key: cord-0000055-1a3sy8ja
authors: nan
title: CLINICAL VIGNETTES
date: 2003-04-03
journal: J Gen Intern Med
DOI: 10.1046/j.1525-1497.18.s1.20.x
sha: a037a1a6fe76f1c43e33a639231b9874cb655f88
doc_id: 55
cord_uid: 1a3sy8ja

nan

LEARNING OBJECTIVES: Recognize that the presenting features of amyloidosis are protean and depend on the organ systems involved. Recognize that cardiac involvement is common in primary amyloidosis and that symptomatic heart involvement carries a poor prognosis. CASE INFORMATION: 66 year old man without PMH presented 8 months of progressive exertional dyspnea and fatigue. Evaluation revealed volume overload with anasarca and signs of biventricular heart failure. Laboratory studies revealed renal insufficiency with a creatinine of 1.8 and 2+ proteinuria. serum protein electrophoresis with immunofixation showed a monoclonal IgA kappa paraprotein; urine protein electrophoresis was unremarkable. Echocardiogram revealed an ejection fraction of 20%. Right ventricular function was moderately reduced and right and left ventricular hypertrophy was noted. ECG showed atrial fibrillation with a ventricular response of 105 BPM and low voltage. Pt. underwent right heart catheterization with endomyocardial biopsy. Tissue stained positive with crystal violet and Congo red with characteristic green birefringence under polarization microscopy. This result together with the paraprotein established the diagnosis of AL amyloidosis. IMPLICATIONS/DISCUSSION: Amyloidosis is a disease characterized by extracellular accumulation of insoluble protein fibrils in various organs and tissues. Classification of amyloidosis is based on the nature of the precursor proteins that form the fibril deposits. AL amyloidosis (primary) is a plasma cell dyscrasia in which clonal plasma cells in the bone marrow produce monoclonal immunoglobulin light chains. Clinical manifestations reflect the organ systems involved with kidney and heart involvement being most common. Clinically evident cardiac involvement occurs in up to 50% of patients with AL amyloid and often leads to significant cardiac dysfunction. Diastolic dysfunction is caused by diffuse infiltration of the left ventricular myocardium with resultant stiffening and impaired relaxation and usually precedes systolic dysfunction. Systolic dysfunction results from replacement of functional myocardial tissue with amyloid protein. The conduction system can be affected by amyloid infiltration as well, leading to conduction disturbances, arrhythmias or sudden death. ECG findings include low voltage, conduction abnormalities such as AV block, atrial fibrillation and pseudoinfarct patterns. This case demonstrates a classic presentation of AL amyloidosis with significant cardiac involvement. AL amyloidosis has a median survival of one to two years but patients with symptomatic heart involvement have a median survival of only six months. LEARNING OBJECTIVES: Recognize the importance of counseling patients who have received previous valve replacements that continued intravenous drug use may disqualify them from lifesaving interventions. CASE INFORMATION: A 44 year-old presented with progressive dyspnea, fevers and substernal tightness. He had a endocarditis requiring porcein valve replacement in 1993. He started using intravenous cocaine and heroin weekly one month prior. He had a fever of 40 C and a holosystolic murmur. Blood cultures grew steptococcus viridans. Transesophageal echocardiography showed aortic valve vegetations on all leaflets and a ring abscess. Toxicology screen was positive for cocaine. Ampicillin and gentamicin were initiated. After six weeks of therapy, the aortic vegetations and blood cultures persisted. Cardiothoracic surgery was consulted, but declined intervention, citing the likely recidivistic drug use and futility of care. IMPLICATIONS/DISCUSSION: Surgical intervention in active intravenous drugs users is an issue of ethical debate. Ninety percent of heroin users will reuse even after successful rehabilitation. Continued intravenous use represents a hundred-fold increased risk of recurrent endocarditis. The apparent futility of surgical intervention in this setting has prompted surgical services to adopt a``one strike and you are out policy.'' This is almost a certain death sentence for patients meeting surgical criteria. The ethics committee was involved but could not establish ethical grounds for challenging surgery's decision. The precedent of withholding organ transplantation from continuing drug users was applied. Physicians should counsel patients who have received previous valve replacements that continued intravenous drug use may disqualify them from lifesaving interventions. Added emphasis on rehabilitation following valve replacement may be the only sure method to avoid this dilemma. 

A 53 year-old woman presented with four months of weakness and a rash. The weakness was progressive, symmetric, and proximal. The muscles of both her upper and lower extremities were affected. The erythematous rash was located on the inner thighs and arms bilaterally. She could not raise her arms and had difficulty holding her head erect; her leg weakness prohibited standing independently. Sensation and reflexes were not affected. She had normal serum electrolytes and complete blood count. Her AST was 200 U/L, ALT 78 U/ L, ALKP 52 U/L, CK 7021U/L, and ESR 29 mm/hr. Her TSH, hepatitis panel, ANA, rheumatoid factor, anti-DS DNA, c-ANCA, and p-ANCA were normal. A muscle biopsy of left thigh showed vasculitis and perifascicular atrophy and necrosis. Methylprednisolone and methotrexate were initiated with resolution of her symptoms. An age-appropriate screen for cancer was negative. IMPLICATIONS/DISCUSSION: The diagnosis of dermatomyositis/polymyositis (DM/PM) requires a high degree of clinical suspicion, as it is established based on the combination of clinical, laboratory, and muscle biopsy findings. This patient demonstrated the proximal muscle weakness characteristic of DM/PM. Other causes of proximal muscle weakness, including electrolyte abnormalities, hypothyroidism, inclusion body myositis or drug induced (HMG CoA reductase inhibitors or steroids) were excluded by history and laboratory data. Perifasicular inflammation suggests dermatomyositis; perimysial inflammation is characteristic of drug-induced myositis. Diagnostic criteria for dermatomyositis include symmetric proximal muscle weakness, elevated serum muscle enzymes, perifasicular inflammation on muscle biopsy, and rash. The classic dermatologic findings of PM/DM include mechanic's hands (synthetase AB subset), heliotrope lids, Gottron's sign and shawl sign . Physicians should be aware that most cases of DM/PM present without the classic findings of DM/PM. Systemic corticosteroids are used for treatment. Immunosuppressive agents are used in cases refractory to corticosteroid treatment. Due to an association with underlying malignancy, an age and gender appropriate cancer screen should be performed in all patients diagnosed with dermatomyositis.

A CASE OF PREGNANCY, HYPOXIA, AND TOO MUCH PROTEIN. R.A. Andrews 1 , E.L. Salerno 2 ; 1 University of Connecticut, Farmington, CT; 2 University of Connecticut, Columbia, CT (Tracking ID #76994) LEARNING OBJECTIVES: 1) Discuss diagnosis, eitiology, and management of pulmonary alveolar proteinosis. CASE INFORMATION: A.G. is a 29 year old female 15 weeks into her fourth pregnancy who presents for diagnosis and treatment of severe hypoxia. Ten weeks prior to admission, she begins having progressive dyspnea on exertion, non-productive cough, weakness, fatigue, nausea, and diarrhea, but no fevers and occassional chills. Two days prior to admission she is referred to the emergency room for severe hypoxia. Patient denies problems with previous pregnancies and is HIV negative. Past medical history and social history are essentially unremarkable. At presentation, she is afebrile with a blood gas on room air that shows a PaO2 of 64. Cardiovascular exam is benign, but diffuse course rales are heard on lung exam. The patient has perioral and acral cyanosis and clubbing. Chest xray shows a diffuse patchy alveolar infiltrate. HCT is 49.3 with normal chemistries and negative D-dimer. Patient is placed on a non-rebreather mask at 100% and started on broad spectrum antibiotics. On day two, she is transferred to intensive care with a PaO2 of 54 on 100% oxygen. Video-assisted thorascopic biopsy is obtained providing the diagnosis of pulmonary alveolar proteinosis. Patient then undergoes whole-lung lavage with improvement in chest xray and PaO2 saturation. IMPLICATIONS/DISCUSSION: Pulmonary alveolar proteinosis (PAP) is a non-inflammatory disease of the lungs affecting men more than women (2:1) typically between 30 and 50 years of age. The primary defect is either a failure to degrade, or increased production, of surfactant causing an accumulation of amorphous proteinaceous material within the alveoli. The exact eitiology remains unclear. Patients generally present with dyspnea on exertion, 30% are asymptomatic. Common symptoms are dry cough, weight loss, malaise and fatigue. Rales are present in 50% of cases. Typical xray findings reveal perihilar alveolar infiltrates with typical``bat wing'' appearance. Diagnosis is made from BAL (bronchioalveolar lavage) or lung biopsy. Lavage produces a milky effluent composed of amorphous granular material that stains PAS (periodic acid-Schiff) positive. On biopsy, inflammatory cells are rare and there is no fibrosis. Alveoli are congested with proteinaceous material and dysfunctional macrophages. Standard of care is whole-lung lavage with 30±40% of patients resolving with only one lavage while the majority of patients require repeat lavage at 6±12 month intervals. Newer treatments include high doses of GM-CSF (granulocyte macrophage-colony stimulating factor) and possibly bone marrow transplant. Prognosis of PAP has been shown to be a 74% 5-year survival. LEARNING OBJECTIVES: 1. Recognize the long term complications after heart surgery for congenital defect in childhood. 2. Appreciate that patients living in precarious conditions need careful management that goes beyond an initial impression, although the risk of somatizing exists. CASE INFORMATION: A 25 year old male asylum-seeker, living in Switzerland for a month, with a history of surgical repair of a pentalogy of Fallot 20 years before with no subsequent complications, presented with breathing-related chest pain responsive to paracetamol, exertional dyspnoea and orthopnoea ± on the same day that five of his compatriots living in the same asylum-seeker centre located in a public bomb shelter with the same symptoms! He was in good general health, his blood pressure was 93/66 mmHg, and he had a regular heart rate of 100 beats/min and a respiratory rate of 25/min. His chest was slightly asymmetrical, with slight arching of the left hemithorax, the sternotomy scar appeared normal, the apical impulse was widened and pulsations were apparent across the whole sternal and left parasternal area (Harzer's sign). Auscultation revealed a holosystolic, non-radiating crescendo murmur of 3/6 in the left parasternal area. Diastole was free and peripheral arteries were normal. Laboratory tests were within normal limits, excluding acute conditions such as pulmonary embolism or cardiac ischaemia. The ECG revealed sinus tachycardia, a vertical frontal axis of the QRS complex and complete right bundle branch block. A transthoracic echocardiogram revealed a voluminous mass with an echo-dense border and an echo-poor centre adjacent to the free wall of the right ventricle, no vascularized (free of internal blood flow), exerting an obvious compression on the right ventricle, the intraventricular pressure being estimated at 80 mmHg based on the high-velocity severe tricuspid regurgitation. Magnetic resonance imaging and computed transverse tomography confirmed the presence of a hypodense mass, in close contact with the pericardium (Fig. 1 & 2) . The severe compression of the right ventricle prompted the surgical removal of this mass. The mass was adhering to the rib cage and the free wall of the right ventricle. Bacteriological investigation revealed the presence of an abscess with coagulase-negative staphylococci. Postoperative progress was uneventful, and the medium-term outcome favourable. No abnormal cavity was visualized during transthoracic echocardiography at the 3-month postoperative control. IMPLICATIONS/DISCUSSION: While infections are known to occur after sternotomy, usually involving coagulase-negative staphylococci, the formation of an abscess in the anterior mediastinum several years after the intervention appears to be exceptional. This diagnosis came to mind only after the more common postoperative complications, e.g. pseudoaneurysm or pericardial haematoma, and the wide range of possible diagnoses covering tumours, infections and malformations of the anterior mediastinum had been considered. Although the signs and symptoms were not very specific and potentially psychogenic in a patient living in precarious conditions, we were inclined to consider a wide range of differential diagnoses, given the patient's history.

care, her pulmonary status gradually returned to baseline and she was tapered off phenytoin without subsequent seizure activity. IMPLICATIONS/DISCUSSION: There are very few reports of a pulmonary embolus (PE) presenting as seizure. Given the acuity of onset of this patient's symptoms and the severity of her initial respiratory acidosis, as well as the lack of neurologic findings, we presume that her seizure represents the onset of her pulmonary embolus, though we can not definitively establish causal relationship. Clinical suspicion of PE may be compromised by the attribution of symptoms to the seizure, such as tachypnea, tachycardia, and hypoxia. The initial evaluation of seizure patients is primarily neurologic, delaying the diagnosis of a cardiopulmonary syndrome. In this particular case, the patient's medical history played a key role in the delayed diagnosis of PE, as her pulmonary symptomatology was attributed to asthma, despite the fact that she had been well controlled on minimal medication prior to admission, and that her clinical signs did not completely resolve with the treatment of her exacerbation. Furthermore, this young, active woman had low risk for thromboembolic disease, especially in the setting of a negative evaluation for hypercoaguability. She did use oral contraception, but this particular medication includes only 0.10mg levonorgestrel and 0.2mg ethinyl estradiol and the patient was a nonsmoker. Thromboembolism should therefore be considered in any patients with acute dyspnea, evidence of cerebral hypoperfusion, hypoxia, or unexplained seizure, even in the setting of pulmonary pathophysiology. year-old healthy female who presented to the emergency department after having her first seizure. She was found by her son in bed with jerking of her left upper extremity. When she regained consciousness she found that she bit her tongue and had urinary incontinence. She was well up until three days before when she developed a constant low-grade headache. Her last menstrual cycle was three months before presentation although she reports some light vaginal bleeding one week prior. Per the patient she had no sexual activity for six months. Physical exam on admission was significant for blood pressure of 145/82 and 1+ ankle edema. The neurological exam was completely normal. The patient did not know she was pregnant on admission but an initial beta-HCG was 12,700. Her urinalysis showed 3+ proteinuria. An ultrasound confirmed the presence of a 30 week gestation fetus. A head CT showed low attenuation lesions in both subcortical parietal lobes and in the left frontal lobe. The patient was transferred to Labor and Delivery with the presumptive diagnosis of eclampsia. She received intravenous magnesium sulfate and steroids to enhance fetal lung maturity. The next day after some fetal distress she delivered a viable male infant via cesarean section. Her vaginal bleeding one week prior to admission was due to placental abruption. IMPLICATIONS/DISCUSSION: Eclampsia is not commonly encountered in the practice of internal medicine but it should be considered in the evaluation of a new-onset seizure disorder in women of reproductive age. It has an incidence of approximately 5 cases per 100,000 live births. It is characterized by generalized seizures or coma in the presence of preeclampsia (hypertension, edema, proteinuria) . It is most common in nulliparous women in the teenage years and early twenties and in women over 35. More than 20% of cases occur before 30 weeks gestation, and 75% of cases occur at term or within 48 hours of delivery. It remains the second most common cause of maternal death in the United States. Treatment consists of oxygen, intravenous magnesium and antihypertensive medications. Anticonvulsant medications may be given for recurrent seizures. The fetus should be delivered promptly. Unfortunately this woman did not recognize that she was pregnant therefore she did not receive any prenatal care. This case underscores the importance of pregnancy testing in all women of reproductive age with a new-onset seizure disorder to expedite the diagnosis. Eclampsia should be part of the differential diagnosis in the evaluation of a new seizure disorder in all women of reproductive age unless she proves not to be pregnant. Early recognition and treatment of this disorder can prevent some potentially devastating consequences.

WHAT IS THE MEANING OF TRISMUS? H.A. Batal 1 , R.H. Harris 1 ; 1 Denver Health Medical Center, Denver, CO (Tracking ID #74878) LEARNING OBJECTIVES: 1) Identify the differential for trismus. 2) Recognize the acute presentation of tetanus. CASE INFORMATION: A 20 yo previously healthy Mexican native presented with 4 days of left cheek spasm associated with pain. He denied any trauma, abrasions or lacerations, thought that he had received his vaccines as a child, and denied any systemic symptoms such as fever or myalgias. He also denied sore throat or dental pain and did not have a personal or family history of neurologic problems, including tics. He had bitten his tongue a number of times due to his left cheek spasm and was finding it difficult to eat solid food, although his intake of liquids was adequate. On examination he had normal vital signs and did not appear to be in any distress. He spoke through slightly clenched lips, but was handling his secretions without difficulty. He had no apparent spasms or tics involving other muscle groups. His neurologic exam was normal, although he refused to protrude his tongue, as he was afraid that he would bite it. His exam showed poor dentition but no localizing dental infection and no evidence of pharyngeal abscess. Submandibular and parotid glands were non-tender. He was noted to have spasm of his left masseter muscle, and broke a tongue blade when an attempt was made to keep his mouth open for examination. He was only able to open his jaw approximately 2 cm. Laboratory examination showed a normal CBC, calcium, and electrolytes. A dental consultant was unable to find any underlying odontogenic etiology for the patient's trismus. Dental radiographs and head MRI were unrevealing. Because the diagnosis of acute tetanus was entertained, the patient was admitted for 48 hours of observation during which time his symptoms did not change. He was discharged with a diagnosis of trismus of unknown etiology and therapy with tegretol at 200 mg bid was initiated. IMPLICATIONS/DISCUSSION: Trimus is defined as spasm of the masticatory muscles, with difficulty in mouth opening, and is a characteristic early symptom of tetanus commonly referred to as lockjaw. The differential diagnosis of trismus is limited and besides acute tetanus includes odontogenic infections, peritonsilar abscess, strychnine poisoning, and drug-induced dystonic reaction. In addition, trismus can be confused with the jaw claudication seen in temporal arteritis as well as the pain of trigeminal neuralgia. Widsom tooth (3rd molar) infections are the most common odontogenic cause of trismus and notably can present without evidence facial swelling. Acute tetanus is important to recognize because it can progress to death as a result of respiratory failure, but the prognosis can be favorable if supportive treatment is initiated promptly. Predictors of inadequate immunity are older age, birth outside the US, low educational status, and poverty. LEARNING OBJECTIVES: To recognize the presentation and therapy of thyrotoxic periodic paralysis. CASE INFORMATION: A 26 yo Latino male was brought to the ER complaining of 12 hours of progressive upper and lower extremity weakness to the point that he could no longer get out of bed. The symptoms began with leg cramps shortly after a family picnic. He had no complaints of abnormal sensation, difficulty breathing or swallowing. He denied recent illness or vaccinations, or ingestion of canned food. He also denied past medical problems, medications, or illicit drug use. His mother and sister had hypothyroidism. The examination showed an alert, well developed male with a mildly enlarged thyroid, but no tremor or lid lag. Strength in the upper extremities was 3/5, and 2/5 in the lower extremities. Deep tendon reflexes were 1 plus bilaterally, and the cranial nerve exam was normal. Labs were remarkable for Na 142, K 1.8, Cl 111, CO2 20. A TSH was drawn. The EKG showed SR with flattened T waves and prominent U waves. After a total of 120 meq of combined IV and PO KCL, the serum K was 5.1 and the patient's symptoms and EKG findings had completely resolved. The following day, the TSH and FT4 returned at <0.03 and 2.48 respectively, consistent with hyperthyroidism. The patient was diagnosed with thyrotoxic periodic paralysis. Propranolol was initiated and a thyroid scan scheduled as an outpatient. Despite compliance with medications, the patient returned to the ER with a recurrence of symptoms after a large Christmas dinner. The iodine uptake scan showed a mildly enlarged gland with homogeneously increased uptake: 20 % (5±17%) at 4h, and 48 % (8±30%) at 24 hours, consistent with Graves disease. Therefore, the patient was treated with radioactive iodine ablation. Four months into followup, the patient was doing well, but had become hypothyroid. IMPLICATIONS/DISCUSSION: Thyrotoxic periodic paralysis is a well described disease in up to 2 percent of all Asian men afflicted with hyperthyroidism. However, it is being increasingly recognized in patients of other racial backgrounds including Native Americans, Latinos and rarely Caucasians or those of African descent. This disorder is caused by overactivity of the Na-K-ATPase channel in the presence of increased thyroid hormone, which shifts potassium intracellularly. The inital treatment involves modest potassium supplementation and non-selective beta blockers. The more common familial periodic paralysis is related to the Na-Ca channel, and presents in a similar fashion, frequently after a carbohydrate rich meal or exercise. It is important for clinicians to understand that thyrotoxicosis of any etiology is an underlying cause of hypokalemic periodic paralysis because treatment of the thyroid disorder will also prevent further paralytic episodes.

