Team C: medicine, geriatric medicine, medical management & administration, and ophthalmology.

READ BEFORE SIGNING: PHYSICIAN LIABILITY AND MEDICAL NECESSITY CERTIFICATION. James Bernick, MD. San Jacinto Methodist Hospital, Baytown, Tex.

Senior patients frequently inform their geriatricians: "If you order it, Medicare will pay." The demand by our patients for items such as powered scooters, oxygen therapy, and home health care appears unending. Payment to the nonphysician supplier is dependent on physician documentation of medical necessity. Typically, physicians initiate the order for home services essential to their patients' functional independence. Unfortunately, geriatricians are approached by patients' families and other well intentioned providers requesting services for which the patient does not qualify or the proposed treatment is likely detrimental. Federal law prohibits unsolicited telephone contacts by suppliers to patients. However, if provided services are considered unnecessary, the certifying physician is responsible. Both state and federal statutes contain criteria determining patient eligibility for covered benefits. Home health statutes mandate the patient be confined to home, a treatment plan established, the patient be un der the care of a physician, and recertification occur within 2 months. Patients receiving home oxygen therapy must have arterial oxygen saturation below 89%. Hospice care defines "terminally ill" as patients with a life expectancy of 6 months or less. If the reviewing agency establishes a pattern of unnecessary services, the certifying physician encounters possible liability for fraud, medical malpractice, or violation of antikickback laws. Improperly filed claims and false statements may be considered fraud and expose the physician to civil or criminal sanctions. In addition, the physician may be excluded from participation in federal health care programs. A State Board of Medical Examiners could take action against a physician for unprofessional or fraudulent conduct. Improper physician certification may result in a malpractice claim. Recent case law held that a physician patient relationship existed for purposes of medical malpractice even though the volunteer hospice physician did not deal directly with the patient. Stark laws and antikickback statutes prohibit physician referral to a home health agency or other entity in which the physician has financial interest. The legitimate needs of senior patients are supported by home health care and equipment. Although physicians do not bill for these covered benefits, they may be held accountable for unnecessary services. By reviewing for appropriate documentation before signing CMN forms, geriatricians assure their patients of proper care and avoid potential liability.

POLYARTERITIS NODOSA PRESENTING AS AN ACUTE CEREBROVASCULAR ACCIDENT (CVA) IN A YOUNG MAN. Paul J. Bennett, MD, Jackson J. Yiwri, MD, and Mukta Panda, MD. University of Tennessee--Chattanooga.

To understand the differential diagnosis of CVA in young patients. To recognize clinical features and proper diagnosis of polyarteritis nodosa (PAN). A 24-year-old black man with a questionable history of multiple sclerosis presented to the ER with acute onset of right-sided weakness, slurred speech, and dysphagia. The patient denied any visual symptoms, headache, fevers, or recent illnesses. On examination, the patient was afebrile, pulse rate 60/mm, and BP 180/128 mm Hg, neck was supple without bruits, and a 2/6 systolic murmur was noted at the apex. No skin lesions were noted. On neurologic examination, the patient had dysarthria, right facial droop, and right hemiplegia. Routine laboratory work was unremarkable with a normal CBC, metabolic panel, and sedimentation rate. Urinalysis revealed 2+ proteinuria with benign sediment. LP revealed no oligoclonal bands. An MRI of the brain revealed a recent deep left-sided infarct involving the internal capsule as well as a small aneurysm of a temporal branch of the right middle cerebral artery. Hypercoalguable workup was negative, p-ANCA was negative, but myeloperoxidase antibody was positive. Echocardiogram revealed mild left ventricular hypertrophy with normal LV function. Cerebral and renal angiography revealed innumerable aneurysms involving almost all branches of medium-sized arteries, A biopsy of the sural nerve with accompanying vasculature confirmed the diagnosis of PAN. The patient was treated with steroids, monthly pulse dose cytoxan, and aggressive physical therapy. Nine months later, he shows marked improvement and no further neurologic insults. PAN is a systemic vasculitis involving small and medium-sized arteries and is more common in middle-aged men. Any organ can be affected but skin, peripheral nerves, joints, intestinal tract, and kidney are most commonly involved. The onset of disease can be abrupt or gradual and usually involves symptoms such as fever, malaise, palpable purpura, infarctive ulcers, joint pain, and livedo reticulais, though multiple m ononeuropathies are the most typical neurologic manifestation. The sedimentation rate is usually elevated, but, as in our case, it can be completely normal antibody to hepatitis B surface antigen can be positive. Tissue biopsy confirms the diagnosis. Untreated, the 5-year mortality rate is greater than 85%. High-dose steroid therapy has improved the 5-year mortality to 30% to 45%, and the addition of immunosuppressive has reduced relapses. Plasmapheresis offers no additional advantages. Treatment of any associated viral illness (hepatitis, HIV) should be part of the initial therapy.

VERTEBRAL OSTEOMYELITIS AND DISCITIS AS PRESENTING FEATURES OF BRUCELLOSIS. George Yacoub, MD, Adel Salama, MD, and Deborah Demicco, MD. University of Virginia School of Medicine, Roanoke-Salem Internal Medicine Program, Roanoke, Va.

Brucellosis is a rare disease in the United States with approximately 100 cases reported every year. This case report deals with a 35-year-old white male who presented to the ER with severe low back pain. He started to have back pain when he slipped at work and hit his back three months prior to his current presentation. MRI of the lumbo-sacral spine, following the fall, showed a small central L4-5 disc protrusion. He was treated with muscle relaxants and analgesics without significant improvement. He noted occasional chills, diminished appetite, and 20 lb. weight loss over the last few weeks. He denied fever and night sweats. Past medical history was not contributory and he never used IV drugs. The patient was a native from Iraq but he had been living in the United States for the last 4 years. He used to raise cows in Iraq and occasionally drank unpasteurized milk. Physical examination revealed normal temperature and tender lumbar vertebrae. Additional investigations revealed normal white count, ESR of 30, n egative blood cultures, positive PPD and normal chest x-ray. A repeat MRI suggested L4-5 discitis and L4/L5 vertebral osteomyelitis. Fluoroscopic guided needle biopsy revealed mild acute and chronic inflammation. Routine cultures, gram stain, AFB, fungal smears of the aspirate were all negative. Brucella cultures grew brucella abortus. Serology showed brucella abortus IgG titer of [greater than] 1:2560 and IgM titer of 1:640. In conclusion, particular attention should be paid to unusual pathogens as causative agents of common medical problems especially in patients from areas with known endemic diseases.

