November
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BEACON Imagine the possibilities. You’ve heard of the Beacon Grant.
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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 Steven L. Thomas Demetropoulos, E. Joiner, MD President Steven L. Demetropoulos, James A. Rish, MD President-Elect J. Clay Hays, Jr., MD Secretary-Treasurer Lee Giffin, MD Speaker Geri Lee Weiland, MD Vice Speaker Charmain Kanosky Executive Director
JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual). Periodicals postage paid at Jackson, MS and at additional mailing offices. CORRESPONDENCE: Journal MSMA, Managing Editor, Karen A. Evers, P.O. Box 2548, Ridgeland, MS 39158-2548, Ph.: (601) 853-6733, Fax: (601)853-6746, www.MSMAonline.com. SUBSCRIPTION RATE: $83.00 per annum; $96.00 per annum for foreign subscriptions; $7.00 per copy, $10.00 per foreign copy, as available. ADVERTISING RATES: furnished on request. Cristen Hemmins, Hemmins Hall, Inc. Advertising, P.O. Box 1112, Oxford, Mississippi 38655, Ph: (662) 236-1700, Fax: (662) 236-7011, email: cristenh@watervalley.net POSTMASTER: send address changes to Journal of the Mississippi State Medical Association, P.O. Box 2548, Ridgeland, MS 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© 2012 Mississippi State Medical Association.
NOVEMBER 2012
VOLUME 53
NUMBER 11
Scientific Articles Abstracts from Research Day Sponsored by the American College 356 of Physicians for the University of Mississippi Medical Center Department of Medicine Dominique Pepper, MD and Calvin Thigpen, MD et al.
Concepts in End-of-Life Care - Introduction Death: An Important Part of Life Rachael W. Faught, DO; Sarah M. Gaugler, DO and Sharon P. Douglas, MD
Top 10 Facts You Should Know about Secondary Causes of Diabetes Mellitus
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President’s Page A Good Death
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Steven L. Demetropoulos MD, MSMA President
Editorial An Interview with Dr. Randy Easterling, President, Mississippi State Board of Medical Licensure
of the MSMA Since 1959
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Richard D. deShazo, Associate Editor
Related Organizations Mississippi State Department of Health
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University of Mississippi Medical Center School of Medicine Literati Medicus- The M3/M4 Humanism in Medicine Book Club at the University of Mississippi School of Medicine
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Mississippi Rising: A Preventive Health Symposium - MS Chapter, ACC
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Departments From the Editor Uncommon Thread
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Asclepiad Hugh A. Gamble, II, MD
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About The Cover: Underpass Cathedral —“The building which is fitted accurately to its end will turn out to be beautiful, though beauty is not intended.” This statement can well apply to the underpass featured in our cover photograph. Passing under this structure en route home from work, Dr. Stanley Hartness, Jackson family physician, was struck by the strong sense of perspective and captured this view on a less busy afternoon. After the photo was developed, Dr. Hartness could envision an altar and pews just as easily completing the setting, hence the title. Dr. Hartness is an associate editor of the Journal MSMA and a past-president of the Association. r VOL. LIII
Official Publication
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Honey E. East, MD; Jose S. Subauste, MD; Ayush Gandhi, MD and Christian A. Koch, MD
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NOVEMBER 2012 JOURNAL MSMA 353
From the Editor
A
good death has long been the hope of mankind. In one of humanity’s earliest surviving literary works, the ancient Mesopotamian Epic of Gilgamesh, the hero Gilgamesh’s animalistic friend Enkidu dreams that he will die a slow, ignoble, immensely painful death at the hands of the gods. He laments: “Oh Gilgamesh, some destiny has robbed me of the honor fixed for those who die in battle. I lie now in slow disgrace, withering day by day, deprived as I am of the peace that comes to one who dies suddenly in a swift clash of arms”(7, iv, 110-4). In this long ago poem, Enkidu is seeking a good death, and central to the tale is Gilgamesh’s realization that death is an inescapable part of life for all but the gods. These thousands of years later, mankind is still seeking a good death. We physicians are taught to battle disease, and death comes as a defeat or failure. But cannot even death be a “medical success?” Physicians, the old joke says, bury their mistakes, but we also bury our successes. In quality end-of-life care, we physicians are not managing a patient’s death; rather we are managing the final stages of someone’s life. It is a period hugely important for the patient. The patient-physician bond is stronger in end-of-life care than any other place in the
practice of medicine. The art of medicine, that combination of scientific knowledge, empathy, compassion, communication, skill, and presence, emerges in quality end-of-life patient care more than anywhere else. With the sickest and most vulnerable 5% of patients accounting for 50% of all healthcare spending, end-of-life care, an extraordinarily complex issue, will continue Lucius M. Lampton, MD Editor to shape our evolving healthcare system. However, the secret of a good death is the secret of everyday care of our patients. As Harvard’s Francis Peabody observed in 1921: “The secret of care of the patient is caring for the patient.” There is no better gift we can give our patients and no better use of our physician skills than to relieve the suffering and provide quality medical care in the final stages of life. This issue of your Journal begins the discussion of better end-of-life care. Expect the conversation to continue. Contact me at lukelampton@cableone.net. —Lucius M. Lampton, MD JMSMA Editor
Journal Editorial Advisory Board R. Scott Anderson, MD, FACR Chair, Journal Editorial Advisory Board Radiation Oncologist and Medical Director, Anderson Regional Cancer Center, Meridian 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, FAAP, FACS 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 Thomas E. Dobbs, MD, MPH Health Officer, District VII/VIII Mississippi State Department of Health, Hattiesburg Sharon Douglas, MD Immediate Past Chair, AMA Council on Ethical & Judicial Affairs, Professor of Medicine and Associate Dean for V A Education, University of Mississippi School of Medicine, Associate Chief of Staff for Education and Ethics, G.V. Montgomery VA Medical Center, Jackson Daniel P. Edney, MD Executive Committee Member, National Disaster Life Support Education Consortium, Internist, The Street Clinic, Vicksburg
Owen B. Evans, MD Professor of Pediatrics and Neurology University of Mississippi Medical Center, Jackson Maxie L. Gordon, MD Assistant Professor, Department of Psychiatry and Human Behavior, Director of the Adult Inpatient Psychiatry Unit and Medical Student Education, University of Mississippi Medical Center, Jackson Scott Hambleton, MD Medical Director Mississippi Professionals Health Program, Ridgeland John Edward Hill, MD, FAAFP Residency Program Director North Mississippi Medical Center, Tupelo John D. Isaacs, Jr., MD Infertility Specialist, Mississippi Fertility Institute at Women’s Specialty Center, Jackson Kent A Kirchner, MD Nephrologist G.V. Montgomery VA Medical Center, Jackson 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, FACS Editor, Annals of Plastic Surgery Medical Director JMS Burn and Reconstruction Center, Brandon John F. Lucas,III, MD Surgeon Greenwood Leflore Hospital
354 JOURNAL MSMA NOVEMBER 2012
Gailen D. Marshall, Jr., MD, PhD, FACP Professor of Medicine and Pediatrics, Vice Chair for Research, Director, Division of Clinical Immunology and Allergy, Chief, Laboratory of Behavioral Immunology Research The University of Mississippi Medical Center, Jackson Alan R. Moore, MD Clinical Neurophysiologist Muscle and Nerve, Jackson Paul “Hal” Moore Jr., MD, FACR Radiologist Singing River Radiology Group, Pascagoula Jason G. Murphy, MD Surgeon Surgical Clinic Associates, Jackson Ann Myers, MD Rheumatologist Mississippi Arthritis Clinic, Jackson Jimmy L. Stewart, Jr., MD Program Director, Combined Internal Medicine/ Pediatrics Residency Program, Associate Professor of Medicine and Pediatrics University of Mississippi Medical Center, Jackson Samuel Calvin Thigpen, MD Hematology-Oncology Fellow, Department of Medicine University of Mississippi Medical Center, Jackson Thad F. Waites, MD, FACC Clinical Cardiologist, Hattiesburg Clinic Chris E. Wiggins, MD Orthopaedic Surgeon Bienville Orthopaedic Specialists, Pascagoula John E. Wilkaitis, MD, MBA, CPE, MS Chief Medical Officer Brentwood Behavioral Healthcare, Flowood
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Representing Physicians NOVEMBER 2012 JOURNAL MSMA 355
• Scientific Articles • Abstracts from Research Day Sponsored by the American College of Physicians for the University of Mississippi Medical Center Department of Medicine [Each year, there are annual scientific presentations made by house-staff in training at UMMC. The Journal has published some of these as the editors felt the information presented would be of interest to our readers. In this issue, we publish abstracts from a recent research day sponsored by the American College of Physicians for the University of Mississippi Medical Center Department of Medicine. We are grateful to Dominique Pepper, MD and Calvin Thigpen, MD for putting these together. Please let us know if you find them useful, so we can make decisions about publishing similar abstracts in the future.] —Richard D. deShazo, Associate Editor 1.
Getting to the GIST of the GastrointestinaI Bleed: A Case Report
2.
A Mitral Mystery: Disparate Response to R-CHOP of Diffuse Large B-Cell Lymphoma Lesions in a Patient with AIDS
3.
Double Trouble: Paraneoplastic Hypercalcemia-Hyperleukocytosis Syndrome in Cutaneous Squamous Cell Carcinoma
4.
Normal Alkaline Phosphatase in Active Paget’s Disease of Bone
5.
Hemolytic Havoc: HELLP, DIC, and TTP in a Patient with Intrauterine Fetal Demise
6.
Cutting to the Chase: An Unusual Complication of Cocaine Use
7.
Brainstorm: A Case Report of Anti-N-Methyl-D-Aspartate Receptor Antibody Encephalitis
8.
Inflammation Gone Awry: Pyoderma Gangrenosum in Newly Diagnosed Crohn’s Disease
9.
Don’t Play With Mismatches: Acute Hemolytic Reaction During Allogeneic Stem Cell Infusion for High Risk Myelodysplastic Syndrome
10. Confusion Abounds: Posterior Reversible Encephalopathy Syndrome in the Setting of Inflammatory Breast Cancer 11. Now You See It, Now You Don’t: Evans Syndrome in a Patient Suspected To Have Lymphoma 12. A Mean Spleen: Splenic Sequestration Crisis in a 53-year-old with Sickle Cell Disease 13. Adding Fuel to the Fire: A Case of Severe Hypercalcemia in the Setting of Extrapulmonary Sarcoidoisis 14. Transarterial Chemoembolization (TACE) Associated Pancreatitis and Gastric Ulceration 15. Flail Chest: New Treatment for a Paradoxical Problem 16. Acute CVA in the Setting of Graves’ Thyrotoxicosis and Moyamoya: A Rare Combination
356 JOURNAL MSMA NOVEMBER 2012
1. Getting to the GIST of the Gastrointestinal Bleed Stewart Boyd, MD1; Stephanie Tanner, MD2; Naveed Ahmad, MD3; Sumanth Daram, MD3; John J. Sheehan, MD3 Department of Medicine, University of Mississippi Medical Center; 2Department of Pathology, University of Mississippi Medical Center; 3Division of Digestive Diseases, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi. Corresponding author: Stewart Boyd, MD, PGY-3, Department of Medicine, University of Mississippi Medical Center (saboyd@umc.edu). 1
Introduction Soft tissue sarcomas are extremely rare and account for approximately 1% of all adult malignancies.1 80% of soft tissue sarcomas that arise from the gastrointestinal (GI) tract are gastrointestinal stromal tumors (GIST) – tumors which have shown significant improvements in median survival since the development of Imatinib.2 Common presenting symptoms include abdominal discomfort, GI bleeding, and anemia.3 We report the case of a 79-year-old woman who presented with melena. Case Description A 79-year-old female presented to the emergency department with melena associated with blood clots. She denied any hematemesis, abdominal pain, or excessive NSAID use. She had recently commenced warfarin after diagnosis of a left lower extremity deep vein thrombosis. The patient was found to have an INR of 2.7 and a hematocrit of 27. The patient was admitted to the hospital for further evaluation. Esophagogastroduodenoscopy (EGD) revealed a large ulcerated submucosal mass in the fundus of the stomach. Computed tomography (CT) of the abdomen and pelvis showed a 9cm x 6cm x 7cm mass in the greater curvature of the stomach. Deep biopsies performed during the EGD were interpreted as a gastrointestinal stromal tumor (GIST) positive for CD 117(c-kit) and CD 34. The patient underwent partial gastrectomy. Post operative PET CT of chest, abdomen, and pelvis showed no evidence of residual disease or metastasis. Given the tumor cytologic characteristics and size, a 12-month course of Imatinib was prescribed. Discussion Tumors originating from the upper GI tract rarely cause severe upper gastrointestinal bleeding (less than 3%). Gastrointestinal bleeding is a common adverse event associated with the use of warfarin for chronic anticoagulation. This case demonstrates how an adverse effect of her medication revealed a potentially fatal disease. With resection and treatment with Imatinib, this patient should have a good clinical outcome. References 1.
Jemal A, Murray T, Samuels A, et al. Cancer statistics 2003. Cancer J Clin. 2003;53:5.
2.
Benjamin R, Pisters PWT, Helman LJ, et al. Abeloff’s Clinical Oncology, ed 4, Abeloff MD (ed). Philadelphia: Churchill Livingstone; 2008:2009-2056.
3.
Savides TJ, Jensen DM, Cohen J, et al. Severe upper gastrointestinal tumor bleeding: endoscopic findings, treatment, and outcome. Endoscopy. 1996;28:244.
2. A Mitral Mystery: Disparate Response to R-CHOP of Diffuse Large B-cell Lymphoma Lesions in a Patient with AIDS
J. Kevin Bridges, MD; James Hamilton, MD; S. Calvin Thigpen, MD; Kenneth Bennett, MD; Carolyn Bigelow, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Kevin Bridges, MD, PGY-3, Department of Medicine, University of Mississippi Medical Center (jbridges@umc.edu). Introduction Due to its aggressive nature, diffuse large B-cell lymphoma (DLBCL) may be discovered in unusual locations, particularly in those with a pre-existing immune compromised condition such as AIDS. We present a patient with widespread diffuse large B-cell lymphoma with involvement of the mitral valve that produced multiple management dilemmas and responded to R-CHOP in an incongruent manner. Case Description A 34-year-old female with AIDS and an absolute CD4 count of 79 presented to our facility with lower extremity weakness and overflow incontinence. Physical exam confirmed cauda equina syndrome. CT of the body identified a pericardial effusion, a filling defect in the left atrium, extensive thrombosis of the portal veins, multiple hepatic hypodensities, a large pelvic mass, and soft tissue filling of the lumbar vertebral canal and sacral foramina. MRI of the spine confirmed compression of the cauda equina
NOVEMBER 2012 JOURNAL MSMA 357
by an epidural mass. Biopsy of the liver mass yielded a diagnosis of DLBCL, and lumbar puncture was negative. Echocardiogram demonstrated a 3.5 cm x 2.5 cm mobile mass on the anterior leaflet of the mitral valve prolapsing into the left ventricle on diastolic filling and a circumferential pericardial effusion that required drainage. Cardiothoracic surgery was consulted for mitral valve replacement. However, due to potential abdominal compartment syndrome related to the portal vein thrombosis and the consequent possibility of an open abdomen in an immune compromised patient, surgery was deferred. After careful consideration, rituximab was given with CHOP chemotherapy. Radiation was also administered to the lumbosacral spine, and anticoagulation was initiated. Over the course of the next several days, the patient became increasingly tachycardic. Repeat echocardiogram at that time, and after her second cycle of R-CHOP, showed a marginal increase in size of the mitral valve mass despite significant improvement of her other lesions and resolution of her cauda equina syndrome. Discussion This case presents several unusual challenges: 1) a mitral valve thrombus (likely from tumor) in the presence of portal vein thrombosis; 2) a CD4 count in the controversial range of 50-100 for giving rituximab; 3) spinal fluid negative for lymphoma despite extensive involvement of the vertebral canal causing cauda equina syndrome; and, even more curiously, 4) widespread response to treatment without response at the critical valvular lesion. Treatment plans include reconsideration of mitral valve replacement since the disparate response of the valvular lesion could be secondary to high blood flow velocity not allowing adequate duration of exposure to high concentrations of chemotherapy.