AN ATYPICAL CASE OF POLYARTERITIS NODOSA. B.N. Batson 1 , J.W. Blackston 1 , C. Subramony 1 ; 1 University of Mississippi Medical Center, Jackson, MS (Tracking ID #75156) LEARNING OBJECTIVES: Recognize the clinical and lab findings of polyarteritis nodosa. Perform an appropriate workup when polyarteritis nodosa is suspected. CASE INFORMATION: A 46 y/o BM was transferred complaining of abdominal pain for 4 days that had not improved with conservative treatment. Outside x-rays demonstrated dilated loops of bowel without obstruction. He denied fever, chills, nausea, and vomiting but reported fatigue, anorexia, and a 40-pound weight loss over the past 6 months. He also reported progressive weakness and numbness of both legs which limited ambulation. Physical was significant for BP of 178/114 and a diffusely tender abdomen without guarding, rebound or mass. He had faint bowel sounds and was heme positive on rectal. He had 2/5 strength in bilateral hip, knee, and ankle flexors and extensors. Sensation was diminished in both feet up to mid-shin. Reflexes and Babinski's were normal. CXR was negatvie except for blebs, but KUB showed multiple dilated loops of bowel with air-fluid levels. Lab included WBC 14.1, Hct 27, and plts 417. BUN was 23 and creatinine 1.2. Total protein was 6.7 with albumin 2.3. Hep BsAg was positive; p-ANCA was negative. On HD#2, CT abdomen showed a 9x5cm right lower quadrant mass, moderate ascites, and patchy kidney enhancement with wedged-shaped hypodensities. Renal ultrasound showed normal kidney size with inhomogeneous architecture. On HD#3, sural nerve biopsy was suspicious for mononeuritis multiplex. Later on HD#3, a mesenteric arteriogram was normal. By HD#4, the patient had decreased abdominal pain with stable hematocrit, but creatinine had risen to 2.7. On HD#5 colonoscopy was normal. He then had an MRI-guided biopsy of the RLQ mass which yielded only red blood cells. On HD#8 surgical exploration found bloody ascites and an 8x10cm mass of the ileocolonic junction requiring hemicolectomy. Ascitic cytology was negative for malignancy. Pathology of the mass showed extensive polyarteritis nodosa involving the small-and medium-sized submucosal and mesenteric arteries. IMPLICATIONS/DISCUSSION: While this patient exhibited many classic symptoms of polyarteritis nodosa, his workup of that suspected diagnosis was confounded by an abdominal mass and false-negative mesenteric arteriogram. One must remember that the diagnosis of PAN is best made with tissue biopsy of an involved organ system. While a positive p-ANCA is suggestive of PAN, and a mesenteric arteriogram showing pseudo-aneurysms is sufficient for diagnosis, both of these tests are positive in less than 50% of patients with known polyarteritis nodosa.

normalize. Magnetic resonance angiography of the abdomen revealed severe stenosis of the distal left renal artery consistent with FMD. The patient underwent contrast-enhanced renal artery angiography that confirmed the diagnosis. Balloon angioplasty of the stenotic left renal artery was performed. The day after angioplasty, the patient's plasma renin decreased to 50 microU/ml and BP to 130/70. IMPLICATIONS/DISCUSSION: Renovascular hypertension should be suspected in patients with age of onset before 20 or after 50 years, severe or refractory hypertension, acute rise in BP over previously controlled hypertension, rise in plasma creatinine concentration especially after starting an angiotensin-converting enzyme (ACE) inhibitor, abdominal bruit, absence of family history of hypertension, a unilateral small kidney, and recurrent acute pulmonary edema or unexplained heart failure. RAS may result from FMD or atherosclerotic disease. FMD most commonly affects women between the ages of 15 and 50 and accounts for less than 10% of cases of RAS. Atherosclerosis is responsible for the other 90% of cases. Gadolinium-enhanced magnetic resonance angiography is the best noninvasive imaging modality to diagnose RAS with 100% sensitivity and 95% specificity. Renal angiography is the gold standard to confirm the diagnosis. Percutaneous angioplasty is the treatment of choice for renovascular hypertension secondary to FMD. Patients with hypertension secondary to atherosclerotic RAS should be treated with aspirin, cholesterol-lowering agents, and smoking cessation. ACE inhibitors and diuretics can be used to control hypertension but should be avoided in the presence of bilateral stenosis. Balloon angioplasty is less successful in atherosclerotic RAS but placement of stents improves the success rates. Surgical revascularization should be considered in patients who fail angioplasty. LEARNING OBJECTIVES: 1. Identify a likely cause of recurrent painful blistering diseases in young adults 2. Identify the classical presentation, manifestations and prognosis of Epidermolysis Bullosa 3. Recognize the main management issues in caring for Epidermolysis Bullosa patients CASE INFORMATION: A 19 y/o latina woman presented for evaluation of painful blisters over her left hand and both feet after recent initiation of jogging. She reported a history of recurrent painful blisters affecting both her hands and feet since childhood. More severe blistering occured in areas where her skin was rubbed. Steroid creams provided no improvement. Lesions in the past healed over about a month, leaving hyper-pigmented scars. This current flare involved both her feet and left hand, but no other area. Systems review was negative. Other family members were not affected. She took Tylenol with hydrocodone for pain. On examination the patient had multiple blisters, 2±3 cm in diameter, mostly on the plantar surface of both feet. The soles of her feet were thickened and pigmented in circular patch-like forms. The blisters were exquisitely tender to touch. Initial differential diagnosis of this patient's condition included bullous pemphigoid, dermatitis herpetiformis, porphyria cutanea tarda and bullous SLE. A skin biopsy performed by a dermatologist demonstrated histologic separation of the basal layer. After immunohistochemistry, a diagnosis of epidermolysis bullosa, simplex form, was made. IMPLICATIONS/DISCUSSION: Epidermolysis Bullosa (EB) is the term given to three major groups of approximately 16 variants of rare dominant and recessive genetic diseases in which minor trauma causes non-inflammatory blistering (mechanobullous disease). There are as many as 150,000 Americans afflicted, mostly children, but variants present up to third decade of life. Those with medium to more severe kinds of EB can live into their thirties. Mortality is predominantly related to suprainfections. Management consists of all efforts to avoid trauma, particularly to the hands and feet via mittens and soft slippers. Adequate long-term pain control is a crucial aspect of taking care of EB patients, as is prevention and early treatment of supra-infections of the blistering lesions. Clasically all EB variants are resistant to all therapy, though literature reports exist of rare responders to treatment with Phenytoin, a known collagenase inhibitor, as well as IVIg. Genetic counseling is essential and fetal skin biopsy techniques have been developed for prenatal diagnosis. The diagnosis of glucagonoma was confirmed by pathologic examination. Upon removal of the tumor, her rash subsequently cleared without any complications. IMPLICATIONS/DISCUSSION: Glucagonoma syndrome is a rare syndrome with an estimated incidence of about 1 in 20 million people. It occurs with equal frequency in men and women and is usually detected between 40 to 60 years of age. The syndrome is caused by excessive production of glucagon by the alpha-secreting cells of the pancreas. Patients may have a characteristic rash, called``necrolytic migratory erythema'', that involves the perioral and perigenital regions. There may also be accompanying glossitis, angular chelitis, and blepharitis. The rash usually responds poorly to topical treatment. The only curative treatment for the syndrome is surgery. Glucagonoma syndrome should be considered in any patient with: 1) newly diagnosed diabetes and 2) a rash that does not resolve with proper topical treatment and is consistent with necrolytic migratory erythema. 10% of all strokes. There is a much broader differencial of disorders that cause infarction in younger people. Full evaluation is required to determine an underlying cause to treat patients accordingly and prevent recurrence. As opposed to stroke in the elderly which are often due to atherosclerosis and embolism, only 40% of strokes in the young are accounted for by these two etiologies. Other important causes include dissection, vasculitis, blood disorders, pregnancy, mitral valve prolapse, migraine, and patent foramen ovale. Given this patient had simulanteous anterior and posterior strokes, some of these etiologies are more likely, including: proximal emboli or a disseminated process such as vasculitis, blood disorder or drug use. This young person's stroke was a result of cocaine use. Proposed mechanisms by which cocaine causes stroke is that it induces vasoconstriction, vasospasm, hypertension and/or vasculitis. Case reports have documented stroke secondary to cocaine use in patients who had infarction in multiple distributions. Several of these cases were confirmed to have cocaine-induced vasculitis on autopsy despite having had negative MRA. LEARNING OBJECTIVES: To distinguish the toxicity of``crystal meth'' (methamphetamine) from other syndromes in a patient presenting with psychomotor agitation and tachycardia. CASE INFORMATION: A 22 year-old male with unremarkable PMH presented to the ED via ambulance with the acute onset of diaphoresis, tachycardia, and restlessness. He had been in police custody for approximately 48 hours, and charged with public intoxication. After his symptoms developed, he admitted to ingesting a``2 gram rock of crystal meth'' to avoid charges of illegal drug possession. Physical exam revealed an anxious but alert WM, BP 119/72 mm Hg, HR regular at 179 bpm, unlabored RR 16 per min., rectal temp T 99.3 degrees F, and O2 sat. 97% on RA. Auscultation of his chest was clear and his neurologic exam was nonfocal; but he was tremulous, pale, and his skin cold and clammy. He required substantial benzodiazepine doses to achieve sedation: diazepam 5mg IV en route to the ED, and a total of 8mg IV lorazepam and 14mg IV midazolam in the ED. The patient was electively intubated for``airway protection.'' His hospital course was uneventful; he was extubated within the first day of admission and transferred back to incarceration in 2 days. CPK levels were normal in the ED, but subsequently increased to ten times the ULN. A serum toxicology screen was positive for amphetamines and cannabinoids, and negative for salicylates, acetaminophen, methanol, ethanol, and ethylene glycol. Confirmatory testing revealed a serum methamphetamine level of 80,000 ng/dL. IMPLICATIONS/DISCUSSION: Delayed methamphetamine toxicity, defined as symptom onset 48 hours after ingestion, has not been previously reported in the medical literature. The crystalline form of methamphetamine, also known colloquially as``crank,'' is a stimulant drug of abuse that is usually nasally inhaled, snorted, or smoked. It is rapidly absorbed from any mucous membrane and produces almost immediate metabolic and psychotropic effects. This patient reported orally ingesting the drug in a plastic container, thus with gastrointestinal transit time and even partial digestion of the container, the drug may have been easily absorbed later in the distal GI tract. Alcohol withdrawal with incipient delirium tremens may also explain his presenting symptoms, but his markedly elevated CPK, a usual laboratory finding with acute methamphetamine overdose, and strongly positive serum methamphetamine level at the time of maximal symptomology, suggest methamphetamine toxicity as the etiology of his distress. This case stresses the need for medical personnel to obtain complete drug exposure histories from agitated patients, including explicit questioning with regard to drug ingestion stemming from attempts to conceal illegal activities.

CARDIAC TAMPONADE DUE TO SEVERE MYXEDEMA. J. Blonsky 1 , V. Shivaswamy 1 , K. Hoskison 1 , R. Sekhar 1 , D. Perry 1 ; 1 University of Oklahoma, Tulsa, OK (Tracking  ID #75122) LEARNING OBJECTIVES: Recognize hypothyroidism as cause for cardiac tamponade. Diagnosis of cardiac tamponade secondary to hypothyroidism. Treatment of cardiac tamponade caused by severe tamponade. CASE INFORMATION: We report a 53-year-old male with an enlarging right testicle, progressive dyspnea, severe dependent edema, and cold intolerance. Physical examination revealed faint heart sounds, ascites, ankle jerks with delayed relaxation, and an enlargement of the right scrotum consistent with a hydrocele, and a clinical diagnosis of cardiac effusion with tamponade was entertained. Further evaluations revealed low voltage complexes on the EKG, and marked cardiomegaly on a Chest Roentgenogram with bilateral pleural effusions. An echocardiogram showed a large pericardial effusion with signs of early tamponade, and a pericardial paracentesis drained 1400ml of exudate. Pericardiocentesis led to significant clinical improvement. To confirm a unifying diagnosis thyroid functions were diagnosed of profound hypothyroidism with a TSH of 52.5 iu/ml. The patient responded well to thyroid hormone replacement therapy, and demonstrated continued recovery at clinic follow-up visits. The scrotal swelling was confirmed as a hydrocele by ultrasound. Hypothyroid effusions involving the pleural, pericardial, and peritoneal cavities have been described, but uncommon clinically. Pericardial effusions tend to be large, and asymptomatic, as the slow temporal progression permits compensation due to pericardial stretching. The clinical presentation suggests chronic cardiac failure and constrictive pericarditis with pleural effusion, ascites, and anasarca. EKG findings include bradycardia and microvoltage complexes. Treatment with thyroid hormone replacement is nearly always followed by steady regression of the effusion. Pericardiocentesis is indicated for tamponade, after a confirmatory echocardiogram. This presentation illustrates the importance of detecting hypothyroidism as cause for cardiac tamponade. Prompt diagnosis is vital to prevent cardiogenic shock, and includes early suspicion on the basis of a detailed physical examination, and rapid diagnosis by thyroid functions and echocardiography. Evacuation of the pericardial fluid, and thyroid replacement therapy leads to complete regression and resolution of the condition. IMPLICATIONS/DISCUSSION: Hypothyroidism may lead to cardiac tamponade. Prompt diagnosis is vital to prevent cardiogenic shock. Complete resolution of pericardial fluid following evacuation and thyroid replacement therapy.

A HISPANIC MAN WITH LYMPHADENOPATHY AND EOSINOPHILIA. D. Bolger 1 ; 1 Johns Hopkins University, Baltimore, MD (Tracking ID #76421)

LEARNING OBJECTIVES: 1. Recognize the clinical features of Kimura's disease. 2. Recognize that a constellation of nonspecific clinical signs can represent a specific entity when pursued. 3. Develop a differential diagnosis for lymphadenopathy and differentiate accordingly. CASE INFORMATION: A 63 year old man born in the Dominican Republic but residing in New York City for 30 years presented to a medical clinic with 2 years of right neck swelling. The gentleman initially noticed a small, painless bump in his neck. The bump enlarged to an eventual size of 8cm by 14cm. Similar bumps also arose in the right neck, left neck, and right axilla. Eventually the predominant lesion became painful and itchy. The patient felt healthy otherwise, denying fevers, fatigue, and weight loss. The patient had a history of hypertension, PPD positivity with negative CXRs, and remote microscopic hematuria. He was taking hydrochlorothiazide and prazosin for his hypertension. He was married with 2 children. A He traveled to the Dominican Republic every year for holiday. No other travel was noted. His physical exam was remarkable for a mobile nodular mass 8cm  14cm in the right anterior cervical neck. There were discrete subcutaneous nodules on both sides of the neck. There was lymphadenopathy in the left neck and right axilla. The nodules and lymph nodes were mobile and firm but without fluctuance. There was no hepatosplenomegaly or other lymphadenopathy present. Pertinent labs included a wbc count of 8100/mm3 with 38% eosinophils (absolute eos count 3078) IgE levels were high at >1800kIU/L. HIV test was negative. Excisional biopsy of lymph node revealed follicular hyperplasia with distinct lymphoid follicles with surrounding fibrosis, abundant eosinophils, post-capillary venules, no granulomas or necrosis, and preserved architecture. Cultures and smears were negative for AFB, fungi, bacteria, and Reed-Sternberg cells. Flow cytometry was negative for lymphoma. In addition, skin snips from the patient were negative for microfilariae. The patient was started on prednisone with rapid resolution of lymphadenopathy, however this recurred when prednisone was tapered. The patient was restarted on full dose prednisone and scheduled for curative radiotherapy. IMPLICATIONS/DISCUSSION: Kimura's disease is a rare disease usually seen in Asian men. They present with lymphadenopathy of the head and neck and eosilophilia. Pathology reveals preserved lymph node architecture with necrosis, predominant eosinophils, endothelial venules, and capsular fibrosis. Often lymphadenopathy is attributed to an infectious agent or malignancy. As this case illustrates, there are other causes to consider. A thorough evaluation and exclusion of important entities such as Hodgkin's disesase, extra-pulmonary TB, and Cat Scratch Disease is critical. Histological evaluation often provides a definitive diagnosis, but not always. The pathology along with the clinical signs (features) were required for the diagnosis in this case. osteomyelitis and an epidural phlegmon. Magnetic resonance imaging (MRI) showed cord compression. Needle biopsy of the abscess was performed, yielding prurulent material. In consultation with Infectious Disease and Pulmonary services, empiric treatment for TB was held as it could mask a pyogenic process. By the eleventh hospital day, needle biopsy failed to grow organisms. Polymerase chain reaction (PCR) results of the biopsy aspirate was positive for mycobacterium tuberculosis (M.Tb) and the patient began therapy with isoniazid, rifampin, pyrazinamide and ethambutol. He subsequently underwent surgery for spinal stabilization and was discharged on an 18 month course of antibiotics. IMPLICATIONS/DISCUSSION: Low back pain is the fifth leading reason for medical visits in the United States. A careful history identifies``danger'' signals of infection or malignancy, such as constitutional symptoms, immunosuppression, age and unremitting nocturnal pain unrelieved by recumbency. In Pott's disease, systemic symptoms are often absent, and patients do not undergo testing until the process is advanced. CXR is not useful in diagnosis since more than 50% of patients do not have lung disease. The primary focus starts in the anteroinferior aspect of the vertebral body of the thoraco-lumbar spine. Local destruction leads to collapse, disc herniation and cord compression. Likewise, a tuberculous abscess, seen in more than 50%, can impinge and compress the spinal cord. CT, myelography, and MRI are useful in diagnosis. While biopsy and culture are sensitive and specific, serology and PCR are useful for timely diagnostic confirmation. Literature reports culture sensitivity for mycobacterial detection is improved by culture media supplemented with oleic acid, albumin, dextrose, and catalase, however detection is not specific to M. Tb. PCR of fixed, paraffin-embedded tissue samples, was shown to have sensitivity and specificity of 94% and 83% respectively. In summary, TB remains a major public health problem. Before the disease can be treated it must be recognized. TB should be considered in cases of spinal osteomyelitis. Early institution of therapy reduces morbidity and mortality.

ASTHMA OR ARE WE MISSING SOMETHING. C. Borrego 1 , E. Flenaugh 1 , D. Norman 1 , J. Henao 1 ; 1 Morehouse School of Medicine, Buford, GA (Tracking ID #74416)

LEARNING OBJECTIVES: Diagnosis and Treatment of Pulmonary Blastoma. CASE INFORMATION: This patient is a twenty-seven year old black male who has a past medical history of asthma since eight years old. He is a non-smoker. He states that eight months ago he started to work at a police impound. Where he states he was exposed to a lot of dust. Six months later he started having shortness of breath, cough with whitish to yellowish sputum, and wheezing with associated left lateral chest pain. He then went to the hospital were he was treated for an asthma exacerbation with improvement and subsequently discharged. He then returned with chest pain, left sided rated 8/10 and admitted. On physical exam blood pressure was 90/43, pulse 97, respirations 20, and temperature 97.3 degrees Fahrenheit. Room air pulse oximetry was 97%. He has decreased breath sounds on the left hemithorax. Otherwise physical exam was normal. Chest x-ray showed left lung to be completely opacified by tumor mass or pleural effusion, with some cystic components. CT scan off chest showed a large soft tissue mass completely replacing the left lung of mixed density most likely representing a neoplastic process such as sarcoma, invading and obstructing the left main bronchus. The bronchoscopy showed the right lung to be patent and 3 cm below the carina going to the left main stem bronchus, the airway was completely occluded by a tumor mass in the lumen. Endo bronchial biopsy was performed at that time, which revealed pulmonary blastoma, monomorphic epithelial type (well differentiated fetal adenocarcinoma). IMPLICATIONS/DISCUSSION: Pulmonary blastoma is hard to be diagnosed before operation. The main symptoms can be cough, expectoration. This tumor is extremely rare and manifest's a mixture of epithelial and mesenchymal neoplastic cells. This is a low grade tumor that consists of immature embryonic epithelial elements forming tubules and glands and primitive lung structures, surrounded by a malignant-appearing mesenchymal stroma. Other tumors with better differentiated background mesenchymal elements or neuroendocrine cells in the stroma have also been reported and may represent part of this tumors spectrum. These tumors presents in children and adults and most commonly appear as parenchymal masses. Pulmonary blastoma is more common in women, and is usually diagnosed by surgical resection. This is usually curative, although if late relapses and metastasis occur they are usually not curable. For palliative treatment radiation therapy may be used, and a role for chemotherapy is not defined. LEARNING OBJECTIVES: Acute Myeloid Leukemia (AML) is an exceedingly rare diagnosis to find in association with Acute Intermittent Porphyria (AIP). Only one case report documents such an occurrence. CASE INFORMATION: We present the case of a 61-year-old man with a long-standing history of known Acute Intermittent Porphyria, (AIP) diagnosed in 1996, who was admitted to the internal medicine service for treatment of pharyngitis and severe dehydration. He had never undergone any chemotherapy and his AIP was fairly well controlled, with only four exacerbations noted including the sentinel episode. At presentation for his current admission the patient described fatigue and increasing retropharyngeal pain associated with deglutition, which had steadily progressed during the preceding three days. His CBC was significant for hemoglobin of 10.6 g/dl, WBC of 170.4/mm3, and a platelet count of 102,000/mm3. The differential was 24% segmented neutrophils, 0% bands, 3% lymphocytes, 57% monocytes, and 7% blasts. The patient had hepatosplenomegaly and a global petechial skin rash. Bone marrow studies were done to characterize the underlying etiology. Cellularity to fat ratio was 100:0 with normal bony spicules. Myelofibrosis was completely absent, and granulopoiesis was increased with an abnormal appearance. The blast estimate was greater than 20%. Over the subsequent week the patient experienced a rapid clinical decline with worsening coagulopathy. In accord with decisions made by the patient, his family, and consulting hematologists, chemotherapy was not instituted. AIP is the most common and most severe of the porphyrias.

IMPLICATIONS/DISCUSSION: Although there are case reports of AML occurring with other hepatic porphyrias, there is only one known prior case report of AIP and AML occurring in tandem. This represents the second known incidence of these two disorders occurring simultaneously.

SARCOIDOSIS PRESENTING AS CERVICAL CORD SYNDROME. D. Bradley 1 , E. Lower 1 , R. Baughman 1 , L. Coberly 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #73947) LEARNING OBJECTIVES: To recognize that sarcoidosis is a rare but treatable cause of spinal cord lesions that can mimic malignant tumors of the spine clinically and radiologically. CASE INFORMATION: A 53 year-old African American male presented with a six month history of worsening neck pain, progressive upper and lower extremity weakness, and difficulties with bowel and bladder function. He also noted severe fatigue and a 30 pound weight loss over the last eight months. Physical examination was remarkable for flaccid paralysis of his right upper extremity, 3/5 strength of his left upper extremity, and 3/5 strength of his lower extremities. He had decreased rectal tone. Significant laboratory findings included a normal CBC, chemistry panel, and liver function studies. Calcium was elevated at 11.5 mg/dL (nl 8.4±10.2), an ACE level was normal. Cerebral spinal fluid studies were unremarkable. MRI of the spine showed extensive abnormal signal involving the entire cervical cord extending through T3 with diffuse, patchy nodular enhancement and edema from C3±C7 suspicious for malignancy. CT of the chest revealed mediastinal adenopathy. Biopsy of subcarinal lymph nodes showed noncaseating granulomas consistent with sarcoidosis. The patient was treated with high dose corticosteroids and IV cyclophosphamide (off label use as a steroid sparing agent) with marked improvement. Repeat MRI six months later was normal. IMPLICATIONS/DISCUSSION: The spinal cord is involved in less than 1% of patients with sarcoidosis. It is rarely the first manifestation of disease. Sarcoidosis of the spinal cord can be can be clinically and radiologically indistinguishable from a malignant tumor of the spine. Definitive diagnosis requires pathologic examination of the spinal cord lesions or, as in our patient, other associated lesions such as hilar adenopathy. Prompt treatment with high dose corticosteroids is essential to a favorable outcome. Steroids may need to be continued indefinately. There has been some success using steroid-sparing agents such as cyclophosphamide to decrease the dose and duration of steroid therapy. Sarcoidosis is a treatable condition that should be included in the differential diagnosis of spinal cord lesions.

