of life in patients with heart failure. J Card Fail. 2007;13(8):643-648. 30. Parshall MB, Schwartzstein RM, Adams L, et al. Update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;185(4):435-452. 31. O’Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. New Engl J Med. 2011;365:32-43. 32. Bruera E, Kim HN. Cancer pain. JAMA. 2003;290(18):2476-2479. 33. Glare P, Miller J, Nikolova T, Tickoo R. Treating nausea and vomiting in palliative care: A review. Clin Intervent Aging. 2011;6:243-59. 34. Lane DA, Chong AY, Lip GY. Psychological interventions for depression in heart failure. Cochrane Database Systematic Review. 2005;(1): CD003329.

16. Captopril Multicenter Research Group. A placebo-controlled trial of captopril in refractory chronic congestive heart failure. J Am Coll Cardiol. 1983;2:755-763. 17. Wong M, Staszewsky L, Carretta E, et al. Signs and symptoms in chronic heart failure: Relevance of clinical trial results to point of care-data from Val-HeFT. Eur J Heart Fail. 2006;8:502-508. 18. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomised intervention trial in congestive heart failure (MERIT-HF). Lancet. 1999;353:2001-7. 19. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. N Engl J Med. 1996;334:1349–55. 20. Effectiveness of spironolactone added to an angiotensinconverting enzyme inhibitor and a loop diuretic for severe chronic congestive heart failure (the Randomized Aldactone Evaluation Study [RALES]). Am J Cardiol. 1996;78:902-7. 21. Pitt B, Zannad F, Remme WJ, Cody R, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999;341:709-17.

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22. Taylor AL, Ziesche S, Yancy C, et al. Combination of isosorbide dinitrate and hydralazine in blacks with heart failure. N Engl J Med. 2004;351:2049-2057.

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23. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study. N Engl J Med. 1986;314:1547–52.

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24. Sindone AP, Keogh AM, Macdonald PS, et al. Continuous home ambulatory intravenous inotropic drug therapy in severe heart failure: safety and cost efficacy. Am Heart J. 1997;134 889–900.

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25. Hauptman PJ, Mikolajczak P, George A, et al. Chronic inotropic therapy in end-stage heart failure. Am Heart J. 2006;152:1096. e1-1096.e8.

26. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term mechanical left ventricular assistance for end-stage heart failure. N Eng J

10 JOURNAL MSMA January 2014

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• Top Ten Facts You Need to Know • About Obese Adults Admitted to Hospital

Dominique J. Pepper, MD; Michael Brewer, DO; Christian A. Koch, MD ntroduction

The CDC defines obesity as a BMI ≥ 30 kg/m2 (body mass index [weight in kilograms divided by height in meters squared]).1 This definition is useful for obesity screening but does not necessarily separate ‘metabolically healthy’ obese individuals from those with high cardiovascular risk.2,3 In 2008, the cost of health care due to obesity in the United States of America (USA) exceeded $147bn.1 In 2011 Mississippi had the highest prevalence of self-reported obesity among adults (34.9%) in the USA.1 Obese adults admitted to the hospital pose several unique diagnostic and therapeutic challenges. The purpose of this article is to alert clinicians to these challenges. 1. Cardiac: Obesity increases the risk of systemic hypertension, pulmonary hypertension, autonomic dysfunction, and a prolonged QTc interval,4-7 all of which may complicate hospitalization and outcomes following surgery. A longer duration of abdominal obesity increases subclinical coronary heart disease and its progression through midlife.8 Paradoxically, mortality following acute myocardial infarction decreases with increasing BMI. The increased age of those with a normal BMI drives this paradox.9,10 Obese adults in acute heart failure often have normal BNP levels.11 2. Respiratory: Oxygen and non-invasive ventilation (continuous positive airway pressure [CPAP] or bilevel PAP) improve chronic daytime hypercapnia and hypoxia in adults with obesity hypoventilation syndrome.12-14 In obese adults with postoperative atelectasis due to lung or abdominal surgery, CPAP reduces the risk of pneumonia and intubation.15 In intubated adults, obesity does not increase mortality but does prolong time on mechanical ventilation and duration in the ICU.16 Author Information: Chief Resident, Department of Medicine, University of Mississippi School of Medicine, Jackson (Dr. Pepper); PGY-2 Resident, Department of Medicine, University of Mississippi Medical Center, Jackson (Dr. Brewer); Professor, Division of Endocrinology, Director, Endocrine Tumor Program, Cancer Institute, University of Mississippi Medical Center, Jackson (Dr. Koch). Corresponding Author: Dominique J Pepper, MD, Chief Resident, Department of Medicine, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216 Telephone: (601)9845601, (dpepper@umc.edu).

3. Gastrointestinal: Central adiposity correlates with an increased risk of gastroesophageal reflux disease, cholecystitis, and non-alcoholic fatty liver disease (NAFLD).17,18 NAFLD affects nearly one-third of Americans,19 and increases the risk of cirrhosis, liver-related death, and drug toxicity. Cytochrome p450 enzymes, located primarily in the liver, metabolize almost two thirds of the 200 most commonly prescribed drugs. 20 4. Endocrine: Appropriate endocrine screening and early recognition of endocrine emergencies in obese adults is lifesaving.21 Hyperosmolar hyperglycemic state (HHS), myxedema coma and acute adrenal insufficiency should be suspected in the appropriate clinical setting. The American Diabetes Association defines HHS as blood glucose >600 mg/ dl, pH >7.30, bicarbonate >15 mmol/l, and serum osmolality >320.21 Clinicians should suspect HHS in middle-aged, obese patients with type 2 diabetes presenting with polyuria, polydipsia and weight loss. Myxedema coma should be considered in unresponsive obese adults with a history of hypothyroidism, previous thyroidectomy or previous radioactive iodine treatment.22 Acute adrenal insufficiency should be suspected in obese adults on steroid replacement with failure to increase the steroid dose after experiencing an acute stress episode.23 Overt signs and symptoms of Cushing syndrome (central obesity, hypertension and hypokalemia) and polycystic ovarian syndrome (central obesity, acne and hirsutism) should prompt appropriate testing.24,25 5. Rheumatologic: Obesity increases the mechanical load on weight-bearing joints, predisposing to osteoarthritis.26 Critically ill obese adults have impaired mobilityduring inpatient admission, which may lead to muscle de-conditioning. Timely initiation of physical therapy during recovery may prevent unnecessary falls and their complications. Pressure care with the aid of bariatric beds may reduce skin breakdown. 6. Oncology: Obese adults have increased rates and later stages of cancer, particularly colon cancer and estrogen sensitive cancers (endometrial and breast).27,28 Clinicians need to perform age-appropriate cancer screening in a timely manner among obese adults. 7. Radiology: There is often a lack of suitably sized stretchers and wheelchairs to transport obese patients to radiology departments. Lipomatosis, which involves the gut and the mediastinum in obese adults, poses several challenges in diagnostic imaging quality, including image acquisition,

January 2014 JOURNAL MSMA 11

and image interpretation.29,30 The weight limit of the imaging table or the aperture diameter of the MRI scanner may preclude diagnostic imaging causing diagnostic delays in life-threatening illnesses. Acquired images may be suboptimal because of soft-tissue artifact, or the need to alter the timing, duration, or protocol of contrast administration.29,30

8. Pregnancy: Extremely obese adult women are more likely to have gestational hypertension, gestational diabetes, shoulder dystocia, cesarean section, birth weight ≥ 4000 gm, neonatal metabolic abnormality, neonatal ICU admission and still-birth.31

12. Mokhlesi B, Tulaimat A. Recent advances in obesity hypoventilation syndrome. Chest. 2007;132(4): 1322-1336.

9. DVT prophylaxis: The risk of deep vein thrombosis increases in immobile obese adults admitted to the hospital, and appropriate prophylaxis is necessary. In patients with hypercortisolemia, the risk of DVT increases further.32 The optimal prophylactic dose for deep venous thrombosis in obese adults is not known.