DIABETIC NEUROPATHIC CACHEXIA. Lala A. Cornelius, MD, and Craig Wierum, MD. University of Tennessee, Nashville, Baptist Hospital.

A 55-year-old dentist recently diagnosed with diabetes mellitus presented with a 40 lb weight loss, impotence, chronic loose stools, and burning sensation in the distal lower extremities over 3 months. His diabetes was well controlled with an oral hypoglycemic agent but he lost another 30 lb. His symptoms became increasingly severe, and pain developed in the proximal lower extremities. He complained of severe insomnia and depression. He appeared cachectic with generalized muscular wasting and decreased muscle strength in the lower extremities. Sensation was decreased to light touch and pinprick in the feet and ankles but vibratory sensation was intact. Lie had normal cognitive function and affect but was emotionally labile and depressed. He had an extensive evaluation for possible malignancy, amyloidosis, porphyria, infection, and endocrine and neuromuscular diseases, all of which was negative. At the end of 1 year, he had lost approximately 93 lb (more than 30% of his body weight). Then his sleep, neuropathi c symptoms and affect began to improve spontaneously. Within 5 months, he regained more than 70% of his weight but continued to complain of significant weakness. Within 1 year, he was back to his normal weight and maintained it for 2 years. He continues to have parasthesias in the lower extremities but his diabetes is well controlled on an oral agent and he returned to his former occupation of dentistry. Diabetic neuropathic cachexia is a rare syndrome. first described in 1974 by Ellenberg. Thirty cases were reported after his original publication. It is usually seen in men with mild diabetes in their sixth and seventh decades of life and is characterized by rapid substantial involuntary weight loss and is not related to diabetes control. There is significant anorexia, depression, and peripheral neuropathy but no microvascular complications of diabetes. The pathophysiology remains unclear. The overall prognosis is good and symptoms generally resolve spontaneously within a year.

VISUAL ACUITY ASSESSMENT IN LONG TERM CARE: NURSING DOCUMENTATION VS. OPHTHALMOLOGISTS EVALUATION. Ann Rybolt, MD, Robert Enzenauer, MD, Scott Sheldon, MD, Diana Allen, MSW, and Neema Doshi, PhD. Chattanooga, Tenn.

The visual impairment score for long term care (LTC) residents is determined by a registered nurse completing the Minimum Data Set (MDS). This assessment is designed to identify potentially reversible impairments and to indicate areas for further assessment. Accurate assessment is crucial for devising optimal care plans. We assessed the accuracy of visual acuity recorded on the MDS. Visual acuity was determined at the bedside by ophthalmologists (the gold standard). Whenever possible, formal visual acuity was performed using a Snellen near card with refractive correction. When a patient was unable to cooperate, the visual acuity was estimated by the ophthalmologist after examining the retina and optic nerve with a direct and indirect ophthalmoscope. The ophthalmologists scored visual acuity as 0 (best) to 4 (worst) based on current Health Care Financing Administration definitions for MDS data in section D.1. Data were available for 142 residents. Using the ophthalmologists rating as the gold standard, the sen sitivity, specificity and 95% confidence limits of the nurses' rating on the MDS were calculated at each level of impairment. The sensitivity of the nurse-rendered MDS in predicting the gold standard for the level of impairments for 0,1,2,3,and 4 were 39.1%, 52.4%, 34.0%, 13.5%, and 35.7%, respectively. Of the 52 residents highly to severely impaired , nursing identified only 14 (26.9%), and of these 52 highly to severely impaired, 10 (19.2%) were rated on the MDS as 0 ("adequate") vision and 15 (28.8%) as "1" (sees large print). Nursing assessment of vision on the MDS was inaccurate in determining visual acuity in LTC patients. Of particular concern is the failure to recognize high levels of impairment which could be reversible or amenable to adaptations to decrease disability and improve quality of life.

MASSIVE HEMOPTYSIS ASSOCIATED WITH CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME. Subramanyam Chittivelu, MD. Pulmonary Critical Care Medicine Division, Department of Medicine, Texas Tech University Medical Center, Amarillo.

A 31-year-old Hispanic woman was admitted to the medical ward for severe hypertension, anemia, anorexia, and nausea. The patient had been tiring easily and feeling weak since the delivery of her 8-month-old third child.

The patient denied any history of early trimester abortions, DVT, thrombocytopenia, or SLE. The patient denied any medical history of HTN, DM, HIV, TB, or UTI. She denied any history of use of aspirin or NSAIDs. She had no history of allergies to either certain foods or medications. Physical examination was remarkable for tachycardia and tachypnea and systolic murmur due to severe anemia. Lungs, abdomen, extremities, skin, and neurologic examinations were normal. Initial laboratory work revealed anemia, thrombocytopenia, and elevated PTT, ESR, BUN, and creatinine. Serologic tests were positive for RF, ANA, and dsDNA, and antiphospholipid antibodies. IV steroids were started for lupus nephritis. Renal biopsy was delayed due to risk of bleeding. The patient started experiencing dyspnea and productive cough. Sputum was noted to be blood tinged initially, which became frank hemoptysis. These symptoms were progressed rapidly into acute respiratory failure with massive hemoptysis requiring an ICU transfer. The ches t x-ray obtained in ICU showed an ARDS pattern and CT scan of chest showed a diffuse multinodular pattern. Bronchoscopy was negative for any mucosal abnormalities or endobronchial lesions. Diagnosis of catastrophic antiphospholipid syndrome was made, and the patient started on IV cyclophosphamide. Rapid resolution of pulmonary symptoms and radiographic features occurred. She was extubated in 2 days and hemodialysis was started for the renal failure. Further workup was negative for HIV, antiglomerulo basement antibodies, C-ANCA, P-ANCA, TB, or other infective agents. The patient returned several weeks later to ICU with seizures, renal failure, and hemoptysis. All were improved with the combination of cyclophosphamide and supportive treatment. Acute and severe pulmonary hemorrhage in a patient with antiphospholipid syndrome can occur due to diffuse alveolar hemorrhage (DAB), which can respond dramatically to the cyclophosphamide.