ZOSTER SINE HERPETE: A CASE OF MASKED DIAGNOSIS. J. Bratcher 1 , S. Patel 1 , K. Cynamon 1 , J. Andrieni 1 ; 1 Lenox Hill Hospital, New York, NY (Tracking ID #75529)

LEARNING OBJECTIVES: 1) Expand the differential for abdominal pain; 2) Diagnose an atypical presentation of herpes zoster in the absence of skin lesions; 3) Recognize that zoster sine herpete is a clinical diagnosis. CASE INFORMATION: A 58 year-old male with history of nephrolithiasis presented with abdominal pain, fever, and chills. Physical exam was significant for low-grade fever and left upper quadrant tenderness. Radiographic studies revealed a 5.3 Â 4.6 cm dissecting aortic aneurysm at the level of the diaphragm, and a separate dissection of the right common iliac artery. The patient was admitted with a diagnosis of an infected aortic aneurysm and evaluated by vascular surgery. The patient continued to complain of left upper quadrant pain, described in a definite dermatomal distribution along the left lower costal margin with radiation to the left flank. Despite absence of any physical evidence of rash, the description was suggestive of herpes zoster. Varicella titers were then ordered and positive IgM titers were revealed. Zoster sine herpete was diagnosed, and the pain spontaneously resolved without medical intervention. On follow-up, the patient remains asymptomatic, never having developed a rash, and repeat CT scans reveal stable aneurysms. IMPLICATIONS/DISCUSSION: Herpes Zoster (Shingles) is a reactivation of varicellazoster virus, which lies dormant in the dorsal or cranial nerve ganglia. Upon recurrence, patients typically have a prodrome of fever, along with pain or tingling in the affected dermatome (50% thoracic, 20% cervical, and 10% lumbosacral). In most cases, the virus creates vesicles along the dermatome after three days, which then crust and resolve within two to three weeks. A small percentage of patients, however, develop acute segmental neuralgia, with a concomitant rise in varicalla IgM antibodies in the absence of skin lesions. This is zoster sine herpete, and as our case illustrates, patients can be initially misdiagnosed with a host of other illnesses, including myocardial infarction, cholecystitis, appendicitis, or diverticulitis. Very little has been published concerning zoster sine herpete since many cases spontaneously resolve without ever having reached the diagnosis. In this particular case, a CT of the abdomen revealed a dissecting aortic aneurysm, which was unrelated to the patient's chief complaint. By relying more on physical exam, the patient's description of the pain, and prior radiographic studies, the diagnosis might have been made more efficiently. This case stresses the importance of history and physical exam in the clinical diagnosis of zoster sine herpete. Otherwise, the diagnosis can be masked by confounding information. ventricular response. CXR (photo to be included) disclosed severe tension pneumothorax with complete collapse of the left lung and slight mediastinal shift to right. Emergent placement of a chest tube resulted in re-expansion of the lung, and stabilization. The patient did well and was discharged from the hospital 2 days later. IMPLICATIONS/DISCUSSION: Use of complementary/alternative medicine, often in concert with``mainstream'' medical treatment, is common and widely practiced in the United States. Acupuncture is effective as sole or adjunctive therapy for management of many types of pain, and is generally regarded as safe. The current vignette describes a case of tension pneumothorax directly attributable to acupuncture treatment. Traumatic injury from acupuncture is rare, but review of the medical literature discloses numerous reports of adverse events resulting from acupuncture treatments. Pneumothorax is the most commonly reported traumatic injury, especially among patients predisposed by presence of COPD; other risks include cardiac tamponade, peripheral nerve injury, and injury to blood vessels including pseudoaneurysm formation. Non-traumatic adverse effects of acupuncture include infections (hepatitis and other blood-borne diseases, as well as reports of septicemia and endocarditis.) The overall safety profile of acupuncture is positive, but patients and physicians should be aware of potential risks of treatment. State laws vary widely regarding requirement for certification; referral to licensed or certified medical acupuncturists is recommended. year-old woman presented with one month of fevers, evanescent rash, myalgias and arthralgias, severe fatigue, and anorexia with 20 pound weight loss. Examination disclosed T 39.48C, tender posterior cervical lymphadenopathy, no obvious synovitis, and a salmon-colored macular exanthem on the lower extremities. CBC showed normocytic anemia (Hgb 9.8,) slight leukocytosis (WBC 11.1 with 82.3% granulocytes,) normal LFTs except for slight elevation of AST, normal BUN/Cr, UA, and CXR. Further tests revealed ESR 90, negative ANA and RhF, and ferritin >2000. Further diagnostic workup included negative PPD, negative blood cultures, normal echocardiogram, normal CT scan except borderline mediastinal lymphadenopathy and mild hepatosplenomegaly, and negative titers for HIV, EBV, CMV, and Lyme disease. Lymph node biopsy disclosed reactive node with no evidence of a clonal population of cells. The patient was diagnosed with AOSD and had minimal response to aspirin. She was treated with steroids and is presently minimally symptomatic on hydroxychloroquine and NSAID. IMPLICATIONS/DISCUSSION: AOSD is a rare disease (incidence 1.6 cases/million persons/yr) that highlights the importance of clinical history and physical examination, since there is no definitive test to make the diagnosis. Diagnostic criteria have been proposed (will be delineated.) ASOD usually follows one of three patterns: self-limited (monophasic) disease with complete resolution of symptoms within one year, intermittent (polyphasic) course with complete remission between flares, or persistent active disease, with chronic destructive arthritis. First line treatment is aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs;) patients with more severe disease may respond to steroids. There are no controlled trials of immune modulating drugs in ASOD. Reports exist of success using methotrexate to control systemic symptoms; other agents used (all off-label) include gold salts, azathioprine, cyclophosphamide, cyclosporine, sulfasalazine, and intravenous immune globulin. Recent reports suggest etanercept and infliximab may have benefit in patients not responding to other therapies. A 74 year old white female presented with a 3 day history of`d ifficulty getting out of a chair'', dyspnea on exertion and``tea colored'' urine. Her past medical history was significant for depression and hypercholesterolemia. Her past medications included simvastatin (40 mgs po qd) and nefazodone (150 mgs po bid). She had been started on the nefazodone 3 months ago for treatment of depression and shortly thereafter developed a fever, nausea/vomiting and muscle spasms. Physical examination revealed significant weakness of the proximal musculature: 3/5 strength in the shoulder abductors and 2/5 strength in the hip flexors. Her laboratory data revealed: CK 37,050, AST 1,744, ALT 1,029, BUN 17, Creatinine 0.8 , Urinalysis: SpGr 1.020, pH 6.0, protein 100, large blood, granular casts. The nefazodone and simvastatin were discontinued and a forced bicarbonate diuresis was initiated. Polymyositis was suspected and steroids were started empirically pending the outcome of testing. An EMG showed no evidence of an underlying myopathy). ANA and an anti-Jo-1 antibody tests were negative. A muscle biopsy showed age-appropriate atrophy but no necrosis of myocytes and no evidence of lymphocytic infiltrate, thus ruling out the diagnosis of polymyositis. Her renal function remained normal throughout the hospitalization. Her CPK was 1,776 eight days after admission and she gradually regained strength in her proximal muscle groups. She was thought to have developed rhabdomyalyis secondary to a drug interaction between simvastatin and nefazodone. IMPLICATIONS/DISCUSSION: To our knowledge, this is the second case report of an adverse event associated with the concomitant use of simvastatin and nefazodone. Simvastatin is metabolized via the CYP3A4 system and nefazodone is a direct inhibitor of CYP3A4 enzymes. While myositis and rhabdomyolysis are adverse events associated with simvastatin monotherapy, we speculate that the introduction of nefazodone into this patient's regimen sufficiently inhibited the CYP3A4 system to cause an increase in serum simvastatin concentration that was adequate to cause rhabdomyolysis. Therefore, we would recommend avoidance of CYP3A4 inhibitors such as nefazodone in those receiving simvastatin therapy.

COLON CANCER, WITH ANGIOGRAPHIC EVIDENCE OF VASCULITIS. I.D. Bucaloiu 1 , S. Dubagunta 1 , K.K. Pachipala 1 , N.R. Kamal 1 , F. Fata 1 ; 1 Geisinger Medical Center, Danville, PA (Tracking ID #76029) LEARNING OBJECTIVES: 5-Fluorouracil (5-FU) is one of the most commonly used chemotherapeutic agents in clinical oncology practice, alone or in different combinations. In stage III colorectal cancer, 5-FU based therapy has been shown to be associated with a survival benefit. We report a case of ischemic small bowel injury in a patient who received adjuvant chemotherapy with Oxaliplatin, 5-FU and LV and was found to have angiographic evidence of vasculitis in the superior mesenteric artery (SMA) territory. CASE INFORMATION: A 73 year-old male underwent a left hemicolectomy for Stage III colon cancer. He was enrolled in an adjuvant chemotherapy research protocol consisting of 5-FU 500-mg/m2 intravenous (IV) weekly boluses each over 1 hour, LV 500-mg/m2 IV weekly infusions each over 2 hours and Oxaliplatin (OP) 85 mg/m2 IV infusions every 2 weeks for 6 weeks followed by two weeks of rest. After the third weekly dose of cycle one of 5 FU/LV he presented with weakness, diarrhea, crampy abdominal pain and poor appetite. His abdomen was distended and he had heme positive stools. Stool cultures and clostridium difficile toxin antigen were negative. He was not neutropenic. Colonoscopy revealed dusky edematous changes in the ascending colon and focal ulceration with patchy submucosal hemorrhages in the distal ileum. Biopsies of the colon mucosa showed densely neutrophilic infiltrates of the lining epithelium and associated mild focal cryptitis. A SMA angiogram was performed and it revealed beading in ileal branches, consistent with the ischemic territory. Vasculitis serologies were negative. The patient was treated conservatively with hydration and IV antibiotics and later he was rechallenged with a 20% reduction of 5-FU dose with no recurrence of his symptoms in 12-month follow-up. IMPLICATIONS/DISCUSSION: Our patient had superficial erosions and ulcerations in the ileum as well as an ischemic appearance of the colon. The characteristic findings of``beading'' on the angiogram suggest an underlying ischemic mechanism related to 5 FU based therapy. This case will add to the series of patients reported with 5-FU induced vascular injury to the small bowel.

THROMBOTIC THROMBOCYTOPENIC PURPURA AND EXTENSIVE BONE MARROW NECROSIS SECONDARY TO METASTATIC SIGNET RING CELL ADENOCARCINOMA. I.D. Bucaloiu 1 , J. Brady 1 , S. Walker 1 , K.K. Pachipala 1 ; 1 Geisinger Medical Center, Danville, PA (Tracking ID #76352) LEARNING OBJECTIVES: Although rare, the association between Thrombotic Thrombcytopenic Purpura and extensive Bone Marrow Necrosis can be the presenting picture of metastatic adenocarcinoma. CASE INFORMATION: A previously healthy 49 years old male was transferred from another hospital with a two-week history of severe, intractable back pain, short-term memory loss fatigue and shortness of breath. On exam he was afebrile, icteric and had multiple ecchymoses on the trunk. Complete blood count revealed severe anemia and trombocytopenia, with serum hemoglobin of 4.6 g/dl, a platelet count of 16 Â 109/L and white blood bell count of 3.22 x 109/L. There was evidence of severe hemolysis with serum lactate dehydrogenase of 2659 U/L and Serum Haptoglobin of 7 mg/dL. Direct Coombs test was negative. The absolute reticulocyte count was 42.6 K/uL. The peripheral smear revealed schystocytes and thrombocytopenia. A CT scan of chest, abdomen and pelvis showed splenomegaly, and was otherwise unremarkable. The initial bone marrow aspirate and biopsy revealed extensive necrosis of bone marrow with marked reduction of normal hematopoietic elements. Flow cytometry was negative for a clonal lymphoid proliferation. The repeat contralateral iliac crest biopsy revealed among the extensive necrosis, small aggregates of highly atypical cells with pleomorphic hyperchromatic nuclei. Some cells had signet ring morphology and they stained positive with mucicarmin and cytokeratin stains, which indicate a carcinomatous origin. The patient received multiple blood transfusions, high dose steroids and plasmapheresis, but none of these interventions had a significant impact on the clinical course. His delirium worsened, developed respiratory failure and expired on the 7th day of hospitalization. IMPLICATIONS/DISCUSSION: Massive bone marrow necrosis is known to occur in the context of malignancy, usually hematopoietic, lymphomas, leukemias, but also solid tumors. At the same time TTP has been reported to occur in the setting of neoplasms, especially adenocarcinomas, usually gastric, pancreatic and breast. The association of TTP and massive bone marrow necrosis, although rarely reported in the literature may represent as illustrated in our case report the heralding picture of metastatic cancer. It is important for physicians to be aware of this association as it forces one to search for an unapparent neoplasm. and pelvis with subsequent abdominal MRI confirmed cavitary lesions in the left upper lobe and revealed a 12 Â 10 Â 7.5 cm adrenal mass. A serum ACTH was low at 3 pg/mL (normal 9± 52 pg/mL) and a serum free morning cortisol of greater than 50 mcg/dL (normal 6±20 pg/mL) confiming a diagnosis of Cushing syndrome. Urine catacholamines were normal. The adrenal mass was later surgically removed with pathology confirming a diagnosis of adrenocortical carcinoma. Sputum cultures obtained by bronchoscopy grew significant colonies of Nocardia Farcinica and Nocardia Nova. The patient was started on intravenous trimethoprimsulfamethoxazole for six weeks followed by oral therapy. IMPLICATIONS/DISCUSSION: Nocardiosis is a rare finding in immunocompromised patients with an estimate of 500±1000 new cases per year. Most cases involve the lung with inhalation as the mode of entry. Although an immunocompromised state predisposes patients to Nocardia infection, steroid use is considered to be an independent risk factor. Our patient, while not taking exogenous steroids, did have very high levels of endogenous cortisol. Definitive diagnosis is typically made by routine culture of an isolated specimen. The most effective treatment for Nocardiosis remains speculative and is based mostly on small retrospective studies and case reports. Trimethoprim-sulfamethoxazole demonstrates synergy against Nocardia and general consensus supports high doses of this drug initially followed by long-term treatment with lower doses for up to one year due to the high degree of recurrence of disease. As demonstrated in this case, one should consider Cushing syndrome as a risk factor for the development of Nocardia infections. year-old man presented with one day of abdominal and back pain. He was a daily heroin user and his last injection was two hours prior to presentation. During his evaluation, he became uncooperative and combative, subsequently leaving against medical advice. Two hours later he was found disoriented on the street. His temperature was 39 C; he had nuchal rigidity and tenderness to palpation over the lumbar spine. There were no murmurs, purpura, or petechiae. He rapidly developed respiratory failure and was intubated. Blood, urine, and CSF cultures grew methicillin-resistant Staphylococcus aureus. He received seven days of vancomycin, and rifampin, After stopping a seven day course of antibiotics, his fever returned. A repeat lumbar puncture revealed persistently positive MRSA. Vancomycin and rifampin were restarted , and his fever resolved. An MRI of the lumbar spine demonstrated pyomyosits of the paraspinal muscles. He received 42 days of vancomycin and rifampin with clinical improvement. IMPLICATIONS/DISCUSSION: Back pain in the intravenous drug user, especially when associated with fever, must prompt high suspicion for meningitis, discitis, oteomyelitis of pyomyositis. Although meningitis from Staphyloccocus aureus is usually secondary to neurosurgical procedures, intravenous drug users are susceptible to staph CNS infections due to their frequent innoculation and impaired immunity. With the increased availability of antibiotics on the street, methicillin-resistant Staphyloccocus aureus is increasingly becoming a community acquired pathogen. As this case illustrates, serious CNS infections in an intravenous drug user may warrant empiric vancomycin until definitive cultures return. Staphyloccocus aureus bacteremia requires at least two weeks of intravenous antibiotics; longer courses are required for deep-seated infections. A secondary focus should always be sought, as Staph is a rare primary infection. This case illustrates the importance of maintaining a high degree of suspicion for Methicillin-resistant Staphyloccocus aureus in intravenous drug users presenting with back pain and fever.

MITOCHONDRIAL TOXICITY AND HIV THERAPY. S. Burridge 1 , L. Coberly 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #75159) LEARNING OBJECTIVES: Recognize the clinical presentation of mitochondrial toxicity secondary to nucleoside reverse transcriptase inhibitors. CASE INFORMATION: A 43-year-old white male with AIDS presented with altered mental status, nausea, vomiting, right upper quadrant pain and myalgias. Medications included didanosine, efavirenz, lopinavir/ritonavir and stavudine. His temperature was 101.28F, HR 120, BP 135/85 and RR of 26. Physical examination was significant for bitemporal wasting, oral thrush, dry oral mucosa, ketotic breath, pain to palpation in the right upper quadrant and a liver span of 20cm. There were no identified sources of infection. Laboratory examination was significant for sodium 126mmol/L, potassium 5.1mmol/L, chloride 88mmol/L, and bicarbonate 13mmol/L. Lactate was markedly elevated at 9.9mmol/L. Transaminases were 111 IU/L and 128 IU/L, alkaline phosphatase was 209 IU/L and total bilirubin was 4.10 mg/ dL. Triglycerides were greater than 1,000 mg/dL. Abdominal CT revealed hepatomegaly with fatty infiltrate. Medication toxicity was suspected and HAART therapy was discontinued. Riboflavin supplementation was initiated. IMPLICATIONS/DISCUSSION: Mitochondrial toxicity is a rare syndrome that has been reported in patients treated with nucleoside reverse transcriptase inhibitors, particularly zalcitabine, didanosine, and stavudine. The diagnosis is clinical. Patients present with nausea/ vomiting, abdominal pain, weight loss, malaise, fatigue, dyspnea and sometimes fever. Laboratory evaluation reveals lactic acidosis, hypertriglyceridemia and elevated liver enzymes. Imaging studies demonstrate hepatomegaly with fatty infiltration. The mechanism of mitochondrial injury is postulated to be inhibition of the mitochondrial gamma polymerase, the enzyme that directs the replication of mitochondrial DNA. The mitochondria are unable to replicate, the citric acid cycle is blocked and lactate production increases. Fatty acid oxidation is inhibited leading to accumulation of lipid droplets. Treatment involves the administration of mitochondrial supportive therapy such as riboflavin, thiamine, ubiquinone and acetyl-carnitine in addition to the cessation of antiretroviral therapy. Unrecognized, this syndrome carries a 60% mortality attributed to worsening acidosis with resulting cardiovascular collapse or progressive hepatic failure. (Tracking ID #76589) LEARNING OBJECTIVES: To recognize the dilemma posed by an inconclusive MRI in cases of intracerebral mucormycosis and to emphasize the need for brain biopsy. CASE INFORMATION: A 42 year-old male with HIV presented with a five-day history of headache, fever, left sided weakness and multiple falls. Physical exam showed a left sided, central, facial nerve palsy, weakness and left sided hyperreflexia. The patient's CD4 count was 56. Cryptococcus, toxopolasmosis, tuberculous meningitis, atypical infectious agents and lymphoma were considered in the working differential diagnosis. CT scanning and CSF analysis were negative. MRI revealed a mass in the right basal ganglia with associated edema and a midline shift. An MRI guided brain biopsy showed mucormycosis. In spite of amphotericin B therapy he expired ten days later. IMPLICATIONS/DISCUSSION: Mucormycosis in an immunocompromised host with HIV has rarely been described in the literature. Notably, in such cases neither CT nor MRI scanning is sufficient to make the diagnosis. In these instances, surgical exploration is mandatory and can provide crucial diagnostic information.

DOWN BUT NOT OUT. S. Agresta 1 , J. Canterbury 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77016) LEARNING OBJECTIVES: 1. Recognize an under-diagnosed cause of rhabdomyolysis. CASE INFORMATION: A 55 year-old obese man presented with severe shortness of breath after being found at his nursing home. His morbid obesity (550 pounds) confined him to a wheelchair. On the evening prior to admission, he fell from his wheelchair without a loss of consciousness or traumatic injury. A nursing aid found him twelve hours later. At presentation, he complained of diffuse pain; he noted associated shortness of breath but no chest pain or palpitations. His heart and breath sounds were normal; pitting edema extended to the knees. His vital signs were normal. His urine was scant (less than 10 cc/hr) and dark brown in color. His CPK was 35,000 U/L, BUN 75 mg/dL and creatinine 2.1 mg/dL. IMPLICATIONS/DISCUSSION: Although rhabdomyolysis is usually seen with crush injuries or toxic myopathies, prolonged stasis and extended isometric contraction as occurs with seizures should also prompt immediate evaluation for the syndrome. A timely diagnosis is essential, as the degree of renal tubular necrosis is proportional to the time and duration of tubular exposure to the myoglobin pigment. Aggressive diuresis decreases this exposure time; this is the main focus of treatment. The color of the urine (brown as opposed to yellow or clear) predicts the pigment concentration in the tubules, and is a better measure of severity and treatment efficacy than the CPK level. Early diuresis, with or without alkalinization, should be maintained until the urine is consistently clear. Acute renal failure is often attributed to the primary disease (sepsis, MI) in patients found down. Rhabdomyolysis should be excluded as an independent cause of renal failure in all patients found down for an undetermined or prolonged period of time.