3. Double Trouble: Paraneoplastic HypercalcemiaHyperleukocytosis Syndrome in Cutaneous Squamous Cell Carcinoma Cory Carter, MD; S. Calvin Thigpen, MD; Kimberly Harkins, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Cory Carter, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center (cbcarter2@umc.edu). Introduction Fewer than 30 cases of humoral hypercalcemia of malignancy (HHM) secondary to primary cutaneous squamous cell carcinoma (SCC) have been documented. In only a few cases is hypercalcemia concomitant with hyperleukocytosis, a finding known as hypercalcemia-hyperleukocytosis syndrome. When compared to patients with hypercalcemia alone, the survival of patients with hypercalcemia-hyperleukocytosis syndrome appears to be shorter. Case Description A 54-year-old African-American male with recurrent cutaneous abscess formation – at the site of a proximal right thigh mass – presented with three days of altered mental status. A previous biopsy of the mass demonstrated moderately to well-differentiated SCC. On initial presentation to our hospital, his serum calcium was 15.9 mg/dl and his WBC count was 15,800. A CT of the head showed multiple low-density lesions suspicious for metastatic disease, and a CT of the abdomen and pelvis revealed a large loculated mass in the medial right thigh with local invasion. A PET scan did not show any areas of hypermetabolic activity in the lung. The patient received aggressive IV hydration as well as bisphosphonate and calcitonin therapy. 25-hydroxy vitamin D and PTH levels were both below normal range, and a parathyroid hormone-related protein (PTHrP) level was elevated. These findings best represented paraneoplastic production of PTHrP from a primary cutaneous SCC. The patient experienced only mild improvement of his mental acuity and minimal response to treatment of his hypercalcemia. He declined palliative chemotherapy and radiation therapy and was discharged to a hospice where he died several days later. Discussion Although HHM has been identified in a significant number of primary SCC of the lung, it has only rarely been reported with cutaneous SCC. Even more exceptional is the presence of concomitant hyperleukocytosis syndrome. We present a case of hypercalcemia-hyperleukocytosis syndrome likely due to cutaneous SCC of which only a small number of cases have been reported. This case supports the finding that the presence of this combined paraneoplastic process is a poor prognostic indicator. Future studies may indicate that the presence of hypercalcemia-hyperleukocytosis syndrome may independently predict survival when compared to standard TNM staging.
358 JOURNAL MSMA NOVEMBER 2012
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4. Normal Alkaline Phosphatase in Active Paget’s Disease of Bone Sarah E. French, MD1; Jose Subauste MD1,2 Division of Endocrinology, Department of Medicine, University of Mississippi Medical Center; 2Medical Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center. Corresponding author: Sarah French, MD, Endocrinology Fellow, Department of Medicine, University of Mississippi Medical Center (sfrench@umc.edu). 1
Introduction Paget’s disease of bone affects approximately 1% of the US population over the age of 40 years. Since most cases are diagnosed incidentally by increased levels of alkaline phosphatase,1 the diagnosis of Paget’s disease of bone is difficult when the level of serum alkaline phosphatase is normal. Case Description A 78-year-old white male with asbestosis and status post left lower lung lobectomy for a lung mass with benign pathology was noted to have a new right upper lobe lung mass on CT thorax, concerning for malignancy. When a CT-guided fine needle aspiration biopsy and thoracentesis were non-diagnostic, a metastatic work-up was commenced. A lucent lesion was found in his left tibia by plain radiographs, and the lesion was active on nucleotide bone scan. Due to concern for possible metastatic disease, a bone biopsy was performed which showed no evidence of carcinoma. However, the pathology report noted remodeling with prominent osteoclastic activity consistent with Paget’s disease of bone. Serum calcium and alkaline phosphatase were both normal: 10.2 mg/ dL (8.8-10.5 mg/dL) and 111 units/L (38-126 units/L) respectively. Further work-up of the right upper lobe lung mass revealed benign pathology. As his tibial lesion was in a weight-bearing bone and he reported bone pain, daily treatment with risedronate 30mg daily was initiated. However, his bone pain persisted despite 3 months of therapy, so alendronate 40mg daily for 6 months was commenced. His bone pain improved and therapy was stopped. The patient remained stable for 4 years until increased bone along his left anterior tibia was noted. An MRI of his lower extremity was consistent with active Paget’s disease so treatment with 6 months of alendronate was recommenced with subsequent improvement of his Paget’s disease. Throughout treatment, his serum alkaline phosphatase level remained within normal limits. Discussion Normal serum alkaline phosphatase levels may be seen in the monostotic form of Paget’s disease of bone or only when a small volume of bone is affected, as was the case in this patient.1 Intensive bisphosphonate therapy to maintain normal alkaline phosphatase levels does not confer any clinic benefit over symptom-driven bisphosphonate therapy, but guidelines recommend re-treatment with bisphosphonates when there is symptom relapse/persistence or biochemical relapse.2,3 In patients with normal serum alkaline phosphatase levels, other markers of bone turnover such as bone-specific alkaline phosphatase or procollagen type 1 N-terminal propeptide may be useful to monitor metabolic bone activity.4 References 1.
Gkouva L, Andrikoula M, Kontogeorgakos V, et al. Active Paget’s disease of bone with normal biomarkers of bone metabolism: a case report and review of the literature. Clin Rheumatol. 2011;30:139-144.
2.
Langston AL, Campbell MK, Fraser WD, et al. Randomized trial of intensive bisphosphonate treatment versus symptomatic management in Paget’s disease of bone. J Bone Miner Res. 2010;25:20-31.
3.
Selby PL, Davie MV, Ralston SH, et al. Guidelines on the management of Paget’s disease of bone. Bone. 2002;31:366-373.
4.
Ralston SH, Langston AL, Reid IR. Pathogenesis and management of Paget’s disease of bone. Lancet. 2008;372:155-163.
5. Hemolytic Havoc: HELLP, DIC, and TTP in a Patient with Intrauterine Fetal Demise Jacob Graham, MD; S. Calvin Thigpen, MD; Zeb K. Henson, MD; Carolyn Bigelow, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Jacob Graham, MD, PGY-1, Department of Medicine, University of Mississippi Medical Center (jgraham@umc.edu). Introduction Preeclampsia or eclampsia complicated by the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP)
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is often disastrous for both mother and fetus. It can occur simultaneously with disseminated intravascular coagulation (DIC), particularly with placental abruption or retained fetal products, and it can be difficult to distinguish from another less common complication of pregnancy, thrombotic thrombocytopenic purpura (TTP). These distinctions must be made early in the course because both DIC and TTP require treatment beyond delivery of the fetus. Case Description A 22-year-old African American female with a 23-week intrauterine pregnancy presented to our university hospital in transfer with eclampsia and laboratory evidence of HELLP. At admission, the patient was found to have intrauterine fetal demise and underwent induction of labor and delivery, with approximately 20% placental abruption noted, followed two hours later by dilatation and curettage for retained fetal products. Concomitantly, the patient was noted to develop profound anemia as well as thrombocytopenia, leukocytosis with bandemia, lactic acidosis, acute renal failure, and a mild coagulopathy. Review of the peripheral smear revealed no schistocytes. Treatment and supportive care for HELLP and DIC were initiated, including dexamethasone, antibiotics, hemodialysis, and multiple transfusions of packed red cells, platelets, and fresh frozen plasma. After three days of minimal improvement, peripheral smear was reviewed again; schistocytes were abundant. Plasma exchange for TTP was initiated. Over the next two weeks, her course was complicated by volume overload requiring intubation for 72 hours. Her overall condition and microangiopathic hemolytic anemia, though, did improve. At two-week outpatient follow-up, her renal function had improved to baseline. Discussion This case highlights potential diagnostic difficulties surrounding three hemolytic conditions associated with pregnancy and serves as a unique example of their presence simultaneously or at least in close succession. Care of the pregnant woman with HELLP, with or without intrauterine fetal demise, requires serial monitoring of platelet counts, laboratory indicators of hemolysis, and the peripheral smear after delivery to ensure that neither DIC nor TTP has developed or been concurrent.
6. Cutting to the Chase: An Unusual Complication of Cocaine Use Andrea McCann; Dominique J. Pepper, MD; Lance Atchley, MD; Jericho Bell, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Dominique J Pepper, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center (dpepper@umc.edu.). Introduction In the 1960s, levamisole was developed as an antihelminthic and an immunomodulatory drug but has since been discontinued due to serious side effects, such as vasculitic skin necrosis and agranulocytosis.1-3 Levamisole is now used to cut cocaine; up to 70% of cocaine seized in the United States is contaminated with levamisole. Here we report a non-fatal case of levamisoleassociated vasculopathy. Case Description A 48-year-old African-American female with type II diabetes mellitus, hypertension, rheumatoid arthritis, and recent cocaine use presented to the emergency room. Her chief complaint was a skin rash which first appeared on her right ear and then spread over a 3-day period to involve her left ear, her maxillae, her right breast, her abdomen and the lateral aspects of her upper arms and thighs. At each location, the rash began as an erythematous macule which enlarged to form a purpuric center with an erythematous border. The rash on her abdomen encircled her umbilicus with a radial measurement of 10–12 cm. All her skin rashes were associated with mild pruritis and tenderness. Associated symptoms included mild chest pain, shortness of breath, and occasional chills. Physical exam was unremarkable except for her numerous skin lesions which caused her considerable emotional distress. No oral or vaginal ulcers were present. Laboratory tests revealed leukopenia, anemia, and a positive urine drug screen for cocaine. The initial differential diagnoses were an autoimmune vasculitis and a fixed drug eruption due to lisinopril, hydrochlorathiazide, metformin, or gabapentin. Upon admission to hospital, all the patient’s medications were stopped, oral and topical steroid therapy was commenced, and a 5 mm punch biopsy of an early lesion on her lateral thigh was performed. Histopathology showed fibrin thrombi within the vessels of the superficial venous plexus as well as a minimal perivascular lymphocytic infiltrate. These findings, in the context of recent cocaine use and the characteristic skin rash, are typical of levamisole-associated vasculopathy. Thus, we were able to counsel the patient to avoid cocaine and improve her adherence with her antihypertensive and diabetic medications. Discussion Our case emphasizes the importance of a thorough clinical interview and clinico-pathological correlation. Recreational cocaine use may result in unusual clinical manifestations, such as a purpuric skin rash, which necessitates a high level of clinical
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suspicion. When confronted by a skin rash in a patient who uses cocaine, a clinician should always consider levamisole-induced vasculopathy. References 1.
Lionel ND, Mirando EH, Nanayakkara JC, et al. Levamisole in the treatment of ascariasis in children. Br Med J. 1969;4(5679):340-341.
2.
Perk K, Chirigos MA, Fuhrman F, et al. Some aspects of host response to levamisole after chemotherapy in a murine leukemia. J Natl Cancer Inst. 1975;54:253256.
3.
Rongioletti F, Ghio L, Ginevri F, et al. Purpura of the ears: a distinctive vasculopathy with circulating autoantibodies complicating long-term treatment with levamisole in children. Br J Dermatol. 1999;140:948-951.
7. Brainstorm: A Case Report of Anti-N-Methyl-D-Aspartate Receptor Antibody Encephalitis Dane Ballard, MD; George Abraham, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Dane Ballard, MD, PGY-1, Department of Medicine, University of Mississippi Medical Center (rdballard@umc.edu ). Introduction Anti-N-Methyl-D-Aspartate receptor (NMDAR) antibody encephalitis is a newly recognized syndrome that causes severe psychotic and neurologic symptoms which rapidly prove fatal if not recognized and treated early. A single institution has reported over 400 cases in just over 3 years suggesting that it may be the most common antibody associated with encephalitis. Here we present a case of NMDAR encephalitis that occurred as a paraneoplastic manifestation of bilateral ovarian teratomas. Case Description A 16-year-old female presented to the Emergency Room after an altercation with her father. Her mother reported a one-week history of psychotic symptoms including insomnia, severe agitation, combativeness, and auditory hallucinations. The patient was confused, lacked insight, and exhibited a tangential thought process. She was discharged from the Emergency Room to a pediatric mental health facility where she was started on haloperidol, olanzapine, and depakote. Five days after admission she developed a fever of 105 degrees Fahrenheit, exhibited diffuse muscular rigidity, and became unresponsive. She was admitted to the medical ICU, intubated, and treated with dantrolene for presumed neuroleptic malignant syndrome. After 4 days of supportive care and failure to improve on dantrolene, a CT abdomen was performed and revealed bilateral ovarian masses consistent with ovarian teratomas. A lumbar puncture was performed and sent to the Mayo Clinic for work-up of a suspected paraneoplastic syndrome. On day twelve of her hospital course, the tumors were resected; pathology later confirmed the masses to be poorly differentiated teratomas. The patient was treated empirically for NMDAR encephalitis with intravenous immunoglobulin and plasma exchange; however, she did not improve with therapy: She remained unresponsive and exhibited choreiform movement which was unsuccessfully treated with haloperidol, phenobarbital, and ziprasidone. Thirty-five days after admission she was weaned from the ventilator, and one week later the NMDAR antibody returned positive. Several days later she was discharged from the ICU to the general ward. She remains unresponsive and does not follow commands. Discussion This case was diagnostically and therapeutically challenging and highlights the masquerading nature of this disease. We emphasize the importance of ruling out organic causes of psychosis, especially in young adults and children. We also stress the need to develop more rapid diagnostic tests for serum and cerebrospinal fluid.
8. Inflammation Gone Awry: Pyoderma Gangrenosum in Newly Diagnosed Crohn’s Disease Eric Reiners, MD; Zeb Henson, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Eric Reiners, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center (ereiners@umc.edu).
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Introduction Crohn’s disease affects 2-6% of the population and is characterized by transmural gastrointestinal inflammation. Pyoderma gangrenosum is a rare ulcerative cutaneous condition that has been described as an extra-intestinal manifestation of inflammatory bowel disease occurring in 2% of patients with Crohn’s disease. Here we describe a young pregnant woman with newly diagnosed Crohn’s disease and pyoderma gangrenosum. Case Description Our case is of a 26-year-old African-American woman with a history of iron deficiency anemia who presented with a three month history of abdominal cramping, nausea, vomiting, and bloody diarrhea. She was diagnosed with Crohn’s disease based on endoscopy findings and pathology from colonic biopsies. Her skin infection was initially treated with antibiotics but was ultimately diagnosed with pyoderma gangrenosum based on sterile wound cultures of the purulent material. Subsequently, antibiotic therapy was de-escalated, and our patient was discharged from the hospital on Humira injections. Upon followup, her Crohn’s disease was in remission and her skin lesions had healed. Discussion Interestingly, our patient’s pregnancy preceded the onset of Crohn’s disease and skin lesions. Pyoderma gangrenosum is a rare complication of Crohn’s disease and is often misdiagnosed. Delay in correct treatment can result in disfigurement, while treatment of the underlying inflammatory bowel disease will often cause resolution of pyoderma gangrenosum. However, early treatment with immunosuppressants could be detrimental if infection is present.