CHOLESTEROL EMBOLI SYNDROME OCCURRING AFTER ADMINISTRATION OF TISSUE PLASMINOGEN ACTIVATOR. Sharolyn Hoover Baldwin, MD, and John Musa, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

A 64-year-old man with history significant for hypertension and tobacco abuse presented to Keesler Medical Center complaining of acute onset of retrosternal chest pain and shortness of breath. He was diagnosed with an acute myocardial infarction and thrombolysed with tissue plasminogen activator. Admission creatinine was 3.0, attributed to chronic hypertension. On day one, creatinine rose to 3.4. Twenty-four hour urine collection revealed 500mg protein. Renal failure worsened and urine output decreased. Livedo reticularis was noted on day six. Peak absolute eosinophil count was 2,130. Anticoagulation was discontinued. By day 9 the creatinine had risen to 8.4 and patient had ischemia of several digits of the left foot. Renal biopsy revealed cholesterol emboli clefts in the small parenchymal arteries. One year later he remains dialysis-dependent. Cholesterol emboli syndrome is usually caused by instrumentation of atheromatous arteries. To date only eighteen cases of cholesterol emboli syndrome following the use of thrombolytic agents have been reported. Pathogenesis results from disruption of atheromatous plaques that spill lipid contents into the bloodstream. Atheromatous debris then lodges in medium to small sized arteries resulting in downstream tissue ischemia. The kidney is frequently involved with acute or progressive renal failure, peripheral eosinophilia, bland sediment and absence of proteinuria. Skin involvement is classically livedo reticularis. Therapy is supportive and loss of renal function tends to be permanent. Our case highlights the need to monitor for such events in the setting of thrombolytic therapy.

LEWY BODY DEMENTIA. Sharolyn Hoover Baldwin, MD, and Eleanor Avery, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

A 78-year-old woman presented with a decline in Folstein Mini-mental Status Examination (MMSE) from 28/30 to 19/30 in one year. Laboratory and radiologic studies were non-diagnostic for structural or metabolic causes of dementia. Three months after presentation she suffered a mandibular fracture from a fall. Two months later she developed hand and head tremor and mask facies consistent with Parkinsonism. Nine months after presentation waxing and waning somnolence was noted. Eleven months after presentation she began to have visual hallucinations. Therapy with olanzapine was initiated which resulted in abrupt worsening of symptoms, including increased rigidity resulting in multiple daily falls, frequent visual hallucinations and a 55-hour period of insomnia. Resolution of acute symptoms occurred after withholding all medications. Lewy body dementia is the second most common cause of dementia, yet remains rarely diagnosed. Diagnostic criteria include dementia with fluctuation of symptoms, visual hallucinations and spontaneous Parkinsonism. Supportive diagnostic features include frequent falls, syncope, transient loss of consciousness, neuroleptic sensitivity, systematized delusions and non-visual hallucinations. Treatment of lewy body dementia requires trial of levo-dopa for Parkinsonism, and non-neuroleptic treatment of hallucinations including trazodone or valproate. Neuroleptic medications are associated with increased rigidity, and should be avoided. This case illustrates a classic presentation of lewy body dementia with adverse response to neuroleptic medication. Our case highlights the importance of precise diagnosis of dementias presenting in the elderly.

ALCOHOLIC DEMENTIA, AN UNDERRECOGNIZED, REVERSIBLE CAUSE OF DEMENTIA IN THE ELDERLY A CASE REPORT. Roger Wood, MD, and Robert Kruger, MD. Wilford Hall Medical Center, Lackland AFB, Tex.

Alcoholism is one of the most common truly reversible causes of dementia among the elderly. Alcoholism accounts for up to 6% of all dementias and is frequently underrecognized due to lack of physician inquiry and awareness. Among seniors, heavy alcohol use increases blood pressure, risk of head and neck cancer, osteoporosis, GI bleed and can interact with many medications. A 78-year-old female with a past medical history of presumed Alzheimer's dementia presented to WHMC with productive cough, purulent sputum, shortness of breath, fevers, chills and fatigue. Social history revealed a positive alcohol history of two to three alcoholic beverages/day. On physical exam the patient was cachectic, oriented only to herself and place, not to time with a mini-mental status exam of 21 (consistent with outpatient scores). She had bibasilar crackles on auscultation and chest x-ray revealed bilateral lower lobe infiltrates. During the five day hospitalization for treatment of pneumonia, the patient had improvement in her mental status with MMSE improving to 24-25. Ethanol is known to cause cognitive deficits attributed to direct neurotoxic effects on the brain. Neurotoxic effects include cortical atrophy, enlargement of lateral ventricles and loss of cortical neurons. CT and MRI studies often show increased size of cerebral sulci and increases in width of inter-hemispheric and Sylvian fissures. Radiographic changes and cognitive deficits may improve as drinking is discontinued, suggesting partial reversibility. Given the potential for improvement of radiographic changes and reversal of cognitive deficits, physicians should be more thorough in gathering social histories regarding alcohol abuse in the elderly. If an alcohol history is present, abstinence should be encouraged and treatment offered to potentially reverse cognitive deficits and other harmful effects on this population.