Sarno G, Räber L, Onuma Y et al. Impact of body mass index on the five-year outcome of patients having percutaneous coronary interventions with drug-eluting stents. Am J Cardiol. 2011;108(2):195-201.

10. Uretsky S, Messerli FH, Bangalore S et al. Obesity paradox in patients with hypertension and coronary artery disease. Am J Med. 2007;120(10):86370. 11. Noveanu M, Breidthardt T, Cayir S et al. B-type natriuretic peptideguided management and outcome in patients with obesity and dyspnea-results from the BASEL study. Am Heart J. 2009;158(3): 488-95.

13. Tamanna S, Ullah MI. Top 10 facts you should know: About how to improve CPAP compliance for the treatment of obstructive sleep apnea. J Miss State Med Assoc. 2012;53(7):220-1. 14. Tamanna S, Ullah MI. About obstructive sleep apnea. J Miss State Med Assoc. 2011;52(1):12-3. 15. Pessoa KC, Araújo GF, Pinheiro AN et al. Noninvasive ventilation in the immediate postoperative of gastrojejunal derivation with Roux-en-Y gastric bypass. Rev Bras Fisioter. 2010;14(4):290-5. 16. Martino JL, Stapleton RD, Wang M et al. Extreme obesity and outcomes in critically ill patients. Chest. 2011;140(5):1198-206. 17. Beddy P, Howard J, McMahon C et al. Association of visceral adiposity with oesophageal and junctional adenocarcinomas. Br J Surg. 2010;97(7):1028-34.

10. Pharmacology: Pharmacokinetic data in obese patients do not exist for most drugs. In situations where such information is available, clinicians should design treatment regimens that account for any significant differences in the drug clearance and the volume of distribution in the obese (based on the lipophilic and hydrophilic tendencies of the drug).33 Careful discussions with the hospital pharmacist to decide whether to dose obese adults on ideal, actual or adjusted body weights are necessary.

18. Ahrens W, Timmer A, Vyberg M et al. Risk factors for extrahepatic biliary tract carcinoma in men: medical conditions and lifestyle: results from a European multicentre case-control study. Eur J Gastroenterol Hepatol. 2007;19(8):623-30.

Conclusion

22. Garber JR, Cobin RH, Gharib H et al. Clinical practice guidelines for hypothyroidism in adults. Endocr Pract. 2012;18(6):988-1028.

All adults admitted to the hospital should be screened for obesity, which poses significant inpatient challenges.34 Early identification and timely treatment of obesity-related illnesses may prevent complications and reduce the high cost of health care.

References 1.

CDC 2013 Adult Obesity Facts http://www.cdc.gov/obesity/data/adult. html [Accessed November 27, 2013].

Ahima RS, Lazar MA. Physiology. The health risk of obesity--better metrics imperative. Science. 2013 Aug 23;341(6148):856-8.

3. Melcescu E, Griswold M, Xiang L, Belk S, Montgomery D, Bray M, Del Ben KS, Uwaifo GI, Marshall GD, Koch CA. Prevalence and cardiometabolic associations of the glucocorticoid receptor gene polymorphisms N363S and BclI in obese and non-obese black and white Mississippians. Hormones (Athens). 2012 Apr-Jun;11(2):166-77. 4.

Seip RL, Mair K, Cole TG et al. Induction of human skeletal muscle lipoprotein lipase gene expression by short-term exercise is transient. Am J Physiol. 1997;272:E255-61.

Vinik AI, Maser RE, Ziegler D. Autonomic imbalance: prophet of doom or scope for hope? Diabet Med. 2011;28(6):643-51.

Dimkpa U, Oji JO. Relationship of body mass index with haemodynamic variables and abnormalities in young adults. J Hum Hypertens. 2010;24(4):230-6.

Baba R, Koketsu M, Nagashima M et al. Adolescent obesity adversely affects blood pressure and resting heart rate. Circ J. 2007;71(5):722-6.

Reis JP, Loria CM, Lewis CE et al. Association between duration of overall and abdominal obesity beginning in young adulthood and coronary artery calcification in middle age. JAMA. 2013;310(3):280-8.

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19. Wieckowska A, Feldstein AE. Diagnosis of nonalcoholic fatty liver disease: invasive versus noninvasive. Semin Liver Dis. 2008;28(4):38695. 20. Williams JA, Hyland R, Jones BC, Smith DA, Hurst S, Goosen TC, Peterkin V, Koup JR, Ball SE. Drug-drug interactions for UDPglucuronosyltransferase substrates: a pharmacokinetic explanation for typically observed low exposure (AUCi/AUC) ratios. Drug Metab Dispos. 2004;32(11):1201-8. 21. Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(12):2739-48.

23. Seetho IW, Wilding JP. How to approach endocrine assessment in severe obesity? Clin Endocrinol 2013;79(2):163-7. 24. Koch CA. Endocrine hypertension: what is new? Rev Port Endocrinol Diabetes Metab. 2012;7(2):52-61. 25. Nieman LK, Biller BM, Findling JW. The diagnosis of Cushing’s syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008;93(5):1526-1540. 26. Conde J, Scotece M, López V, Gómez R, Lago F, et al. Adipokines: novel players in rheumatic diseases. Discov Med. 2013;15(81):73-83. 27. Reeves GK, Pirie K, Beral V et al. Cancer incidence and mortality in relation to body mass index in the Million Women Study: cohort study. BMJ. 2007;335(7630):1134. 28. Tao W, Lagergren J. Clinical management of obese patients with cancer. Nat Rev Clin Oncol. 2013 Jul 16. doi: 10.1038/nrclinonc.2013.120. [Epub ahead of print]. 29. Ghanem MA, Kazim NA, Elgazzar AH. Impact of obesity on nuclear medicine imaging. J Nucl Med Technol. 2011;39(1):40-50. 30. Vannier MW. CT clinical perspective: challenges and the impact of future technology developments. Conf Proc IEEE Eng Med Biol Soc. 2009;1909-12 31. Crane JM, Murphy P, Burrage L et al. Maternal and perinatal outcomes of extreme obesity in pregnancy. J Obstet Gynaecol Can. 2013;35(7):60611. 32. Stuijver DJ, van Zaane B, Feelders RA et al. Incidence of venous thromboembolism in patients with Cushing’s syndrome: a multicenter cohort study. J Clin Endocrinol Metab. 2011;96(11):3525-32. 33. Hanley MJ, Abernethy DR, Greenblatt DJ. Effect of obesity on the pharmacokinetics of drugs in humans. Clin Pharmacokinet. 2010;49(2):71-87. 34. Pickkers P, de Keizer N, Dusseljee J et al. Body mass index is associated with hospital mortality in critically ill patients: an observational cohort study. Crit Care Med. 2013;41(8):1878-83.