9. Don’t Play With Mismatches: Acute Hemolytic Reaction During Allogeneic Stem Cell Infusion for High Risk Myelodysplastic Syndrome S. Calvin Thigpen, MD; J. Kevin Bridges, MD; Stephanie Elkins, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Calvin Thigpen, MD, Hematology/Oncology Fellow, Department of Medicine, University of Mississippi Medical Center (sthigpen@ umc.edu). Introduction Allogeneic stem cell transplantation from an HLA matched donor is occasionally performed when there is an ABO mismatch with the recipient. We report a patient with high-risk myelodysplastic syndrome (MDS) and high-risk co-morbidities who experienced an acute hemolytic reaction during stem cell infusion despite efforts to prevent this occurrence. Case Description A 63-year-old Caucasian male with an artificial aortic valve, MDS, and multiple cytogenetic abnormalities presented for conditioning chemotherapy and allogeneic stem cell transplant. The patient, who was maintained on full dose heparin throughout his transplant, was blood group O positive while his HLA matched unrelated donor was blood group A positive. The patient’s anti-A titer was 1:64 prior to admission. He, therefore, underwent plasmapheresis twice which reduced his anti-A titer to 1:16. Also, red blood cell reduction was performed on the donor’s stem cell product. Despite these measures, after 45 mL of stem cell product had infused, the patient developed chest tightness, shortness of breath, back pain, pink urine, fever, and tachycardia. The infusion was stopped. Intravenous fluids and furosemide were administered. Labs reflected active hemolysis. After 90 minutes, the stem cell infusion was resumed at a much slower rate and, 17 hours later, completed. The patient subsequently developed renal failure over the following week and eventually required renal replacement therapy. Additionally, his course was complicated by alveolar hemorrhage and respiratory failure, necessitating cessation of his heparin. He eventually recovered and was discharged to a long-term acute care facility. Discussion This case highlights several challenging scenarios: 1) infusion of stem cells from an HLA matched, but ABO mismatched, donor; 2) management of an acute hemolytic reaction when the patient must have a blood product in order to survive; 3) stem cell transplant in a patient with an artificial heart valve; and 4) management of the potential sequelae of an acute hemolytic reaction and of stem cell transplant. In the years to come, continued improvements in processing and preparation of stem cell products offer hope for fewer complications with ABO incompatible transplantation.
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10. Confusion Abounds: Posterior Reversible Encephalopathy Syndrome in the Setting of Inflammatory Breast Cancer CR. Kelly Waespe, MD; S. Calvin Thigpen, MD; Darryl Hamilton, MD; Ralph Vance, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Calvin Thigpen, MD, Hematology/ Oncology Fellow, Department of Medicine, University of Mississippi Medical Center (sthigpen@umc. edu). Introduction Posterior Reversible Encephalopathy Syndrome (PRES) may present with a variety of neurologic signs, including confusion, visual disturbance, seizures, headaches, and occasionally focal motor or sensory deficits. Among the possible triggers of PRES is the recent use of immunosuppressive or cytotoxic medications. While several instances of PRES have been described in patients who have recently received chemotherapy for a variety of malignancies, we were unable to identify in the literature any cases in a patient with inflammatory breast cancer. We report one such patient here who had recently been treated with cyclophosphamide and doxorubicin. Case Description A 50-year-old Caucasian female with recurrent metastatic estrogen- and progesterone-receptor positive inflammatory breast cancer presented with three weeks of progressive confusion, visual changes, right upper extremity weakness, and ataxia. Treatment of her malignancy prior to metastatic recurrence had included neo-adjuvant docetaxel and cyclophosphamide, modified radical mastectomy, chest wall radiation, and hormone therapy with tamoxifen and subsequently letrozole. Upon being found to have evidence of cancer in her liver, thoracic vertebrae, and right acetabulum, the patient underwent one cycle of doxorubicin and cyclophosphamide. Twenty-two days later she developed the aforementioned neurologic symptoms. MRI of the brain revealed bilateral cortical edema and patchy enhancement consistent with severe PRES. Neurology was consulted, and because of the concern for leptomeningeal carcinomatosis, a cisternal spinal puncture was performed. The cerebrospinal fluid analysis was negative for malignancy. The patient’s blood pressure was aggressively controlled to avoid further complicating PRES, and she slowly began to recover. On hospital discharge, approximately six weeks after initial symptoms, her memory was improved as were her gait and the use of her right upper extremity. Because she had previously tolerated cyclophosphamide chemotherapy well, it was felt that her PRES was most likely secondary to doxorubicin. Discussion Given that its symptom complex is broad, PRES is a diagnosis of exclusion, particularly when there is a possibility of metastatic spread of malignancy. In this patient, metastatic involvement of the CNS could not be proven, and MRI findings, which were consistent with PRES, resolved as the time interval since the administration of doxorubicin lengthened. This case represents the first reported instance, known to us, of the development and resolution of PRES in a patient with inflammatory breast cancer.
11. Now You See It, Now You Don’t: Evans Syndrome in a Patient Suspected To Have Lymphoma Bobby W. Tullos; Sarah M. Gaugler, MD; S. Calvin Thigpen, MD; Zeb Henson, MD; V. E. Herrin, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Bobby Tullos, 4th year medical student, Department of Medicine, University of Mississippi Medical Center (btullos@umc.edu). Introduction Evans syndrome is an autoimmune disorder characterized by concomitant autoimmune hemolytic anemia and immune thrombocytopenia. Although more frequent among children, Evans syndrome may occur in adults as an idiopathic illness or be associated with a malignancy or an autoimmune disorder. Here we report a rare adult case of Evans syndrome, strongly suspected to have a lymphoproliferative disorder. Case Description A 57-year-old female with rheumatoid arthritis presented to the emergency department with recent worsening of chronic night
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sweats and cough. On exam, wheezing and diffuse lymphadenopathy were present, and laboratory work-up revealed eosinophilia, Coombs-positive anemia, reticulocytosis, thrombocytopenia, and a polyclonal gammopathy. A review of the peripheral smear confirmed the presence of spherocytes, a hallmark of autoimmune hemolytic anemia. Systemic steroids were given with dramatic improvement of her cough, lymphadenopathy, and all laboratory abnormalities. Axillary lymph node biopsy was performed two days after the initiation of steroids, but pathology revealed only an abnormal lymphoid population suspicious for, but not diagnostic of, a non-Hodgkin lymphoma. Subsequent bone marrow biopsy revealed a hypercellular marrow with increased immature cells but no definitive evidence of malignancy. Anti-nuclear antibody testing was positive, but no specific antibodies were elevated. HIV and viral hepatitis tests were negative. Over the course of the next six weeks, the patient’s eosinophil count, hemoglobin, and platelet count normalized as her dose of oral prednisone was slowly tapered. Her lymphadenopathy and wheezing completely resolved as did her cough and night sweats. Regular clinic visits are planned for surveillance for recurrence of any abnormalities or development of a lymphoproliferative disorder. Discussion Most cases of Evans syndrome are idiopathic with a minority being associated with a malignancy or autoimmune disorder. Our case is unique in that it involves Evans syndrome 1) in an adult, 2) who presented with multiple common manifestations of lymphoma, but 3) who, likely because of an overwhelming response to treatment of her immune cytopenias, has not been diagnosed with a malignancy. A diagnosis of lymphoma once the steroid taper is complete would provide further evidence for the efficacy of corticosteroids in lymphoproliferative disorders.
12. A Mean Spleen: Splenic Sequestration Crisis in a 53-Year-Old with Sickle Cell Disease Kelly J. Wilkinson, MD1; S. Calvin Thigpen, MD1,2; Frank J. Criddle, MD1; John T. Lam, MD3 Department of Medicine, University of Mississippi Medical Center; 2Division of Hematology, Department of Medicine, University of Mississippi Medical Center; 3Department of Pathology, University of Mississippi Medical Center. Corresponding author: Kelly Wilkinson, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center (kjeanes@umc.edu). 1
Introduction Splenic sequestration crisis is a potentially fatal complication of sickle cell disease that occurs when trapped sickled cells cause acute enlargement of the spleen and prevent the return of blood flow to the circulation. Autosplenectomy usually occurs before adulthood; therefore, crises affect patients with sickle cell disease very early in life because the spleen is still present. Case Description A 53-year-old African American female with a history of sickle cell disease and chronic hepatitis C presented to the emergency room with a one-week history of severe diffuse pain, greatest in her mid-back and abdomen. The patient stated this was typical for her sickle cell crises. Physical exam was significant for abdominal tenderness in all four quadrants and splenomegaly. Labs revealed a hemoglobin of 6.1 g/dL, unchanged from just two months prior. Occasional sickle cells were seen on peripheral smear. She was admitted to the general medicine service for treatment of her presumed sickle cell crisis. Just twelve hours later her hemoglobin had decreased to 2.9 g/dL with peripheral smear showing no sickle cells. Upon further examination, the patient’s diffuse abdominal pain had localized to her left upper quadrant, and her previously palpable spleen was markedly increased in size. Splenic sequestration crisis was diagnosed at that time. Multiple units of packed red blood cells were transfused over the next few days, and her hemoglobin eventually stabilized. Surgery was consulted, and outpatient splenectomy was planned. The patient’s pain, however, precluded discharge, and her blood counts gradually declined. In light of these developments, inpatient splenectomy was pursued. Pneumococcal, Haemophilus, and meningococcal vaccinations were administered, and open splenectomy was performed after it was determined intra-operatively that laparoscopic resection was not possible. Afterward, her left upper quadrant pain was significantly improved, and her hemoglobin remained stable until discharge. Pathologic evaluation confirmed splenic sequestration. She has not required further hospitalization for sickle cell crises. Discussion There are three uncommon aspects that make this case interesting: 1) a patient with sickle cell disease having survived to the age of fifty-three, 2) the presence of a spleen at this age, and 3) the occurrence of a splenic sequestration crisis. As this case demonstrates, a splenic sequestration crisis should be considered as a potential etiology for abdominal pain in sickle cell patients of any age.
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13. Adding Fuel to the Fire: A Case of Severe Hypercalcemia in the Setting of Extrapulmonary Sarcoidoisis Andrea Green; Rebecca Chick, MD; Eric Reiners, MD; Vikas Majithia, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Andrea Green, 4th year medical student, Department of Medicine, University of Mississippi Medical Center (agreen@umc.edu). Introduction Hypercalcemia arises in 11% of patients with sarcoidosis with clinically significant hypercalcemia occurring in only 5% of patients. Hypercalcemia is rarely the presenting symptom of sarcoidosis.1 The highest reported calcium value in the literature of a patient with sarcoidosis is 14 mg/dl.2 We present a unique case report of a patient who was admitted for hypercalcemia of 18.9 mg/ dl. Further inquiry into the patient history revealed a three-month history of Vitamin D replacement therapy provoking a calcium level not normally seen in patients with sarcoidosis. Case Description A 56-year-old African-American female presented to clinic with a several month history of fatigue, constipation, depression, dyspnea as well as an episode of syncope. She had experienced a 70-lb weight loss, several non-healing leg ulcers and nodules on her wrists/ankles for last 4 years. Her systemic examination was non-diagnostic. The laboratory testing was significant only for severe hypercalcemia (18.9 mg/dl). She was admitted to inpatient service for further work-up and treatment. The elevated calcium was successfully treated with IV fluids and IV pamidronate. Radiographs and CT scans showed widespread bilateral lung opacities with numerous nodules and significant areas of consolidation, nodular liver contour,’ and hepatosplenomegaly with multiple lowdensity lesions. Standard workup for other causes of hypercalcemia was unrevealing. The patient’s ACE level was elevated at 213 ug/L, and biopsies of skin ulcers, nodules, liver, and lung revealed granulomatous inflammation and non-caseating granulomas. A diagnosis of sarcoidosis was made, and she was treated with prednisone 1 mg/kg/day with an excellent clinical, radiographic, and laboratory response. It was discovered that 3 months prior to this presentation, she had been given weekly high dose (50,000 IU) vitamin D replacement in response to a documented 25-hydroxyvitamin D level of 14.1 ng/ml. Discussion Although significant hypercalcemia can be seen in up to 5% of cases of sarcoidosis, this case is unique as severe hypercalcemia (>15mg/dl) as a sole presenting sign has not previously been described. Most cases of patients presenting with calcium levels >14 mg/dl are considered to have hypercalcemia of malignancy until proven otherwise.1 In this patient, 25-hydroxyvitamin D levels were diminished, secondary to active sarcoidal macrophages depleting the available stores. Therefore, active sarcoidosis complicated by vitamin D replacement therapy contributed to an extreme elevation of calcium ultimately leading to the correct diagnosis. References 1. Iannuzzi M, Rybicki B, Teirstein A. Sarcoidosis. N Engl J Med. 2007;357:2153-2165. 2. Karnchanasorn R, Salkonda M, Aldasoqi S, et al. Severe Hypercalcemia and Acute Renal Failure: An Unusual Presentation of Sarcoidosis. Case Reports in Medicine. 2010:423659.
14. Transarterial Chemoembolization (TACE) Associated Pancreatitis and Gastric Ulceration Kamel Gharaibeh, MD; Sumanth Daram, MD; Kenneth Ball, MD; Roland Garretson, MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Kamel Gharaibeh, MD, PGY-1, Department of Medicine, University of Mississippi Medical Center (kgharaibeh@umc.edu). Introduction Transcatheter arterial chemoembolization (TACE) is an established modality for treatment of unresectable hepatocellular carcinoma (HCC). Common complications after TACE are post-embolization syndrome (fever, abdominal pain, nausea, vomiting) and transient impairment of liver and kidney functions. Rarely, ischemic damage involving extra-hepatic organs may occur. This may take the form of gastrointestinal tract ulceration, acute cholecystitis, and acute pancreatitis. We present a very rare case of acute pancreatitis and ischemic gastric ulceration developing after TACE in a patient with HCC.
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Case Description A 69-year-old man with HCC and cirrhosis secondary to chronic hepatitis C was admitted to the hospital for severe abdominal pain a few hours after TACE of the left hepatic artery. He had previously undergone an uneventful TACE of the right hepatic artery a few months prior. After admission to the hospital, he was noted to have melena and acute blood loss anemia along with pre-renal azotemia. CT scan of the abdomen and pelvis revealed changes consistent with acute pancreatitis and duodenitis. An elevated serum lipase level corroborated the CT findings. An upper GI endoscopy performed 2 days later revealed multiple gastric and duodenal ulcers of ischemic etiology. Our patient was managed conservatively and was discharged home in a few days. Discussion To our knowledge, this is the first case of a patient developing two ischemic complications secondary to TACE. Selective catheterization of the tumor vessels is the established standard in TACE. Ischemia is important in the development of acute pancreatitis and GI tract ulcers. The proposed mechanism of these complications is inadvertent embolization through collateral vessels or regurgitation of chemotherapeutic agents to the arteries of other organs To prevent these complications, the catheter tip should be placed as close to the distal branches of the hepatic artery as possible, although a highly selective procedure may not be possible in all patients. Treatment of GI tract ulcers and acute pancreatitis in this setting is not different from what could have been for other etiologies.