LISTEN TO ME, NOT MY THYROID. E. Chan 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77077) LEARNING OBJECTIVES: 1. Listen to the patient's previous history to establish appropriate management decisions. 2. Use the history of the patient's symptoms to distinguish Graves disease from propylthiouracil allergy. CASE INFORMATION: A 23 year-old woman presented with recurrent palpitations, muscle weakness and dyspnea. She had a past history of Graves disease but had refused propylthiouracil therapy. She had a heart rate of 130, and a temperature of 104 F. There was right eye exophthalmos, a diffusely enlarged thyroid. A venous hum was heard over the thyroid; she had proximal muscle weakness and hyperreflexia. The thyrotropin levelwas 0.06U/ ml and the FT4 was 17.01 g/dl. She was treated with with potassium iodide, propylthiouracil and propranolol with resoluton of her symptoms. Three days later, she developed severe generalized arthralgias and myalgias with progressively deteriorating muscle strength and swelling of her fingers. Her anti-nuclear antibody, anti-histone antibody, and acetylcholine receptor antibody were negative. The anti-striated muscle antibody, rheumatoid factor and p-ANCA were also negative. The propylthiouracil was discontinued based upon the hypothesis that the new symptoms were due to an allergic response, Her symptoms resolved the following day. Upon further questioning, she noted a similar reaction to a previous treatement with propythiouracil as the cause of her non-compliance with this therap. A subtotal thyroidectomy, resulted in complete resolution of her symptoms. IMPLICATIONS/DISCUSSION: The appropriate management decision is often obtained by listening to the patient. In the thrill of treating Graves's disease, the reason for the patient's previous non-compliance with propylthiouracil was ignored. Although an allergic reaction to propylthiouracil is rare, it is characterized by arthralgias, myalgias, anxiety and tachycardia when it occurs. Distinguishing this reaction from continued symptoms of Graves's disease requires a meticulous history. Thyroidectomy is the treatment of choice in patients who are unable to tolerate propylthiouracil therapy. Carefully listening to why patients have declined previous therapy is important in preventing recurrence of previous adverse effects.

included rolling and lifting weights on an exercise ball. After returning home he became nauseated, diaphoretic, weak, and experienced excruciating left flank pain followed by an episode of watery diarrhea. His symptoms worsened and he presented to the emergency room the following morning. Physical examination at that time revealed a well-nourished man in marked distress secondary to intractable pain. There was significant tenderness to minimal palpation and percussion in his lower left quadrant and over his left costovertebral angle region. An initial computerized tomography (CT) of the abdomen showed an insignificant left renal cyst. Laboratory evaluation was significant for leukocytosis with a left shift, mild normocytic anemia, slightly elevated creatinine and CPK, and urine which showed pyuria but was sterile. Overnight he experienced fever and worsening pain with apparent peritoneal signs. The next morning a chest x-ray was done which showed no evidence of pneumonia. CT of the abdomen was repeated. In view of the patient's declining condition, this subsequent CT was read as a possible abscess. Aspiration of the renal abscess grew Streptococcus pneumoniae, as did all blood cultures. Predisposing factors for pneumococcal bacteremia were excluded. He recovered fully after a two-week course of ceftriaxone and four weeks of levofloxacin. IMPLICATIONS/DISCUSSION: Streptococcus pneumoniae is a very uncommon pathogen in renal abscesses. Extrapulmonary pneumococcal infection is most often metastatic from the lung. No respiratory disease was noted in our patient. Only two published cases of Streptococcus pneumoniae renal abscesses have been reported. These will be discussed, one in full detail. The etiology of our patient's Streptococcus pneumoniae continues to be a mystery. Two hypotheses will be presented. LEARNING OBJECTIVES: Often uncommon diseases present initially in the primary care setting, and appropriate referral and diagnosis are essential. The following case illustrates an unusual skin condition seen in a primary care setting in order to expand the generalist physician's differential diagnosis of dermatologic conditions associated with renal failure. CASE INFORMATION: The patient is a 36-year-old woman with a history of type I diabetes complicated by renal failure for which she underwent a kidney-pancreas transplant ten years ago. Her transplanted kidney remained functional until three months prior to presentation, at which time hemodialysis (HD) was initiated. Within one month of starting HD, she developed thickening and hardening of the skin on her left hand, which rapidly expanded to involve the entire left arm, and the right hand and arm. Within two months, the feet, lower legs, buttocks, and areas of the back had areas of skin hardening. The face, abdomen, and chest were spared. These areas of skin hardening were associated with minimal overlying skin changes, but she developed burning paresthesias during this time for which she was treated with oxcarbazepine. A skin biopsy confirmed the diagnosis of nephrogenic sclerosing dermopathy (NSD), with the findings of increased numbers of dermal spindle cells and thick collagen bundles in the reticular dermis. IMPLICATIONS/DISCUSSION: NSD was first described in September 2000 in a case series of 14 patients with a fibrotic skin condition resembling scleromyxedema. Each patient had a history of renal failure and 12 of the patients were receiving HD at the time of diagnosis. Patients displayed skin thickening and hardening with overlying brawny skin discoloration, which was localized to the torso and limbs with sparing of the face. Several patients complained of painful paresthesias beginning with the onset of skin hardening. In each case, the skin condition has been progressive with no known effective therapy. The etiology of NSD is unclear, but infectious agents or toxic agents (toxins in the dialysate, endogenous toxins not cleared by dialysis) have been proposed. Resolution of the skin lesions occurred in one case when HD was stopped following resolution of acute tubular necrosis. Through accurate referral and diagnosis of patients, more can be learned about the etiology, prevention, and treatment of NSD. Early recognition of NSD may allow early referral for transplantation to prevent progression of disease on HD, although there is not definitive evidence to date that NSD regresses following transplantation. A 58 year old Mexican man presented with progressive shortness of breath and a dry cough for over 1 month. Review of systems was positive for dyspnea on exertion, three pillow orthopnea, and an eight pound weight loss. His past history is noncontributory, and he uses no medication, tobacco or alcohol. On physical exam breath sounds were decreased with bilateral rales 1/2 way up. He was tachycardic with a loud P2, a jugular venous pressure of 10cm and 2+ edema to the shins. Chest x-ray showed bilateral pleural effusions; right greater than left. Echocardiogram revealed an ejection fraction of 70% with pulmonary hypertension. Laboratories were significant for a normocytic anemia with low iron, TIBC and reticulocyte count; ESR 116; urinalysis with trace protein and 20 red cells; and negative serologies for hepatitis B/C, HIV, and coccidiodes. CT chest was negative for pulmonary embolism and infiltrate. Diagnostic thoracentesis removed 200cc of hazy fluid with pH 7.48, 1250 white cells (81% lymphocytes) and cultures negative for bacteria, fungi and acid fast bacilli (AFB). Cytology was negative for malignant cells. Rapid reaccumulation later prompted removal of another 1L of fluid. A tuberculin skin test was 8 mm but sputum AFBs were negative. Further work-up revealed a positive ANA (1:2560 titer) and strongly positive anti-Smith antibody with negative anti-dsDNA and ANCA. He was diagnosed with SLE and started on prednisone 40 mg daily with resolution of the effusion and improvement in pulmonary hypertension. IMPLICATIONS/DISCUSSION: Pleural effusion is the initial manifestation in 1%, and pleurisy in 3%, of SLE patients, more often in those with late-onset (after age 50). Lupus pleuritis usually presents as pleuritic chest pain with fever, cough and dyspnea but rarely with massive effusions. Pleural symptoms may precede other manifestations of SLE by months or years, particularly in men. To diagnose pleural effusions caused by lupus pleuritis, one must rule out other causes including pulmonary embolism, congestive heart failure, infections (i.e. parapneumonic or tuberculous), and malignancy. Effusion ANA titer detection is a very sensitive but nonspecific test while anti-DNA antibodies or LE cells in the pleural fluid are diagnostic but not very sensitive. Treatment includes NSAIDs for mild cases and systemic corticosteroids for more severe cases. Early diagnosis and prompt treatment can greatly decrease morbidity from this disease. year old man presents with complaints of progressive leg swelling, erythema, 30 lb weight loss, and severe bilateral hip pain over 3 months. He initially noted several fluid filled blisters and pedal edema that spontaneously resolved. Over the next several weeks he described progressive bilateral hip pain requiring the use of crutches for ambulation. The month prior to admission the patient was bed bound secondary to pain. He denied other constitutional symptoms. Of note, he had eliminated fruits and vegetables from his diet 3 years ago. The patient had emigrated from Ethiopia 35 years ago. Physical exam revealed poor dentition, a perifollicular petechial rash of his lower extremities, hyperpigmentation of his upper thighs and bilateral lower extremitity edema. MRI was significant for lower extremity soft tissue edema and osteoporotic femoral heads with abnormal marrow signal. Laboratory values were notable for a normocytic anemia, normal coagulation panel, and electrolyte panel and a Vitamin C level of <0.12 mg/dL. Punch biopsy of the petechial lesions demonstrated perifollicular hemorrhage and corkscrew hair follicles. Vitamin C supplemenation 1000mg per day was initiated with resolution of symptoms over several weeks. Repeat MRI of his LE noted resolution of soft tissue edema and improving osteoporosis. IMPLICATIONS/DISCUSSION: Symptoms of scurvy have been described as early as 1500 BC by the ancient Egyptians. In contemporary history, epidemics have been described in the Renaissance era, when sailors were frequently affected, and during the 19th century, by those who experienced the Great Potato Famine, American Civil War armies, and the California Gold Rush communities. A cofactor and strong reducing agent, vitamin C is crucial to numerous biochemical pathways including collagen synthesis, norepinephrine synthesis, prostaglandin synthesis, and antioxidant function. Collagen synthesis disruption in particular leads to the clinical syndrome of scurvy including ecchymoses, bleeding gums, petechiae, and arthralgias. Other signs and symptoms include muscle pain, microcytic anemia, decreased wound healing, mood disturbances, and anorexia. While scurvy occurs rarely in the US, typically it is seen in elderly or alcoholic patients and those with diets devoid of fruits and vegetables. Sudden cardiac death has been reported in these patients however, morbidity and mortality largely occurs as a result of hemorrhage which can occur in any organ. Skin biopsy findings of perifollicular hemorrhage and follicle corkscrewing are pathopneumonic for the disorder. Symptoms typically improve over days to weeks with the addition of Vitamin C to the diet. Prognosis is excellent with timely diagnosis and treatment.

NOT JUST ANOTHER DIARRHEA: A CASE OF SECONDARY AMYLOIDOSIS ASSOCIATED WITH LYMPHOMA. J. Chowdhury 1 , A. Gomez 1 ; 1 UCLA San Fernando Valley, Sylmar, CA (Tracking ID #76168) LEARNING OBJECTIVES: 1) Recognize lymphoma as a chronic inflammatory state that can be associated with secondary amyloidosis 2) Distinguish between primary and secondary amyloidosis. CASE INFORMATION: A 44 year old Hispanic male with non-Hodgkin's lymphoma, diagnosed and treated in Mexico with chemotherapy and radiation five years ago presents with five months of large volume, watery diarrhea. He had four to six episodes of blood-tinged diarrhea per day, with abdominal cramps, nausea and vomiting. The patient had anorexia with a twenty pound weight loss, orthopnea and bilateral lower extremity edema. His blood pressure was 60/palp, pulse 88, and he was afebrile. He had dullness to percussion and decreased breath sounds over the left lower lobe as well as 1+ pitting edema in BUE and 2+ pitting edema in the BLE. A CBC was normal, BUN 38, creatinine 1.3, PT 29.6, INR 2.47, PTT 47, albumin 1.4, AST 10, ALT 13, alkaline phosphatase 153, total bili <0.1, LDH 762. Urinalysis showed small blood, 3+ proteinuria, 2 rbc's and 3 wbc's. CXR showed a left-sided pleural effusion. The patient was admitted to the ICU and started on IV steroids and pressors. Thoracentesis revealed a transudate with many lymphocytes, but no malignant cells. CT scans revealed a mass in the left upper lobe of the lung and left hemithorax volume loss, colon dilation to 6 cm and small bowel dilation to 3 cm. Biopsy of the lung mass revealed Hodgkin's lymphoma. Bone marrow biopsy was positive for both crystal violet and Congo Red, suggesting amyloidosis. Rectal biopsy showed friable mucosa and revealed apple green birefringency when viewed with Congo Red stain, confirming the diagnosis of gastrointestinal amyloidosis. Unfortunately he succumbed to the disease a week later while on steroids and chemotherapy. IMPLICATIONS/DISCUSSION: Both primary and secondary amyloidosis present in a variety of ways, including heavy proteinuria, edema, hepatosplenomegaly, hematochezia, congestive heart failure, and carpal tunnel syndrome. Secondary, or AA, amyloidosis occurs in chronic inflammatory states, such as rheumatoid arthritis, inflammatory bowel disease, or osteomyelitis. However, reports of an association with lymphoma are rare. Obtaining a good past history for chronic inflammation is nevertheless important when diagnosing AA amyloidosis. The only disease linked to primary, or AL, amyloidosis is multiple myeloma. Once the diagnosis of amyloidosis is made from tissue biopsy, the distinction between primary and secondary amyloidosis is made based on the presence of a chronic inflammatory state in secondary amyloidosis or the presence of certain paraproteins, found in about 90% of primary amyloidosis. We diagnosed this patient as secondary amyloidosis based on his history of lymphoma.

``MY TOOTH IS KILLING ME!'': OVER THE COUNTER ANALGESIC RISKS AND HEPATITIS C. E. Coffey 1 , E. Schneider 1 ; 1 Hennepin County Medical Center, Minneapolis, MN (Tracking ID #76561) LEARNING OBJECTIVES: 1. Recognize increased risks of acetaminophen and nonsteroidal antiinflammatory drugs (NSAIDs) for patients with Hepatitis C. 2. Recognize importance of adequate medical and medication history, even for common complaints. CASE INFORMATION: 50 year old male presented to a walk-in clinic seeking medication for a two week old toothache. Nonprescription pills at home didn't help. He also reported 2 days of nausea, vomiting, loose bowel movements, diffuse myalgias, generalized weakness. He denied alcohol, infectious contacts. PMH included hepatitis C, alcohol and cocaine use. Physical exam remarkable only for an ill appearing male with an abscessed tooth and mild abdominal tenderness. Labs included K 3.8, BUN 32, creatinine 2.9, ALT 3460, AST 2575, bilirubin 5.1, alk p'tase 135, lipase 111, INR 1.4. Acetaminophen level 52. Salicylate level was not elevated. He later admitted to taking up to 20 tablets of naproxen and acetaminophen a day over the last few days. He was admitted to the medicine service, and improved with acetylcysteine and supportive care. He was counselled about acetaminophen use. A dentist extracted the abscessed tooth before discharge. IMPLICATIONS/DISCUSSION: Acetaminophen and NSAIDs are associated with increased transaminases in patients with hepatitis C. Renal failure has been associated with NSAIDs and with paracetamol poisoning.This case illustrates that the presenting problem isn't always the most serious. The non-pain symptoms, past history and specific information on his self medication were keys to diagnosis. Given potential toxicities of analgesics, patients with hepatitis C are well advised to seek advice for pain issues rather than self medicating.

DIAGNOSIS AND TREATMENT OF POST PRANDIAL NAUSEA, ALLERGY AND EOSINOPHILIA. D. Coleman 1 , J.S. Scolapio 1 , J.R. Cangemi 1 , J.C. Guarderas 1 ; 1 Mayo Clinic Jacksonville, Jacksonville, FL (Tracking ID #76262) LEARNING OBJECTIVES: Eosinophilic gastroenteritis, is a disorder characterized by infiltration of eosinophils into the mucosa of the gastrointestinal tract. As a clinical entity with recognizable symptoms it is a rare disorder. Here we discuss the extensive treatment course of a refractory case of eosinophilic gastroenteritis. CASE INFORMATION: A 16-year-old male patient who presented with post-prandial fullness and nausea. He had a history of seasonal allergies, asthma, and peripheral eosinophilia. Endoscopy of the stomach with mucosal biopsies revealed predominate eosinophils. A diagnosis of eosinophilic gastroenteritis was made. He was treated with a proton pump inhibitor (Prilosec) an oral cromolyn (for gastrointestinal symptoms), initially. After no response, he began on high dose prednisone with a gradual taper, with clinical response, to every other day prednisone indefinitely. Several years later, he again experienced symptoms of dysphagia, early satiety, nausea and occasional vomiting. He had been compliant with his medications. The oral steroids (20 mg every other day) had not been tapered because of recurrent symptoms upon dose reduction. As a result of his prolonged predisone use, bone mineral analysis was performed and showed signs of early osteoporosis. He was treated with Fosamax 5 mg a day, vitmain D 50,000 IU twice a week, and Calcium 1000 mg a day. A trial of an elemental nutrition formula was attempted in hopes of reducing his gastrointestinal eosinophilia. Although his peripheral eosinophil count significantly decreased on this elemental diet (Vivonex) he was unable to continue with it because of its poor taste. Given his refractory symptoms and continued risk of complications from chronic steroid use he was treated with Interferon Alpha, starting at a low dose and gradually increased to a dose of 1 million units per day. His peripheral blood eosinophils initially dropped from 5410 to 1020 but then slowly began to increase. In early 2002 his gastrointestinal symptoms recurred and his peripheral blood eosinophils began to rise. He had been compliant with medications. Because the majority of his symptoms were gastroesophageal, we elected to try oral flonase. Since this newest therapy was begun, he has experienced a marked drop in peripheral blood eosinophils (the lowest to date) and his gastrointestinal symptoms have markedly improved. IMPLICATIONS/DISCUSSION: This case is unique because it illustrates an unusual approach to a refractory case of eosinophilic gastroenteritis. Most known and reported therapies had failed in our patient with the exception of high dose steroids and, more recently, oral Flonase. Unfortunately his dependence upon corticosteroids resulted in the serious sequelae of osteoporosis. Although a systemic illness with marked peripheral eosinophils, the symptomatology of this patient was predominantly gastrointestinal. RAPIDLY PROGRESSIVE HEPATOSPLENOMEGALY. K. Cooke 1 , S. Rusch 1 ; 1 University of Illinois, Peoria, IL (Tracking ID #76040) LEARNING OBJECTIVES: Discuss the differential diagnosis of rapidly progressive hepatosplenomegaly while highlighting a typical presentation of an uncommon lymphoma. CASE INFORMATION: A previously healthy 32-year-old woman initially presented to her primary care physician with pleuritic left shoulder pain and a normal physical exam. Laboratory results then included platelets of 104,000/L; alkaline phosphatase of 125 U/L; alanine aminotransferase of 58 U/L; and aspartate aminotransferase of 65 U/L. Two weeks later, the patient returned with acute onset of fevers, fatigue and nausea. Physical examination was benign except for marked hepatosplenomegaly. The liver was palpable 11cm below the right costal margin and the spleen 5cm below the left costal margin. Laboratory results included platelets of 42,000/L; alkaline phosphatase of 1,045 U/L; alanine aminotransferase of 285 U/L; and aspartate aminotransferase of 610 U/L. Admission computed tomography showed diffuse homogenous enlargement of the liver, spleen and kidney with a few mildly enlarged retroperitoneal lymph nodes. Serologic evaluation was negative for hepatitis A, B and C viruses, cytomegalovirus, Epstein Barr virus, herpes simplex virus, toxoplasmosis and human immunodeficiency virus. Bone marrow biopsy on day two of admission was negative for malignancy, infection and amyloid. Screening for antinuclear antibody and extractable nuclear antigen antibodies was negative. The patient's history did not reveal risk factors for unusual infections or toxins. Noninvasive doppler ultrasound was not consistent with Budd Chiari. Blood cultures were negative and alpha-fetoprotein level was within normal limits. During the ensuing four days, the patient rapidly deteriorated with additional liver enlargement of 4cm, falling platelet count and metabolic acidosis. On day five of admission, a transjugular liver biopsy demonstrated alphabeta-hepatosplenic T-cell lymphoma. IMPLICATIONS/DISCUSSION: Rapidly progressive hepatosplenomegaly is not widely discussed in the literature. However, reviewing MEDLINE and EMBASE databases, one can conclude that it is most common in hematologic malignancies and infection. The above typical presentation of an uncommon peripheral T-cell lymphoma illustrates that lymphoma can present without lymphadenopathy or bone marrow involvement. Hepatosplenic T-cell lymphoma is an aggressive cancer with a poor prognosis. Despite aggressive treatment, our patient died on the 28th hospital day.

A PAIR OF PAINFUL HANDS. A. Cooper 1 ; 1 University of Pennsylvania, Philadelphia, PA (Tracking ID #73721) LEARNING OBJECTIVES: 1. To review the American College of Rheumatology diagnostic criteria for rheumatoid arthritis (RA). 2. To discuss initial treatment of newly diagnosed RA. CASE INFORMATION: A 39 y/o homeless woman with a past medical history significant for hypertension, diabetes, hepatitis C, and asthma on no medications was admitted to the inpatient psychiatric unit for depression with suicidal intent. The medicine service was consulted for evaluation of hand pain. The patient had been having 2 months of progressively worse pain in both her hands, as well as 1 month of swelling and morning stiffness lasting 90 minutes before improvement. The symptoms made it difficult for her to make a fist or hold her cigarette. Over the last 1 week, all of her symptoms markedly increased. Additionally, she recently noted a sensation of numbness and tingling in her first three fingertips of the right hand that wakes her from sleep. The patient denied any fevers, chills, night sweats or other joint involvement. She denied dry eyes or mouth, as well as urethritis/vaginitis. Review of systems in detail was otherwise negative. Social history was significant for a 20 pack year smoking history. Family history was noncontributory. Physical exam was significant for bilateral symmetric swelling, mild erythema and boggy tenderness of 8 proximal interphalangeal joints. There was no involvement of the distal interphalangeal joints or thumbs and minimal tenderness of the MCP joints. There was no wrist tenderness. Remainder of the joint exam was unremarkable. Remainder of the physical exam was significant for a blood pressure of 130/90, mild expiratory wheezes bilaterally at the lung bases, and a positive Phalen's sign. Pertinant negatives included a temperature of 97.9, moist mucous membranes, no cardiac murmurs, no rashes or nodules and a negative Tinel's sign. Laboratory results were significant for normal electrolytes, renal function, TSH, WBC and hemoglobin levels. The ESR was normal at 9. Anti-Scl 70, dsDNA, and complement levels were normal. The ANA was weakly positive at 1:160. The patient had a positive RF of 104 IU/mL (normal 0±29 IU/mL). Parvovirus IgM was negative, as were Hep B serologies and HIV. IMPLICATIONS/DISCUSSION: Discussion: This patient was diagnosed with early moderately severe RA. The American College of Rheumatology criteria for diagnosis of RA were initially developed to help classify patients for clinical studies. However, they have proved useful in diagnosis as well. The guidelines are as follows: A patient has RA if at least 4 of these criteria are met (the 1st 4 of which must have been present at least 6 weeks): 1) Morning stiffness, usually lasting at least 1 hour before maximal improvement. 2) Arthritis of at least 3 or more joint areas. 3) Arthritis of hand joints. 4) Symmetric arthritis. 5) Rheumatoid nodules. 6) Serum rheumatoid factor. 7) Radiographic changes±erosions, unequivocal bony decalcification adjacent to affected joints. Radiographic changes are present in 15% of patients in the 1st year of disease, in >90% of patients after the 1st 2 years. The initial diagnosis of RA may be difficult because early RA may satisfy few of the diagnostic criteria. Additionally, systemic lupus erythematosis, Sjogren's syndrome, and mixed connective tissue disease may also commonly present with a positive rheumatoid factor, and may be difficult to differentiate from RA early in the course of illness. Finally, seronegative RA, or RA presenting in a single large joint such as the knee, poses it's own obvious diagnostic dilemma. The diagnosis of RA is supported by findings of carpal tunnel syndrome, as seen in this patient, as well as weight loss, fever, anemia, serositis, pulmonary nodules and peripheral neuropathy. Therapy for RA is usually initiated with non-steroidal antiinflammatory drugs (NSAIDs). Prednisone is added for rapid improvement when severe joint symptoms are present, and is usually tapered after inflammation is controlled. Disease modifying anti-rheumatic agents (DMARDs) are added if symptoms are not controlled with NSAIDs, if symptoms are moderate or severe in nature, or if radiographic changes are present. DMARDS are medications that have been proven to reduce the rate of bony destruction in RA. The most common DMARD used for initial treatment is methotrexate, started at a dose of 7.5 mg/week. The maximum dose of methotrexate is 25 mg subcutaneously/week. It is important to monitor patients for methotrexate toxiticy including liver function tests (cirrhosis), pulmonary symptoms (interstitial lung disease), and bone marrow toxicity. LEARNING OBJECTIVES: 1) Apply epidemiologic factors to decisions of whether to screen for hepatocellular carcinoma (HCC) in chronically Hepatitis B-infected individuals. 2) Recognize the limitations of current screening modalities for HCC. CASE INFORMATION: An asymptomatic 23 year-old male student presents to clinic after being told by a former sexual partner that he had``given her an infection.'' He has no significant past medical or surgical history. His review of systems is negative. He was born in China and immigrated to the United States at two years of age. He uses a half-pack-per-day of tobacco, alcohol to intoxication 1±2 times per week, no recreational drug use. His physical examination is normal. His laboratory values are significant for being hepatitis B (HBV) surface antigen positive, surface antibody negative, core antibody positive, e antigen negative, and HBV viral load undetectable. Hepatitis C and Human Immunodeficiency Virus (HIV) are negative. His liver function tests are all within normal limits.