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January 2014 JOURNAL MSMA 13

• Special Article • King David, Son of Jesse: The World’s First Parkinson’s Patient …Observations from November 2013

avid, the shepherd boy who slew Goliath, was first described in Jewish Scripture from 1000 BC. Later in life, he composed many songs, prayers, and praises that make up a large part of the Book of Psalms in current Jewish and Christian Holy Bible(s). The Muslim world recognizes him as a prophet, and the Qur’an has a named chapter attributed to David (“Zabur”). The story of David and Goliath is well known in the secular world and, indeed, is the title of a current best seller.1 Thus, for the devout as C. Randle Voyles, MD well as for the secular irreligious, King David, son of Jesse, has become a major reference point as part of the world’s culture. Now, 3000 years later, it appears that he also may have been the world’s first described person with Parkinson’s disease. Furthermore, his most important battle for world history is little known. Parkinson’s disease is a common degenerative process related to a decrease of available dopamine (a neurotransmitter that “fires” nerve endings) in an area in the base of the brain called the substantia nigra. The onset of symptoms is slow and gradual, and the diagnosis is made most frequently at age 61-62. “Early onset” Parkinson’s does occur as highlighted by the American movie star Michael J. Fox. The most clearly recognized presenting complaint is a unilateral tremor in a finger or hand. However, there are many other subtle non-specific symptoms - often recognized in retrospect – such as loss of smell (anosmia), slowness of movement (bradykinesia), and deterioration in hand-writing (micrographia). Later symptoms include the characteristic change of gait (shortened steps with shuffling and loss of free arm swing, usually unilaterally initially). While Parkinson’s occurs in both sexes and all occupations, there is a preponderance in males (notably in type A personalities), and the neurodegenerative effects may be more readily recognized in individuals with occupations which require physical dexterity and stamina. Early on, the combination of symptoms can lead to weakness and exhaustion with moderately difficult tasks; later, there are major impediments with ordinary motor activities. When the effects of progressive motor disorder lead to a named diagnosis, the newly diagnosed member of Club Parkee (Parkinson’s diagnosis) faces dilemmas: Do I tell? Do I keep on, not tell and hope no one notices? Should I take early retirement? Will retirement be forced on me? Very few have asked how this relates to King David….

Unique aspects of the history of David…. The Scriptures of The Holy Bible record more about the ages of events in the life of David than perhaps any other Biblical character…… We know that he encountered Goliath as a “shepherd boy” in his late teenage years…… He became King of Judah at about age 30 and led his troops into many battles as the kingdom of Israel expanded. He reigned as King David for 40 years, seven years in Hebron and 33 years in Jerusalem. He ceased leading his troops into battle after a little known life-threatening event at about age 61….. David suffered from an unnamed progressively deteriorating condition prior to his death at age 70……. The throne was then passed to his son Solomon, who also served as king for the next 40 years. When David used a slingshot to kill the Philistine giant Goliath, he made a place in history that persists to this day. What is less well-known but more important for the history of the world is his later encounter with another Philistine giant from the family of Goliath….. and his name was Ishbi-Benob. At that encounter on the battlefield, King David (now 61 years old) was specifically reported in the literature as having become “weak and exhausted” in battle; he was about to be slain by the sword of Ishbi-Benob but was dutifully rescued by his trusted warrior named Abishai who killed Ishbi-Benob. At that juncture, David’s men rendered a directive that was specifically recorded: “You are not going out to battle with us again! Why risk snuffing out the light of Israel.”(NLT).2 Methods: A forensic investigative literary review mandates a careful analysis of the recorded facts interspersed with some degree of creative thinking and extrapolation. To assign a modern day diagnosis to an individual almost 3000 years earlier

14 JOURNAL MSMA January 2014

might be called weird, nutty or whimsical ideation. After all, James Parkinson did not describe the “shaking palsy” until 1817. Thus, I plead not just for the reader’s forbearance as I take a bit of liberty and editorial privilege but would ask that you read the following with the “trusting” assumption that the retro-active diagnosis of Parkinson’s disease is correct. What are the clues from old literature that support a current diagnosis? More importantly, what difference does it make? Are there potential benefits for individuals with Parkinson’s or with any unfavorable diagnosis? How good is your imagination? Just suppose for the sake of argument that you are both a seer and sage in King David’s entourage on a spring day in 940 BC. As long term counsel, you have a unique insight into the mindset of the aging Parkinsonian King David as he prepares for battle as the Alpha Male, Type A CEO of the Israeli forces. You had tried to provide wise counsel in personal matters earlier which he dismissed and suffered severe personal consequences. You recognize that his sense of self-worth makes it obligatory that he maintain his role as leader in the battlefield as he proclaims, “Am I not the one God designated to slay the Goliath? Surely, He wishes for me to slay Ishbi-Benob.” However, the combination of bradykinesia, muscle stiffness and loss of agility – even in the face of dogged determination – sets the stage for the Biblically-described “weakness and exhaustion” and failure in the battle field. King David has passed his prime! He may even be a liability. You try to console David as his supporting officers have the uncomfortable task of relieving the highly respected king of his responsibilities on the battlefield – the very role that had made him unique in the history of the world. (Club Parkee, what was the name of your Ishbi-Benob???) More important for world history is what happened after the forced retirement for David. When he relinquished his role as leader of the forces, he likely felt an initial emptiness with severe despair and some depression; paradoxically, he may have also been relieved. History records that he left his warrior role to lead his people and write much of what we know as the book of Psalms. He provided the father-mentor role for his son Solomon who built the Temple at Jerusalem and wrote the books of Proverbs, Ecclesiastes, and Songs of Solomon. For the Christian world, he set the stage for and offered prophecy for the coming of the Christ child. Thus, on review, David’s early “retirement” from physical warfare was followed by literary contributions that helped shape the culture of most of the world. In spite of the neurodegenerative process that we now suspect to be Parkinson’s disease, his major contribution came after his initial mandatory retirement from what he considered his major role in life. Club Parkee, take notice!