15. Flail Chest: New Treatment for a Paradoxical Problem Janelle Bennett, MD; Bavin Dalal, MD
All authors affiliated with the Department of Medicine, University of Mississippi Medical Center. Corresponding author: Janelle Bennett, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center ( jabennett3@umc.edu). Introduction Flail chest is the paradoxical movement of a segment of the chest wall caused by fractures of 3 or more ribs.1 In flail chest, acute respiratory distress is commonly observed from the increased work in breathing often necessitating intravenous analgesia, supplemental oxygen, and mechanical ventilation for hypoxemic or hypercapneic respiratory failure.2 Reported cases of the use of noninvasive ventilation for management of flail chest is limited. Here we report a case of acute respiratory distress due to flail chest that we successfully managed with noninvasive bilevel positive airway pressure (BiPAP) ventilation. Case Description An 89-year-old white male with hypertension, coronary artery disease, and previous stroke presented to the emergency department with progressive worsening of shortness of breath for one week following a recent fall. He was unable to complete full sentences without pausing and complained of pain over his left thorax. He was afebrile and normotensive. Oxygen saturation was 97% on 100% non-rebreather. Physical exam revealed paradoxical chest movement over his left lower thoracic region. CT of his thorax displayed lung contusions and fractures involving the 6th, 7th, 8th, and 9th left ribs. Initial arterial blood gas revealed a pH of 7.28, pCO2 46 and pO2 71 on 2LPM O2. Repeat arterial blood gas after two hours showed worsening hypercapnea with a pH of 7.16 and PCO2 of 68. Non-invasive ventilation (BiPAP 15/5 with FiO2 30%) was initiated, and after two hours his arterial blood gas improved (pH 7.340, pCO2 38, and pO2 85). Pain control was achieved with intravenous narcotics. The patient’s respiratory status continued to improve, and he was successfully weaned to 2L nasal cannula over the next 12-16 hours. He was transferred from the ICU to the general medical ward the following day and discharged from the hospital shortly thereafter. Discussion Only one prior case report has described an adult patient receiving BiPAP for flail chest.3 The use of non-invasive ventilation, such as CPAP, in patients with hypoxic respiratory failure lowers mortality rate and reduces nosocomial infections with a similar length of ICU stay, compared to invasive positive pressure ventilation.4 In our patient, the use of BiPAP provided pneumatic stabilization. After ensuring adequate pain control, we were able to wean BiPAP successfully, and the patient was discharged promptly from the hospital. References 1. Duff JH, Goldstein M, McLean AP, et al. Flail chest: a clinical review and physiological study. J Trauma. 1968;8:63–74. 2. Craven KD, Oppenheimer L, Wood LD. Effects of contusion and flail chest on pulmonary perfusion and oxygen exchange. J Appl Physiol. 1979;47:729. 3. Abisheganaden J, Chee CBE, Wang YT. Use of bilevel positive airway pressure ventilatory support for pathological flail chest complicating multiple myeloma. Eur Respir J. 1998;12:238–239. 4. Gunduz M, Unlugenc H, Ozalevli M, et al. A comparative study of CPAP and IPPV in patients with flail chest. Emerg Med. 2005;22(5):325-329.
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16. Acute CVA in the Setting of Graves’ Thyrotoxicosis and Moyamoya: A Rare Combination Janelle Bennett, MD; Sarah French, MD; Shema R Ahmad MD All authors affiliated with the Department of Medicine, University of Mississippi Medical Center, Corresponding author: Janelle Bennett, MD, PGY-2, Department of Medicine, University of Mississippi Medical Center ( jabennett3@umc.edu). Introduction Graves’ disease is the most prevalent autoimmune disorder in the United States.1 The association between Graves’ disease and stroke is well established; however, its pathophysiology is controversial.2-7 Moyamoya disease is a rare cerebrovascular disorder characterized by stenosis or occlusion of the terminal portions of bilateral internal carotid arteries. Stenosis or occlusion may progress to the proximal portion of the anterior or middle cerebral arteries to be accompanied by the formation of net-like collateral vessels.8,9 Here we report an acute cerebral infarction in a patient with Graves’ thyrotoxicosis and Moyamoya disease. Case Description A 29-year-old African-American female with a history of bilateral carotid stenosis and right MCA infarction three months prior with no residual neurologic deficits presented with a five-hour history of left-sided weakness. On initial examination, left facial weakness, dysarthria, a flaccid left upper extremity, decreased left lower extremity strength, and a positive Babinski’s sign were noted. She also had tachycardia, lid lag, a diffuse goiter, and onycholysis. CT of her head showed a hypodensity in the right frontal lobe compatible with remote infarction. CT angiogram showed significant narrowing and irregularity of bilateral supraclinoid carotid arteries, bilateral MCA, and bilateral ACA arteries (more severe on right) as well as extensive medial and lateral lenticulostriate collaterals bilaterally. Cerebral arteriogram supported angiographic findings. Laboratory work-up was significant for TSH 0.005 IU/mL (range 0.27-4.20 IU/mL), free T4 greater than 6.5 ng/dL (0.93-1.70 ng/dL), and anti-thyroid peroxidase antibody 409 IU/mL (0-5.6 IU/mL). On thyroid ultrasound, the gland was diffusely enlarged and heterogenous with a micronodular pattern and increased blood flow throughout. No discrete nodules or masses were identified. The patient was treated with aspirin and dipyridamole. She also received methimazole 30mg twice daily, Lugol solution, and propranolol for her hyperthyroid state. Neurosurgery plans for Encephalo-Duro-Arterio Synangiosis (EDAS) after discharge. Discussion Case reports of concurrent Graves’ disease and Moyamoya are limited. The combination of both diseases may certainly intensify susceptibility to cerebral ischemia. In published cases, the thyrotoxic state was usually treated with thyroid medications (rather than radioablation) while the cerebral artery stenosis of Moymoya was treated by Encephalo-Duro-Arterio Synangiosis (EDAS) or encephalomyosynangiosis (EMS).10 One reported case of concurrent Moyamoya and Graves’ disease was successfully treated with steroids and plasmapharesis with no neurosurgical intervention necessary.11 With the increasing recognition of concurrent Moyamoya and Graves’ disease, cerebral angiography should be considered in a patient with focal neurologic symptoms and Graves’ disease. References 1.
Jacobson DL, Gange SJ, Rose NR, et al. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol. 1997;84:223-243.
2.
Fazekas JF, Graves FB, Alman RW. The Influence of the Thyroid on Cerebral Metabolism. Endocrinology. 1951;48:169-174.
3.
Liu JS, Juo SH, Chen WH, et al. A case of Graves’ disease associated with intracranial Moyamoya vessels and tubular stenosis of extracranial internal carotid arteries. J Formos Med Assoc. 1994;93:806-809.
4.
Ni J, Gao S, Cui LY, et al. Intracranial arterial occlusive lesion in patients with Graves’ disease. Chin Med Sci J. 2006;21:140-144.
5.
Colleran KM, Ratliff DM, Burge MR. Potential association of thyrotoxicosis with vit B and folate deficiencies, resulting in risk for hyperhomocystinemia and subsequent thromboembolic events. Endocr Pract. 2003;9:290-295.
6.
Iso H, Moriyama Y, Sato S, et al. Serum total homocysteine concentrations and risk of stroke and its subtypes in Japanese. Circulation. 2004;109:2766-2772.
7.
Siegert CE, Smelt AH, de Bruin TS. Superior sagittal sinus thrombosis and thyrotoxicosis. Possible association in two cases. Stroke. 1995:26:496-497.
8.
Suzuki J, Takaku A. Cerebrovascular “Moyamoya” disease. Disease showing abnormal net-like vessels in the base of the brain. Arch Neurol. 1969;20:288-299.
9.
Burke GM, Burke AM, Sherma AK, et al. Moyamoya disease: a summary. Neurosurg Focus. 2009;26(4):e11.
10. Malik S, Russman A, Katramdos A, et al. Moyamoya syndrome associated with Graves’ Disease: a case report and review of the literature. J Stroke Cerebrovasc Dis. 2010;12:1-9. 11. Utku U, Asil T, Celik Y, et al. Reversible MR angiographic findings in a patient with autoimmune Graves’ disease. Am J Neuroradiol. 2004;25:1541-1543.
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• MSDH • Mississippi Reportable Disease Statistics
September 2012 Figures for the current month are provisional
Totals include reports from the Department of Corrections and those not reported from a specific District. For the most current MMR figures, visit the Mississippi State Department of Health website: www.HealthyMS.com.
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A Good Death
H
ere is a tale of two patients. The first patient was a 75year-old diabetic who had hypertension. She had both legs amputated above her knees. She was on dialysis because of end-stage renal disease and was sent to the emergency department because she had both a low heart rate and a low blood pressure. She was not mentating very well and would answer only a few simple questions. Her Steven L. Demetropoulos, MD heart rate was in the low forties, and her blood pressure was eighty systolic. 2012-13 MSMA President It looked like she was in a third degree heart block. When the family arrived, we talked to them about her code status. They wanted her to be a full code. I explained to them that this could mean intubating the patient and breathing for her on the respirator as well as giving her medications to keep her blood pressure elevated and possibly even a pacemaker. I explained to them that these measures probably would not change the course of her chronic illnesses at all. The family was still adamant that she was to be a full code. She did have increased respiratory depression. She was intubated and placed on a respirator. She was admitted to the intensive care unit and a temporary pacemaker placed, but she died about three days later alone, paralyzed, and on a respirator. It was after visiting hours in ICU, and no one was with her. The second patient was a patient who was diagnosed with acute leukemia. He went into the hospital for one month for chemotherapy to see if he would go into remission. The remission failed. He was given a ten or fifteen percent chance to have some other type chemotherapy that could possibly prolong his life a little bit. He chose to come home to his family. He was put on hospice and spent a week surrounded by his family and then died with all the family members present at his home. So what is the difference in the two deaths? One death you could see as being a more dignified and peaceful passage into death. There was a sense of closure and an ability to say goodbye. The other death was a death in which a person was alone. It was filled with more painful procedures, needle sticks, tubes, and all these things that really reduce the dignity of a person. Somehow as a country we are going to have to come to grips with our end-of-life issues. We spend an inordinate amount of the whole entire Medicare budget in the last thirty days of a person’s life. That time is often spent in a hospital instead of at home with friends or family. It is often an undignified experience with tubes in every orifice, and oftentimes the patient is connected to ventilators and unable to either speak or know. If patients had the choice to understand what the end of their life would look like, they certainly wouldn’t choose a more painful, undignified exit from this life. But on a regular basis, as an emergency physician, I see family members making decisions about their loved ones that are more reflective of what they want rather than what the patient wants. They oftentimes want to keep momma or daddy alive at any cost despite the fact that they have chronic debilitating diseases with very poor quality of life. So what can we do as physicians? (1)
First of all we can talk to our patients and make sure that we know what their desires and wishes are before they get to the point where they become debilitated or unable to make a decision. We can make sure that discussion takes place with their family members as well so that they understand the kind of experience the patient wants to have at the end of their life.
(2)
We can make sure that they sign the appropriate documents— the DNR orders or the living will and make sure that everything that patient wants done at the end of life is specified so there is no question as to the extent of medical treatment they desire.
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We can do a better job of promoting the hospice and palliative care services, and let people know that this is a way in which patients can stay at home; that they can be made comfortable; their anxiety can be allayed, and they can be in a familiar place; and they can spend as much time with their family and friends as possible.
(3)
Death doesn’t have to be something that is avoided or denied or ignored but can once again be something that is sacred, that is part of every life, that is filled with dignity, that honors the person and is one which we would call a good death.
J
ust what the doctor ordered
SPINACH & MUSHROOM RISOTTO
After providing recipes for several salads, I’ll progress to a dish that can be served as a side or a main course. This month’s recipe is a mushroom and spinach risotto. I usually start out with one small onion, add a teaspoon of garlic, and sauté together in olive oil. Add one box of mushrooms (I prefer the Portobello mushrooms). Then I use one cup of Arborio rice to three cups of chicken broth. Gradually add the chicken broth as you cook the rice. It cooks, over about a 20-minute period of time, until the liquid is all gone. About three or four minutes before the liquid is gone, I add my spinach. I usually use two packages because we like a lot of spinach in our dish. Add the spinach, and let it sauté down. Just before the risotto is ready, I add about one cup of Parmesan cheese. The spices I generally add are one tablespoon of ground basil and one teaspoon of oregano and salt and pepper to taste. This makes a great vegetarian meal or you can throw in some shrimp about three minutes before it is done to make a great shrimp risotto. As well, you can serve it as a side with sausage or steak. For variation, you could replace the mushrooms and spinach with butternut squash or asparagus. Bon appetit!
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374 JOURNAL MSMA NOVEMBER 2012
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• Scientific Article • The two “tales” shared in the preceding President’s Page, “A Good Death,” are familiar to all of us and reflect daily experiences for some of us. As the survival curve for Americans has shifted to the right and the majority of deaths are now associated with chronic rather than acute disease, planning for death has become as logical as planning for life’s other transitions. As the author says, “Death is a part of life.” The frustrations and concerns expressed by health care providers at every level come through in this editorial. There are also suggestions that we as physicians have a missing skill set in dealing with end-of-life issues. The President’s Page by Dr. Steve Demetropoulos (p. 371) is a perfect introduction to a series of articles by Sharon Douglas, MD and colleagues from UMMC and the Sonny Montgomery VA Medical Center on end-of-life medicine in the Journal MSMA, the first of which begins here. Dr. Douglas, a Mississippian and pulmonary/critical care specialist, serves on the Department of Veterans Affairs National Ethics Advisory Commission and is immediate past chair of the American Medical Association’s Council on Ethical and Judicial Affairs. These articles will help us better navigate through the issues of appropriate medical care, advanced directives, end-of-life counseling, ethical decision making, and the stress we all experience as we work through end of life care with our patients, our families, and ourselves. There is a knowledge and data base that has developed over the last two decades that addresses the issues raised in this editorial in a practical way. We are not alone in assisting our patients in their search for “a good death.” —Richard D. deShazo, MD, Associate Editor
Series: Concepts in End of Life Care Introduction - Death: An Important Part of Life Rachael W. Faught, DO; Sarah M. Gaugler, DO and Sharon P. Douglas, MD
“To everything there is a season, and a time to every purpose under the heaven: a time to be born, and a time to die...” Ecclesiastes 3:1-2 Introduction Americans expect their physicians to be competent to care for them at end-of-life.1 A landmark study in 1995 on endof-life care decision making revealed severe deficiencies in this area.2 Since that time, end-of life care focused studies have led to a rapid evolution of thought, skill, standards of care, and increasing competence in this area. For instance, physicians must recognize that dying is part of life. During this critical time of life, the dying part, patients want physicians’ presence more than ever. This article will review key points on caring for dying patients. To follow in the series will be articles on specific topics regarding end-of-life care of patients, including Author Information: Internal Medicine Resident, University of Mississippi Medical Center (Dr. Faught and Dr. Gaugler). Pulmonary Physician, Professor of Medicine, Department of Medicine, University of Mississippi Medical Center (Dr. Douglas). Corresponding Author: Sharon P. Douglas, MD, G.V. (Sonny) Montgomery VA Medical Center, 1500 East Woodrow Wilson Avenue Jackson, MS 39216 Phone: (601) 364-1355 (spdouglas@umc.edu).