Observational studies show that among perinatally-infected individuals, incidence of HCC begins rising in young adulthood (20±30 years of age). Among those who are infected later in life the incidence of HCC begins rising at 40 to 50 years of age. Other major risk factors for HCC include presence of cirrhosis, e-antigenemia, exposure to other hepatotoxins including alcohol and tobacco, and co-infection with hepatitis C virus. HCC screening is usually done at 6±12 month intervals. Common modalities used include serum alpha fetal protein (AFP), ultrasound (US), and computed tomography (CT). The usefulness of AFP is limited by sensitivity (approximately 60%) and specificity (approximately 85%). Thus, US or CT must be used in conjunction with AFP. Ultrasound, the most widely-used modality, has a variable sensitivity determined by operator experience, reported to be 35% to 84%. CT, with less operator-dependent variability and sensitivity greater than 90%, is the most expensive of screening modalities. Given the limitations of existing screening methods and overall small survival-benefits of current widely-available treatments, the cost-effectiveness of HCC screening has been questioned. There are no randomized studies assessing cost-effectiveness of HCC screening. Non-randomized studies have shown conflicting results. Thus, although a recent survey of U.S. hepatologists showed that 84% of respondents screen for HCC in individuals with cirrhosis, no official guidelines have yet been provided by the National Cancer Institute (NCI).

ALONG CAME A SPIDER . . . . . . CAUSING UNUSUAL ULCERS. N. Correia 1 , R. Abou Jawde 1 , S. Baghdasarian 1 , S. Schmitt 1 ; 1 Cleveland Clinic Foundation, Cleveland, OH (Tracking ID #76813) LEARNING OBJECTIVES: To emphasize the extensive differential diagnosis of lower extremity (LE) ulcers, the incidence of pyoderma gangrenosum (PG) following trauma and the importance of accurate diagnosis, we present a case in which lesions that appeared following a spider bite were intially treated as infection. CASE INFORMATION: A 59 year old man presented with non-healing painful left LE ulcers. He was bitten by a spider after which he noted a small red tender spot over his shin that progressed to an ulcer with purulent drainage. He was treated with oral and intravenous antibiotics, local wound care and surgical debridement without improvement. During treatment he developed a new ulcer on the same leg and an inflamed nodule over the contralateral malleolus. IMPLICATIONS/DISCUSSION: PG, a deforming ulcerative skin disease, usually presents with erythematous nodules or vesiculopustules on the legs. The lesions undergo a rapidly destructive necrotizing process to form large ulcers with surrounding erythema. Although frequently associated with inflammatory bowel disease or immunosuppression, in adults PG can occur spontaneously, following trauma (including spider bites), or in association systemic diseases. Biopsy confirmed the presence of PG in our patient and he improved dramatically on prednisone.

SARCOIDOSIS PRESENTING AS TESTICULAR MASS: CASE REPORT AND REVIEW OF THE LITERATURE. L. Corsino-Nunez 1 , M. Kam 1 , C. Kaye 1 ; 1 Wayne State University, Detroit, MI (Tracking ID #75657) LEARNING OBJECTIVES: To recognize sarcoid presenting as a testicular mass. CASE INFORMATION: Sarcoidosis a chronic multisystem disease of unknown etiology characterized by noncaseating granulomas. The most commonly involved organs are the lungs, lymph nodes, skin, uvea, liver and bone. Sarcoidosis of the male urogenital tract is uncommon. Physicians need to be aware of this occurrence especially in males with a known history of sarcoidosis. Case: A 31 y/o African American male presented to the Emergency Department complaining of dyspnea, fever and night sweats. Past medical history was significant for asthma. Admission physical exam was remarkable for bilateral, nontender, mobile, cervical lymph nodes and a right testicular mass. Chest-x-ray revealed mediastinal and bilateral hilar lymphadenopathy. Computarized Axial Tomography scan of the chest, abdomen, and pelvis was consistent for bilateral lymph nodes in the axillary and inguinal region. Ultrasonography of the right testicule was done and showed marked enlargement of the right epididymus and small hydrocele. Biopsy of one of the submandibular lymph node revealed non-caseating granulomas. A right orchiectomy was performed. The pathology report was consistent with non-caseating granuloma involving the epidiymis and focal testicular parenchyma. The spermatic cord was free of granulomatous inflammation. IMPLICATIONS/DISCUSSION: Discussion: Sarcoidosis with testicular involvement is rare. Only 0.2% of patients with sarcoidosis have urogenital involvement. Forty-three cases have been described in the English language medical literature. We want to enhance physicians' awareness of urogenital sarcoidosis and include in the differential diagnosis of a palpable testicular mass. The treatment for urogenital sarcoid is corticosteroids, identical to systemic sarcoid. Review of the literature shows that a great unnecessary percentage of patients with testicular sarcoid have undergone orchiectomy. Thus awareness of this condition may result in prevention of this radical approach in males who present with sarcoidosis and a testicular mass. LEARNING OBJECTIVES: To recognize Pott±Puffy Tumor as a complication of sinusitis. CASE INFORMATION: Pott±Puffy Tumor is defined as subperiostial abscess and osteomyelitis of the frontal bone seen as a complication of frontal sinusitis. With the advent of antibiotics, Pott±Puffy Tumor is a rarely recognized entity. A 31 y/o white female, previously healthy until one day prior to admission, presented with frontal headaches, dull in nature that progressively worsened, associated with remarkable forehead swelling, and dizziness. One week prior to admission she received a two-week course of cefuroxime for frontal sinusitis. Her past medical history was significant for fibrodysplasia of the ethmoidal sinus during childhood requiring five surgical interventions. Admission physical exam was remarkable for forehead swelling with tenderness over the frontal bone and absence of fever. Computerized axial tomography scan of the head revealed opacification of the frontal sinus. The frontal sinus was drained and a purulent discharge was obtained. Gram stain and culture showed no organisms or growth. Frontal headache and swelling improved after drainage. She was placed on ampicillin/sulbactam for a total of two months. She was scheduled for frontal sinus obliteration after completing the antibiotics. IMPLICATIONS/DISCUSSION: Pott±Puffy tumor represents a rare complication of frontal sinusitis. Only 21 cases have been reported after the antibiotic era, of wish 7 have presented in adults. The importance of making this diagnosis is to prevent expansion of the infection to the brain. We would like to highlight the importance of making an accurate diagnosis, especially in patients treated for frontal sinusitis. Five cases in which no organisms have been identified are reported in the literature. This entity can be successfully treated with antibiotics and drainage. LEARNING OBJECTIVES: Recognize the importance of secondary causes for hypertension. CASE INFORMATION: A 51 year old diabetic gentleman with obstructive sleep apnea treated with CPAP and a long-standing history of hypertension came to our clinic for a routine visit. Despite five anti-hypertensive medications, blood pressures remained near 180/100. This prompted a search for secondary hypertension. Studies were negative for renal vascular disease and pheochromocytoma as well as primary hyperaldosteronism. Despite preserved renal function, Nephrology consultation was obtained with the resulting suggestion that this may be a case of occult noncompliance. However, the patient regularly attended appointments and filled all of his antihypertensives in a timely manner. This convinced us to look further into additional possible rare causes for secondary hypertension. On one subsequent follow-up visit, the patient did complain of jaw changes and a thick tongue. He has coarse facial features, a large fleshy nose and large tongue along with multiple skin tags and large hands. The constellation of hypertension, sleep apnea, diabetes, and a documented history of carpal tunnel syndrome, along with his complaints and findings raised the possibility of acromegaly as a reason for refractory hypertension. For the initial workup, a screening insulinlike growth factor 1 level was then ordered, which returned at 2.5 times the normal range. A subsequent confirmatory glucose tolerance test with measurement of growth hormone levels then failed to show GH suppression with a glucose load, supporting the diagnosis of acromegaly. IMPLICATIONS/DISCUSSION: Acromegaly is a somatic growth and proportion disorder with elevated levels of GH and ILGF-1 found as hallmarks of this syndrome. It is most often caused by GH-secreting pituitary tumors. Some of its features include skeletal overgrowth, arthropathy, skin changes, cardiovascular disease and respiratory dysfunction. Hypertension is one important complication of acromegaly, with the prevalence of hypertension in acromegalic patients estimated to be about 35%, although there is no consensus in the medical literature regarding the exact mechanisms involved in its pathogenesis. While hypertension is a common condition treated by internists, fewer than 5% of cases are found to have secondary causes. This case highlights the need to consider rare causes of hypertension in patients resistant to treatment, and demonstrates why acromegaly should be considered in the differential.

THE TUMOR THAT MELTED AWAY. J. Cunningham 1 , M. Panda 1 ; 1 University of Tennessee±Chattanooga Unit, Chattanooga, TN (Tracking ID #76984) LEARNING OBJECTIVES: 1. To recognize the similarity in the radiographical and clinical presentation of pulmonary blastomycosis and neoplasms. 2. Stress the importance of a high index of suspicion to avoid misdiagnosis and unnecessary invasive diagnostic procedures. CASE INFORMATION: 57 year old white female with a 40 pack/year history of tobacco abuse presented with persistent cough, mucoid and occasionally bloody sputum for 2 months. She denied fever, chills, night sweats, dyspnea, or recent travel. Her vital signs and room air oxygenation were normal. Physical exam revealed diffusely diminished breath sounds with no accessory muscle use or clubbing. Labs were normal except for a normocytic anemia, and thrombocytosis. CXR showed a right upper lobe infiltrate. CT revealed a large right hilar structure surrounding the distal main stem bronchus with impingement, infiltrative changes surrounding the mass, and an enlarged precarinal lymph node. An endobronchial biopsy and aspiration of the mass revealed no neoplastic cells. Gram stain was negative, and cultures revealed no fungal growth after 28 days. Aspiration smears from the precarinal area were nondiagnostic, but smears from the postcarinal area revealed Blastomyces dermatitidis. She was treated with Itraconazole with complete resolution on repeat CT scan after 6 months. IMPLICATIONS/DISCUSSION: Blastomycosis is a pyogranulomatous infection that can involve many organ systems, but primarily affects the lungs. Infection results from inhalation of the Blastomyces conidia, which may be asymptomatic or present in ways indistinguishable from TB, bacterial pneumonia, ARDS, histoplasmosis, and most ominously bronchogenic carcinoma. Most cases occur in areas surrounding main waterways in North America. Demographics indicate no specific sex, age, race, occupation or seasonal predilection, but exposure to soil is a common factor linking infections. Blastomycosis radiographically mimics many lung diseases with carcinoma being the most common primary diagnosis. Definitive diagnosis is made by isolation in sputum smears or growth in sputum culture which may take up to 30 days. Bronchoscopy requires special considerations in order to obtain a higher yield of fungus. Treatment with lidocaine inhibits growth & limiting concentration to 1g/dL has been recommended. B. dermatitidis can be missed on H&E specimens, so silver or PAS stains should be used. If no diagnosis results invasive thoracoscopy or thorocotomy are often done hastily before the fungus has had time to grow in culture because of the common presentation of Blastomycosis and carcinoma. Blastomycosis infection has been known as``the great masquerader'', therefore, it is very important for physicians to be familiar with the epidemiology in order to develop an index of suspicion for the fungus in endemic areas. Thus, patients can be spared from the distress of undergoing unnecessary testing and invasive surgical procedures. year old Latino male presented to the emergency room with a five day history of severe sharp, pulsatile left sided neck pain, worsened with exertion and head movement with flexion and lateral rotation. This neck pain waxed and waned in intensity throughout the five days prior to admission. The patient reported weakness and numbness of the left arm, which he had used while driving to the emergency room. This weakness resolved with lowering of the left arm. He denied having associated headaches or visual disturbances. The patient was afebrile with a blood pressure of 127/76. Physical examination revealed marked tenderness upon palpation over the left carotid artery. Carotid artery bruits were not present on auscultation. No thyroid tenderness, enlargement, or nodularity was evident. Funduscopic examination, evaluation of cranial nerve function, and assessment of motor and sensory function in the upper and lower extremities were within normal limits. The patient was admitted for treatment of possible left carotid artery dissection and anticoagulation therapy with unfractionated heparin was initiated. An MRI/MRA of the neck was subsequently performed to evaluate for carotid artery dissection. No abnormal flow voids or evidence of dissection were noted. A sonogram of the neck failed to reveal evidence of dissection. ESR was 5, CBC was within normal limits. The diagnosis of carotidynia was made, and the patient's symptoms resolved with prednisone and NSAIDS. IMPLICATIONS/DISCUSSION: Carotidynia is an idiopathic neck pain syndrome arising from the cervical carotid artery resulting in unilateral neck pain that frequently radiates to the ipsilateral face and ear and sometimes to the head. Facial pain is a common primary symptom and carotid artery tenderness and overlying soft tissue swelling are the major physical findings. Two forms of this disorder have been described, an acute form that results in a monophasic illness usually lasting less than two weeks and tending not to recur, and a chronic recurring form which manifests as a vascular headache variant, responsive to antimigraine therapy. Both forms are responsive to the administration of corticosteroids. An evaluation for structural disease of the carotid arteries should be considered in patients with ipsilateral neck pain. MRI/ MRA of the neck has proven highly sensitive. Other imaging modalities to consider include ultrasound and angiography. The diagnosis of carotidynia should be considered only after careful evaluation for other etiologies of neck pain. Considerations for ipsilateral neck pain in the region of the carotid artery near its bifurcation include carotid dissection, migraine headache, thyroiditis, aneurysm of the carotid system, neck neoplasms, or rarely, temporal arteritis.

AN UNUSUAL CAUSE OF CHEST PAIN: SPONTANEOUS PNEUMOTHORAX. S. Daud 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73682) LEARNING OBJECTIVES: 1) Recognize spontaneous pneumothorax as an etiology of chest pain. 2) Describe the typical presentation of spontaneous pneumothorax 3) Recognize the treatment options and prognosis of spontaneous pneumothorax. CASE INFORMATION: A previously healthy seventeen year-old male was seen in the emergency department for complaints of chest pain. His pain was described as a sharp pain above his nipples, bilaterally, which initially had occurred at rest. The pain was neither exacerbated nor relieved by movement or deep inspiration. There were no associated palpitations nor diaphoresis or vomiting. He was taking no medications, but smoked marijuana weekly for the past few months. He occasionally smoked cigarettes, but never consumed alcoholic beverages. There was no family history of coronary artery disease, hypercoagulable states, or vasculitis. Examination revealed a 5 H 11 HH young man in mild distress. His weight was 60 kg, his respiratory rate was 16, and his heart rate was 84. He had no oral lesions and had normal dentition. The cardiac exam revealed normal heart sounds and no murmurs. The lungs were clear to auscultation and had a normal percussion note. The abdomen was scaphoid and non-tender. There was no peripheral edema. Electrocardiogram and pulse oximetry were normal. A chest roentgenogram revealed bilateral apical pneumothoraces. They were estimated to be 10% each. Bilateral apical drainage catheters were placed and the patient's symptoms resolved. The patient was admitted to the hospital for observation. IMPLICATIONS/DISCUSSION: Primary spontaneous pneumothorax is defined as a pneumothorax without a precipitating factor such as trauma, in a patient without clinically evident lung disease. It typically occurs in tall, thin males between 10 and 30 years of age. The use of smoking tobacco has been reported to increase the risk in men by as much as a factor of 20 in a dose dependent manner. Subpleural bullae are found in virtually all patients; their mechanism of formation is not completely understood, but is thought to be related to degradation of elastic fibers in the lung. This process is thought to be accelerated by smoking. The primary spontaneous pneumonthorax results in a decrease in vital capacity, and an increase in the alveolar-arterial oxygen gradient, leading to hypoxemia. Because underlying lung function is normal, hypercapnia is not usually seen. Most patients present with ipsilateral pleuritic chest pain occurring at rest. Tachycardia is frequently the only abnormal physical finding. The diagnosis is confirmed by the identification of a thin, visceral pleural line displaced from the chest wall on chest roentgenography. Treatment with observation, needle aspiration, or drainage through a chest tube all have been advocated. The average rate of recurrence is about 30%, with pulmonary fibrosis, asthenic habitus, and history of smoking all thought to be risk factors for recurrence. (Tracking ID #73698) LEARNING OBJECTIVES: 1) Recognize the common causes and workup of diffuse pulmonary infiltrates. 2) Recognize the usual presentation of desquamative interstitial pneumonitis. CASE INFORMATION: A 45 year-old male with a history of COPD and multiple pneumonias within the past year was admitted to the hospital for complaints of cough productive of yellow sputum, fevers, chills, and worsening shortness of breath. He was found to be febrile and hypoxemic, and have a leukocytosis with a predominance of neutrophils. A chest x-ray showed the presence of diffuse interstitial infiltrates. He was admitted to the hospital and treated for pneumonia with antibiotics and bronchodilators for 11 days without significant improvement. Sputum and blood cultures were negative for bacterial pathogens. Computed tomography (CT) of the thorax showed ground-glass opacities in all lung fields, worse on the right. Pulmonary function testing revealed mild restrictive disease with decreased lung volumes and decreased DLCO. He did not improve clinically and was scheduled for open lung biopsy. Pathology revealed the diagnosis of desquamative interstitial pneumonitis. He was started on Prednisone 60mg daily, had significant clinical improvement and was discharged from the hospital. CT of the thorax performed one month later showed near-complete resolution of the ground-glass infiltrates. IMPLICATIONS/DISCUSSION: The differential diagnosis of a patient with diffuse pulmonary infiltrates is broad. Acute diffuse lung diseases (less than 4±6 weeks in duration) include infection, pulmonary edema, pulmonary hemorrhage, hypersensitivity pneumonitis, and acute eosinophilic pneumonia. Chronic diffuse lung diseases include idiopathic pulmonary fibrosis, sarcoidosis, pneumoconioses, and interstitial lung disease associated with connective tissue diseases. Desquamative interstitial pneumonitis (DIP) is one of the distinct clinical and histopathological entities belonging to the family of idiopathic interstitial pneumonias. The average age of onset is about 45 years of age, and a male preponderance has been noted. Cigarette smoking has been linked consistently to this diagnosis. The typical presentation is an insidious onset of dyspnea and cough. Chest roentgeography often shows a diffuse pattern of reticulonodular opacities, with CT showing a ground-glass appearance. Pulmonary function testing shows a restrictive pattern. Diagnosis is best made with lung biopsy demonstrating the characteristic appearance of alveolar filling by mononuclear cells and thickening of the alveolar septa. Pateints are generally treated with corticosteroids until symptoms are improved at which point they are tapered slowly. Data are lacking regarding the optimal duration of treatment and prognosis of DIP. A 44 year old African American woman presented with the acute onset of shortness of breath and substernal chest pain with radiation of the pain to the neck and left arm. She was diagnosed with acute myocardial infarction with positive CK and isoennymes and troponin-T. Initial ECG did not indicate an acute injury pattern, however ST-T wave change in V5 and V6 suggested lateral ischemia. Platelet count on initial presentation was 36,000. Her initial Hgb was 9.2. No previous laboratory data were available to review. She was initially treated with aspirin, low molecular weight heparin, and GIIB/IIIA inhibitors. Subsequent to this her blood count was repeated and platelet count had dropped to 11,000. At this time her peripheral smear was reviewed and 20±25 schistocytes were identified per high power field. The case was discussed with the Hematology division and plasmapheresis was initiated within 12 hours. After two double volume exchange transfusions, her platelet count had rebounded to 50,000 and her LDH was falling as well. Her platelet count slowly continued to improve over the course of her hospitalization. At discharge on hospital day #8, her platelet count was 236,000. At no point did the patient have renal dysfunction, neurologic symptoms, or fever. IMPLICATIONS/DISCUSSION: TTP is characterized by arteriolar lesions in various organs that contain platelets and fibrin. This results in MHA, and thrombocytopenia. The tissue hypoxia that ensues is responsible for the symptoms. Myocardial vessel involvement may be a cause of sudden death in some patients. However the isolated involvement of myocardial vessels is rare, especially when there is no of involvement of renal and cerebral vessels. TTP is treated with plasmapheresis initially. The disease is now 90% survivable if therapy is initiated promptly. Before this therapy was available, TTP had a 90% mortality. Plasmapheresis is conducted until platelet count, LDH, and MHA resolves. At that time, pheresis is gradually weaned. Those patients who relapse can be treated with corticosteroids, cyclophosphamide, or vincristine. Splenectomy is also an option. LEARNING OBJECTIVES: 1. Diagnose B12 deficiency on clinical grounds 2. Recognize the relationship between H. pylori infection and B12 deficiency 3. Assess potential complications of B12 deficiency. CASE INFORMATION: A 65 year old male was admitted to our hospital with a two month history of progressive gait instability, weakness and bilateral lower extremity numbness. He was unable to walk without assistance, was totally dependant for activities of daily living, had recently become incontinent of urine and had developed severe constipation. He also complained of mild numbness, tingling and weakness in his upper limbs, and had difficulties with hand motor control. He denied fevers, myalgias, pain, involuntary limb movements, headaches, or trauma, however he did have a forty pound weight loss over the previous three months. He had no significant past medical history and was on no medications. Physical exam showed no cranial nerve defects, mild proximal weakness and proprioceptive loss, with severe, diminished lower extremity strength, proprioception, vibration and sensation. Lower extremity tendon reflexes were brisk with positive Babinskis. Bilateral crackles at mid lung fields were evident on chest exam. Laboratory values on admission were significant for hemoglobin of 10.8 g/dl, mean corpuscular volume of 106.8 fL, and B12 of 75 ng/L (190±900). Arterial blood gas on 2L of oxygen showed pH of 7.456, PCO2 of 40.4, and PO2 of 69.0. With the laboratory diagnosis of B12 deficiency, a homocysteine level was obtained and was significantly elevated at 188 mmol/L (0±13). Chest X-ray showed extensive bilateral reticular infiltrates and small bilateral effusions. Due to these findings, a computed tomography of the chest was done which revealed left apical bullae, extensive ground glass opacities, and multiple filling defects in the interlobar and branch arteries consistent with pulmonary emboli. Lower extremity Doppler ultrasound confirmed deep vein thrombosis (DVT). An esophagogastroduodenoscopy was ordered to help determine the cause of the B12 deficiency. This showed mild chronic gastritis and H. pylori organisms. Serum studies for intrinsic factor and parietal cell antibodies were negative. He was treated with intravenous B12, triple therapy for H. pylori, anti-coagulation and oxygen support, however his respiratory status declined over the next three to four weeks and he died approximately one month after admission. Autopsy confirmed sub acute combined degeneration in the spinal cord and organizing thromboemboli with diffuse alveolar damage of the lungs. IMPLICATIONS/DISCUSSION: This case demonstrates a cascade of events that most likely began with the relatively common finding of H. pylori gastritis. Our patient then developed B12 deficiency, which has a known association with this infection. This in turn contributed to elevated homocysteine by interfering with its conversion to methionine. This contributed to a hypercoagulable state and in combination with immobility from the B12 deficiency induced sub acute combined degeneration, led to the DVT and pulmonary emboli. This directly contributed to the patient's respiratory decline. This case demonstrates that when H. pylori gastritis is confirmed, the association between this infection, B12 deficiency and hyperhomocysteinemia should be considered, as this can have profound consequences. 3) Discriminate between opiate dependence and addiction. CASE INFORMATION: A 29-year-old male with a history of hemophilia and hepatitis C presented with recurrent episodes of crampy abdominal pain over the past seven months. He denied fevers, chills, nausea, vomiting. There was no change in bowel habits or alteration of the pain with food or defecation. He denied previous surgeries or intravenous drug use. Physical exam showed no fever, heart rate 106, dilated pupils, diaphoresis, and a soft abdomen with voluntary guarding. The patient had undergone an extensive prior workup for these symptoms including CT scanning, colonoscopy, and upper endoscopy-all of which were normal. On our further review we learned that the patient had been taking two narcotic medications prescribed from different doctors. He described occasionally taking these medications for pain control, but was unaware both were narcotics. His symptoms completely resolved after starting a low dose methadone taper, and the patient was grateful for ending a seven-month cycle of pain. IMPLICATIONS/DISCUSSION: The symptoms of opiate withdrawal can include sweating, headache, nausea/vomiting, abdominal cramping, diarrhea, dilated pupils, piloerection, insomnia, agitation, and anxiety. Opiate withdrawal can occur from chronic prescription narcotic use, but may go unrecognized by patients and physicians. In our patient with hemophilia, prescription narcotics rather than NSAIDS were given for minor pains. His abdominal pain along with dilated pupils and diaphoresis suggested withdrawal leading to a more extensive review of his medication use. Despite using his medications as prescribed, his chronic use led to physical dependence. Addiction is defined as the compulsive use of a substance despite negative consequences. Dependence, however, does not usually have the psychological associations that are seen in addiction, making it harder to recognize. Nonetheless, patients with physical dependence can experience severe distress, as did our patient. Opiate withdrawal causing abdominal pain remains a diagnosis of exclusion and other serious causes should always be ruled out. LEARNING OBJECTIVES: 1. Discuss approach to fever in travelers 2. Recognize Dengue fever presentation 3. Realize importance of controlling mosquito vectors. CASE INFORMATION: 23 year old male with no prior history presents with 3 days of fever, malaise, headache and body aches. He returned to the US 6 days prior after a month-long backpacking trip in Brazil. His fever has no pattern and is relieved with Ibuprofen. His headache is bitemporal with some associated photophobia and neck pain. His body aches are generalized but most severe in the lower back. He denied HIV risk factors and review of systems is negative. He did not receive any vaccines or prophylactic medications. His bp is normal, pulse 70, and temperature 38.6 degrees Centigrade with malaise and a maculopapular rash over the trunk. Otherwise exam was negative. At this point the differential included flu, malaria, typhoid fever, leptospirosis, acute HIV, and Dengue fever. Laboratory investigation revealed a mild leukopenia with normal platelet count. CSF, HIV p24 Ag, thick and thin smear, RPR were all negative. Dengue titer came back positive for serum ELISA IgM. He was treated symptomatically with resolution of symptoms within a week's time. IMPLICATIONS/DISCUSSION: Dengue fever is caused by a single stranded RNA virus in the family Flaviviridae (found throughout the tropics) and transmitted to humans by the Aedes aegyptia mosquito. With urbanization and subsequent inadequate waste and water management, Dengue incidence is increasing in South America and the Caribbean. There is a disease spectrum with Dengue ranging from a relatively non-specific illness, to Dengue fever (acute illness with leukopenia, headache, malaise, myalgias/arthralgias) to Dengue hemorrhagic fever (the above plus positive tourniquet sign, thrombocytopenia, and increase vascular permeability) to Dengue shock syndrome (the above plus hypotension and narrow pulse pressure). Diagnosis of Dengue is usually by isolation of the virus or serologic testing such as ELISA for IgM. Dengue fever is typically self-limited with symptoms lasting appoximately 7 days. Warning signs for Dengue shock syndrome include sustained abdominal pain, persistent vomiting, change of level of consciousness, and a sudden decrease in platelet count. Dengue has 4 serotypes and repeat infection with another serotype is more likely to casue severe disease. In addition to improved mosquito control, a vaccine is currently being developed.