ORTHOSTATIC HYPOTENSION AND BRADYCARDIA AS A CAUSE OF REVERSIBLE DEMENTIA. Michael Zane, DO, and Eleanor Avery, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

An 86-year-old man with a medical history of sick sinus syndrome, coronary artery disease, hypertension, and chronic renal insufficiency presented to a civilian physician in June 1998 for progressive memory loss. Folstein Mini Mental Status examination (MMSE) was 11/30 consistent with moderate to severe dementia. Vitals were BP of 95/45 and HR of 56. Evaluation for reversible causes revealed a normal TSH, B12, RPR, CT of head, and a MCV of 106, however, there was no history of alcohol use. Not soon after being seen, the patient was hospitalized for symptomatic bradycardia and third-degree heart block and a pacemaker was placed. At follow-up there was a subjective improvement in the dementia. Patient presented in February 1999 with complaints of dizziness. Vitals indicated orthostatic hypotension and fludrocortisone was started. An MMSE in May 1999 was 28/30 with normal vitals. Two more office visits after this showed similar findings. We hypothesize that his cognitive deterioration was a result of impaired ce rebral perfusion. Our patient's evaluation did not reveal a traditional, potentially reversible cause of dementia. However, correction of conditions, bradycardia, and orthostatic hypotension that decreased cerebral perfusion resulted in measurable and sustained improvements in the MMSE. Dementia will become an increasingly important health care problem as the population of older adults escalates. In conclusion, our case shows that it is important to identify reversible, partially reversible, and treatable factors that may cause or contribute to a dementing process.

LUNG ABSCESS: PATHOGENESIS, DIAGNOSIS, AND TREATMENT. Prakash Ramanathan, MD, and Robert J. DiBenedetto, MD. Department of Internal Medicine Education, Memorial Health University Medical Center, Savannah, Ga.

Despite extensive work focused on identifying the microbiologic agents of lung abscess, delay in diagnosis and selection of appropriate antimicrobial agents are important factors affecting mortality. This review describes the chronologic progression of a lung abscess, various modalities of diagnosis, and appropriate therapeutic decisions. An extensive literature search of the PUBMED and MEDLINE databases was conducted for the terms "lung abscess" and "pneumonia." References from the identified articles were also evaluated. This review substantiates and emphasizes the importance of identifying lung abscess as a major cause of morbidity and mortality. Appropriate medical intervention can effectively alter long-term survival and prognosis of patients with lung abscess.

UPPER EXTREMITY DEEP VENOUS THROMBOSIS: THE KEESLER EXPERIENCE. Capt Amy D. Strassburg, MD, and Capt Craig A. Kovitz, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

This study was designed to analyze the clinical characteristics of patients seen at the Keesler Medical Center (KMC) from 1997-2000 with a diagnosis of upper extremity deep venous thrombosis (DVT). Inpatient records from 1997-2000 were searched for the diagnostic code DVT. Ninety-nine records with this diagnosis were found and reviewed to further delineate those with upper extremity DVT. Information on patient demographics, etiologies, treatment and complications were then gathered from these records. Eleven records were identified with a diagnosis of upper extremity DVT. Two of these were excluded due to a true diagnosis of thrombophlebitis. Of the nine remaining cases, five were female and four male with an age range of 22-75. Four of the thromboses were right-sided, one in an axillosubclavian (AS) distribution and one internal jugular (IJ). The other five were left-sided: two in an AS distribution, one IJ and two with multi-vessel involvement. Upper extremity swelling was the most common presenting symptom . Duplex ultrasonography was the most used diagnostic tool. Five patients were treated with unfractionated heparin (UFH) in the hospital followed by outpatient warfarin maintenance. One patient was initially treated with UFH, but was sent home prior to achieving a therapeutic international normalized ratio (INR) with enoxaparin and warfarin. One case required multiple attempts at thromblysis as well as rib resection (due to Paget-Schroetter disease) in addition to standard UFH/warfarin therapy. The patient with a septic thrombembolism was treated with IV vancomycin as well as UFH. The one remaining patient received comfort care only in compliance with his wishes. Complications in this patient population included an inpatient case of heparin induced thrombocytopenia. No patients suffered a pulmonary embolus. Suspected etiologies/associated hypercoagulable states include one case of Paget-Schroetter disease, six cases involving instrumentation, five cases with underlying malignancies and one patient with a Prot ein S defect. Upper extremity DVT has become an increasingly recognized diagnosis. Upper extremity DVT accounts for 9.1% of DVTs found at KMC during the study period. The incidence as well as other characteristics of our DVT cases, with the exception of complication rate, analyzed in the retrospective chart review are similar to that found in other recent reviews of the topic.

SCLERAL PERMEABILITY OF CARBOXYAMIDOTRIAZOLE (CAI). C. A. Self, MD, L. P. J. Cruysberg, MD, J. B. Sanders, MD, E. C. Kohn, MD, P. Yuan, PhD, A. J. Franklin, MD, PhD, and H. F. Edeihauser, PhD. University of Tennessee College of Medicine, Chattanooga Unit; Emory University, Atlanta, Ga; and National Institutes of Health, Washington, DC.