palliative care, Do Not Resuscitate (DNR), advance directives, and bereavement. Average life expectancy in the early 1900s was 50 years. Death typically came quickly, often as a result of infectious diseases or accidents.1 Today nearly half of the deaths in the United States, accounting for all age groups, are caused by heart disease (25%) and cancer (23%). Almost three quarters of all deaths occur among persons aged 65 years or older, but 29% of deaths now occur over the age of 85. Common causes of death vary according to age group. The majority of child mortality (1-19 yrs) is caused by unintentional injuries. In contrast, chronic diseases account for five of the six leading causes of death between the age of 45 and 64.3
Mississippi Department of Health Data Death, as defined by the Mississippi State Health Department, is either “(a) irreversible cessation of circulatory and respiratory functions or (b) irreversible cessation of all functions of the entire brain, including the brain stem.” 4
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The Mississippi State Department of Health Vital Statistics Report for 2010 reported a total of 28,950 deaths in Mississippi, averaging 79 deaths per day. Of the nearly 29,000 deaths, 19,730 were Caucasian and 9,220 were non-white. Persons 75 years of age and older had the highest contribution to the death rate with 13,983 deaths. The incidence of death was equal between men and women. Consistent with nationally reported data, the two leading causes of death in Mississippi are heart disease (26.1%) and malignant neoplasms (21.6%). Accidents, although contributing significantly fewer deaths (5.8%), remain the third most common cause of death in the state.4
Physicians’ Roles in Death and Dying Pronouncing death has long been the responsibility of the physician. Although no formal protocol exists for pronouncing death, there is consensus that it should involve (1) identifying the patient, (2) performing an examination to assess response to stimuli, spontaneous respirations, heart sounds, pulses, pupillary response, and (3) the pronouncement and documentation of death and time of death.5 While the pronouncement of death once mastered is relatively straightforward, the complexity of end-of-life care is often underestimated. Our roles as physicians entail providing the best quality of life possible for our patients. What is less emphasized, yet equally important, is that we also provide quality healthcare during the process of dying. It is difficult to define what constitutes a “good death.” Hales et al6 reviewed research on the quality of death and dying. The conclusion of their review is that a good quality death is multidimensional and very subjective. Factors influencing a patient’s perception of death and dying include cultural background, religious beliefs, type and stage of disease. Patrick, et al7 studied improving the quality of death and dying. They emphasized controlling pain and symptoms, providing an at-home death, and effective communication. Unfortunately, dying at home is not achieved in a majority of patients. Preparing for an at home death is facilitated in patients with chronic and progressive disease processes that will likely cause their death. As a patient becomes terminally ill, relief of pain and suffering become increasingly important and can outweigh the benefits of treating the illness itself. When asked, terminally ill patients have also suggested that other important aspects of the dying process include having a designated decision maker, knowing what to expect about physical condition, maintaining dignity, having someone who will listen, being able to say goodbyes, and having one’s financial affairs in order. Other psychosocial and spiritual aspects are important as well.8 The patient’s goals for care are the priority, as psychosocial, emotional, and spiritual goals may be as important as physical needs.9 Such goals may include saying goodbyes, financial planning, unresolved business, personal death planning, personal reflection, finding spiritual meaning, coming to peace with God, and praying. A multidisciplinary approach to end-of-life care for patients is
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Major Points about Death: ·
Death is an important part of life and patients want their physician present during this time.
·
The two leading causes of death in Mississippi and the nation are cardiovascular disease and cancer.
·
Death does not just happen to the patient. It also happens to the patient’s community.
·
The definition of a good death, or a death with quality, is individualized to the patient. The patient’s wishes should be important to the physician and the health care team.
·
Suffering is not limited to the physical but also includes social, emotional, and spiritual components.
· Physician self-awareness and venue for personal debriefing about death and dying is imperative.
· Ministering to patients and their families at the end-of-life is a powerful experience. Physicians should not take this duty lightly.
· A health care team approach to end-of-life care for patients and families is important.
· Proficient skills for end-of-life care are important for physicians.
· Managing death well can be very fulfilling for physicians and health care teams.
often needed to address these goals. Clergy, social workers, palliative care providers, nurses, volunteers, and others can be helpful to patient and family. Early and effective communication is a cornerstone in facilitating a good death for a patient and for their loved ones. Such communication should include symptom expectation, knowledge of disease progression, and patient wishes as they approach death. Physicians should be willing listeners. This can help in providing adequate palliation and will also aid in providing an at-home death for appropriate patients. Communication is also crucial to patient and family satisfaction. A patient’s perception of a good quality death will be influenced by how well they feel a physician listened and understood their goals of care. There is no one set definition of a “good death.” The goals of care for the dying patient must be individualized and end-of-life care is a dynamic process best negotiated among patient, family, and the health care team.8
Dealing with Death Most physicians enter the medical profession with focus on healing, and ideally that is what they wish to do. However, physicians must understand that the death of a patient should not be considered as a personal defeat. Some of the most fulfilling experiences physicians can have may be caring for the dying and their families. It is a powerful place to be, an awesome privilege. In this role there is often much more gratitude from those so served than from those cured. Care of dying patients has a moral, psychological, and interpersonal intensity that distinguishes it from other areas of medical care.10 It is normal for physicians to be moved by the deaths of patients. It is also important to be introspective and aware of personal attitudes, feelings, and expectations regarding death as we process these experiences. Many physicians experience stress, sadness, and guilt caused by caring for dying patients. Maladaptive coping mechanisms may lead to burn out and other forms of emotional distress.11 Physicians need a safe venue to debrief about their own emotions related to death so that they can develop appropriate coping mechanisms. Such a safe environment may be as simple as discussion with a trusted colleague or a senior physician. In the case of physicians in training, the training program should support a safe environment for physicians-intraining to debrief and obtain emotional support. Senior or attending physicians should teach and model both excellent
patient care and appropriate self care in managing dying patients as wisdom of experience can be invaluable to younger physicians in any healthcare setting. Self care can include good health care for oneself, opportunities for relaxation, exercise, interests outside of medicine, spiritual reflection, and fellowship with family and friends. Pride must not keep physicians from seeking or receiving emotional support related to caring for dying patients.
Education on End-of-life Care Issues surrounding death and dying are some of the most challenging for patients, their families, and also for physicians. Physicians must have the courage, character, and medical expertise to engage and communicate well with patients and their families as there is no time that medical guidance and support are needed more. Providing aggressive palliative care and comfort measures can often be as important as, or even more important at times than, life-extending procedures and therapies. Since the SUPPORT study2 in 1995 revealed shortcomings in end-of-life care, medical schools and residency programs have increased education on end-of-life care. It will be increasingly important as America’s population ages for physicians to have proficient end-of-life skills. We hope to provide skill sets in this series of articles that will be mutually beneficial to patients and physicians.
“to cure sometime, to relieve often, to comfort always” —Edward Livingston Trudeau
References 1.
EPEC Project Web Site. Available at: http://epec.net. Accessed June 26, 2012.
2.
SUPPORT Investigators: A controlled trial to improve care for seriously ill hospitalized patients. JAMA 1995;274:1591-1598.
3.
National Center for Health Statistics (US). Health, United States, 2010: With Special Feature on Death and Dying. Hyattsville (MD): National Center for Health Statistics (US); 2011 Feb. http://www.ncbi.nlm.nih. gov/books/NBK54374/. Accessed June 26, 2012.
4.
http://msdh.ms.gov/phs/stat2010.htm. Accessed July 9, 2012.
5.
Ferri FF. Practical guide to the care of the medical patient. eighth edition. 2011 Mosby, Inc. Chapter 1, B, 10.
6.
Hales, S, Zimmerman, C, Rodin, G. The Quality of Dying and Death. Arch Intern Med. 2008; 168(9):912-918.
7.
Patrick, D, Curtis, R, Engelberg, R, Neilsen, E, McCown, E. Measuring and Improving the Quality of Dying and Death. Ann Intern Med. 2003; 139:410-415.
8.
Steinhauser KE, Christakis NA, Clipp EC, McNeilly M, McIntyre L, Tulsky JA. Factors Considered Important at the End-of-life by Patients, Family, Physicians, and other Care Providers. JAMA. 2000; 284(19):247682.
9.
Bailey FA. The Palliative Response. Menasha Ridge Press. 2005:4.
10. Snyder, L. American College of Physicians Ethics Manual. 6th ed. Ann Intern Med. 2012;156(1):73-104. 11. Redinbaugh EM, Sullivan AM, Block SD, et al. Doctors’ emotional reactions to recent death of a patient: cross sectional study of hospital doctors. BMJ. 2003;327(7408):185.
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• Editorial • An Interview with Dr. Randy Easterling, President, Mississippi State Board of Medical Licensure Richard D. deShazo, MD, Associate Editor
W
e understand you are a Mississippi native. Can you tell us how you came to be a physician and a family medicine doctor?
I had always been interested in medicine growing up. I was a master’s level counselor at the Gulf Coast Mental Health Center in 1976 and 1977. While serving in that role, I saw that physicians seem to play a central role in the treatment of all patients. At that point, I decided to go to medical school. While in medical school, I did my family medicine rotation with Dr. Walter Rose in Indianola. I found his practice and the specialty of family medicine fascinating. That was certainly a driving force that led me into family medicine. You have served many roles in the MSMA, and we are aware of your service there. How did you end up on the Mississippi State Board of Medical Licensure? What is your role there? I have always been interested in the role the licensure board plays in our state. In 2006, I asked Governor Haley Barbour to appoint me to an opening on the board. He was kind enough to do so. Governor Phil Bryant reappointed me in 2012. The appointments are for 6-year terms. I have served on the executive committee of the board for the last four and half years and became president of the board four months ago. You have received a lot of public attention recently concerning problems with opiate overuse and abuse in the state. How did you get interested in this area? I am a Diplomate with the American Board of Addiction Medicine and have practiced addiction medicine along with family medicine for the last 25 years. While serving on the licensure board, we have seen a dramatic increase in the number of physicians prescribing opioids for non-malignant pain. This has also become a national epidemic. I have seen a dramatic increase in the last number of years in admissions to my chemical dependency unit for opioid addiction. Two years ago, almost all adults admitted were for cocaine and alcohol addiction. Now, that has changed, and significant numbers admitted are for prescription opioid addiction. As we understand it, it is your opinion that there are concerns on both the physician and patient side of our problem with opiates. Could you fill us in on that? Presently, we are in the midst of an opioid addiction epidemic. Ninety-nine percent of all the hydrocodone written in the world is written in the United States. (Do Americans have 99% of the pain in the world?) Hydrocodone is the most commonly prescribed drug in America. There is enough hydrocodone prescribed in the United States annually to give every man, woman, and child 5 mg of hydrocodone every 4 hours for 30 days. The problem is we have too many physicians prescribing opioids for chronic non-malignant pain and too many patients taking them, selling them, and diverting them. You have been quoted in the newspaper as saying there is no indication for opioids other than for pain associated with cancer. How did you reach that conclusion, and on what scientific data is it based? It is important to point out that there is very little evidence, if any, for long-term effectiveness in treating chronic nonmalignant pain with opioids. The fundamental question is where is the scientific data that using short-term opioids for chronic non-malignant pain is effective? We all know that the potential for harm is significant. Sixty-six percent of all patients in the United States that take opioids for 90 days are taking opioids 5 years later. There is also evidence that use of opioids for as little as several months on a continuous basis might create opioid induced hyperalgesia. This is a condition where pain paradoxically worsens as opioid doses increase. This condition results from a hypersensitivity of nerve receptors and actually makes pain worse as an individual increases their opioid consumption. Purdue Pharmacy promulgated the idea that chronic non-malignant pain should be treated with opioids over a decade ago. Interesting enough, Purdue Pharmacy is one of the prime producers of hydrocodone.
378 JOURNAL MSMA NOVEMBER 2012
If there are physicians in the state who are abusing opiates, what is the Board of Medical Licensures process for stopping their ability to prescribe opiates? The Mississippi State Board of Medical Licensure has a number of well-qualified investigators. When a complaint is filed with the board, we begin an investigation that may well take months, if not years. We collect information, work with the DEA, and the Mississippi Bureau of Narcotics, and create a case against the physician. The case is then presented to the executive committee, and we call the physician in and take appropriate action. This may well result in a hearing which could result in the physician’s license being revoked and/or suspended. Is the board aware of physicians who are contributing to this problem, yet have not yet received appropriate disciplinary action for that? Yes, each physician has the same rights that every other citizen has in the United States. For us to take action, we should, and do, build a case documenting inappropriate prescribing. As I said, this may take months, if not as long as a year. We do not call physicians in on a whim; there must be a preponderance of evidence that they are overprescribing. What are your thoughts about chronic pain management for patients with chronic rheumatic and orthopedic problems? What non-opiate approaches do you think are best? Is there a consensus among the board about pain management? Do experts in this area consult the board? In terms of dealing with chronic rheumatic and orthopedic problems, there are a number of medications available prior to prescribing opiates. 1) Nonsteroidal anti-inflammatory medicines can be highly effective. 2) The Neurontin and Lyrica medications also have been found to be effective. One can also use Cymbalta, Ultram, and Toradol. As with any medication, all of these should be used in appropriate dosage and combinations and in response to the individual patient’s chronic pain situation. In terms of a consensus among the licensure board about pain management, there is a general feeling that there are too many physicians writing opioids for chronic non-malignant pain. There is not a total agreement by board members as how to handle this problem, but it is an issue that we are grappling with on a daily basis. The board has certainly consulted with experts in the area of pain management. Is there a relationship between the Board of Licensure and the Board of Pharmacy? If so, how does this affect your thought process and plan for management of opiate use? There is an ongoing relationship with the Board of Medical Licensure and the Pharmacy Board. There has been an advisory committee formed that represents medicine, nursing, pharmacy, law enforcement, the licensure board, the nursing board, etc. This advisory committee has met on several occasions in order to advise the pharmacy board about the Prescription Monitoring Program. This is an ongoing effort and a work in progress. Pharmacists in the state see this as a problem as do we physicians. There is a commitment on their part to work with physicians to try to alleviate this epidemic. How do you manage patients with chronic pain in your medical practice? What suggestions would you give to other primary care physicians who frequently see these folks? I have a small number of chronic pain patients in my practice. As mentioned above, I use nonsteroidal antiinflammatories, Neurontin, Lyrica, Cymbalta, and other treatment modalities. I also use a combination of the above. There are rare occasions, in my opinion, where long-acting opioids may be used for chronic orthopedic and rheumatic pain, but these should be used very judiciously and in very specific patients. The suggestion that I would give other primary care physicians in terms of treating chronic pain is very simple. Realize that these medications are very addictive, and the risk may well outweigh the benefits. Find a good pain management physician and use them as consultants as we do cardiologists, gastroenterologists, etc. Simply be aware that these medications are very powerful and often times can cause more harm than good. r
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NOVEMBER 2012 JOURNAL MSMA 379
• Top 10 Facts You Should Know • About Secondary Causes of Diabetes Mellitus Honey E. East, MD; Jose S. Subauste, MD; Ayush Gandhi, MD and Christian A. Koch, MD [We see so much obesity induced diabetes in Mississippi that we have to remind ourselves that there are other causes and look for them when appropriate. Dr. East and her colleagues have done a good job bringing us up-to-date on secondary causes of diabetes and refreshing our memories on this important topic.] —Richard D. deShazo, Associate Editor
Introduction Endocrinopathies or medications may alter beta cell function (insulin secretion), insulin sensitivity, and body weight/ composition to cause secondary diabetes. In some cases, these alterations are self-inflicted, for instance in hormone abuse in the setting of anti-aging therapies with growth hormone (GH), testosterone, dehydroepiandrosterone (DHEA) or doping.1 Endocrinopathies associated with secondary diabetes include disorders of the pituitary, thyroid, or adrenal gland, and/or (gastroenteropancreatic) neuroendocrine tumors.2 Endocrine disruptive chemicals have also been implicated in promoting the development of diabetes mellitus.3 Medications associated with inciting diabetes mellitus may affect glycemic control by effects on beta cell function (amount of insulin secretion), insulin resistance at sites of insulin action, i.e. liver, muscle, fat, or body composition (muscle, bone, fat).