BLOOD IS THICKER THAN WATER: THE MANAGEMENT OF HYPERVISCOSITY IN ADULTS WITH CYANOTIC HEART DISEASE. A. DeFilippis 1 , S. Aaberg 1 ; 1 Emory University, Decatur, GA (Tracking ID #76037) LEARNING OBJECTIVES: 1. Recognize the clinical presentation of hyperviscosity syndrome in patient with chronic hypoxia. 2. To recognise the complications of phlebotomy in the treatment of erythrocytosis of cyanotic heart disease. 3. To recognise the appropriate use of hydroxyurea in the treatment of erythrocytosis of cyanotic heart disease. CASE INFORMATION: A 19-year-old male with uncorrected tetralogy of Fallot presented to the emergency room after a ground level fall after climbing two steps. The fall was preceded by two episodes of lightheadedness. He denied vertigo, bowel or bladder incontinence, chest pain, dyspnea, or palpitations. At presentation, he was afebrile with a pulse of 90 beats per minute, blood pressure of 117/63, 30 respirations per minute and an oxygen saturation of 79%. Physical examination was remarkable for a well developed, alert and oriented male in no distress, clubbing in all digits, normal S1 and S2 heart tones with a II/VI early systolic ejection murmur heard throughout the chest; a cardiac heave over the left side of the chest, no jugular venous distention, no peripheral edema or crackles. Chest radiograph revealed a large bootshaped heart and right-sided aortic arch. EKG was notable for a normal sinus rhythm with left axis deviation and right atrial enlargement. Remarkable laboratory values were hemoglobin of 24g/dL and a hematocrit of 76 %. The patient was phlebotomized 500ml of blood and discharged from the hospital after remaining in normal sinus rhythm and asymptomatic for 24 hours. IMPLICATIONS/DISCUSSION: Complications of chronic hypoxia including erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses or stroke and endocarditis are among the most common consequences of cyanotic heart disease in adults. The compensatory erythrocytosis of cyanotic heart disease can become pathologic by causing an increase in blood viscosity, which decreases perfusion, resulting in a decrease in total oxygen delivery and an increased risk of veno-occlusive/hyperviscosity syndrome. Treatment of hyperviscosity secondary to erythrocytosis in cyanotic heart disease is controversial. Data suggest that phlebotomy has the potential to increase exercise capacity, reduce the symptoms of hyperviscosity syndrome and reduce the potential increased risk of vasoocclusive disease in selected patients with polycythemia secondary to cyanotic heart disease. Unfortunately, repeated phlebotomy can quickly lead to iron deficiency. Microcytic erythrocytes produce higher viscosity than normocytic erythrocytes at comparable hematocrits putting patients at high risk for vasoocclusive events. There is limited data on the use of hydroxyurea to suppress erythrocytosis in this patient population. Thus we concluded that until newer approaches to decreasing the hematocrit, without causing iron deficiency anemia, are shown to be safe and efficacious, phlebotomy should only be used for the acute resolution of hyperviscosity symptoms; and the use of hydroxyurea should be limited to recurrently symptomatic patients.

CARDIAC SARCOID AND RISK OF SUDDEN DEATH. A. DeFilippis 1 , A. Palacio 1 , D.W. Brady 1 ; 1 Emory University, Decatur, GA (Tracking ID #76794) LEARNING OBJECTIVES: 1. Recognize the clinical presentation of cardiac sarcoid. 2. Treat cardiac sarcoid and its inherent risk for sudden cardiac death. CASE INFORMATION: A 58-year-old female with cutaneous sarcoid presents to the emergency room with a 3 month history of progressive dyspnea on exertion. She also reports a 2-week history of proximal nocturnal dyspnea, cough, 2-pillow orthopnea and lower extremity edema. She denies chest pain, fever, chills, or palpitations. Her past medical history includes hypertension, diabetes, hypercholesterolemia and obstructive sleep apnea. On presentation, she was afebrile, pulse 106, blood pressure 120/60, respiratory rate of 28 and oxygen saturation of 88% on room air. Physical exam was significant for S3 gallop, normal pulmonary exam, lower extremity edema and several silver dollar size hyperpigmented lesions on her legs. Routine laboratory testing was unremarkable, chest radiograph revealed mild cardiomegaly as compared to a normal radiography 1 month earlier. EKG revealed a new right conduction system block as compared to a normal EKG 2 years earlier. High resolution CT scan was negative for pulmonary embolus and deep venous thrombosis but revealed multiple enlarged mediastinal lymph nodes. Echocardiogram was notable for hypokinetic lateral and inferior wall motion, new from a normal dobutamine stress echocardiogram 2 years earlier. Cardiac catheterization revealed normal coronary angiography, an ejection fraction of 20% and regional wall motion abnormalities, which lead to a cardiac biopsy that revealed non-caseating granulomas consistent with active cardiac sarcoid. The patient improved with diuresis and systemic afterload reduction. She was started on a 6-month course of prednisone and equipped with an automated internal cardiac defibrillator with rescue pacing, prior to discharge from the hospital. IMPLICATIONS/DISCUSSION: Dyspnea and cough are amongst the most common clinical presentations of sarcoid but are attributed to pulmonary rather than cardiac pathology. Although less than 10% of sarcoid patients demonstrate symptoms secondary to cardiac sarcoid, cardiac involvement is found in up 76% of sarcoid patients at autopsy and accounts for 50% of the mortality in this patient population. The most common presentation of cardiac sarcoid, found in approximately 50% of patients, is arrhythmias or cardiac conduction abnormalities as a result of granuloma formation in the conduction system. Sarcoid granulomas in the ventricular myocardium may lead to ventricular arrhythmias in as many as 22% of patients with sarcoid. Granulomas in myocardium can result in diastolic or systolic dysfunction and has accounted for 25±75% of the deaths in some studies of cardiac sarcoid patients. Endomyocardial biopsy is highly specific but due to the non-homogeneous pattern of infiltration will only lead to a diagnosis of cardiac sarcoid in approximately 20% of cases. With arrhythmias or cardiac conduction abnormalities accounting for 30±65% of the deaths inpatients with cardiac sarcoid, automated internal cardiac defibrillators (AICD) with rescue pacing are standard of care in survivors of deadly arrhythmias. Although no trials have assessed the efficacy of AICDs in the absence of ventricular tachyarrhythmias, many advocate their use in all cases of known cardiac sarcoid; others reserve the use to patients with EKG abnormalities by standard of Holter monitor testing. Treatment of the underlying pathological process with immunosuppression is controversial and void of any large randomised trials to access efficacy. A small uncontrolled study demonstrated improvement and/or reversal of EKG abnormalities in greater than 50% of patients treated with corticosteroids. In one retrospective study of patients with cardiac sarcoid, 5-year survival was increased from 10% to 75% with the use of corticosteroids. Opponents to the use of corticosteroids raise concern that corticosteroids convert granulomas to scar tissue increasing the risk of aneurysms. Cardiac transplant has been successful with recurrent disease possible but rare.

A WOMAN FROM CAMEROON WITH FEVER, ABDOMINAL PAIN AND EOSINOPHILIA. K. Dendrinos 1 ; 1 Boston University, Boston, MA (Tracking ID #75960) LEARNING OBJECTIVES: Review the Differential Diagnosis of Eosinophilia, Evaluate Fever of Unknown Origin. CASE INFORMATION: A 70 year old woman, recently emigrated to the U.S., presents to this hospital complaining of fever and chills for the past 3 months. She also complained of right and left upper quadrant pain. These complaints originally began in her home country of Cameroon, she came to the U.S. one week prior to her initial admission. During her first admission, she was febrile daily to 101 degrees Fahrenheit. Her exam was notable for right upper quadrant abdominal tenderness. Her laboratory examinations were significant for a CBC with an eosinophilia of 43%, that would peak later that month at 60%. Suspicion was high for a parasitic infection. Serologies would later be positive for multiple parasites endemic to Cameroon. She was treated with a wide array of antibiotics, including anti-tuberculosis medications, anti-fungals, and anti-helminthics. Her clinical course deteriorated and she died in the intensive care unit. On autopsy, she was found to have widely disseminated lymphoma involving nearly every organ system. IMPLICATIONS/DISCUSSION: This case initially appeared to be a classic presentation of a parasitic infection: a patient with fever and eosinophilia from an endemic area with positive serologies. It presents a chance to review the differential diagnosis of eosinophilia, and to again rethink the work-up of a fever of unknown origin. This case again demonstrates that``common things occur commonly'' (even when the patient comes from an unfamiliar part of the world). It also demonstrates the importance of keeping the differential diagnosis open, especially when the therapy instituted according to the initial dianosis fails.`L OCKING'' IN THE CASE FOR PREVENTIVE IMMUNIZATIONS. J. Derby 1 , C. Manhart 1 , C. Murphy 1 ; 1 Creighton University, Omaha, NE (Tracking ID #74723) LEARNING OBJECTIVES: Recognize that there are many patients at risk who have not received a primary series in tetanus. Distinguish a differential diagnosis of tetany. Manage a tetanus infection. CASE INFORMATION: A 71 year old female with no significant past medicial history and on no medications presented to the ER complaining of waking up in the middle of the night and being unable to move for the last 24 hours due to muscle stiffness. On initial exam she had marked neck stiffness with muscle spasms triggered by light touch and deliberate speech. A CT scan was unremarkable. A trial of IV diphenhydramine was administered to rule out a dystonic reaction. Stychnine levels and tetanus antibodies were drawn ( both later reported as negative). Over the next few hours obvious trismus developed. Her muscle spasms spread inferiorly to involve her abdominal wall, and her upper and lower extremities demonstrated lead pipe rigidity. The patient was intubated prophylactically and IV diazepam was begun. The patient was given tetanus immunoglobulin as well as a Td vaccination (since the illness is not protective). Metronidazole was administered IV. IMPLICATIONS/DISCUSSION: The majority of reported cases of tetanus in the US are in patients over the age of 60 years old. Currently, nearly 50% of elderly patients in the United States have non-protective titers. This is attributed to waning immunity in patients who have not received booster shots. Additionally, many elderly never received the primary series as children (which was not available until the 1950's). This patient had received one booster without a primary series which did not protect her,but may have prevented her mortality. Many immigrants as well, may have never received the primary tetanus series. Physicians must be diligent in immunizing at-risk groups and ensure that all patients whos tetanus immunization status is unknown receive a primary series. LEARNING OBJECTIVES: To analyze an interesting presentation of rhinocerebral mucormycosis and review current diagnostic and treatment modalities. CASE INFORMATION: The patient is a 26 yo African American male with a past medical history significant for Type I Diabetes Mellitus who presented with a chief complaint of leftsided facial swelling for nine days. He stated that the onset of facial swelling occurred over few hours and that the progression was rapid. Pt reported subjective fevers and chills. He denied upper respiratory or sinus-related symptoms. He initially presented to an outside hospital after two days of facial swelling. There he underwent a sinus CT that revealed mucosal thickening involving the left ethmoid, maxillary and ethmoid sinuses. He was treated with a seven day course of Rocephin and Cleocin. The patient was in DKA at the time of presentation and was treated for two days per hospital DKA protocol. On the day of discharge from this outside hospital the patient presented to our institution reporting that the facial swelling had not improved with prior therapies. Additionally, he complained of bilateral blurry vision with increased sensitivity to light. On physical examination the patient was afebrile. HEENT examination was significant for left-sided facial swelling with infraorbital involvement, a greenish-yellow discharge from the left medial canthus and left nares, photophobia and a necrotic plaque of the hard palate. The patient was unable to medially deviate his left eye. Laboratory work revealed a normal white cell count and differential, and a normal chemistry panel with the exception of an elevated serum glucose of 256. The differential diagnosis at this point included among other conditions fungal sinusitis, bacterial sinusitis, lymphoma and Wegener's granulomatosis. MRI of brain revealed extensive paranasal sinus opacification with abnormal dural enhancement extending from the left sphenoid sinus to involve the left cavernous sinus, left middle cranial fossa and left fifth cranial nerve with no intracranial, parenchymal or orbital involvement. The patient underwent a nasal biopsy that revealed multiple hyphal elements consistent with Mucormycosis. The patient was started on Amphotericin B at 1.5/mg/kg/day and underwent extensive surgical debridement. Although no orbital involvement was confirmed on MRI, the patient's cranial nerve palsy and opthalmoplegia were understood to be a manifestation of rhino-orbital mucormycosis. The hospital course was complicated by acute renal failure, septic shock, diabetic ketoacidosis and cardiac arrest. While serial MRIs showed no regression of disease, the patient was medically stabilized, and showed clinical improvement over an eight week hospital course. However, the patient's vision loss and opthalmoplegia did not improve with treatment. IMPLICATIONS/DISCUSSION: Rhizopus oryzae accounts for 90% of rhinocerebral mucormycosis. Patients in DKA are highly susceptible because the acidic, glucose rich environment provides a perfect medium for growth. The clinical presentation includes classic sinusitis symptoms and signs along with nasal necrosis (38%) and palatal or gingival necrosis (14%) as in the case of our patient. The diagnosis of mucormycosis is histologic, and it is the only fungus that can be seen with H & E stain. The mainstays of treatment are surgical debridement and reversal of predisposing factors. While lipid containing formulations allow for higher doses to be given due to reduced toxicity there may be problems with delivering the complex to infarcted tissue and obtaining effective concentrations. Administration of intravenous Amphotericin B along with alternative routes such as aerosolized and CSF perfusion pathways is an aggressive treatment modality. Hyperbaric oxygen is an accepted, but not commonly utilized adjuvant to treatment. Even with early detection and treatment the overall mortality rate in patients with rhinocerebral mucormycois remains high. A 59 year old homosexual Caucasian male presented with complaints of b/l hearing loss, tinnitus and vertigo for several months prior to presentation. Patient had an audiogram performed which showed moderate to severe symetrical sensorineural hearing loss. Patient did not have a history of recent aminoglycoside use and was not a diabetic. He was worked up with thyroid stimulating hormone, sedimentation rate, coagulation tests, rheumatoid factor and anti-nuclear antibody titers which were all within normal limits. PPR was positive at 1:16 and MHA-TP was positive at 4+. He refused an HIV test. Patient subsequently received a lumbar puncture which was positive for VDRL . He was thus diagnosed with neurosyphilis and admitted to the inpatient medicine wards where he received a 14 day course of IV Penicillin. Hearing loss improved with treatment of the neurosyphilis. IMPLICATIONS/DISCUSSION: Neurological manifestations of syphilis can occur during any phase of this disease as the central nervous system is seeded during spirochetemia. Up to forty percent of patients infected with Treponema pallidum will have cns involvement. Although neurosyphilis can be aymptomatic, symptomatic neurosyphilis can present earlier as syphilitic meningitis or later in the infection, can have a meningovascular or parenchymatous pesentation. Cranial nerve involvement, especially of cranial nerves II±VIII, can be seen. Syphilitic otitis is a form of neurosyphilis that can present as deafness, vertigo and/or tinnitus and should considered in patients who present sensorineural hearing loss. If treated early, syphilitic otitis may be curable, but can lead to irreversible damage if untreated. CASE INFORMATION: 78 years old man with coronary artery disease, emphysema and alcoholism presents with short of breath and palpitations. He had clear chest film, but was found to be in rapid atrial fibrillation and controlled with diltiazem. On day 3 of hospital stay, his mental status deteriorated and rapidly went into delirium tremens. He subsequently had temperature spike to 103.0(F) with associated leukocytosis. His oxygen saturation became very unstable and eventually requiring mechanical ventilation. He repeat chest X-ray showed right lower lobe consolidation. His sputum gram stain showed 4+ small gram negative rods which was identified to be Pasteurella Multocida. He had been a long time avid deer hunter and has three dogs which he is in close contact with. He was treated with a third generation cephalosporin and his condition slowly improved. His subsequent CT of chest revealed left lung nodule. The biopsy of the nodule was consistent with squamous cell carcinoma of the lung. IMPLICATIONS/DISCUSSION: Pasteurella Multocida is common organism in many domestic and wild animals. Human Pasteurella is a major pathogen in wound infections due to animal bites. Greater than 70% of the reported cases of Pasteurella Multocida pneumonia occurred in patients with non-traumatic exposure to colonized animals.