Introspection from a member of Club Parkee

This Jackie Meena painting, a favorite of her husband Al’s, is a landscape acrylic composition which embodies a central crucifix. The multi-talented Jackie composed this work while teaching a class in North Carolina. A personal commentary from surgical mentor Albert L. Meena, MD is referenced 8 in this article. Dr. Meena’s obituary appears in this issue of the Journal. — Photo by Dr. Randy Voyles

There are not so subtle clues in David’s writings that offer a glimpse into the life of one plagued by Parkinson’s disease around 1000 B.C. These clues are more readily apparent to the attentive members of Club Parkee whose walk is both intensely introspective and, perhaps, a bit unstable. For example, one hindered by the gait disturbances of dopamine deficiency might anticipate that David would record: “He makes my feet like the feet of a deer and sets me securely on the heights; you widen a place beneath me for my steps and my ankles do not give way.”3 Furthermore, David would proclaim, “He will not allow your foot to slip; your Protector will not slumber.”4 The psychological changes associated with an early suspicion of Parkinson’s are often more difficult to face than any initial physical impairment, especially if one is dethroned as a mighty warrior. David’s initial effects of Parkinson’s were certainly non-specific and prompted questions like: “What is wrong with me? Am I just getting old too fast? Am I over-reading my symptoms? Am I becoming demented?” The psychological load must have been particularly troublesome as the onset is insidious… yet progressive. With current radiological imaging (DAT scans and enhanced PET scans), the diagnosis of Parkinson’s can be conclusive in many (but often it is not). A confirmed diagnosis is sometimes paradoxically a mixed relief (“My symptoms have a real explanation.”) However, any initial relief is fairly quickly offset by the implications of Parkinson’s: you have a progressive biochemical deterioration in the base of your brain (or worse); there is no cure; there are medicines that help with the symptoms but they have significant side effects; you will gradually lose physical control of mobility if you live long enough (but, so does everyone else!) ...continued on page 17

January 2014 JOURNAL MSMA 15

Save the Date! May 24-27, 2014 12th Annual CME in the Sand Sandestin Golf and Beach Resort Tentative Agenda Saturday, May 24 9:00 - 4:00 MSMA BOT Meeting 11:00 - 2:00 CME Sessions

Sunday, May 25 9:00 - 1:00 6:30 PM

CME Sessions Welcome Reception with Children’s Activities

Monday, May 26 7:15 8:00 9:00 6:30

- 8:00 -12:30 AM PM

Breakfast with Exhibitors CME Sessions Spouse/Children’s BINGO Family Dinner with Children’s Activities

Tuesday, May 27 7:15 - 8:00 Breakfast with Exhibitors 8:00 -12:30 CME Sessions

For more information visit www.MSMAonline.com 16 JOURNAL MSMA January 2014

...continued from page 15

From despair and despondency to help and hope New members of Club Parkee understand Denial, Despair, Despondency, and Depression! Even King David might find very little solace from his would-be comforters; “Yes, I know it is not cancer! You don’t have to tell me that it could be worse! Yes, I know that there is meaningful Life beyond a diagnosis! Yes, I am blessed with Loving support! Yes, I know that God’s Love will prevail! But my days on the battlefield are over! Don’t you know that self-pity is a rational choice???” David recorded heartwrenching despair in several pleas to God: 1) “My God, My God, why have you forsaken me?”5 2) “How long will you forget me? Forever?... How long will I store up anxious concerns within me, agony in my mind every day?”6 3) “My days are like a lengthening shadow, and I wither away like grass.”7 While self-pity and depression may have been rational responses for David, they were/are also counter-productive responses because a depressive outlook hides help and steals hope! (“I tried it once; it did not help!”8) Son Solomon recorded father David’s admonition in the 12th chapter of Proverbs: “Delayed hope makes the heart sick!” David knew the enemies of Despair and Depression but they ultimately were overcome by Help and Hope. The great warrior realized that he was not the potter but merely the clay. Interestingly, the historical scripture records David’s appeal for Help from the Higher Being and his subsequent prerequisite transition to peace and solace before assuming the most important responsibilities of his life. (Attentive reader, anticipate David’s references to motor disorder in subsequent verses.) 1) “But in my distress I cried out to the Lord… He heard me from His sanctuary.”9 2) “Keep me safe, O God, for I have come to you for refuge…Every good thing I have comes from You.”10 3) “God, renew a steadfast spirit within me..”11 4) A recorded response from God: “Call on Me in a day of trouble; I will rescue you.”12 5) David is consoled and records… “Your word is a lamp for my feet and a light on my path.”13 6) “I will bless the Lord who guides me; I know the Lord is with me… I will not be shaken.”14 7) “You delivered me from death, even my feet from stumbling to walk before God in the light of life.”15 8) “I love the Lord because He heard my appeal… and rescued my feet from stumbling and my eyes from tears.”16 9) “You have given me hope through Your Word… This is my comfort in my affliction!”17 10) With rejuvenated spirit, David asks “May I be like the rain that falls on fresh cut grass, like spring showers that water the earth.”18

11) “A man’s steps are established by the Lord, and He takes pleasure in his way. Though he falls, he will not be overwhelmed, because the Lord holds his hand.”19

Concluding remarks…. Based on age, our best clinical history, and repeated literary references, it is safe to say King David, son of Jesse, may have had Parkinson’s disease! But maybe… he did not. More importantly, his journey from Despair and Depression to Help and Hope offers utility for Club Parkee as we continue our walk (should I say shuffle?) through life. Members and guests, now enjoy the richly metaphorical message from King David with a bit more insight! The Lord is my shepherd, I shall not want. He maketh me to lie down in green pastures; he leadeth me beside the still waters. He restoreth my soul: He leadeth me in the paths of righteousness for his name’s sake. Yea, though I walk through the valley of the shadow of death, I will fear no evil: for thou art with me; thy rod and thy staff they comfort me. Thou preparest a table before me in the presence of mine enemies: thou anointest my head with oil; my cup runneth over. Surely goodness and mercy shall follow me all the days of my life; and I will dwell in the house of the Lord forever.20

January 2014 JOURNAL MSMA 17

About the author (more accurately labeled as scribe): Dr. C. Randle Voyles is an adjusting transitional surgeon who has early Parkinson’s disease. He readily admits overt plagiarism and duplication of emotional descriptions as outlined by King David, son of Jesse, in the Holy Bible. The parallel of career-altering degenerative changes will be common to many with Parkinson’s and other processes; King David’s recorded response has been helpful to the author-scribe and its reproduction hopefully will be helpful to others. Nothing herein is original except for the consideration of King David’s possible diagnosis. Any questions, critiques, or concerns are appreciated and may be directed to davidsstillwaters@gmail.com. References 1. David and Goliath by Malcolm Gladwell (2013)

11. Psalms 51:10

2. 2nd Samuel 21:15-22

12. Psalms 50:15

3. 2nd Samuel 22: 34-37

13. Psalms 119:105

4. Psalms 121:3-4

14. Psalms 16:8

5. Psalms 22:1

15. Psalms 56:13

6. Psalms 13:1-2

16. Psalms 116:1,8

7. Psalms 102:11

17. Psalms 119:49-50

8. Personal commentary from surgical mentor Albert L. Meena, MD

18. Psalms 72:6

9. Psalms 18:6

19. Psalms 37:23

10. Psalms 16:1-2

20. Psalms 23 (King James version chosen for rich language)

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• President’s Page • SGR – The Gift that Keeps on Giving

James A. Rish, MD 2013-14 MSMA President

ith the new year before us, I hope that everyone had a chance to enjoy the Thanksgiving, Hanukkah, and Christmas holidays. We truly have much for which we can be thankful. However, the flawed SGR formula is not one of them. The sustainable growth rate formula has been in existence since 1997. Its initial purpose was to contain growth in spending on physician services. SGR has been the mechanism that ties physician payment updates to the relationship between overall fee schedule spending and growth in gross domestic product.