Carboxyamidotriazole (CAI) is a drug that has been shown to have antiangiogenic effects in mouse and human cancers. In a mouse model of retinal neovascularization, CAI significantly inhibits new blood vessel growth when given before the formation of abnormal new blood vessels and, when given after, promotes regression of neovascular fronds. Because local therapy is ideal, novel drug delivery systems can be developed if a drug can cross the sclera. Compounds of similar molecular weight (dexamethasone and methotrexate) to CAI have been shown to cross the sclera with permeability constants in the range of 1.83 to 3.91 x 10-6 cm/sec. An hypothesis was formed that CAL would cross the sclera with a similar permeability constant. Moist chamber stored scleral tissue from eye bank eyes was dissected and mounted in a 2 chamber acrylic perfusion apparatus. CAI in differing concentrations and different solvents (40 mm in 20% dimethylsulfoxide (DMSO), 20 mm in 10% DMSO, and 20 mm in 10% ethanol) was placed on the episcler al side of the donor sclera in the first chamber. The uveal surface of the sclera was apposed to the second chamber, which contained basic salt solution (BSS). Samples were obtained at 30-minute or 1 hour intervals from the uveal chamber. CAI traversed the sclera effectively in all three solutions. The permeability constants are 5.59 x 10-6 cm/sec (20 mm in 10% DMSO), 1.44 x 10-6 cm/sec (40 mm in 20% DMSO), and 9.08 x 10-6 cm/sec (20 mm in 100% ethanol). The solutions reached steady state in 6,8, and 22 hours, respectively. CAI is an exciting drug with the potential to help in the management of many common blinding neovascular diseases. The drug crosses human sclera with similar kinetics to dexamethasone and methotrexate. Therefore, a local drug delivery system can be developed to deliver CAI across the sclera to treat human pathologic ocular neovascularization.

MULTIDISCIPLINARY PAIN CONTROL CENTERS DECREASE UTILIZATION OF HEALTHCARE RESOURCES. Janice Livengood, PhD, HSP, Benjamin W. Johnson, MD, DABPM, MBA, and Stephen Bruehl, PhD. Vanderbilt University Pain Control Center, Nashville, Tenn.

Caring for chronic pain patients on a continuing basis can be a source of frustration for the primary care physician. Interventions that only target pain reduction without addressing psychological and social factors are unlikely to result in long-term benefit. Referral to a multidisciplinary pain center (MPC) can reduce stress for the primary care physician while insuring adequate patient care. MPCs typically include pain management physicians, nurse specialists, physical therapists, and psychologists, each of whom specializes in treating different features of the pain experience, yet in an integrated way. This study examined treatment efficacy at the Vanderbilt Pain Center where 86 patients were contacted for follow-up telephone interviews; of these 11 declined to be interviewed and 7 could not be reached. The final sample of 68 patients was predominantly female (68%), married (56%), caucasian (85%), and had at least a high school education (61%). Ages ranged from 15-76, with pain complaints including low back pain (41%), cervical back pain (36%), dorsal back pain (12%), and headache (10%). Sixty-four percent were diagnosed with muscular pain and 61% with neurogenic pain (including patients with both types of pain). Of those interviewed, 77% were pleased with their treatment, 76% reported experiencing decreased pain, 85% felt they could better manage their pain, 28% were taking less narcotic medication, and 45% reported taking no narcotic medication. With regards to healthcare utilization, 60% reported fewer emergency room visits and 41% reported fewer physician visits. Patients also reported a reduction in visits for physical therapy (53%) and for psychological care (59%). Fifty-four percent reported no surgery since treatment, and 64% reported no additional pain treatment following the Vanderbilt Pain Center treatment program. Overall results indicate that MPC treatment resulted in a high level of patient satisfaction and substantial improvement in pain. Overall healthcare utilization after treatment was reduced by half. These preliminary findings are part of a larger outcome study currently being conducted to examine the individual and societal economic implications of multidisciplinary pain treatment.

EMERGING ROLE OF RIBOFLAVIN IN THE TREATMENT OF NUCLEOSIDE ANALOGUE INDUCED TYPE B LACTIC ACIDOSIS. Saundra D. Dalton, MD, Ali R. Rahimi, MD, and Than Win, MD. Department of Internal Medicine Education, Memorial Health University Medical Center, Savannah, Ga.

Type B lactic acidosis is a rare and often fatal complication seen in patients receiving the nucleotide analogues zidovudine, stavudine, didanosine, and lamivudine. We describe a case of a 51-year-old HIV positive woman on three nucleoside analogues. She presented with nausea, vomiting, abdominal pain, and hepatic steatosis. Signs of mitochondrial toxicity were shown by diffuse myopathy and pancreatitis. Serum riboflavin levels documented a deficiency, which was treated with 50 mg riboflavin daily. Immediately after treatment, serum blood urea nitrogen level, lactic acid levels, and arterial blood pH all returned to normal values. Her signs of mitochondrial toxicity also improved after treatment with riboflavin. Successful reversal of her type B lactic acidosis after riboflavin therapy suggested that riboflavin deficiency plays a direct role in the development of nucleotide analogue induced lactic acidosis. It is impossible to predict which patients are predisposed to development of this syndrome. For this re ason, it may be necessary to screen and treat riboflavin deficiency in patients on nucleoside analogues.

SIMVASTATIN-INDUCED LACTIC ACIDOSIS: A RARE ADVERSE REACTION. Anil Goli, MD, Ryland P. Byrd, Jr., MD, and Thomas M. Roy, MD. Division of Pulmonary and Critical Care Medicine, James H. Quillen College of Medicine, Johnson City, Tenn.