Respiratory infection caused by Pasteurella Multocida can range from asymptomatic colonization to otitis media, sinusitis, epiglottitis, pneumonia, empyema and lung abscess. The degree of pulmonary infection depends on the immunity state of the host and can carry a very high mortality. Treatment of choice for Pasteurella Multocida infection is either penicillin, second or third generation cephalosporins, or doxycline. Prolonged antibiotic treatment is warranted in immnocompromised host. 2) To consider macrophagic myofasciitis in patients presenting with proximal muscle weakness and myalgias. CASE INFORMATION: Macrophagic myofasciitis is a syndrome of proximal muscle weakness, pain and fatigue. Clinical presentation is very similar to polymyositis, with proximal muscle pain, weakness, fatigue, fever and ternderness. Macrophagic myofasciitis is distinguished from polymyositis microscopically, with infiltration of the fascia with macrophages in MM. Cardiac involvement is found in over 70% of patients with polymyositis. We report a case of macrophagic myofasciitis presenting with proximal muscle weakness and ventricular tachycardia. A 49 year-old African American female with several months of progressive muscle weakness presents with palpitations and dizziness. Physical examination demonstrated significant proximal muscle weakness with no evidence of a skin rash. Laboratory data revealed a creatinine kinase of 1301 u/liter (normal <2oo), a CK-MB of 41.7 (normal 0± 60) and an aldolase of 40.2 (normal 1.5±8.1). An EKG showed a wide complex tachycardia with a rate of 220. A coronary angiogram was normal and electrophysiologic studies failed to induce ventricular tachycardia. Electromyopathy was consistent with a myopathy and her muscle biopsy revealed macrophagic infiltration of fascia, consistent with a diagnosis of macrophagic myofasciitis. Her ventricular tachycardia was postulated to have arisen from a myofasciitis. After initiation of high dose steroids, her muscle enzymes normalized and no further episodes of tachyarrhythmia occurred. IMPLICATIONS/DISCUSSION: MM is a relatively new muscle disease, with a first case report in 1993 in France. In several ways, it is similar to polymyositis, with bilateral muscle weakness and pain. Both are associated with an altered immune system. Cardiac arrhythmia in polymyositis is fairly common, occurring in over 70% of patients. These arrhythmias are due to an increase in spontaneous and disorganized myopathic contraction. There are no previous reports of cardiac disrhythmias in macrophagic myofasciitis. Most patients respond well to treatment with steroids and/or antibiotics in a few weeks. LEARNING OBJECTIVES: To recognize rare presentations of severe hypothyroidism. CASE INFORMATION: 18 year old African American female presented to the teen pregnancy center secondary to increased abdominal girth and amenorrhea. She also reported fatigue, hair loss, dyspnea on exertion, and sadness. Physical exam was significant for alopecia, a large goiter, markedly distended abdomen with fluid wave, tense edema of the hands, and delayed deep tendon reflexes. Labs were remarkable for a TSH of 240 with undetectable T4 and T3, marked microcytic anemia and an erythrocyte sedimentation rate of 140. CXR revealed a globular pericardial silhouette and ultrasound of the abdomen showed a large amount of ascites. Echocardiogram was unremarkable except for a moderate pericardial effusion. Pelvic ultrasound showed enlarged cystic ovaries, consistent with Van Wky Grumbach syndrome. Peritoneal fluid studies were consistent with myxedematous ascites. Upon further questioning, the patient stated that she had been treated for hypothyroidism as a young teen and had been lost to follow-up for two years. She also had a history of prior suicide attempts and depression. IMPLICATIONS/DISCUSSION: The manifestations of thyroid disorders are many, myxedematous ascites are a well-known but not often seen presentation. Serositis from hypothyroidism may be caused by several things: a capillary leak syndrome resulting from the dearth of thyroid hormones, an SIADH-like picture causing body cavity fluid accumulation, or high hyaluronate concentrations in the body fluid acting as an osmotic attractant. The anemia of hypothyroidism is thought to be caused by either direct bone marrow toxicity, lack of stimulation of erythropoiesis, decreased RBC survival time, and increased 2,3-DPG concentration. Van Wky Grumbach syndrome is a rare condition in which the TSH at high levels acts as an FSH analogue to cause ovarian hyperstimulation/cyst formation. This should be considered when a patient with no known thyroid disease presents with cystic ovaries. year old Hispanic male with no significant past medical history presents to our clinic with a one year history of intermittent bright red blood per rectum and two week history of mild dyspnea on exertion. He has previously been evaluated for the rectal bleed at various clinics and treated with topical hemorrhoidal ointments without relief. Patient denies chest pain, orthopnea, paroxysmal nocturnal dyspnea, abdominal pain, bowel changes, fever, chills, and weight loss. He is a sexually active homosexual. Family history is negative for colon cancer and polyps. Vital signs show temperature 100.3, BP 138/76, HR 75, RR 14. Physical exam is significant for mildly decreased breath sounds in left upper lobe and guaiac positive stool but no palpable rectal mass. Lab results show hemoglobin 10.9, MCV 78.0, and WBC 6.4. HIV test is negative. Colonoscopy with biopsy shows squamous cell cancer. Staging studies including chest x ray and a CT scan of the thorax display a 3.5 cm mass in the left upper lobe and CT pelvis confirms anorectal mass. Biopsy of the lung mass is consistent with a metastatic lesion. He is treated with chemotherapy and undergoes resection of the solitary lung mass. IMPLICATIONS/DISCUSSION: Anal canal carcinoma can be overlooked in young otherwise healthy patients as rectal bleeding is often attributed to hemorrhoids. Squamous cell cancer of the anal canal has a high association with human papilloma virus (HPV) particularly HPV-16. HPV DNA is isolated in 88% of anal cell cancers. Other risk factors include chronic immunosuppressive therapy, HIV, and smoking. Past treatment for anal canal carcinoma involved abdominoperineal resection with permanent colostomy. Cure rates with surgical resection ranged between 40±70%. However, in recent studies, chemotherapy with 5-FU and mitomycin combined with radiotherapy offer a 66±70% cure rate and lower rate of complications. Prognosis is dependent on the size of tumor, distant metastases, and nodal involvement. In conclusion, recurrent rectal bleeding in young patients with associated risk factors warrants a more thorough investigation. year old male presented with ten days of progressive difficulty walking, stating he had weakness in the lower extremities and in his right hand. He also reported slurred speech. Pt had no known medical problems and denied the use of medications, illicit drugs, tobacco or alcohol. Physical examination was significant for 3/5 right lower extremity strength with absent reflexes of the right leg. Sensory exam was grossly intact. The patient had poor performance of finger to nose testing and difficulty with rapid alternating movements. There was severe gait instability. Babinski's sign was bilaterally equivocal. CBC, chemistry panel, ESR, TSH, RPR, EKG were normal. After an unremarkable head CT, an MRI of the head showed a demyelinating pattern involving the middle cerebellar peduncles. The CSF protein, gram stain, culture, cell count, and glucose were within normal limits. On hospital day 4, HIV serology was positive and thus confirmed the clinical diagnosis of PML. CSF testing for JC virus later returned positive. IMPLICATIONS/DISCUSSION: PML is a demyelinating disease associated with infection of the JC virus. An AIDS defining condition, PML may present with rapid or progressive focal neurological deficits, including aphasia, ataxia, hemiparesis, hyporeflexia, and impaired cognition. In AIDS, PML implies a very poor prognosis with a survival expectancy of about six months. The diagnosis of PML is made through a clinical constellation which includes HIV positivity, characteristic MRI findings, and positivity for JC virus in the CSF. MRI findings of PML are similar to those seen in Acute Disseminated Encephalomyelitis (ADEM), a demyelinating process associated with infections or vaccinations in children, but they differ from those seen in Multiple Sclerosis (MS). The MRI with MS typically shows plaques in the periventricular region, corpus callosum, centrum semiovale, and less commonly in the deep white matter structures. There is no specific therapy for PML, and improvement of symptoms relies on increasing CD4 count via antiretroviral therapy. There has also been suggestion of improved clinical response with the addition of Cidofovir, a drug typically used to treat CMV retinitis.

ABDOMINAL PAIN: A CASE OF NARROWLY±FOCUSED DIFFERENTIAL. A.K. Duncan 1 , W.E. Wysokinski 1 , A.K. Ghosh 1 ; 1 Mayo Clinic, Rochester, MN (Tracking ID #74267) LEARNING OBJECTIVES: 1) Recognize the need to expedite the work-up of poorly responding abdominal pain; 2) Recognize that vasculitis could present with diarrhea. CASE INFORMATION: A 72-year-old women was transferred to our hospital for management of her diarrhea and weight loss. Three months prior to admission, she had an episode of upper respiratory tract infection and was treated with a 10 days course of antibiotics. One month prior to entry, she developed profuse diarrhea and malaise. EGD reveled mild gastritis, small bowel follow through and colonoscopy was normal and she was empirically treated with metronidazole for pseudomembranous colitis. She complained of increasing abdominal pain and was found to have air on an upright abdominal film. Exploratory laparotomy revealed necrosis, inflammation and perforation in the small bowel and nodular lesions in the liver. She underwent extensive small bowel resection, cholecystectomy, and liver biopsy. Liver histology was reported to reveal stellate granulomata consistent with Yersinia. However, cultures and serology for Yersinia were negative. She was empirically treated with ciprofloxacin and transferred to our hospital. Examination revealed an elderly woman, with mild dyspnea, and atrial fibrillation with HR of 110/mt. She was mildly icteric, with skin breakdown in the sacral and inter-scapular region. Chest examination revealed bilateral basilar crackles. Abdomen was mildly tender and distended. Neurological examination revealed generalized but asymmetric neuropathy. Re-evaluation of the small bowel biopsy revealed transmural fibrinoid necrosis with granulomatous inflammation typical of polyarteritis nodosa (PAN). EMG was consistent with mononeuritis multiplex. ANCA was negative. Visceral angiogram revealed micro-aneurysms in the spleen, kidney, jejunal and ileal branches. She was initiated on prednisone and pulse cyclophosphamide therapy with rapid improvement in symptoms. On follow-up at 3 months she continues to gain weight and has no new symptoms. IMPLICATIONS/DISCUSSION: PAN affects the gastrointestinal tract in over 40% of cases. PAN cases presenting with acute abdomen has been associated with a high mortality (60%). GI bleeding, perforation, pancreatitis, renal insufficiency, proteinuria, cardiomyopathy and CNS vasculitis are poor prognostic factors. A high index of suspicion and re-examination of a broad differential diagnosis in cases of acute abdomen, could lead to earlier detection of PAN and successful therapy of this potentially fatal condition.

HYPOGLYCEMIA AND HYPONATREMIA: A HIGHER CAUSE. E.J. Dzielak 1 , N.C. Chiappetta 2 ; 1 Dunmore, PA; 2 Moses Taylor Hospital, Scranton, PA (Tracking ID #77122) LEARNING OBJECTIVES: DDX of hypoglycemia W/U of and DDX of primary, secondary and tertiary causes of adrenal insufficiency. CASE INFORMATION: A 74 year-old man with past medical history of hypothyroidism, prostate carcinoma, iron deficiency anemia, paroxysmal atrial fibrillation, and hyponatremia, presented nausea and vomitting. Physical exam was normal. Abnormal laboratory data included a sodium of 125, glucose of 40, and mild normocytic anemia. His hypoglycemia did not correct with exogenous glucose administration. An A.M. cortisol level returned as 1.3. ACTH level was then drawn and returned as 20 pg/ml. Further evaluation to distinguish between secondary and tertiary adrenal insufficiency was preformed with a corticotropin stimulation test. The results of this test confirmed the diagnosis of secondary adrenal insufficiency. IMPLICATIONS/DISCUSSION: Secondary adrenal insufficiency is a deficiency of ACTH from the anterior pituitary gland resulting in a decreased production of cortisol . In the adrenal gland, ACTH stimulates the zona fasiculata, while having minimal affect on the zona glomerulosa. Therefore, manifestations of aldosterone deficiency (hyperkalemia and hypotension) are not present, as this case demonstrated. To confirm adrenal insufficiency, an AM cortisol level of <1.3 is needed. If the cortisol level is greater than 1.3, the diagnosis of adrenal insufficiency could be confirmed by a cosyntropin stimulation test. To distinguish between primary and secondary adrenal insufficiency, an ACTH level should be drawn which should be >100 pg/ml in primary adrenal insufficiency. The Metyrapone and Insulin Induced Hypoglycemia tests confirm secondary adrenal insufficiency. To distinguish between tertiary and secondary adrenal insufficiency, the corticotropin stimulation test is indicated. An absent response from baseline with ACTH and cortisol confirms secondary adrenal insufficiency, while an prolonged and exaggerated ACTH repsonse is consistent with tertiary adrenal insufficiency.

A GASTROINTESTINAL LINK TO OSTEOPOROTIC FRACTURES. L. Eck 1 , C. Jachna 1 ; 1 Kansas University Medical Center, Kansas City, KS (Tracking ID #74458) LEARNING OBJECTIVES: To recognize that celiac disease is commonly associated with low peak bone mass and adult osteoporosis leading to disabling fractures. CASE INFORMATION: A 49 year old white male with a history of multiple atraumatic fractures including a hip fracture at age 22, wrist fracture at age 16, multiple rib fractures and a recent wrist fracture presented for evaluation of osteoporosis. Bone mineral density studies revealed a T-score of À3.1 at the spine, consistent with osteoporosis. On clinical history, the patient reported a long-standing history of approximately eight loose bowel movements per day associated with abdominal cramping. He also reported low body weight through young adulthood and lactose intolerance. Lab studies were notable for an elevated IgG antigliadin antibody of 132 Units, with a reference range of >30 Units being strongly postive for a diagnosis of celiac sprue. Follow up small bowel biopsy revealed villous atrophy consistent with the diagnosis of celiac sprue. IMPLICATIONS/DISCUSSION: Celiac disease is caused by a genetically based inability to digest gluten, a major protein commonly found in grains. Due to the availability of new highly sensitive and specific serologic diagnostic tests, it is increasingly recognized in the United States as a cause of malabsorption. Celiac disease is often asymptomatic but symptoms suggesting the diagnosis include bloating, flatulence, chronic diarrhea and lactose malabsorption. Other than gastrointestional symptoms, celiac disease also has a wide spectrum of extraintestinal manifestations including iron deficiency anemia, low bone mineral density, and dermatitis herpetiformis. In a study of North American adults with celiac disease, 70% of subjects had low bone mineral density, predisposing them to fractures. Other studies have suggested that in subjects with celiac disease, bone manifestations may be more severe in men than in women possibly due to estrogen's protective effects on the bone. Historically, initial screening for celiac disease involved detection of antigliadin antibody. However, more specific serologic tests, including antiendomysial and antitissue transglutaminase antibodies, are now available. Histologic identification of gluten sensitive enteropathy, with characteristic small bowel mucosal abnormalities including villous atrophy, crypt heperplasia, and an increased density of inflammatory cells, still remains diagnostic. The pathogenesis of low bone mass and osteoporosis in celiac disease is multifactorial. The reduction in surface area of the intestinal mucosa may contribute to calcium malabsorption and subsequent secondary hyperparathyroidism leading to increased bone resorption. Vitamin D deficiency is also believed to be common. Those who are undiagnosed during childhood and young adulthood may never achieve peak bone mass. In addition, some researchers suspect that systemic effects of inflammatory cytokines involved in the intestinal mucosa inflammation may also contribute to the development of bone disease. Not only should patients with celiac disease be screened for osteoporosis, but patients with low bone mineral density and no evident osteoporosis risk factors should be evaluated for celiac sprue.

A. El-Sharkawi 1 , S. Kripalani 1 ; 1 Emory University, Atlanta, GA (Tracking ID #75179) LEARNING OBJECTIVES: Hepatitis due to herpes simplex virus (HSV) is an uncommon, but potentially fatal cause of hepatitis that is often not considered in the differential diagnosis of acute hepatitis during pregnancy. Serological tests have limited value in establishing an early diagnosis and a high index of suspicion and early diagnostic tools, such as HSV DNA detection are essential. Early treatment with acyclovir decreases mortaility from herpes simplex hepatitis. CASE INFORMATION: A 19 y/o woman, G2 P1, with no significant PMHx, presented with premature labor at 32 weeks gestation. The initial symptoms were controlled, but over the next several days, the pt developed a cough, dyspnea, RUQ abd pain, and fever of 39C. Evaluation of blood, urine, and amniotic fluid cultures was unremarkable. CXR revealed bibasilar atelectasis versus infiltrate, and she received azithromycin and ceftriaxone for presumptive pneumonia. The pt remained febrile with increasing RUQ pain. Labs revealed declining Hb (7.1), WBC (5.6 with 56% bands), and Plt counts (62,000), with rising liver transaminases (AST 2490, ALT 796), INR 2.5, T. Bili 2.2. RUQ U/S showed hepatomegaly and fatty liver. Considering her worsening condition, obstetrics performed a C-section on hospital day 5.

Post-operatively, the pt was emergently intubated for acute respiratory failure. Physical exam revealed Temp 39.2, HR 146 (reg), BP 107/38, slight RUQ tenderness, liver span 13 cm, no fluid wave or shifting dullness, and 2 vesicular lesions on the Rt upper inner thigh. DDx at this point included HELLP syndrome, acute fatty liver of pregnancy, acute viral hepatitis, pyelophlebitis, portal vein thrombosis, and acute hepatic failure secondary to sepsis. Antimicrobials were changed to ceftazidime, vancomycin, and acyclovir. On hospital day 11, PCR for HSV type 1 and 2 returned positive. In addition, cultures of the vesicular lesions on the patient's right thigh grew herpes simplex. Further questioning of the patient's partner revealed a hx of genital herpes. With the initiation of acyclovir, the pt defervesced and her transaminases decreased. However, she suffered multiple ICU complications, as well as herpes encephalitis. The newborn infant was in the NICU with herpes meningitis. IMPLICATIONS/DISCUSSION: Hepatitis due to herpes simplex virus (HSV) is an uncommon, but potentially fatal cause of hepatitis that is often not considered in the DDx of acute hepatitis during pregnancy. HSV can affect the liver during primary or recurrent infection, although hepatitis during recurrent infection has not been documented in immunocompetent hosts. Review of the literature suggests that HSV hepatitis can present with wide clinical spectrum from mild symptoms to fulminant hepatic failure. However, the initial symptoms are often nonspecific. Therefore, a high index of suspicion and early diagnostic tools, such as HSV DNA detection are essential. Unfortunately, serological tests have limited value for establishing an early diagnosis, though they may be used retrospectively to support the diagnosis. Definitive diagnosis is made with a liver biopsy, but this is frequently not possible because of severe coagulopathy.`J UST A MED REFILL''. S. Elad 1 , G. Applebaum 1 ; 1 University of California, Los Angeles, Sylmar, CA (Tracking ID #74705) LEARNING OBJECTIVES: 1. To recognize the impact the closing of community clinics has had on uninsured and indigent patients. 2. To raise the possibility that short term economic gains resulting from the closure of primary care clinics may result in preventable hospitalizations. CASE INFORMATION:`Maria' is a 56 -year old woman with a past medical history of diabetes, hypertension and hyperlipidemia that came to the hospital urgent care for a`med refill'. She ran out medications 2 months ago after her community clinic was closed secondary to`budget cuts'. Today Maria reports she has noticed increased urination and thirst for the past two weeks and a frontal headache with blurry vision for the past three days. She denies chest pain or shortness of breath. She has not been febrile. Maria had been on two medications for her blood pressure and diabetes, and a pill for high cholesterol. Presently she is completely out of her medications. When questioned why she waited two months to get her medications refilled Maria stated the two hour bus ride and 6 hour wait in the emergency room required her to take time off work she could not afford. On exam, Maria's blood pressure was 190/108 with a pulse of 83. The rest of her cardiac, pulmondary and nuerologic exam was unremarkable except for bilateral decreased visual acuity. Her blood sugar was 275 with sugar and protien in her urine but no ketones. Her anion gap was normal as was her blood count. Maria was given a dose of lisinopril and her headache resolved once her blood pressure decreased to 160/90. She was restarted on her oral diabetes medication. Her medications were refilled and she was instructed to return to urgent care in one week to have her blood pressure and blood sugar rechecked. IMPLICATIONS/DISCUSSION: The national health care crisis has been the topic of many news programs and newspaper articles for the past year. According to the Kaiser Family Foundation approximately 19% of Californians are uninsured. In California, which faces a multi-billion dollar deficit, politicians have been discussing ways to trim costs which have included proposals to close hosptials and clincs. The recent closure of several primary care clinics in Los Angeles County has left many patients like Maria without access to health care. By the time Maria was able to visit the hospitals' urgent care clinic she had run out of medications and both her diabetes and hypertension were poorly controlled. Had Maria required hospitalization at the time of her visit the cost would have been much higher. Maria's primary care visit to the emergency room was entirely avoidable had her clinic not been closed. Much of the short term economic gains obtained by closing county subsidized clinics may later be lost by patients utlizing our emergency rooms for primary care visits. Even in the context of our current financial situation steps need to be taken to ensure that uninsured patients have reasnable access to primary care services outside the hospital setting. LEARNING OBJECTIVES: 1-To recognize fungal vertebral osteomyelitis as an etiology for worsening back pain in patients with history of multiple back surgeries. 2-To consider secondary bacterial infection in patients who fail to respond to appropriate antifugal therapy. CASE INFORMATION: A 48-year-old male presented in January 2001 with worsening back pain, bilateral leg weakness and urinary incontinence. Condition started in 1993 after back injury during demolition job that required multiple back surgeries. Examination was remarkable for bilateral leg weakness and local tenderness over lumbar spine. MRI examination revealed disc space infection at the L3-4 level with adjacent vertebral osteomyelitis. CT guided aspiration of L3-4 space was performed and cultures grew Candida albicans. Treatment was instituted with IV Amphotericin B via Mediport. Therapy was switched to oral fluconazole 400 mg daily. In March 2001, he developed Mediport related Staphylococcus aureus sepsis and was treated with cefazolin for two weeks. Patient was re-admitted in April with worsening back pain. MRI examination revealed worsening inflammatory changes within L3 and L4 vertebral bodies and small epidural abscess. CT guided aspiration was performed and cultures grew methicillin sensitive Staphylococcus aureus. We started treatment with Nafcillin 2 gm IV every 4 hours in addition to fluconazole. Surgical debridement followed by physical therapy and long term IV antibiotics controlled our patient's symptoms. IMPLICATIONS/DISCUSSION: Candidal vertebral osteomyelitis is a rare disease with 65 cases identified in literature. Risk factors have been associated with hyperalimentation, surgical procedures, abdominal surgeries, immunosuppressive therapy and IV drug abuse. The usual mode of spread is hematogenous during episodes of fungemia. The most frequent mode of presentation is severe back pain and diagnosis can reliably be made only when the organism is isolated from the lesion. Both medical and surgical treatment resulted in more favorable outcome for most patients. This case demonstrates the importance of recognizing fungal vertebral osteomyelitis as a cause of worsening back pain in patients with history of back trauma and multiple back surgeries even in the absence of risk factors.