Although this sounds good in principle, the fact of the matter is that it does not work. How many times have we had to go to the halls of Congress in order to avert significant cuts in Medicare reimbursement by virtue of the sustainable growth rate formula? The past decade and a half have brought about a multitude of short-term fixes which have served only to frustrate physicians, create barriers to access for our senior citizens and create budgetary dilemmas for our congress. In 2010 alone we had to go to Congress on four occasions to avoid such drastic cuts in reimbursement. By and large we have been thrown a bone in the form of a 0.5-1.0% update. No one would argue that this is hardly sufficient to cover inflationary forces and ever increasing overhead we have all had to bear in our practices due to perpetual government overregulation. Everyone including our congressional leaders has recognized the flawed nature of the SGR formula. Once again the time has come to lobby Congress in an effort to avoid a 24.4% reduction in Medicare reimbursement scheduled to take place January 1, 2014. However, the difference this time is that there is growing bipartisan and bicameral support for repeal and replacement of the SGR formula. On July 31, 2013, the House Committee on Energy and Commerce voted 51-0 on legislation to repeal the SGR formula. On October 30, 2013, the bipartisan leadership of the House Ways and Means Committee and Senate Finance Committee released a proposal of their joint framework for repealing the SGR formula and replacing it with a new payment formula. There is a keen awareness that the cumulative cost for the updates thus far over the past decade and a half has been approximately $146 billion. Currently a 1% positive update or patch will cost the taxpayers $18 billion which is added to the cumulative cost of replacement. Therefore, every time Congress kicks the can down the road the cost of repeal increases. By virtue of a mathematical error on the part of the Congressional Budget Office (CBO), the estimated cost of full repeal of the SGR formula has been reduced from $243.7 billion to $139.1 billion – a fire sale as it were. We are at a point in which we will have spent as much on patches as would be required to repeal and replace the SGR formula altogether. As with any type of sweeping reform, the devil is in the details. The repeal proposal would permanently repeal the SGR update mechanism, reform the fee-for-service payment system through greater focus on value over volume, and encourage participation in alternate payment models (APM) including a new “value-based performance payment” (VBP) program, bundled payments model, a patient-centered medical home model or accountable care organization. A new VBP program would be budget-neutral and used to adjust payments beginning in 2017. This VBP program essentially combines all the current incentive and penalty programs such as the value-based modifier, PQRS and meaningful use. In addition, the current draft proposal calls for a ten-year freeze on Medicare physician payment which is a tough pill to swallow.

January 2014 JOURNAL MSMA 19

One would rightfully ask why we should support such a deal that includes a ten-year freeze on payment updates. This is tantamount to a significant payment reduction, when one factors in an ongoing increase in overhead and further cumulative cuts in reimbursement which a large percentage of physicians will face compliments of continued/additional sequester cuts and the likes. I think the answer lies in the political process, which is a messy endeavor and accurately likened to making sausage. The fact of the matter is that there is much less of an appetite to avoid cuts in the environment of debt and deficit reduction. Many Capitol Hill experts feel the â&#x20AC;&#x153;status quoâ&#x20AC;? is not likely to be an effective approach going forward, and we will likely see a payment cut in the form of a 1-2% negative update. Keep in mind that what we are dealing with at the current time is a draft proposal, which is likely to undergo significant modification going forward. Your AMA delegation has just returned from the interim meeting in Maryland where we went to Capitol Hill to diligently advocate our concerns regarding the SGR repeal proposal. Your delegation was able to meet and voice our concerns with every Mississippi legislative member and/or his staff. The message to our congressional leaders is that a freeze on payment updates will make it very difficult for our physicians to continue seeing Medicare patients thus limiting access to care for our seniors. We must be able to maintain a certain level of reimbursement relative to our actual practice costs in order to simply pay our bills and sustain our practices. Your MSMA leadership will remain engaged in this discussion and debate as this situation rapidly unfolds. I urge all of you to familiarize yourself with this proposal and discuss your concerns with your legislators. Your comments and concerns are always welcomed and appreciated.

Susan and I would like to extend our wishes for a Happy New Year to you and your family.

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• Clinical Problem-Solving • Three Strikes and You’re Out

Cynthia Colson Garrett, MD

17-year-old African-American male presented to an emergency department with pain and swelling of his left arm. He was a left-handed pitcher for his high school baseball team and had pitched 111 pitches 2 nights ago. The next day he iced his left arm. However, the following day swelling started in his left forearm and hand, and pain radiated to the left humerus and shoulder. He denied joint pain and altered sensation in the hand. He was able to move his fingers but it was painful to do so. He had no significant past medical history and no history of surgeries. He had no history of bleeding disorders. A long differential diagnosis of shoulder pain is possible but a short list of possibilities includes rotator cuff injuries, dislocation of the shoulder, acromioclavicular separation, bursitis, thoracic outlet syndrome and deep vein thrombosis. A venous Doppler ultrasound indicated left axillary and subclavian deep vein thrombosis (DVT). He was transferred to the Family Medicine service of a nearby teaching hospital for further care. Repeat Doppler scan confirmed left axillary and subclavian DVT. The patient was given weight based enoxaparin (Lovenox) and warfarin (Coumadin) for anticoagulation. Color Doppler ultrasound is the screening tool of choice for evaluating for a DVT because of its ease of performance. It also has a sensitivity of 70 to 100 percent and specificity of 93 percent.1 However, it is very unusual to see a young person with a DVT. Therefore, I will obtain a hypercoagulable investigation in spite of the negative personal and family history of bleeding disorders. I will also consult a vascular surgeon for possible intervention. A hypercoagulability panel was unrevealing. However, the patient did have an elevated creatinine kinase concentration of 413 U/L (reference range 38-173 U/L). The elevated creatine kinase concentration is consistent with the diagnosis of axillosubclavian vein thrombosis (ASVT) and subsequent muscle damage. The overall presence of hypercoagulable states, including hyperhomocysteinemia, is a less likely contributor to the condition than anatomic abnormalities but an underlying prothrombotic state may have prognostic implications. Compressive injury appears to be the most critical factor.2 Author Information: Dr. Garrett was a resident in the Department of Family Medicine at the University of Mississippi School of Medicine. Corresponding Author: Cynthia Colson Garrett, MD; Baptist Medical Clinic, 401 Baptist Drive, Madison, MS 39110. (cgarrett11167@yahoo.com).