1. Acromegaly The prevalence of acromegaly has been estimated to be 480 per one million adults.4 It is diagnosed using tests to demonstrate insuppressible GH production The prevalence of diabetes mellitus in acromegalic patients with GH excess and elevated insulin-like growth factor-1 (IGF-1) levels ranges from 19% to 56% in different series, depending on family history of diabetes, aging and changes in body composition, and acromegaly disease duration.5,6 GH increases gluconeogenesis, lipolysis, free fatty acid levels, and insulin resistance in the liver as well as in peripheral tissues. IGF-1 on the other hand, enhances sensitivity to insulin in skeletal muscle.7 Cardiovascular risk in patients with insulin resistance, impaired glucose tolerance, and diabetes mellitus secondary to GH excess normally improves upon normalization of GH and (sex- and age- matched) IGF-1, levels achieved by transsphenoidal surgery, radiation, and/or medical therapy.8 Somatostatin analogues (SSAs) used for medical treatment of acromegaly (and other pituitary disorders including Cushing’s disease) exert different hormonal effects on blood glucose levels including inhibition of insulin secretion. In case of overt hyperglycemia during SSA therapy, insulin is preferred over insulin sensitizers. Regular monitoring of blood glucose levels and glycemic control in acromegalic patients post-pituitary surgery are recommended even in presurgical normoglycemics.9 380 JOURNAL MSMA NOVEMBER 2012
2. Growth hormone deficiency (GHD) has many etiolo-
gies and is primarily related to disorders of the pituitary. Congenital factors include genetic abnormalities such as transcription factor defects (Pit-1, Prop-1, LHX3/4, HESX-1, PITX-2), GH gene defects, GH receptor/post receptor defects, brain structural abnormalities, and midline facial defects. Acquired factors for GHD include pituitary and sellar/suprasellar tumors, pituitary infarction, surgical and nonsurgical trauma, cranial irradiation, central nervous system infection, and others. The diagnosis of GHD includes a GH stimulation test and measuring an IGF-1 level. IGF-1 levels should be sex-and age-matched, as GH and IGF-1 levels decrease with ageing. Adults with lifetime, untreated isolated GHD have reduced beta cell function and a higher frequency of impaired glucose tolerance. The metabolic syndrome is highly prevalent in patients with GHD and may contribute to the increased risk of cardiovascular morbidity and mortality observed in these subjects.10,11 IGF-1 levels appear to be consistenly reduced in subjects with the metabolic syndrome. On the other hand, GH replacement therapy in older GH deficient patients with higher waist circumference may lead to a higher incidence of diabetes mellitus compared to GH deficient younger patients on GH replacement.12
3. Cushing’s Syndrome (CS) is primarily associated
with exogenous glucocorticoid excess (inhaled, topical, oral, parenteral). Endogenous etiologies include ACTH-secreting pituitary lesions, neuroendocrine tumors with ectopic ACTH or CRH secretion, and adrenal tumors secreting excessive glucocorticoids.13 The prevalence of diabetes mellitus in patients with CS varies between 20% and 50%.14 On the other hand, screening obese patients for the presence of CS is not cost effective, as the prevalence of CS in such patients is less than 3%. 2,15 Chronic hypercortisolemia causes central obesity, hypertension, insulin resistance, diabetes mellitus, dyslipidemia, and a prothrombotic state, manifestations of the metabolic syndrome present in most patients with CS. Mortality and morbidity in patients with CS are related to blood pressure and glycemic control.16 Achieving eucortisolemia or blocking the action of cortisol / glucocorticoids at the receptor level help improve glycemic and blood pressure control. In patients with Cushing’s disease, the first line therapy usually consists of removal of the
responsible pituitary adenoma by transsphenoidal adenomectomy.17 Medical therapies include steroidogenesis inhibitors (ketoconazole, metyrapone, etomidate, mitotane which is also adrenolytic), somatostatin receptor analogs like octreotide18 and pasireotide; and type II glucocorticoid receptor antagonists (i.e. mifepristone). In most patients with newly diagnosed Cushing’s disease, transsphenoidal surgery and resection of an ACTH-oma leads to remission in 70-90% of cases with very low morbidity (perioperative mortality < 1.5%, cerebrospinal fluid leak < 8%, meningitis < 3%, central diabetes insipidus < 9%, epistaxis < 6%, syndrome of inappropriate secretion of antidiuretic hormone < 25%), if performed by an experienced surgeon. However, at 10 years after such surgery, there is a risk of recurrence in up to 30% of patients. Hyperglycemia in patients with CS should be treated with metformin and high dose insulin or insulin analogues.
4. Glucagonoma and Somatostatinomas are neuroen-
docrine tumors (NET). In general, any tumor that acquires the ability to produce and secrete hormones that worsen glycemic control (CRH, ACTH, cortisol, GHRH, GH, catecholamines, glucagon, somatostatin, and others) can induce secondary diabetes. We will limit this section to glucagonoma and somatostatinoma. Patients with abdominal pain who undergo an abdominal CT scan with the discovery of a gastroenteropancreatic NET should be referred to both an endocrine surgeon and an endocrinologist with an expertise in endocrine tumors. Glucagonoma is a rare neuroendocrine tumor of the alpha cells of the pancreas that results in up to a 1000-fold overproduction of the hormone glucagon. Diabetes mellitus occurs in 75 to 95% of patients with glucagonoma.19 Other symptoms include dermatitis (necrolytic migratory erythema), abdominal pain, anorexia, diarrhea, and constipation. Insulin resistance in this condition is controlled by diet, oral agents, or insulin, and is not associated with diabetic ketoacidosis, since beta cell function is preserved and insulin secretion is normal. Glucose intolerance also occurs in up to 75% of patients suffering from a somatostatinoma, a rare neuroendocrine tumor of pancreatic delta cells. It is characterized by the triad of diabetes mellitus, steatorrhea, and gallstones.20 Development of glucose intolerance is due to decreased or inhibited insulin secretion caused by excess of somatostatin. DM in these patients is usually mild and complications can be prevented by diet and oral hypoglycemics, with small doses of insulin in some cases. This tumor has a high malignant potential and early tumor removal is very important for survival.
5. Pheochromocytoma and paraganglioma are NETs of the sympathetic and parasympathetic nervous system. If these tumors secret catecholamines, impaired glucose tolerance can be observed in 25%-75% of patients.21 Development of diabetes associated with pheochromocytoma is thought to be due to decreased insulin secretion. However, hyperinsulinemia due to beta receptor stimulation in patients with pheochromocytoma has also been reported. Insulin sensitivity improves after
removing the tumor / adrenalectomy in patients with adrenal pheochromocytoma.22 Pheochromocytomas are rare and make up approximately 5% of incidentally discovered adrenal tumors. The diagnosis should not be made by an adrenal biopsy but rather clinically and biochemically.
6. Primary aldosteronism is a common cause of endocrine hypertension and has been identified in approximately 11% of patients with resistant hypertension. The prevalence of adrenal masses in Japanese patients with type 2 diabetes mellitus is about 5%.23 Aldosterone may also play a role in the pathogenesis of the metabolic syndrome.24 Type 2 diabetes appears to be more prevalent in patients with primary aldosteronism (23%) than in hypertensives without aldosteronism (10%).25 Activation of the mineralocorticoid receptor can impact insulin sensitivity independent of its effects on blood pressure and treating patients with primary aldosteronism to reduce aldosterone excess has been shown to reduce insulin resistance.26 Incidentally discovered adrenal tumors are now common with modern imaging technologies. To sort out whether such tumors produce and secrete hormones, patients with these tumors should be referred to an endocrinologist and endocrine surgeon and a center that allows performing adrenal vein sampling. 7. Polycystic ovarian syndrome (PCOS) is a heterogeneous disorder with menstrual and metabolic abnormalities due to hormonal imbalance. According to different studies almost 50% of women with PCOS are obese, 45% of women have glucose intolerance, and 10% of women have DM type 2. The underlying pathophysiology is still unclear but it is believed that development of diabetes is mainly due to insulin resistance with body weight and composition representing major factors.27 Metformin is the drug of choice for DM in these women as it reduces insulin resistance and also improves ovulation when used together with clomiphene. 8. Obstructive sleep apnea (OSA) is the most common sleep breathing disorder and has multiple neuroendocrine effects. The likelihood of developing DM in a patient with OSA is approximately 1.62 fold and both share common risk factors such as age and obesity. Secondary DM is due to frequent awakening and apneic phases. This causes frequent sympathetic stimulation and cortisol secretion which leads to glucose intolerance, insulin resistance, and testosterone deficiency. CPAP has been shown to improve insulin resistance and glucose metabolism as well as testosterone deficiency.28, 29 In acromegalics with OSA due to tongue enlargement, treatment is more challenging. 9. Testosterone deficiency Men with metabolic syndrome are more likely to develop hypogonadism and vice versa.29,30 The odds of developing DM in men with low testosterone levels were increased 2.7 fold in recent studies. Testosterone deficiency causes fatigue with muscular atrophy which in turn causes decreased levels of GLUT4 transport and insulin recepNOVEMBER 2012 JOURNAL MSMA 381
tors. Therefore, testosterone deficiency can represent a risk factor for cardiovascular disease. Testosterone replacement therapy usually improves insulin resistance. Testosterone deficiency in men can point to the diagnosis of a pituitary tumor.
10. Medications A long list of drugs can induce diabe-
tes mellitus. These include the atypical antipsychotic agents risperidone, olanzapine, clozapine, and quetiapine;31,32 the calcineurin inhibitors including cyclosporine and tacrolimus (reduced insulin production and secretion, beta cell toxicity);33and highly active antiretroviral therapy which can lead to insulin resistance and lipodystrophy.34
Conclusion Secondary forms of diabetes mellitus are commonly overlooked. They usually occur because of reduced beta cell function and/or increased insulin resistance. In many instances (GH deficiency, glucocorticoid excess, polycystic ovarian syndrome, obstructive sleep apnea, testosterone deficiency, atypical antipsychotic drugs), reduced lean body mass plays a role, although good muscle mass with little fat (in acromegalics or in HAART treated patients) can also lead to impaired glucose tolerance and diabetes mellitus. The challenge remains to identify an underlying endocrinopathy in patients with diabetes mellitus. Disease duration before making a diagnosis of secondary diabetes usually is more than 7 years in diabetics, acromegalics, patients with Cushing’s syndrome, primary aldosteronism, and pheochromocytoma. When clues are present, timely referral to an endocrine subspecialist therefore is critical (Table 1).35 References 1.
Geraci MJ, Cole M, Davis P. New onset diabetes associated with bovine growth hormone and testosterone abuse in a young body builder. Hum Exp Toxicol. 2011;30(12):2007-12.
2.
Fierabracci P, Pinchera A, Martinelli S, Scartabelli G, Salvetti G, Giannetti M, Pucci A, Galli G, Ricco I, Querci G, Rago T, Di Salvo C, Anselmino M, Vitti P, Santini F. Prevalence of endocrine diseases in morbidly obese patients scheduled for bariatric surgery: beyond diabetes. Obes Surg. 2011;21(1):54-60.
3.
Lind PM, Zethelius B, Lind L. Circulating levels of phthalate metabolites are associated with prevalent diabetes in the elderly. Diabetes Care. 2012;(7):19-24.
4.
Rosario PW. Frequency of acromegaly in adults with diabetes or glucose intolerance and estimated prevalence in the general population. Pituitary. 2011;14(3):217-21.
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Colao A, Ferone D, Marzullo P, Lombardi G. Systemic complications of acromegaly: epidemiology, pathogenesis, and management. Endocr Rev. 2004;25:102–152.
6.
Fieffe S, Morange I, Petrossians P, Chanson P, Rohmer V, Cortet C, BorsonChazot F, Brue T, Delemer B; French Acromegaly Registry. Diabetes in acromegaly, prevalence, risk factors, and evolution: data from the French Acromegaly Registry. Eur J Endocrinol. 2011;164(6):877-84.
7.
Møller N, Jørgensen JO. Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects. Endocr Rev. 2009;30(2):152-77.
8.
Jaffrain-Rea ML, Minniti G, Moroni C, Esposito V, Ferretti E, Santoro A, Infusino T, Tamburrano G, Cantore G, Cassone R. Impact of successful transsphenoidal surgery on cardiovascular risk factors in acromegaly. Eur J Endocrinol. 2003;148(2):193-201.
9.
Larijani B, Nakhjavani M, Baradar-Jalili R, Akrami SM, Bandarian F. Diabetes mellitus following pituitary adenomectomy in euglycaemic patients with acromegaly. J Coll Physicians Surg Pak. 2005;15:430–432.
10. Oliveira CR, Salvatori R, Barreto-Filho JA, et al. Insulin sensitivity and β-cell function in adults with lifetime, untreated isolated growth hormone deficiency. J Clin Endocrinol Metab. 2012;97(3):1013-9. 11. Akanji AO, Smith RJ. The insulin-like growth factor system, metabolic syndrome, and cardiovascular disease risk. Metab Syndr Relat Disord. 2012;10(1):3-13. 12. Luger A, Mattsson AF, Koltowska-Häggström M, Thunander M, Góth M, Verhelst J, Abs R. Incidence of diabetes mellitus and evolution of glucose parameters in growth hormone-deficient subjects during growth hormone replacement therapy: a long-term observational study. Diabetes Care. 2012;35(1):57-62.
13. Singer J, Werner F, Koch CA, Bartels M, Aigner T, Lincke T, Fasshauer M, Paschke R. Ectopic Cushing’s Table 1. Clinical Features Suggesting a Secondary Form of Diabetes Mellitus syndrome caused by a well-differentiated Headaches, increasing shoe and ring size, coarsening facial Acromegaly ACTH-secreting features neuroendocrine carcinoma of the ileum. Exp Growth Hormone Deficiency Fatigue, body composition change with increasing fat mass Clin Endocrinol Diabetes. 2010;118(8):524-9.