A 53-year-old man presented with nausea, poor appetite, progressive generalized weakness, and malaise of 3 to 4 weeks' duration. His medical history was significant for coronary artery bypass grafting 4 months previously, hypertension, and hyperlipidemia. He denied ethanol and consumption of other alcohol-containing solutions. He also denied illicit drug use, recent traumatic injury, and recent infectious illnesses. The patient had been taking simvastatin 40 mg every day for 3 years. Diltiazem 30 mg QID had been initiated 3 months earlier for blood pressure control. His vital signs were stable. He had no hepatosplenomegaly, abdominal tenderness, or musculoskeletal tenderness. His arterial blood gas values showed a compensated metabolic acidosis (pH 7.37, [Pco.sub.2] 15.2 mm Hg, [Po.sub.2] 88.7 mm Hg). Laboratory data was also significant for an anion gap of 22 and a serum lactate of 8.3 mmol/L. His blood urea nitrogen, creatinine, glucose, and thiamine levels were normal. His blood also tested negative for ke tones, [beta]-hydroxybuterate, methanol, and ethylene glycol. His serum salicylate level was not elevated. There was laboratory evidence of end organ damage of hepatitis and rhabdomyolysis. The patient's simvasta in therapy were discontinued and his acidosis resolved gradually. Simvastatin, a hydroxymethylglutarate coenzyme A (HMG-CoA) reductase inhibitor, is a commonly used cholesterol-lowering agent. The long-term safety profile of simvastatin, established over 10 years of clinical use, is excellent. HMG-CoA reductase inhibitors block 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate limiting enzyme in cholesterol synthesis. However, other important nonsterol compounds, such as coenzyme QIO (CoQIO), are also derived from the same synthetic pathway. CoQ10 is an essential carrier of the mitochondrial respiratory chain that regulates oxidative phosphorylation. HMG-CoA reductase inhibitor have been documented to lower serum concentrations of CoQ10. It has been suggested that the adverse effects caused b y HMG-CoA reductase inhibitors is due to CoQIO deficiency in tissue mitochondria. Documentation of this cause and effect phenomena, however, has been lacking. We offer evidence that lactic acidosis may develop as a complication of simvastatin therapy. Our patient also manifested the well known HMC-CoA reductase inhibitor drug toxicities of rhabdomyolysis and hepatitis. The occurrence of these known adverse events with lactic acidosis in our patient suggests that interference of mitochondrial respiratory chain may indeed play a role in the toxicity of this class of drugs. Whether lactic acidosis is an additional unusual side effect or evidence that mitochondrial dysfunction is the mechanism through which the other toxicities of HMC-CoA reductase inhibitors are manifested remains to be elucidated.

A MAN WITH HEEL PAIN: AN ATYPICAL PRESENTATION OF RENAL CELL CARCINOMA. David A. Gose, MD, L. E. Robertson, MD, and Ali R. Rahimi, MD. Department of Internal Medicine Education, Memorial Health University Medical Center, Savannah, Ga.

Renal cell carcinoma represents 1% to 3% of all visceral malignancies. Since renal cell carcinoma can produce such a variety of symptoms, it is often considered one of the great "mimics" in medicine. We are presenting a case of renal cell carcinoma manifested with heel pain and calcaneous metastasis. A 47-year-old white man with no history of arthritic pain presented with new onset right heel pain. Physical examination was unremarkable. X-ray of the foot revealed a destructive calcaneous bone lesion. Subsequent open biopsy of the lesion was consistent with clear cell carcinoma. Further workup established the diagnosis of bilateral renal cell carcinoma. Renal cell carcinoma is associated with a classic triad, including hematuria, flank pain, and flank mass. Unfortunately, this entire triad is present in only 10% to 20% of cases. Hematuria is the most sensitive finding and eventually develops in approximately 90% of cases. It often can produce constitutional symptoms of malaise, fever, and weight loss, or paran eoplastic syndromes, including polycythemia, hypercalcemia, and hypertension. Renal cell carcinoma most commonly metastasizes to lungs and bone. Renal cell carcinoma has an unpredictable clinical course. Treatment of localized disease is surgical nephrectomy. No chemotherapy agent has been consistently effective in producing regression. Interferon-alfa and IL-2 are used for treatment but have low response rates. Renal cell carcinoma continues to be one of the great mimics in medicine. The best treatment for this disease remains early detection and surgical resection. To our knowledge, this is the first atypical presentation of renal cell carcinoma with calcaneous metastasis reported in the literature.

METHICILLIN RESISTANT STAPHYLOCOCCUS AUREUS (MRSA) ENDOCARDITIS SECONDARY TO TONGUE PIERCING. Peter R. Harding, DO, Michael W. Yerkey, MD, Gregory Deye, MD, and Donald Storey, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

An 18-year-old woman presented with fever, malaise, nausea and anorexia. She was healthy until one week prior to presentation when she allowed an acquaintance to repierce his tongue with her tongue stud. She then rinsed the blood-tinged stud with beer and replaced it in her tongue. Three days later she developed fevers up to 104[degrees] F. She became progressively lethargic and dyspneic. She had no past medical or surgical history and denied IVDU. Physical examination revealed clear lungs, regular tachycardia and II/VI systolic murmur at the LUSB without radiation. She had multiple Janeway lesions and splinter hemorrhages on all extremities. Laboratory evaluation was remarkable for WBC 14,000. ECG and chest x-ray were unremarkable. Transesophageal echocardiogram found a 3 cm mitral valve vegetation. CT and MRI of the brain showed three right-sided, subcentimeter enhancing lesions consistent with emboli. Blood cultures were positive for MRSA. She was treated with antibiotics and underwent emergent mitral valv e replacement and perivalvular debulking surgery. We postulate that a pierced tongue was the portal of entry for S aureus leading to infectious endocarditis (IE) in our patient. Previously, most cases of S aureus IE were community acquired; however, recent liturature suggests a shift to nosocomial acquistion. In addition, community-acquired native valve MRSA IE in non-IVDU is extremely rare. We hypothesize that this patient's IE was a direct result of the unsanitary tongue piercing. This is the first reported case of MRSA IE related to tongue piercing.

THE COMBINED SURGICAL APPROACH FOR ORBITAL DECOMPRESSION IN THYROID EYE DISEASE, AN ANALYSIS OF RESULTS. Steven R. Anderson, MD, FACS. Department of Ophthalmology, University of Tennessee College of Medicine, Chattanooga Unit.

This presentation will discuss the surgical approach to the orbit using a combined orbital and sinus approach. We will cover the surgical anatomy of the normal orbit and sinuses as well as the altered anatomy of the severely congested orbit in thyroid eye disease. The criteria for orbital decompression will be covered as well as necessary ancillary tests that the general ophthalmologist can perform that will help lead to timely referral. Surgical results will be analyzed including appearance, visual acuity, visual fields and patient satisfaction. Complications, pitfalls to surgery and timing of orbital decompression in relation to eyelid surgery and strabismus will be discussed.