22 JOURNAL MSMA January 2014

ASVT is quite rare. The incidence is 2 per 100,000 patients per year.3 As a matter of comparison, ocular albinism has an incidence of 1 per 20,000 per year.4 The term effort thrombosis has also been used to describe Paget Schroetter syndrome as well as spontaneous ASVT. Effort thrombosis refers to the observation that a spontaneous ASVT was an often dramatic, unexpected presentation in an otherwise healthy young individual.3,5,6 It often occurs in a physically active person after unusually strenuous use of the arm and shoulder. This is consistent with the presentation of our otherwise healthy young athlete. On physical exam I did observe that the patient has muscular hypertrophy of the left arm and that it is much more developed than the right arm due to his use and exercise regimen. Chest radiograph showed no abnormalities, and Dopplers and venogram showed only the thrombosed veins. I therefore think that the thrombosis is due to compression of the vein against the hypertrophied muscles and will require vascular surgery intervention. A vascular surgeon confirmed the diagnosis of Paget Schroetter syndrome or effort thrombosis based on examination and the presence of a DVT. Venogram is the gold standard and most accurate test for diagnosis of ASVT.6 As there is no standard approach to treatment of ASVT, the family was informed of the risks and benefits of surgical intervention and informed that the decision must be individualized for the patient. After discussion, they were amenable to the idea of surgery as it was believed to be necessary due to the patient’s desire to pursue his sport past the high school level. A venogram was scheduled for the following day. Thrombolysis and mechanical thrombectomy were performed. After inflation of the axillary vein to a nominal pressure, which drastically improved the lumen, there was only minimal passage of contrast over the first rib and the vein was still obstructed. There was concern that further dilation might rupture the vein so the procedure was terminated. It was the consideration of the surgeon that the vein would probably re-thrombose. Therefore, the plan was amended by the surgery team to perform angioplasty and to keep the patient anticoagulated in order to perform an early first rib resection. The surgery team noted that repeat angioplasty or stenting of the left axillary subclavian vein may still be necessary. The patient’s symptoms improved after thrombectomy and angioplasty. He did complain of some numbness in his fingers and toes bilaterally while in the Post-Anesthesia Care Unit and had some elevated blood

pressure readings. These symptoms resolved spontaneously and did not return. Despite many years of cumulative experience and consensus regarding ASVT or Paget Schroetter syndrome, the treatment of this disorder is still debated.2,3,6 Therapeutic options include anticoagulant therapy, fibrinolytic therapy, surgical therapy and combinations of the above. While surgery is advocated, the timing is a matter of debate as well as duration of longterm anticoagulation and repeat endovascular interventions.2,3,7 Stenting is not thought suitable by many experts because of the elevated compressive forces they would need to withstand, and, therefore, the high risk of stent failure and fracture.3,7 Furthermore, it is noted that most obstructive lesions are external to the vein and not affected by balloon dilation. Stent placement has been found to be an independent risk factor for re-thrombosis.8 If a patient has residual stenosis after thrombolytic venography, they should be considered for surgical exploration and revision. This can usually be done in the next 24 to 48 hours, during which time anticoagulation should be maintained.8 The hospital course was complicated by acute renal failure due to the contrast dye from the venogram. However, after hydration with intravascular fluids the patient’s renal function returned to normal. The idea of stenting was abandoned. The patient was scheduled for a left transaxillary first rib resection on day 8. Anticoagulation was continued but held the day prior to surgery and restarted the day after surgery. Large venous collaterals were noted during the surgery. The patient tolerated the procedure well. His pain was controlled and the symptoms improved. In one study, recurrence of ASVT was especially high in young patients who did not have surgery (23%), while surgical treatment achieved a long-term success rate (93%).2 Another interesting point was that continued participation in athletic activity did not raise the risk for recurrence in a study where thrombolysis and expectant management were used for therapy.2 Our patient did not have the desired therapeutic result after thrombolysis and mechanical thrombectomy, so I think that the aggressive approach our patient chose gives him the maximal chance for unrestricted use of his arm and pursing his baseball career. The prognosis is excellent. The patient was discharged and prescribed weight based enoxaparin and warfarin based on the usual practice of 3 to 6 months of anticoagulation.2,3 He was doing well at his 2 week followup with very little swelling or pain. The patient may require repeat venogram in the future with further angioplasty. The patient returned to school after 2 weeks. At the 4 week followup he was noted to have a 3 centimeter seroma, which was aspirated. A duplex Doppler showed the axillary and subclavian veins to be patent. He was continued on his warfarin and scheduled for a return visit in 3 months. The patient is expected to be able to resume baseball at his prior level of activity. Key Words: Paget Schroetter Syndrome, effort

thrombosis, spontaneous upper extremity venous thrombosis

References 1. Mustafa B, Rathbun S, Whitsett T, Raskob G. Sensitivity and specificity of ultrasonography in the diagnosis of upper extremity deep vein thrombosis: a systematic review. Arch Intern Med 2002; 162:401-404. 2. Weinberg I. Paget Schroetter syndrome. Vascular Medicine: Evidence Based Vascular Medicine Reviews, January 25, 2011. Available at: www.angiologist.com/paget-schroetter-syndrome/3/. Accessed July 12, 2012. 3. Vijaysadan V, Zimmerman A, Pajaro R. Paget-Schroetter syndrome in the young and active. J Am Board Fam Med. 2005; 18(4):314-319. 4.

Wolff K, Johnson RA, Suurmond D, eds. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology 5th ed. New York, NY: McGraw-Hill; 2005

Flinterman LE, VanDer Meer FJ, Rosendaal FR, Doggen CJ. Current perspective of Venous Thrombosis in the Upper Extremity. J Thromb Haemost 2008; 6:1262-1266

Paget Schroetter syndrome, a subset of TOS, UCLA Surgery. Available at: http://www.surgery.ucla.edu/vascular/dx_paget_ schroetter.shtml. Accessed July 12, 2012.

7. Urschel HC, Patel AN. Surgery remains the most effective treatment for Paget-Schroetter syndrome: 50 years’ experience. Ann Thorac Surg. 2008;86(1):254-260. 8.

Lee JT, Karwowski JK, Harris EJ, et al. Long-term thrombotic recurrnce after nonoperative management of Paget-Schroetter syndrome. J Vasc Surg. 2006; 43:1236-1243.

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• In Memoriam • [The Journal of the Mississippi State Medical Association notes with sadness the passing of our MSMA members. If you’re aware of the death of an association member we’ll help you honor them in the pages of the Journal MSMA. We publish obituaries, periodically when we can obtain reliable information. We invite you to help us remember members in the pages of our JMSMA by emailing obituaries to KEvers@MSMAonline.com. High resolution photos (300dpi) are preferred. Note: Photos cannot be faxed.] —Ed.

James Earl McAfee, MD Columbus Dr. James Earl McAfee, 78, passed away October 2, 2013, at his residence. Visitation for Dr. McAfee was held at Lowndes Funeral Home, Columbus. Dr. McAfee was born July 7, 1935, to the late James A. and Willie Thompson McAfee in Dyersburg, TN. He received his doctorate degree from University of Tennessee - Memphis, College of Medicine in 1959. Dr. McAfee moved to Columbus in 1994 to open Baptist Occupational Health Clinic and later opened his own practice Columbus Occupational Medicine, in 2001. He retired in 2009 after practicing medicine for 50 years. He loved to travel out west, especially Estes Park, CO. He enjoyed hunting, reading, spending time with his dog Esko, and especially being a doctor practicing medicine. Dr. McAfee is survived by his sons: David McAfee Griffith, Cleveland, MS and James Kent McAfee, Fort Worth, TX; two grandchildren, close friends, Chris and Traci Wright, Vicky Jones, L.D. Hutt, Robert Tilley and his pet dog, Esko. Memorials may be made to Columbus Lowndes Humane Society, P.O. 85, Columbus, MS 39703.