Cushing’s Syndrome Neuro-endocrine tumors Primary aldosteronism PCOS OSA Testosterone deficiency
Central obesity, moon facies, buffalo hump, purple striae > 1 cm Dermatitis, steatorrhea, HTN, flushing HTN, hypokalemia Menstrual irregularities, infertility, hirsutism Daytime somnolence, obesity, headaches, snoring Erectile dysfunction, decreased libido, fatigue, increasing fat mass
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14. Arnaldi G, Mancini T, Polenta B, Boscaro M. Cardiovascular risk in Cushing’s syndrome. Pituitary. 2004; 7:253–256. 15. Baid SK, Rubino D, Sinaii N, Ramsey S, Frank A, Nieman LK. Specificity of screening tests for Cushing’s syndrome in an overweight and obese population. J Clin Endocrinol
Metab. 2009;94(10):3857-64. 16. Clayton RN et al. Mortality and morbidity in Cushing’s disease over 50 years in Stoke-on-Trent, UK: audit and meta-analysis of literature. J Clin Endocrinol Metab. 2011;96:632-42. 17. Tritos NA, Biller BM, Swearingen B. Management of Cushing’s disease. Nat Rev Endocrinol. 2011;7(5):279-89. 18. Uwaifo GI, Koch CA, Hirshberg B, Chen CC, Hartzband P, Nieman LK, Pacak K. Is there a therapeutic role for octreotide in patients with ectopic Cushing’s syndrome? J Endocrinol Invest. 2003;26(8):710-7. 19. Eldor R, Glaser B, Fraenkel M, Doviner V, Salmon A, Gross DJ. Glucagonoma and the glucagonoma syndrome- cumulative experience with an elusive endocrine tumour. Clin Endocrinol (Oxf). 2011;74(5):593-8. 20. Nesi G, Marcucci T, Rubio CA, Brandi ML, Tonelli F. Somatostatinoma: clinico-pathological features of three cases and literature reviewed. J Gastroenterol Hepatol. 2008;23(4):521-6. 21. Stenström G, Sjöström L, Smith U. Diabetes mellitus in pheochromocytoma: fasting blood glucose levels before and after surgery in 60 patients with pheochromocytoma. Acta Endocrinol (Copenh) 1984;106:511–515. 22. Wiesner TD, Blüher M, Windgassen M, Paschke R. Improvement of insulin sensitivity after adrenalectomy in patients with pheochromocytoma. J Clin Endocrinol Metab. 2003;88(8):3632-6. 23. Hiroi N, Sue M, Yoshihara A, Ichijo T, Yoshida-Hiroi M, Higa M, Yoshino G. Prevalence of adrenal masses in Japanese patients with type 2 diabetes mellitus. Diabetol Metab Syndr. 2010 Dec 20;2:71. 24. Sowers JR, Whaley-Connell A, Epstein M. Narrative review: the emerging clinical implications of the role of aldosterone in the metabolic syndrome and resistant hypertension. Ann Intern Med. 2009 Jun 2;150(11):776-83. 25. Reincke M, Meisinger C, Holle R, Quinkler M, Hahner S, Beuschlein F, Bidlingmaier M, Seissler J, Endres S. Participants of the German Conn’s Registry. Is primary aldosteronism associated with diabetes mellitus?
26. Garg R, Adler GK. Role of mineralocorticoid receptor in insulin resistance. Curr Opin Endocrinol Diabetes Obes. 2012;19(3):168-75. 27. Liang SJ, Liou TH, Lin HW, Hsu CS, Tzeng CR, Hsu MI. Obesity is the predominant predictor of impaired glucose tolerance and metabolic disturbance in polycystic ovary syndrome. Acta Obstet Gynecol Scand. 2012;91(10):1167-72. 28. Lindberg E, Theorell-Haglöw J, Svensson M, Gislason T, Berne C, Janson C. Sleep apnea and glucose metabolism - a long-term follow-up in a community-based sample. Chest. 2012 Apr 12. 29. Ullah MI, Washington T, Kazi M, Tamanna S, Koch CA. Testosterone deficiency as a risk factor for cardiovascular disease. Horm Metab Res. 2011 Mar;43(3):153-64. 30. Singh SK, Goyal R, Pratyush DD. Is hypoandrogenemia a component of metabolic syndrome in males? Exp Clin Endocrinol Diabetes. 2011;119:30-35. 31. De Hert M, Detraux J, van Winkel R, Yu W, Correll CU. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat Rev Endocrinol. 2011 Oct 18;8(2):114-26. 32. Panagiotopoulos C, Ronsley R, Kuzeljevic B, Davidson J. Waist circumference is a sensitive screening tool for assessment of metabolic syndrome risk in children treated with second-generation antipsychotics. Can J Psychiatry. 2012;57(1):34-44. 33. Tillmann FP, Quack I, Schenk A, Grabensee B, Rump LC, Hetzel GR. Prevalence and risk factors of pre-diabetes after renal transplantation: a single-centre cohort study in 200 consecutive patients. Nephrol Dial Transplant. 2012;27(8):3330-7. 34. Gutierrez AD, Balasubramanyam A. Dysregulation of glucose metabolism in HIV patients: epidemiology, mechanisms, and management. Endocrine. 2012;41(1):1-10. 35. Endocrine Hypertension (editors: Koch CA & Chrousos GP), Contemporary Endocrinology Series, Springer, New York, 2013, ISBN: 978-1-60761-547-7 (Print), ISBN: 978-1-60761-548-4 (online).
We specialize in the business of healthcare • • • • • • • •
Results of the German Conn’s Registry. Horm Metab Res. 2010;42(6):4359.
Comprehensive Management Comprehensive Consulting Billing & Accounts Receivable Management Coding & Documentation Practice Assessments & Revenue Enhancement Profitability Improvement Practice Start-ups Personnel Management
Author information: Endocrinologist, Former Fellow, University of Mississippi Medical Center (UMMC), Jackson (Dr. East). Professor, Fellowship Program Director, Division of Endocrinology, UMMC (Dr. Subauste). Resident, Guthrie Robert Packer Hospital, Sayre, PA. (Dr. Gandhi). Professor, Division of Endocrinology, UMMC (Dr. Koch). Corresponding author: Honey E. East, MD; Premier Medical Group of Mississippi, 501 Marshall Street, Suite 208, Jackson, Mississippi 39202.
Journal of the Mississippi State Medic
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Message from MSMA President Steve Demetropoulos, MD
Annual Session
Message from MSMA President Steve Demetropoulos, MD • ANNUAL SESSION
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or the last eight years that I have been on the Board of Trustees of our Association, we have struggled with the problem of how to increase attendance at our annual session. After all, we as an organization do most of our business in this primary meeting. Through the House of Delegates, we put forth proposed resolutions, we discuss them, we vote on them, and then we enact policy from them. The annual session gives us an opportunity to have input in the direction of our organization. Therefore, from that aspect, it is very much a business meeting. In addition, other facets of it are equally important. One is the camaraderie that takes place among doctors when they have an opportunity to visit with each other, discuss important topics, socialize, and visit with old friends. The annual session also provides us with the opportunity to be updated on important issues that affect all doctors in Mississippi. These range from Medicaid to IQH issues to public health issues that affect each of us. Another important feature of our annual session is the educational offering. We try to bring very up-to-date and relevant CME topics that are of broad interest to all doctors regardless of specialty. Therefore, as you can see, our annual session is more than just a business meeting. Over the last eight years, we have tried to increase attendance by moving the annual session to different parts of the state. We have held it in Vicksburg, Biloxi, Oxford, Natchez, Tupelo, and in Destin, Florida. Our most recent meeting was in Point Clear, Alabama. We have also tried to have it in a more resort-friendly environment, which is why we had it at the Beau Rivage in Biloxi and in Point Clear, as well as in Destin. We have tried to make the event more family-friendly. We had children’s programs at the Natchez conference and again at Point Clear. We also had special events that would be of interest to spouses, such as several lectures by authors. Most recently, we featured two World War II veterans, also in an attempt to increase our attendance. We have all struggled with the importance of trying to keep the annual session in Mississippi but we are limited by a couple of considerations: (1) the need for a smoke-free environment and (2) a place where the convention center is in close proximity to the hotel so there would not have to be a lot of driving. Prior to 2005, we consistently had the meeting at the Bay View Hotel in Biloxi. It was separated from the gambling facility across the street at The Grand Hotel. It was a stand-alone hotel with great meeting facilities. It was smoke-free and there were many of children’s activities. Restaurants and shows were also available at The Grand Hotel. Unfortunately, after Hurricane Katrina, that facility has not been fully replaced and so we really have a limited choice within our state with regard to facilities. Our attendance has been flat for the last seven years. We can’t seem to get back up to the level that we were prior to Katrina. At the 2005 Biloxi meeting, we had 214 doctors in attendance. Since then, we have not been able to get much more than 150 doctors to a meeting. The highest number was in Biloxi in 2008 when there were 157 doctors in attendance. Last year we sent out our questionnaire electronically to the membership asking for feedback regarding the annual session. We only had 110 responses. Those generally were in favor of keeping the event within Mississippi. As I have thought about this issue and struggled with whether we should keep the conference in Mississippi, and where to have it, and in what type venue, I believe the overriding consideration should be how we can get the most physicians to the conference. If our primary function is to do the business of the organization, having an adequate number of physicians there to represent our colleagues across the state should be our most important goal. Our staff and Board of Trustees have come up with a new recommendation. We will try to separate the functions of the annual sessions to make them more convenient to attend. We have recommended that the business aspect of the Association be conducted yearly in Jackson on a consistent date each year. This offers a centralized low cost, high tech environment to hold the meeting. The meeting would be conducted on a Friday and Saturday and would be able to accomplish all elections and business of the Association. This format would allow more participation, either in person or by telecommunications, by our membership. Popular social events like the Inaugural Gala and Alliance fundraiser would still be included. The CME and social aspect of the annual session will be held during the family friendly CME in the Sand sponsored by the Young Physicians section. It will be expanded to a weeklong event scheduled each year around Memorial Day. By splitting the meetings, we hope to increase attendance at both events, while saving money and expanding involvement through state of the art telecommunications which is very expensive, and often times unavailable at other locations. This would allow for more virtual interaction during our business meeting. The CME event is held in a resort location and allows for more family events without the pressure of Association business. Our older members have been faithful in coming over the years. We must somehow invigorate the next generation of physicians to assume the mantle of leadership and that means being active and involved in the annual session. Your Board of Trustees will continue to work hard to Increase attendance at this event. Please show your support for this new recommendation by attending our next annual session in August of 2013. We can reinvent annual session, but we need your help to do it. Let us hear from you about the 2013 August 16-17 annual meeting. Log in at MSMAonline.com. Go to “Issues and Forums,” and add your comments under the “Annual Session” heading.
384 JOURNAL MSMA NOVEMBER 2012
• UMC SOM • Literati Medicus- the M3/M4 Humanism in Medicine Book Club at the University of Mississippi School of Medicine Maribeth Porter, MD, Chief Resident Department of Family Medicine, Trident Medical Center / Medical University of South Carolina Jacob Graham, MD, Internal Medicine Resident, Department of Medicine Jerry Clark, PhD, Associate Dean for Student Affairs Sharon Douglas, MD, Professor of Medicine, Department of Medicine University of Mississippi Medical Center, Jackson
The book club developed a lapel pin for its members (left). A list of books that the medical student book club has read since its inception follows on the next page.
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or many, becoming a physician is an ideal established at a young age. The sense of pride at medical school acceptance quickly becomes a reality not initially comprehended: the gravity and awesome nature of this chosen career path. As medical school begins, many long hours are spent learning the basics upon which medical careers are built. Most medical students count down the months until interaction with patients becomes the daily course. During the first two years of curriculum, the ethics lectures, especially the ones discussing clinical dilemmas and the doctor/patient relationship, can be a welcomed addition to the basic science lectures. It is refreshing to discuss subject matters which can leave students with lingering thoughts to ponder. Recommended readings outside the lecture series on topics such as medical ethics, humanism in medicine, professionalism, patient communication, and end-of-life care are often cited. Frequently students scribble down the works hoping to find a chance to read them while realizing that time is a precious commodity. In the Spring of 2008 one third year student decided that her “to-read” list from ethics lectures should become a shared experience with other students. She approached an ethics professor and the medical school leadership for assistance in setting up a student-lead book club to read books with humanism in medicine themes.