CLINICAL MANIFESTATIONS OF ELECTROLYTE DISTURBANCE ASSOCIATED WITH SHORT BOWEL SYNDROME AND CROHN'S DISEASE. Luiz Nascimento, MD, Linda Astalos, SFNP, Susan Craven, RN, A/GNP, Diane Brown, ANP, and Alfredo Pegoraro, MD. Hamlet, NC.

Short bowel syndrome (SBS) has been shown to cause significant electrolyte imbalances with major (and/or minor) clinical consequences. We have identified three patients with SBS with a variable range of clinical manifestations: A) The first patient has shown significant hypocalcemia characterized by tetany - completely corrected by calcium replacement and myocalcin (nasal spray). Hypokalemia (3.1 mEq/L) and hypomagnesemia (1.4 mg/dL) were prominent features; B) The second patient showed visual disturbances including decreased night vision, corrected by antibiotic therapy, most likely associated with improvement of absorption of vitamin A, hypokalemia was not a feature due to end stage renal disease and; C) The third patient presented with proximal muscle paralysis secondary to severe hypomagnesemia (0.6 mg/dL) and hypokalemia (2.4 mEq/L) completely reverted following intravenous replacement of magnesium and potassium. The patient was unable to raise her arms to comb her hair, or to climb up the first step of a stairway. Hyperreflexia and muscle twitching with facial numbness were other findings. The grip was normal bilaterally. Hypocalcemia was a universal finding but phosphate levels were normal or minimally altered in the two patients without renal failure. Two patients had ileostomy - one had ulcerative colitis, one ileostomy secondary to multiple surgeries for pelvic cancer. The third one had severe malabsorption secondary to Crohn's disease. All had chronic diarrhea. Acute and chronic interventions for therapy of electrolytes disturbances are discussed and literature reviewed.

RICHTER'S SYNDROME: A DEVASTATING COMPLICATION OF CHRONIC LYMPHATIC LEUKEMIA. Michael Puruckherr MD, K. Krishnan, MD, Ryland Byrd, Jr., MD, and Thomas Roy, MD. Department of Internal Medicine, East Tennessee State University, Johnson City, Tenn.

Richter's syndrome (RS) refers to the occurrence of diffuse, large cell lymphomas in chronic lymphatic leukemia (CLL). CLL is an indolent but incurable disease due to accumulation of mature lymphocytes. The transformation to Richter's syndrome changes this prognosis dramatically. We describe a 43-year-old man who presented with cervical lymphadenopathy, generalized pruritus, fever and night sweats, intolerance to alcohol and high white cell counts. Bone marrow biopsy and flow cytometry was consistent with B-CLL. He was initially treated with 4 cycles of cytotoxic chemotherapy (chlorambucil/prednisone). Since he was not responding to this regime, he was considered for bone marrow transplantation. Cytoreduction was attempted with a purine analogue, fludarabine, prior to planned bone marrow transplantation. Recurrent herpes zoster infections, neutropenic fever and pancytopenia complicated his course. He also had rectal bleeding and had to undergo a fistulotomy. Most of the lymphadenopathy appeared to decrease in size on fludarabine except for the left inguinal lymph nodes. These nodes were noticeably increasing in size. An excisional biopsy of the inguinal lymph nodes was consistent with large cell lymphoma, i.e., Richter's syndrome. It was decided to change therapy to standard non-Hodgkin's lymphoma chemotherapy, CHOP, (cytoxan, vincristine, adriamycin, prednisone) at this time. There was no response to 2 cycles of CHOP chemotherapy. Clinical and radiological progression of disease in the lymph nodes and also the appearance of new nodular densities in lung and liver were noted. He was due to commence alternate salvage chemotherapy before bone marrow transplantation, but died due to problems related to prolonged myelosuppression and neutropenia. This patient's course mirrors the original description of this condition by Maurice Richter in 1924. RS in CLL is an abrupt deterioration with worsening lymphadenopathy, extranodal involvement, severe constitutional symptoms and an uniformly poor prognosis. Median survival i n RS is less than 6 months. It arises from the same clone as CLL. The mechanisms that determine transformation are not known. No effective therapy is currently available for this devastating complication that arises in a common hematological disease with a generally less aggressive course. Close follow up and regular physical examinations are required even in asymptomatic patients with CLL to identify this complication.

PORTAL VEIN GAS AND PNEUMATOSIS INTESTINALIS. Yazan Abu Qwaider, MD, and Subrarnanyam Chittivelu, MD. Department of Medicine, Texas Tech University Medical Center, Amarillo.

An 80-year-old man was brought to the emergency room by his daughter with fever, dyspnea, and abdominal pain for 1 day. The patient denied any history of nausea, vomiting, diarrhea, or melena. He had not experienced similar complaints in the past. His recent medical history was significant for an abdominal hernia repair 6 weeks earlier, which was complicated postoperatively by right femoral vein thrombosis requiring embolectomy. Other medical history included CHF, AFib, HTN, DM, and dementia. He was taking digoxin, captopril, warfarin, insulin, hydrocodone, dulcolax, hydrochiorothiazide-triamterene, and milk of magnesia. On physical examination, the patient was alert, awake, and well-oriented with blood pressure 120/60 mm Hg, temperature 41.7[degrees]C, pulse rate irregularly irregular at 112/mm, respiratory rate 25/mm, and oxygen saturation 92% on 2 L of oxygen given via nasal canula. Signs of pulmonary edema were evident on lung auscultation. Ivioderate abdominal distention was present without organomegaly or ascites. The remainder of the examination was unremarkable. Routine workup, including the electrolytes, CBC, and UA, was normal. Coagulation panel showed elevated prothrombin time of 72 seconds with INR of 5.49. ECG showed atrial fibrillation. Abdominal and pelvic CT scan showed gas in the liver, portal vein, splenic vein, and walls of small and large bowel without any evidence of perforation of viscera. The patient was admitted into ICU with the diagnosis of portal vein gas (PVC) and Pneumatosis intestinalis (P1). Surgical consult was obtained and patient treated supportively. He recovered without any complications. PVC and PI are relatively uncommon. Most commonly PVG and P1 are associated with surgical and medical conditions such as bowel ischemia, acute abdomen, after GI diagnostic procedures, AM repair, CHF, AIDS, steroid use, etc. In our patient, even though he had multiple risk factors for bowel ischemia, PVG and PI developed without any evidence of ischemic bowel; instead CHF and hydrocodone induce d bowel distention seemed to be the responsible mechanisms for PVC and IV.