Richard C. “Dick” Fleming, MD Meridian

Funeral services for Dr. Richard “Dick” Fleming were held November 18, 2013, at St. Patrick Catholic Church with Father Frank Cosgrove and Father Suresh Thirumalareddy officiating. Interment followed in Magnolia Cemetery. Dr. Fleming, retired doctor of internal medicine and cardiology,

24 JOURNAL MSMA January 2014

died peacefully at his home on Nov. 11, 2013. A lifelong resident of Meridian, he was born on Sept. 28, 1934, to Richard C. and Eloise Hoaf Fleming. Dick graduated from Millsaps College as a premed major minoring in English literature. He attained his medical degree from the University of Mississippi school of Medicine. Following induction into the U.S. Army Medical Corps he served his tour of duty in Vietnam and was discharged honorably having attained the rank of Captain. Returning to Meridian, he joined the medical practice of Dr. Med Scott Brown, one of his early mentors. Richard had many interests. He especially enjoyed traveling with Barbara, and Ireland was a perennial favorite. They enjoyed exploring the culture, food, and sights. He had a great interest in cooking and exploring his genealogy, both paternal and maternal sides. He had a large extended family, many aunts, uncles, and cousins who considered Dick the “go to person” for family history. After retirement, his focus became St. Patrick Catholic Church of which he and his family were lifelong members. His talents were given particularly to the Knights of Columbus in which he was a 4th degree Knight. He served them in many capacities and offices. He is survived by his cousins, Frank McGinn, Patricia McGinn McCauley, and Kathleen McGinn Sealeeky, all of Texas; cousins, Geraldine Fleming Heblon and Roberta, both of Meridian, MS; and all of their families. Preceded in death by parents, Richard Charles Fleming Sr. and Mary Eloise Hoaf Fleming; and a sister, Barbara Ann Fleming. Visitation was held Sunday, November 17th, 2013, at James F. Webb Funeral Home, followed by a prayer service led by Father Frank Cosgrove and Father Suresh Thirumalareddy. A Rosary was recited, led by the Knights of Columbus who served as pallbearers. Memorials may be made to the St. Patrick Catholic School Endowment or the Knights of Columbus, John J. Burns Council 802.

Albert Lloyd Meena, MD Madison Dr. Albert Lloyd Meena, 86, of Madison departed this earthly life peacefully in his sleep and went to be with our Lord and Savior Jesus Christ on Sunday, December 1, 2013 at Baptist Medical Center. A Memorial Service was celebrated at Northminster Baptist Church in Jackson, Mississippi on Friday, December 6, 2013. Visitation preceded the service at the church. Dr. Meena was a native of Clarksdale, Mississippi, graduating from Clarksdale High School in 1945. He joined the Navy and served during World War II. After his Navy service he returned to Mississippi where he studied at the University of Mississippi graduating in 1952. He went on to attend the University Of Indiana School Of Medicine. He returned to Jackson in 1955 when the University Mississippi Medical Center moved from Oxford. He was among the first to graduate from the new school. Dr. Meena established himself as one of the premier surgeons of Mississippi and the Southeast. He became a legend in general surgery, an icon of the highest order of medicine’s integrity and dedication. He was highly esteemed by his peers, and respected and loved by his patients who appreciated his extraordinary compassion along with their treatment. He served the medical establishment with honor and distinction. He served on numerous hospital committees as well as Chief of Surgery. He served on the Medical Staff at MS Baptist Hospital, St. Dominic Jackson Memorial Hospital, River Oaks Health Systems and MS Surgical Center. Dr. Meena was a leader in establishing multiple community organizations such as Jackson Prepatory School and Northminster Baptist Church. He was one of the five founders of the 5-star Hunting Club in Greenwood, Mississippi, and Annandale Country Club of Madison. He was a member of Northminster Baptist church and active in his Sunday School Class and numerous mission-related activities. In his spare time he loved hunting ducks and quail, golfing, and after retirement spent his summers golfing and hiking in the beautiful colors of the trees in the North Carolina Mountains or teaching students to read after school in Jackson. He also loved attending Ole Miss Football games and cheered for the Rebels for over 60 years. He was preceded in death by his parents, Elias and Mamie Meena, his sister, Victoria, and his eldest brother, Edward. Dr. Meena is survived by his loving wife of 47 years,

Jackie Meena, his two children, Katherine Meena Fountain and husband Walter of Madison; and son Walter Lauch Meena of St. Pete Beach, Florida; three grandchildren, Stephen Fountain and wife Cassie of Lafayette, Louisiana; Kelly Kyzar and husband Jake of Madison; Kristen Mason and husband Colby of Ridgeland; great grandchildren, Noah Kyzar, Weslee Kyzar, Meena Fountain, Jon Martin Fountain and Lucy Mason and his Brother Victor Meena of Clarksdale, Mississippi. He is also survived by his nephews Hu Meena, Dickie Meena and his niece Mary Martha Bobo and their children. Dr. Meena lived a life that seemed to be almost without fault. He was a man of great character and will be greatly missed by all. Dr. Meena and his family would like to express their appreciation to the doctors and nurses at Baptist Medical Center and Fresenius Medical Care Jackson for all the prayers and loving kindness shown during his extended illness. In lieu of flowers the family asks that Memorials be made to any of Dr. Meena’s favorite charities: Blair E. Batson’s Children’s Hospital. Stewpot, Northminster Baptist Church, Mississippi’s Children’s Museum or a charity of your choice.

Hildon H. Sessums, Jr., MD Vicksburg Services for Dr. Hildon H. Sessums Jr., 58, of Vicksburg were held Nov. 5, 2013, at Glenwood Funeral Home in Vicksburg with the Rev. Tim Brown officiating. Visitation was at the funeral home and he was buried in Clinton at Lakewood Cemetery immediately following the service. Dr. Sessums was born in Greenwood to Hildon H. Sessums Sr. and Marion Morrison Sessums of Drew, on Nov.13, 1954. He grew up in Prentiss and eventually moved to Clinton. Don was a member of the National Junior Beta Club at Clinton Elementary-Jr. High School for outstanding character and achievement. He attended Clinton High School, where he was a member of the national Beta club all four years. He played on the CHS Golf team four years with his closest buddies, Woody Woods and Mike Mayfield. He received the award of merit for outstanding achievement for being the football manager of the “Arrows” his junior and senior year. He graduated from Clinton High School in 1972 and attended Mississippi College 1972-1976, with a bachelor’s degree in chemistry and a minor in mathematics. He was a member of Alpha Epsilon Delta, an honorary pre-med fraternity, included on the dean’s list, and participated in the honors program. While at Mississippi College, he worked during the summer at the Clinton Police Department. He attended the University of Mississippi School of Medicine 1976-1980 and obtained his medical degree. He then entered a family medicine residency program from 1980-1983,