The Administration of the University of Mississippi School of Medicine and a number of its partners have been quite supportive of the book club since its inception. A good example of this support is realized through an annual grant from the Vicksburg Medical Foundation. Educators understand that co-curricular activities such as the book club are an extension of a good academic program and reinforce the objectives of the school. It allows students to merge facets of their theoretical learning into individual engagement. All students from the M3 and M4 medical school classes were, and still are, invited to join the book club. The initial plan was to read selections to help gain deeper understanding of the medical profession as well as to challenge members to consider others’ views on medicine and humanism issues. Maribeth Porter became the chair for the first M3/M4 humanism in medicine book club named Literati Medicus, and it has continued to flourish. Successors in bookclub leadership have included Jacob Graham and Katie Maxwell followed by Shea Bell, Sangita Goel, Sam Love, and currently Ashley Emerson, Debbie Rigney, Elizabeth Schimmel, and Patrick Williams. Literati Medicus currently meets five to six times a year for dinner and discussion at the Student Union on campus. The discussion is facilitated by a student leader of the book club. One of the ethics professors from the Department of Medicine participates as the faculty advisor. One student
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wrote, “I got involved with the book club because I wanted to get back into reading for pleasure. After years of reading textbooks and power points, the book club got me started with reading again. It was appealing because it combined many things I enjoy-- medicine, ethics, and a glimpse of the more global aspects of the question ‘what am I doing here?’ It also provided a platform to discuss issues and topics that we did not necessarily have time to cover in our regular course work.” The meetings have become more than a discussion about literature. They are an opportunity for students to interact with other students fostering new ideas about the art of medicine. Our gatherings provide a safe environment to share the highs and lows of clinical experiences. We are challenged by opinions different from our own and encouraged to develop our own ideals. We consider patients’ viewpoints and circumstances in hope that we can better serve them. One of the former medical student leaders has realized that residents and fellows also wish to read works other than Medical Knowledge Self Assessment Program, Washington Manual, and Harrison’s Textbook of Medicine, and is currently starting a book club for Internal Medicine residents and fellows. There has been great enthusiasm for the idea even given the increasing claims on trainees’ time. The plan is to read one book related to the practice of medicine every 6-8 weeks and then meet for dinner and discussion at the house of a faculty member. The Medicine Department is supporting these events by providing food and funding some of the books. The first selection will be The Gift of Pain, by Paul Brand and Philip Yancey, a book chosen from the Literati Medicus book list. Literati Medicus has grown in membership and enthusiasm each year. Students feel that this is a rewarding experience and that ultimately they become better physicians for the evenings spent sharing ideas and making lasting friendships over good books. r
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Literati Medicus
Books Read 2008-2012 Blink: The Power of Thinking without Thinking – Malcolm Gladwell The Last Lecture – Randy Pausch Mom’s Marijuana: Life, Love and Beating the Odds – Dan Shapiro Delivering Doctor Amelia: The Story of a Gifted Young Obstetrician’s Error and the Psychologist Who Helped Her – Dan Shapiro The Last Goodnights: Assisting My Parents with Their Suicides – John West The Nazi Doctors – Robert J. Lifton My Own Country – Abraham Verghese The Spirit Catches You and You Fall Down – Anne Fadiman Code Blue: A Katrina Physician’s Memoir – Richard Deichmann The Good Doctors: The Medical Committee for Human Rights and the Struggle for Social Justice in Health Care –John Dittmer How Doctors Think – Jerome Groopman Better: A Surgeon’s Notes on Performance – Atul Gawande Complications: A Surgeon’s Notes on an Imperfect Science – Atul Gawande My Stroke of Insight – Jill B. Taylor When Doctors Become Patients – Robert Klitzman Pathologies of Power: Health, Human Rights, and the New War on the Poor – Paul Farmer An Unquiet Mind – Kay R. Jamison The Man Who Mistook His Wife for a Hat: And Other Clinical Tales – Oliver Sacks Mountains beyond Mountains – Tracy Kidder
• Uncommon • Una Voce Thread • • Birthdays
I
was born on November 14th, but I stopped having birthdays when I was forty. Not as a matter of choice or vanity, but through a simple coincidence. On my fortieth birthday I received the most wonderful present possible, my daughter Allison, and while I didn’t know it at the time, it reduced the entirety of my future birthdays to two words…”and Dad.” When I was forty-one I celebrated my first “Happy First R. Scott Anderson, MD Birthday Allison…and Dad.” As the years passed I had nursery school parties, Barbie cakes, and a cheerleader party complete with high school cheerleaders and football players from my son Dylan’s class. Because Char was preoccupied getting just the right thing for our baby girl, my presents tended to be kind of interesting. One year I got three versions of the same button down shirt with Charlene’s initials embroidered on the sleeve; a few years later it was my grandfather’s initials on the same shirt. Now, don’t suppose that I’m complaining about it; it’s just a natural consequence of sharing a birthday with one of your children. For her part, Allison has always asked for things we could share for her birthday. Like football tickets, or four wheelers, or a new hunting rifle so we could hunt together. You may remember a few years ago when I told you about quitting on a hunt up in Kentucky and driving all night so Allison and I could spend our birthday hunting together. She shot two bucks with one shot that year. This past year was Allison’s sixteenth birthday, and any of you who have had a daughter turn sixteen know that sixteen is NOT an…and Dad… birthday! There was a hall to be rented, a DJ, food to arrange for, and decorations. By the time everything was arranged the party was going to be the night before our actual birthday to accommodate something important, I’m not sure what. But by the time we had set up, had half of the teenagers in town spill drinks and food on the floor and cleaned up the resultant mess, everybody was just about birthday partied out for that particular year. The next night (our real birthday) I was sitting in my recliner watching the news while Charlene and Maddie, our twelve year old daughter, fixed us something to eat in the kitchen for supper. I overheard Maddie whispering, not that quietly, “What do you mean you didn’t get him anything? No presents, no birthday card, no cake…” Thirty seconds later Mat came cruising through the den on her way to the back of the house. She was back there for a while, until Char called us all into the kitchen to eat. It was a good meal, meatloaf and brussel sprouts, which are two of my favorites, and worthy of a birthday dinner any day. Having overheard the whispering, I figured that was that. But before anyone got up to clear the plates, Maddie stood up and announced, “Okay Dad, shut your eyes.” I looked at Charlene. She shrugged. “Alright, now you can open them,” Mat finally said. When I opened my eyes, she was holding out a bowl of vanilla ice cream with a candle stuck in it. “Y’all don’t want any?” I asked. “We’re just going to share yours,” Maddie explained. “That will be wonderful,” I said and stuck a few spare spoons into the bowl. When I looked up, Mat was holding a card in one hand and a gift bag in the other. The card was colored with crayon and lettered with a magic marker. It said, “We all wanted you to have a special birthday card so we made it ourselves.” It was signed, “Your Family” in Maddie’s handwriting. I thanked them all. Holton and Allison looked at each other trying to figure out what was going on. Maddie stood, gift bag extended. The top was stuffed with yellow and pink tissue paper, and each gift was separated in its own layer. The first was my pocket knife, a twin blade Old Timer I’d carried for years. “How did you know? This one’s my favorite!” I said. Maddie smiled. So did Char. Next was a half-empty bottle of my favorite after-shave, then my favorite Alabama cap, and finally a still cold Diet Coke. What dad could ask for a better birthday than that?
NOVEMBER 2012 JOURNAL MSMA 387
When your medical office is short-staffed, you get frustrated.
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e are looking for physicians to join our group to perform Consultative Examinations for Social Security Disability in Mississippi. Part-time or fulltime. No call or weekends. Travel within state will be necessary. Pay is guaranteed regardless of turnout and paid promptly regardless of time of collection. All administrative needs including scheduling, transcription, assisting and billing are provided. Physicians working for us have various background and training including, IM, FP, pain mgt, surgery, orthopedics, neurosurgery, cardiology and general practice. There is minimal risk and stress involved with this position. You will have time to enjoy your life and not be stressed out. Contact
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KEEP MAMA HAPPY. When your office is short-staffed, use the MSMA Online Job Bank!
Susan Gladys 1.866.929.8766 or email susang@tsom.com
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PHYSICIANS NEEDED Internists, Cardiologists, Ophthalmologists, Pediatricians, Orthopedists, Neurologists, Psychiatrists, etc. interested in performing consultative evaluations according to Social Security guidelines.
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DISABILITY DETERMINATION SERVICES 1-800-962-2230 388 JOURNAL MSMA NOVEMBER 2012
MISSISSIPPI RISING A PREVENTIVE HEALTH SYMPOSIUM
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HILTON JACKSON http://www.msacc.org/RegistrationPacket2013.pdf
NOVEMBER 2012 JOURNAL MSMA 389
MISSISSIPPI RISING: A PREVENTIVE HEALTH SYMPOSIUM COURSE OVERVIEW The Mississippi Chapter of the American College of Cardiology is hosting a Preventive Health Symposium to engage health care professionals in promoting a healthier Mississippi. This symposium will address measures that will make a tremendous impact on cardiovascular health in Mississippi. Join fellow colleagues as we work together to raise Mississippi’s standing in national health standards and not only make Mississippians healthier but also significantly lower the cost of delivering healthcare in our state.
SCHEDULE
State Health Officer Mississippi State Department of Health
Sam Dagogo‐Jack, MD, FRCP Professor of Medicine & Director Division of Endocrinology, Diabetes & Metabolism A. C. Mullins Chair in Translational Research Director, General Clinical Research Center University of Tennessee Health Science Center
Friday, February 8, 2013 7:00 PM - *Welcome Dinner
(*Not included in registration fee. Additional registration required)
Saturday, February 9, 2013 7:30 AM Registration and Breakfast 8:00 AM Welcome 8:00 AM Morning Session 11:30 AM Lunch Afternoon Session 1:00 PM 5:00 PM Adjourn
Richard D. deShazo, MD Billy S. Guyton Distinguished Professor Professor of Medicine and Pediatrics The University of Mississippi Medical Center
Dipti Itchhaporia, MD, FACC Chair, Board of Governors, American College of Cardiology( ACC) Robert and Georgia Roth Chair for Excellence in Cardiac Care Director of Disease Management Hoag Memorial Hospital Presbyterian, Newport Beach
Carl J. Lavie, M.D., FACC, FACP, FCCP Professor of Medicine Medical Director, Cardiac Rehabilitation and Prevention Director, Stress Testing Laboratory John Ochsner Heart and Vascular Institute Ochsner Clinical School ‐ The University of Queensland School of Medicine
TARGET AUDIENCE This conference is intended for cardiovascular specialists, internists, family physicians, advanced practice nurses, nurses in cardiology and physicians assistants.
ACCREDITATION
The Health Preventive Symposium is being submitted for 7.5 hours of AMA PRA Category 1 Credit ™.
Michael Mansour, FACC, FACP President MS Chapter American College of Cardiology American College of Cardiology Board of Governors
REGISTRATION Registration for this conference is $50 and includes breakfast, breaks, lunch and CME certificate. Additional registration is required if attending the Welcome Dinner on Friday, February 8, 2013.
HOTEL INFORMATION This conference will be held at the Hilton Jackson. Rooms are available by contacting:
Hilton Jackson 1001 East County Line Road Jackson, MS 39211 601‐957‐2800
FACULTY Mary Currier, MD, MPH
Group Rate: $99 +tax and fees Group Code: MS Chapter, ACC Cutoff Date: January 9, 2013
EVENT REGISTRATION: Name: _____________________________________________________
Professional Initials (Please circle): MD DO NP PA Other _____________
Practice Name:______________________________________________
Preferred address: ___________________________________________
City: _______________________ State: _____ Zip: _________________
Daytime Telephone: _______________ Email:_____________________
Thomas J. Payne, PhD Professor, Department of Otolaryngology and Communicative Sciences Associate Director, ACT Center for Tobacco Treatment, Education and Research University of Mississippi Medical Center
David A. Sabgir MD FACC Founding CEO, Walk with a Doc
Frank W. Smart, MD, FACC, FACP Professor and Chief Section of Cardiology LSU School of Medicine in New Orleans Director of the Cardiovascular Center of Excellence LSU Health Sciences Center
J. Clinton Smith, MD, MPH Professor Emeritus of Pediatrics (Cardiology) University of Mississippi Medical Center Medical Consultant, Mississippi Public Health Institute
Welcome Dinner ‐ $250/Couple Friday, February 8, 2013 – Hilton Jackson Meeting Registration ‐ $50 Saturday, February 9, 2013 – Hilton Jackson
PAYMENT OPTION: Make checks payable to MS Chapter, American College of Cardiology Send completed form and payment to: MS Chapter, American College of Cardiology Attn: Jenny White, PO Box 2548, Ridgeland, MS 39158
QUESTIONS: Contact Jenny White at JWhite@MSMAonline.com or 601‐
853‐6733 x 332.
390 JOURNAL MSMA NOVEMBER 2012
Hector Ventura, MD, FACC
President LA Chapter American College of Cardiology American College of Cardiology Board of Governors Professor of Medicine Medical Director Cardiac Transplant and Heart Failure Ochsner Clinical School ‐ The University of Queensland School of Medicine
Thad Waites, MD, FACC
Immediate Past Chair, Board of Governors American College of Cardiology Director Cardiac Catheterization Laboratories Southern Heart Center (A Service of Hattiesburg Clinic, P.A.)
Janet Wright, MD, FACC Executive Director Million Hearts Department of Health and Human Services (HHS) Centers for Disease Control and Prevention (CDC) Centers for Medicare & Medicaid Services (CMS)
Protecting the practice of medicine The American Medical Association is proud to have helped the Mississippi State Medical Association (MSMA) address concerns that federal interference is diminishing the role of state legislatures and medical boards in licensure and scope-of-practice issues. We believe physicians, not federal government bureaucrats, are best suited to regulate the practice of medicine and make clinical judgments that affect patient health and safety. The AMA and the MSMA support you in the state house, the courthouse and in your practice. Working together with the MSMA, the AMA will continue to make a difference.
Be a part of it. ama-assn.org/go/memberadvocate Please activate your 2013 AMA membership through the Mississippi State Medical Association at (601) 853-6733.
Š 2012 American Medical Association. All rights reserved.
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NOVEMBER 2012 JOURNAL MSMA 391 11/8/12 12:30 PM
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• Asclepiad •
ugh Agnew
Gamble, II, (named after his grandfather) was born in Greenville, Mississippi. With the exception of time away at school, he has lived in Greenville his lifetime. While attending Millsaps College (1965-1969) he met Dawn Pittman. They married in 1969, just weeks before beginning medical school and have been married for 43 years. They have two children. Their daughter Katherine is married to Corey Boozer and lives in Greenville where she is a graphic designer who works from home while being a mother to her two daughters, Leanna (10) and Lauren (6). Their son, Hugh A. Gamble, III, is married to Meredith Green Gamble and lives in Alexandria, Virginia. He is the legislative director and general counsel for U. S. Senator Saxby Chambliss of Georgia. They have one son, Hugh Gamble, IV (1 year). Medicine has always been the family trade. “William Gaston Gamble (my great-grandfather) moved to Guntown, Mississippi, after the Civil War and practiced medicine there until his death. His two sons Hugh Agnew Gamble (my grandfather) and Paul Gaston Gamble (my great-uncle), practiced medicine in Greenville all of their professional lives. Hugh’s only child Lyne Starling Gamble (my father) also practiced in Greenville all of his medical career. He had four sons (Hugh II, Lyne Jr., William and Paul). Hugh II completed training in 1980, and joined his father in his practice at Gamble Brothers and Archer Clinic,” Dr. Gamble explained. The library at MSMA headquarters is dedicated in the memory of our family members who were all Mississippi physicians by Lyne’s four sons. Drs. Hugh, Paul, Lyne and Hugh II have all served as president of MSMA. The family has donated several books to the library including a large number of bound issues of The Mississippi Doctor which evolved into the Journal of the Mississippi Medical Association, in addition to furnishings. “The family hopes that this library will encourage others to donate books that are of interest to MSMA and the practice of medicine in Mississippi,” Dr. Gamble added. Dr. Gamble received his M.D. from the University of Mississippi School of Medicine (1969-1973); General Surgery (1973-1978); Thoracic & Cardiovascular Surgery (1978-1980). “When I came to Greenville, there had not ever been a thoracic surgeon in the Mississippi Delta. I was advised by a senior surgeon in our community that I needed to plan to make a living by practicing general surgery since there was not enough thoracic or vascular surgery to keep me busy. Clearly he was wrong. After about six months, it became obvious that my volume of thoracic and vascular surgery was such that I quit practicing elective general surgery. There are very few surgeons in the country that are able to build a busy practice that is dominated by thoracic surgery. I was able do so because other thoracic surgeons were in the bigger cities hours away,” Dr. Gamble remarked. “Greenville now has two.” When asked about his MSMA presidency, he said, “By far the most memorable activities were those related to tort reform. The month after I was installed as MSMA president I attended a state-wide blood drive at Mississippi Blood Services where I represented MSMA. At about 10:00 a.m., I was informed that the St. Paul Insurance Company had withdrawn from the Mississippi medical malpractice marketplace. By 11:00 a.m., the staff at MSMA had already arranged multiple interviews with the press. Working with the press, the legislature, other stake holders, and our membership, continued aggressively throughout my term as president. As you know, the first part of tort reform was passed by the legislature in 2002. It was quite a year!” Mentored in healthcare issues from birth, Dr. Gamble recalls his childhood. His father and grandfather frequently discussed their medical practices and the issues of organized medicine at the dinner table. “By the time I was in college, my father was serving on the Board of Trustees, and later as president of MSMA when I was at the University. We would usually visit when he was in Jackson, and the hot topics of the day were the subjects of discussion. Needless to say, my father and my grandfather were mentors from a very early age,” he said. “Dr. James D. Hardy was by far the most influential mentor in my surgical training. I, like most of the residents who trained under him, consider him to be an enormous influence in my professional life. He taught me much more than just the art of surgery.” A Diplomate of the American Board of Surgery and Fellow and former Governor of the American College of Surgeons, with professional affiliations and offices too numerous to mention, Dr. Gamble has served our MSMA as an AMA Delegate; Board of Directors: Mississippi Physicians Care Network, Mississippi Foundation for Medical Care (IQH), Mississippi Medical Political Action Committee, and Medical Assurance Company of Mississippi Risk Management Committee. Outside interests: “I enjoy woodworking but do not have the time to do it. I spend most of my leisure time doing yardwork and gardening. While working in the yard, one can almost be guaranteed that no one else will show up; therefore, you have hours of much enjoyed solitude,” he snickers. In closing words to his colleagues, Dr. Gamble says,“Stay engaged. There are evil forces attacking the field of medicine, and unless we are all involved, they will win.” —Karen A. Evers, JMSMA Managing Editor
392 JOURNAL MSMA NOVEMBER 2012
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