POEMS SYNDROME. T.B. Repine, MD, D.P. Mong, MD, and M.K. Koops, MD. Brooke Army Medical Center, Fort Sam Houston, Tex.

POEMS syndrome is a remarkably rare disorder characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes. We present a 70-year-old white man with hypertension who was found to have 100 mg/dL of protein in his urine and an enlarged prostate with a PSA of 9.9 mg/dL during routine primary care screening. Subsequent 24-hour urine showed 1,720 mg protein and urine protein electrophoresis revealed a biclonal M spike of IgG and IgA, which was also found in the serum. The patient's enlarged prostate was diagnosed as stage T1, N0, M0 adenocarcinoma, and he underwent radical prostatectomy. After surgery, he complained of new bilateral lower extremity paresthesias that were attributed to routine use of serial compression devices during his surgical and postoperative course. The paresthesias, however, failed to improve after discharge and progressed insidiously over 8 months to incapacitating peripheral neuropathy, prompting hospital admission. Physical examination also identifi ed diffuse pitting edema, hepatomegaly, lymphadenopathy, and thickened hyperpigmented skin including associated violaceous rhinophyma. EMG confirmed diffuse distal sensorimotor polyneuropathy with evidence of demyelination and secondary axonal degeneration. Bone marrow biopsy showed 10% plasma cells (normal [less than]5%) with lambda light chain restriction. Additional laboratory results were significant for serum TSH of 9.1 IU/mL and FT4 of 0.9 ng/dL, consistent with subclinical hypothyroidism and ACTH stimulation test with a peak 60 minute serum cortisol of 14.4 ug/dL revealing adrenal insufficiency. This constellation of findings fulfilled all five criteria for POEMS syndrome. Also known as Crow Fukase or Takatsuki syndrome, POEMS is an extremely uncommon collection of findings associated primarily with plasma cell dyscrasias. Despite this known association, the underlying causal mechanism and the entire spectrum of protean manifestations are still unknown. Treatment options are limited, though removal or irradiation of a localized plasmacytoma improves patient symptoms dramatically. We performed an exhaustive but unsuccessful search for a plasmacytoma and are now treating our patient with melphalan and prednisone. Unfortunately, his condition has continued to deteriorate. Further study of this unique syndrome is needed to advance both our understanding of the pathophysiology of POEMS syndrome and to develop additional treatment options.

PERCUTANEOUS STENTING OF THE RIGHT PULMONARY ARTERY DUE TO HISTOPLASMA CAPSULATUM MEDIASTINAL FIBROSIS. Ronald N. Wool, MD, and Daniel F. Lee, DO. Department of Medicine, Eisenhower Army Medical Center, Fort Gordon, Ga.

Fibrosing mediastinitis is a rare, insidious disease, with a variable progression, that can produce an extensive fibrotic response in the mediastinum. It is typically due to an infectious etiology, with Histoplasma capsulatum being the most common cause in the United States. The ensuing fibrotic process can lead to compression of mediastinal structures, including the great vessels, airways and esophagus. Until the past decade, medical and surgical therapies offered limited clinical effectiveness, often with high risk. Fiberoptic and stent technologies have allowed less invasive techniques for the treatment of tracheobroncheal and esophageal compression with varying success. Advancements in percutaneous stenting have also allowed successful treatment of superior vena cava syndrome caused by fibrosing mediastinitis. The present case describes the first successful employment of percutaneous angioplasty and stenting of the right pulmonary artery, in a patient with severe stenosis due to fibrosing mediastinitis.

PSUEDALLESCHERIA BOYDJI (P BOYDII) BRAIN ABSCESSES. Capt Julie Mennino, MD, and Capt Donald Storey, MD. Keesler Medical Center, Keesler Air Force Base, Miss.

A 50-year-old man presented following a near-drowning episode secondary to a MVA with hypothermia, shock and respiratory failure requiring intubation. He subsequently developed ARDS and required two days of ventilatory support. Sputum cultures demonstrated Aeromonas sobri and Enterobacter cloacea for which levofloxacin was started. He was discharged one week after his initial presentation. One week later he reported left-sided weakness, lethargy, chills, sweats and right-sided headache. Physical exam revealed dense left hemiparesis with 0/5 strength, left facial droop and left-sided hyporeflexia. CT scan of the head revealed a 2.0-cm abscess in the right frontal-parietal region. MRI showed a 2.5 cm abscess in the right frontal-parietal lobe and 1 cm abscesses in the left occipital and frontal regions. Ceftriaxone, metronidazole and trimethoprimsulfamethoxazole were started. He underwent craniotomy with aspiration and drainage of the right frontal-parietal lobe abscess. Gram stain showed many septated hyphae a nd high dose ketoconazole was started. Cultures demonstrated Scedosporium apiospermium (the asexual form of P boydii) and anti-fungal therapy was changed to high close miconazole. He suffered uncal herniation and died two weeks later. P boydii is the most common fungus infection after near drowning episodes. The majority of cases have involved disseminated disease and CNS involvement in immunocompetent hosts. Treatment of P. boydii brain abscess includes early surgical intervention and high-dose miconazole therapy, as this fungus is resistant to amphotericin B. Outcomes are poor regardless of treatment modality, especially in those patients with multiple abscesses. A high index of suspicion is necessary in near drowning cases to offer these patients any hope of recovery.