January 2014 JOURNAL MSMA 25

working with the McWillie Family Medical center in Jackson. Other medical experience included medical evaluation for Social Security Disability Determination Services and extensive work in Emergency rooms in Central Mississippi. Dr. Sessums served in the medical corps with the Mississippi Army National Guard from 1978-1992. He was awarded the Meritorious Service Medal from the Department of the Defense in June 1989 for outstanding service while serving as company commander, Company C, 106th Forward Support Battalion, Mississippi Army National Guard, Hazelhurst, from March 1987-1989. He was honorably discharged from the Army as a lieutenant colonel before the Gulf War and started practice in 1983 with Vicksburg Family Medical Clinic. He was selected as physician winner of the 1989 Patient Care Award for excellence in patient education, jointly with his partners. In June 1995, he and his partners (Dr. Lee Giffin, and Dr. Sandra Burford) established a private practice, Mission Primary Care Clinic, where he practiced until 2012. He was a past member of the American Medical Association, the American Academy of Family Physicians, the Mississippi State Medical Association, the West Mississippi Medical Society, the American College of Occupational and Environmental Medicine, the Mississippi Foundation for Medical Care, American Diabetes Association, University of Mississippi Alumni Association, the National Rifle Association, the National Guard Association of Mississippi, and other charities. He served on the St. Aloysius Football Parents Supporters and the Warren Central Parents of Football Supporters. He was a member of Crawford Street United Methodist Church. He was preceded in death by his mother, Marion Morrison Sessums; his maternal grandparents, Paul and Mabel Morrison; his aunts, Virginia Morrison Arledge and Katie Sessums Dallas; his father-in-law, John W. Carter, and a nephew, John C. Mckei. He leaves behind three sons, Lt. Hildon H. Sessums III (Courtney) of Oxford, Carter David Sessums of Vicksburg, Robert Anthony Sessums of Oxford; a grandson, Wyatt David Sessums; his father, Hildon H. Sessums Sr.; a sister, Dr. Catherine Sessums both of Hattisburg; his mother-in-law, Ruth F. Carter of Greenwood; sisters-in-law Lin Carter McKei of Pearl, and Jeffie Carter of Greenwood; his wife of 33 years, Lisa Carter Sessums, formally of Greenwood. Pallbearers were Harold Hughes Kent Jr., Harold Hughes Kent III, William Anthony Kent, David M. Sessums, Royce Foster Welburn and Dr. Robert Lee Giffin. Special Thanks to Mission Primary Care Clinic, Vicksburg Convalescent Home, River Region emergency room and staff, Vicksburg Fire Department EMTs and paramedics, Warren County Sheriffs Department, Vicksburg Police Department, University of Mississippi Medical Center,

26 JOURNAL MSMA January 2014

St. Dominic’s Hospital, Alabama Transplant Center of the University of Alabama at Birmingham, Dr. Michael Davis, and a very special thanks to his good friend and partner, Dr. Lee Giffin.

William Bill Spragins, MD Hollandale Graveside services for Dr. William “Bill” Spragins, 68, of Hollandale, were held at Hollandale City Cemetery. He died Wednesday, Oct. 30, 2013, at his home. Arrangements were under the direction of Boone Funeral Home, Leland. After graduating from Mississippi State University, Dr. Spragins attended the University of Mississippi Medical Center, where he received his medical degree. He began his career in Tutwiler and moved to Hollandale where he continued his career until being forced to retire due to illness. “Doc,” as he was known around the community, spent much of his free time coaching his children and their friends in numerous sports, supporting the Deer Creek Warriors, and acting as team physician. His proudest moments came later in life when he became known as “Pop” to his three grandchildren. He is preceded in death by his father, Homer Spragins and a son, Marc Spragins. He is survived by his wife Terri Menotti Spragins of Hollandale; a daughter, Beth Spragins Giachelli (Jeffrey) of Leland; son, Brand Spragins (Randi) of Leland; mother, Imogene Henley of Cleveland; brother, Gene Spragins of Marion, AR; and 3 grandchildren, Will Giachelli and Meg Giachelli, both of Leland, and Brody Spragins of Franklin, TN. The family received friends at Hollandale United Methodist Church after the graveside services. Memorials may be made to Marc Spragins Scholarship Fund, 2596 Highway 12, Hollandale, MS 38748.

Earl Emerson Whitwell, MD Tupelo Dr. Earl Emerson Whitwell, 70, passed away Nov. 8, 2013, peacefully in his sleep. After a 13-year battle with Parkinson’s disease, Earl crossed the veil, finally healed and eternally restored. His life of service and his spirit of generosity were two outstanding hallmarks of his character and the true measurement of a life well-lived. Earl was born in Memphis, Tenn., on July 12, 1943. He grew up in the small town of Senatobia. An Eagle Scout, Earl was an intelligent,

active young man, enjoying all sports but excelling in football. He graduated as the Senatobia High School Valedictorian in the spring of 1961. Accepting a college football scholarship, Earl attended the University of Virginia for two years. He returned to Mississippi to complete his undergraduate work at the University of Mississippi but gained acceptance to the University of Mississippi School of Medicine after his junior year of college. He completed his Doctor of Medicine degree in 1968. He completed his residency in orthopedic surgery in July of 1973, and he was subsequently board certified as a diplomate by the American Board of Orthopedic Surgery in 1974. He became a Fellow of the American Academy of Orthopedic Surgeons in 1977.Dr. Earl moved to Tupelo and began a successful 28 year orthopedic career becoming the founding member of the Tupelo Orthopedic Clinic, practicing from 1973-2001. Active both in the church and the community, Dr. Earl served many local residents over the years, including working with the Tupelo High School football program as team doctor for nearly two decades. He also conducted the Crippled Childrenâ&#x20AC;&#x2122;s Clinic throughout his entire career. He was a member of the American Academy of Orthopedic Surgeons and the Mississippi Orthopedic Society, serving as president in the 1990s. Earl was married to Valerie Argo Whitwell on Dec. 14, 1990, and they were married for 23 years. He was an avid sportsman. He also loved playing golf and watching college

football. A World War II history buff, Earl was a voracious reader and a lifetime learner, imparting wisdom to both family and friends. He was an advisory board member with the Mississippi Chapter of Fellowship of Christian Athletes and the Save a Life Foundation during the 1980s. Most recently, his passion has been serving at The Orchard in Tupelo as a spiritual mentor and discipleship leader, along with serving on the Jeremiah Council for over a decade. The funeral service was held at Nov. 10, 2013, at The Orchard, a United Methodist congregation. The service will be officiated by Bryan Collier, senior pastor of The Orchard. Private burial followed the funeral handled by W.E. Pegues Funeral Home at Tupelo Memorial Cemetery. Earl is survived by his wife, Valerie Argo Whitwell; his three children, Andy Whitwell and his wife, Callie (Dallas), Jenny Christensen and her husband, Paul (Nashville), and Sami Whitwell, currently attending the University of Virginia. He is also survived by his three grandchildren, Luca, Emerson and Peyton, along with his in-laws, Charles and Mickie Argo; his two brothers Joseph W. Whitwell (Atlanta) and Robert Q. Whitwell (Oxford); his niece and nephews; and the rest of his family and friends.Earl is preceded in death by his parents, Joseph Warlick Whitwell and Lucille Bean Whitwell. Pallbearers are Stephen Farmer, Joe Fields, Joey Hutto, Keith Lawrence, Don Leathers, Mitch Massey, Tommy Morgan, John Phillips, Ray Reed, Keith Roberts, Rud Robison and Charles Buddy Wikle. Honorary pallbearers were the members of the Jeremiah Council at The Orchard in Tupelo. In lieu of flowers, memorial donations may be given to the Parkgate Pregnancy Clinic, 100 Park Gate Ext. A2H, Tupelo, MS 38801, or The Orchard, 1379 Coley Rd, Tupelo, MS 38826.

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