A CASE OF STERNOCLAVICULAR JOINT SEPTIC ARTHRITIS. E.H. Elbadawy 1 , K. Gopal 1 ; 1 Fairview Hospital, Cleveland, OH (Tracking ID #76754) LEARNING OBJECTIVES: 1-To recognize the clinical picture of sternoclavicular septic arthritis. 2-To emphasize the importance of early diagnosis and treatment in preventing devastating complications. CASE INFORMATION: A 43-year old white male admitted with 2 days history of worsening dull aching pain, swelling and erythema at the right sternoclavicular joint (SCJ) area. Condition started 2 days after he sustained a fall as he was wrestling with his 8-year old son. Patient denied fever, chills or dyspnea. Past medical history was significant for hypothyroidism and depression. Patient denied IV drug abuse, alcohol intake or smoking. On examination he was febrile at 103 F with pulse of 125 and blood pressure of 146/81. He appeared to be in pain with significant soft tissue swelling, erythema and marked tenderness over the right SCJ. Range of motion of the right shoulder was severely limited due to pain. Initial laboratory evaluation revealed WBCs of 12.5 k/AL and ESR of 56. Therapy was initiated with imipenem 500 mg IV every 6 hours for possible SCJ septic arthritis because of history of penicillin allergy. SCJ aspiration was unsuccessful in obtaining any fluid. Computed tomography scan revealed soft tissue swelling around the right SCJ with no evidence of fluid collection. Three-phase bone scan showed increased soft tissue activity and delayed bony uptake involving the right SCJ area. Blood cultures drawn on admission grew methicillin-sensitive Staphylococcus aureus and therapy was switched to cefazolin 2 grams IV every 8 hours. Patient reported significant improvement is his symptoms after 3 days of intravenous antibiotics and was discharged home on cefazolin 2 gm IV for total of 4 weeks. Follow-up one week later revealed complete resolution of the soft tissue swelling, tenderness and erythema with painless full range of motion of his right shoulder. IMPLICATIONS/DISCUSSION: Sternoclavicular septic arthritis accounts for 1±9% of septic arthritis cases. Predisposing factors include IV drug abuse, DM, central venous catheters and trauma. Aspiration of the joint can be helpful in confirming the diagnosis and guiding treatment. Unfortunately, the failure rate with this method is high due to the technical difficulty in aspirating the small joint space, as in our patient. Clinical diagnosis requires a high index of suspicion in any patient presenting with swelling and pain around the SCJ. Spread of infection can lead to superior vena cava obstruction, mediastinitis and septic shock. Early diagnosis is critical in order to prevent life threatening complications.

M. Eskildsen 1 , K. Lasser 1 ; 1 Cambridge Hospital, Cambridge, MA (Tracking ID #74000) LEARNING OBJECTIVES: 1. To recognize the common side effects of atypical antipsychotics. 2. To learn about a previously unreported complication of these drugs. CASE INFORMATION: A 39-year-old man with a history of hepatitis C, schizophrenia, and past alcohol abuse was admitted with worsening abdominal pain and distension over one month, accompanied by vomiting and watery diarrhea. He stated that he had been sober for two years. His only medications were risperidone at 8 mg daily, and olanzapine at 10 mg daily. His psychiatrist had decreased the olanzapine dosage and attempted to discontinue his prescription one year prior to admission due to poor response, but the patient had refused to do so for unclear reasons. Physical exam revealed a temperature of 37.8C; and a distended, diffusely tender abdomen, without signs of ascites or peritoneal irritation. Laboratory evaluation was remarkable for triglycerides that were over 3800 mg/dl, our lab's upper limit of measurement, and a lipase of 250 U/l. Serum glucose was 553 mg/dl, with no prior readings in the diabetic range. A computed tomography of the abdomen indicated mild pancreatitis with no biliary obstruction. On admission, after discontinuing both medications, we gave him intravenous fluids and nothing by mouth, as well as patient-controlled analgesia with intravenous morphine. Upon discharge, one week later, he was pain-free, and his triglycerides and glucose decreased to 308 and 250 mg/dl, respectively. Of his antipsychotics, risperidone alone was resumed before discharge, up to a dose of 8 mg daily two months later. He has remained without abdominal pain, with serum triglycerides in the 300 range, and persistent diabetes mellitus treated with metformin. IMPLICATIONS/DISCUSSION: A MEDLINE search yielded two reports of pancreatitis associated with olanzapine, and two with risperidone. Hyperlipidemia, including elevated triglycerides, is a side effect of both drugs, although it is more commonly observed with olanzapine. However, this is the first described case of pancreatitis in relation to either of these two drugs that has been associated with massive hypertriglyceridemia, and we have reported it as an adverse event to the FDA. Because he has tolerated risperidone well after discharge, olanzapine seems more likely to have precipitated his pancreatitis, although a synergistic mechanism between the two drugs is another possibility. This case illustrates the need for close monitoring of lipids and glucose in patients taking atypical antipsychotics. 

A 28 year old white male with no significant past history was referred for preoperative clearance for left foot amputation. Patient had non-healing ulcers on his left heel and ankle for 1 month with no response to antibiotics. One year prior, he had a flulike illness, hematuria and painful left testicle which resolved spontaneously except for a persistent dry cough. CXR revealed a spot on the left lung. His TB skin test was negative. The patient denied hematospermia, weight loss, night sweats, trauma, neurologic or GI symptoms. On exam he was a healthy appearing male with previously unnoticed 2 crusted, raised lesions measuring 2.5 Â 2.5 cm on the left arm. These lesions had not been documented during his earlier visit notes though patient admitted to having these lesions for many months. He also had 3 left foot lesions, 1 on the heel and 2 draining lesions on the left malleolus. A plain film of left ankle revealed a lytic area in the distal tibial metaphysis. Bone scan was consistent with acute osteomyelitis. Biopsy of left bony lesion revealed chronic inflammation & giant cells but negative AFB stains and routine cultures. On H & E stain, a multinucleated, thick double contoured wall of yeast with single, broad-based buds was visualized consistent with BD. The patient had complete resolution of all skin lesions and CXR after 6 months of itraconazole treatment. IMPLICATIONS/DISCUSSION: BD is a fungus found in the soil and causes multisystemic pyogranulomatous disease. Blastomyces in endemic in areas bordering Mississippi and Ohio river basins and the Great Lakes. Initial infection is usually via the lungs, can be asymptomatic in 50% of patients or be mistaken for the flu or pneumonia. Pulmonary manifestations include involvement of upper lobes with cavitation, mass lesion with productive cough, hemoptysis, dyspnea, pleuritic chest pain, low grade fever, night sweats, and weight loss. Skin lesions are usually painless, nonpruritic, hyperkeratotic, ulcerative plaques on the face or extremities and may involve mucosa of nose, mouth and larynx. Other common sites of involvement include bone, genitourinary tract or CNS. If untreated, the clinical course can be months to years with remissions, exacerbations and progression in size. The rapid method of diagnosis is visualization of budding yeast in KOH mounts of pus from lesions. Definitive diagnosis is by growth of organism in culture. Treatment consists of 6 months of itraconazole in immunocompetent patients. Amphotericin B is used in patients who are pregnant, seriously ill & immunocompromised, with CNS infection or progressive disease on itraconazole. Our case stresses the importance of a thorough history and physical for appropriate management especially in a disease that is known as the great masquerader.

NECROTISING FASCIITIS. C. Eze 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77055) LEARNING OBJECTIVES: 1. Recognize the signs of deep fascial infections. 2. Use the physical examination to prompt timely surgical intervention for necrotizing fasciitis. CASE INFORMATION: A 21 year-old Hispanic-speaking man presented with four days of left leg pain, swelling and fever after a spider bite. He had a temperature of 103 F, a heart rate of 128, and a blood pressure of 128/70. His left lateral leg was warm, edematous and tender. There was a 1 cm ulcer without drainage or necrosis. The pulses, sensation and range of motion of were normal. A plain film of his leg showed no soft tissue air or bone involvement. His WBC count was 22,000; the remaining laboratory values were normal. Blood cultures were obtained and he was empirically started on gatifloxacin due to a penicillin allergy. After 48 hours, he showed no improvement. Bullae and ecchymosis were noted on the second day; he lost sensation of the overlying skin on the third day. His antibiotic coverage was broadened to include coverage for MRSA. An MRI revealed fluid collections between the muscle and fascia consistent with necrotizing fascitis. An emergent fasciotomy and posterior compartment release were peformed. Wound cultures grew group A Strep. and Strep. milleri. IMPLICATIONS/DISCUSSION: The timely diagnosis of necrotizing fasciitis is important to preventing tissue damage, systemic toxicity, limb loss or death. Cellulitis not responsive to antibiotics, or the appearance of ecchymosis, bullae or anesthesia should prompt consideration of this diagnosis. The physical examination reflects the deep fascial structured damaged by the advancing infection. Ecchymosis, bullae and anesthesia reflect the damaged vessels, skin planes and nerves. While MRI is useful, establishing a timely pre-test probability prompting surgical exploration is the gold standard for making the definitive diagnosis. The closed space of deep fascial infections renders them immune from systemic antibiotics; treatment requires immediate surgical release. Antibiotics only buy time for surgical intervention.

AUTONOMIC DYSFUNCTION AFTER HEAD TRAUMA. C. Eze 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77084) LEARNING OBJECTIVES: 1. Identify the subtle presentation of autonomic dysfunction in the elderly. 2. Recognize the association between autonomic dysfunction and spinal cord lesions. CASE INFORMATION: An 81-year-old man presented with acute confusion following six months of progressive lower extremity weakness. He had fallen two weeks prior resulting in a periorbital hematoma. A CT had been obtained on two prior ER visits to exclude a sub-dural hematoma, and was negative on both occasions. His initial blood pressure was 122/60 mmHg with a pulse of 84. Fifteen minutes later his blood pressure dropped to 64/42 with a pulse of 134. Intravenous fluids resulted in a blood pressure of 175/104 mmHg with fifteen minutes. Ten minutes later his blood pressure again declined to 55/39 mmHg He was placed on an epinephrine drip with an immediate and sustained response of his blood pressure to 169/101 mmHg. His examination was notable for flat neck veins, no S3, and normal lung sounds. His reflexes were absent in both lower extremities without a Babinski's response; his upper extremity reflexes were 1+. His laboratory values, including cortisol, were normal. The EKG revealed atrial fibrillation. There was no subdural hematoma on repeat head CT. Owing to the suspicion of autonomic insufficiency, cervical-spine X-ray was obtained, revealing compression fractures involving the C4 to C7 vertebrae. He was admitted to the ICU and neurosurgery was consulted. IMPLICATIONS/DISCUSSION: Wide hemodynamics variations should prompt consideration of autonomic dysfunction, that should in turn prompt suspicion for an occult spinal cord lesion. This is especially true in elderly patients who may not be able to verbalize cervical pain. Hypertention and bradycardia may result from spinal cord reflexes unopposed by central regulatory mechanisms. Support of vascular tone with vasopressors is critical to resuscitation. This case emphasizes the importance of a careful cervical spine evaluation in all falls involving the elderly. LEARNING OBJECTIVES: To recognize that high dose simvastatin monotherapy, although having an excellent safety profile, can cause significant rhabdomyolysis, acute renal failure and hepatitis in the right patient population. To recognize that the addition of a potent or weak cytochrome P450 inhibitor is not needed for the significant adverse effects of simvastatin to occur. CASE INFORMATION: A 62 y.o. woman developed increasing myalgias, malaise, shortness of breath and dyspnea on exertion over 1 week and left lower extremity swelling. Medications included simvastatin 80mg daily with normal baseline transaminase levels and diltiazem for the past year. CXR revealed mild bilateral pulmonary edema and an ultrasound of the left lower extremity revealed no deep vein thrombosis. Exam revealed in ill appearing female in moderate distress secondary to myalgias, mild rhonchi bilaterally, normal heart tones and bilateral lower extremity dependent edema (Lt>Rt). Laboratory studies: alkaline phosphatase 177, AST 1511, ALT 224, LDH 1396; creatinine 5.6 (baseline 1.4±1.7); BUN 92; potassium 5.6; phosphate 6.5; calcium 8.8; creatinine phosphokinase >20,000; troponin <0.05; CKMB 171; TSH wnl; uric acid 8.0. Urinalysis revealed a large amount of blood with only 4±10 red blood cells. Simvastatin was discontinued. Aggressive treatment with sodium bicarbonate, intravenous hydration and hemodialysis was begun. Over a sixty-plus day hospital course, the patient's renal failure resolved (baseline creatinine now 2.2±2.4) and transaminases normalized. The patient was eventually discharged to home to continue physical rehabilitation with no permanent requirement for hemodialysis. IMPLICATIONS/DISCUSSION: Simvastatin's long term safety profile is excellent. Simvastatin induced rhabdomyolysis is reported with low incidence (0.6% in one study involving 80mg of simvastatin) and it is seldom associated with acute renal failure or hepatitis. Myopathy and rhabdomyolysis increases with dose and with concomitant use or addition of potent cytochrome P450 3A4 (CYP450) inhibitors, i.e. fibrates, cyclosporine, azathiaprine. A baseline severe renal insufficiency (creatinine clearance by the Cockroft-Gault method, 17cc/ min) and a urinary tract infection treated with a fluoroquinolone 2 days prior, combined to increase the risk of this patient developing rhabdomyolysis. Published reports of simvastatin induced myopathy involve the addition of potent or weak CYP450 inhibitors. Our patient had been stable on high dose simvastatin and diltiazem (a weak CYP450 inhibitor) for over 1 year prior to presentation and did correlate with the addition of known CYP450 inhibitors. Additionally unique, this is the first reported case involving the combined toxicities of rhabdomyolysis, acute renal failure and hepatitis with high dose simvastatin monotherapy. 2) Recognize the dangers of rapid correction of hyponatremia. CASE INFORMATION: A 56 year-old man with a history of alcohol abuse was admitted to an outside hospital with altered mental status. On exam, the patient was disoriented, but neurological exam was otherwise nonfocal. Computerized tomography (CT) of the head was unremarkable. Laboratory results revealed hyponatremia with sodium of 104 mmol/L. The patient was given hypertonic saline, and the sodium was corrected to 123 within the first 24 hours. The patient was then transferred to our facility for continuation of his care. Physical examination on arrival revealed multiple focal neurological findings including bilateral eye deviation to the left, neck deviation to the left, absent gag reflex, and poor motor coordination with spastic movement of all extremities. The patient's speech was severely dysarthric and unintelligible. Magnetic resonance imaging (MRI) of the brain showed enhancement of the motor cortex of both cerebral hemispheres and enhancement of the frontal eye fields on the left with sparing of the adjacent sensory cortex. In consideration of the MRI findings, neurology consultation was sought. The patient's severe dysarthria, dysphagia, ataxia, and optic apraxia were attributed to extrapontine (as opposed to central pontine) myelinolysis from rapid correction of the patient's hyponatremia. IMPLICATIONS/DISCUSSION: Severe symptomatic hyponatremia should be treated with hypertonic saline, but with a correction in plasma sodium of not more than 1±2 mmol/liter/ hour and a maximum increase of 8 mmol/liter during the first 24 hours. Our patient's sodium was corrected from 104 to 123, with an increment of 19 within 24 hours. Rapid correction may result in osmotic demyelination or central pontine myelinolysis, which is characterized by flaccid paralysis, dysarthria, and dysphagia. Isolated extrapontine myelinolysis is extremely rare, with only two cases reported in the literature. The neurologic deficits depend on the anatomical location of osmotic demyelination. Treatment is supportive, and recovery is slow within weeks to months. Gradual correction of hyponatremia is important because aggressive correction can cause not only central pontine myelinolysis but also the unusual manifestation of extrapontine myelinolysis. LEARNING OBJECTIVES: 1) Construct a differential diagnosis of chronic ataxia. 2) Review the etiology, presentation, and prognosis of paraneoplastic cerebellar degeneration. CASE INFORMATION: A 55-year-old male ex-smoker with no significant past medical history presented to clinic with paresthesias of the right upper and lower extremities, followed by gradual onset of ataxia, diplopia, and dysarthria over a period of five months. The patient also reported weight loss and a chronic dry cough. The patient had no history of toxic exposures or family history of inherited ataxias. Physical exam revealed optical dysmetria, truncal ataxia, finger-to-nose dysmetria, and dysdiadochokinesis. The patient's speech was severely dysarthric, and sensation was decreased on the right upper and lower extremities. Magnetic resonance imaging (MRI) of the brain was normal. HIV and RPR serologies were negative, and TSH was within normal limits. Lumbar puncture revealed paraneoplastic antibodies, including anti-Hu, anti-P/Q type calcium channel, and anti-acetycholine receptor. Computerized tomography (CT) of the thorax demonstrated a 2 cm left hilar mass. Bronchoscopy and endobronchial biopsy were negative, but subsequent thoracotomy and biopsy revealed small cell lung carcinoma (SCLC). IMPLICATIONS/DISCUSSION: The differential diagnosis of chronic ataxia includes primary and metastatic neoplasms, paraneoplastic syndromes, progressive multifocal leukoencephalopathy, multiple sclerosis, hypothyroidism, tabes dorsalis, inherited ataxia syndromes, vitamin E deficiency, toxic exposures, and stable gliosis due to stroke or demyelination plaque. In approximately 80% of cases with paraneoplastic cerebellar degeneration, the underlying tumor is SCLC. Fifty-one percent of patients with cerebellar degeneration and SCLC have detectable anti-Hu antibodies. Other antibodies found in paraneoplastic cerebellar degeneration include anti-P/Q calcium channel, anti-Yo, anti-Ma1, anti-Tr, and anti-CV2, but their exact sensitivities and specificities are not yet known. Therapy is supportive, and symptoms usually do not improve with immunosuppression or treatment of the tumor. In conclusion, paraneoplastic cerebellar degeneration with paraneoplastic antibodies should be considered in all patients with chronic ataxia without other predisposing etiologies. LEARNING OBJECTIVES: 1. Discuss the presentation of primary bacterial peritonitis. 2. Recognize group A beta-hemolytic Streptococcus as a rare but serious cause of primary peritonitis. CASE INFORMATION: A 52 year old woman presented to the Emergency Room with a four day history of fevers, chills, and profuse watery diarrhea with associated crampy lower abdominal pain. She denied any nausea, vomiting, cough, dysuria, or headaches. She denied any recent travel or sick contacts, but noted that the symptoms began hours after having eaten at a Chinese restaurant. Her past medical history was remarkable for a prior appendectomy, she was on no medications, and her family history was significant only for colon cancer in her mother. Her exam revealed a temperature of 38.7 C, a blood pressure of 72/40, and a pulse of 112, with abdominal tenderness and guarding in both lower quadrants. Labs showed a white cell count of 5.7 (with a bandemia of 52), a potassium of 2.4, a bicarbonate of 15, a Blood Urea Nitrogen of 52, and a creatinine of 3.7. Liver function tests, amylase, lipase, and urinalysis were all normal. Fecal leukocytes were absent and her abdominal film showed only a few air-fluid levels. It was the impression of all clinicians involved that the patient's presentation was most consistent with acute infectious diarrhea and profound dehydration complicated by renal failure and electrolyte derangement. Following aggressive hydration with IV crystalloids, the patient's blood pressure improved to 120/80 and her heart rate slowed to 88. After blood, urine, and stool cultures were taken, she was started on IV ciprofloxacin for empiric treatment of her presumed acute infectious diarrhea. She continued to have diarrhea over her hospital course, but her abdominal pain and temperature curve lessened, and she appeared to be improving clinically. All cultures (including c. difficle and giardia screens) had returned negative. On hospital day four, her fever and abdominal pain worsened and her abdomen became distended, rigid, and equisitely tender. An abdominal CT showed diffuse thickening of her colon with ascites and dilated loops of small bowel. An emergent exploratory laparotomy was performed and several liters of cloudy yellow ascites were drained. A nectrotic mesenteric lymph node filled with pus was resected and her abdomen was irrigated with several liters of saline. Gram stains of both the pus from the lymph node and the ascitic fluid revealed gram positive cocci in chains, and she was promptly started on IV clindamycin. Cultures of the ascites and pus grew group A betahemolytic Streptococci, and she was continued on the clindamycin. She continued to improve over her hospitalization and made a full and healthy recovery. IMPLICATIONS/DISCUSSION: Primary bacterial peritonitis occurs as a result of bacterial infection of the peritoneal cavity and is distinguished from secondary peritonitis by the absence of any underlying cause or demonstrable abdominal source. The onset is often rapid and insidious, and is marked by the appearance of fever, nausea, abdominal pain, and diarrhea. The patient typically has abdominal rigidity and rebound with features of systemic inflammation (tachycardia, hypotension, tachypnea, etc.) which may progress to frank shock. Streptococcus pyogenes, or group A Streptococcus, is a very common human pathogen, with up to 15% of asymptomatic individuals carrying the bacterium (typically in the upper respiratory tract). However, primary bacterial peritonitis due to Streptococcus pyogenes is exceptionally uncommon with very few adult case reports documented in the literature. It may be slightly more common in women, with asymptomatic colonization of the genital tract acting as a portal of entry. The diagnosis is often made only at laparotomy and despite the profound morbiditiy associated with the disease, rapid initiation of the appropriate antibiotics usually results in a successful cure.

EUREKA! A TREATABLE CAUSE OF DIZZINESS. E.J. Favus 1 , R. Ambrosino 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73835) LEARNING OBJECTIVES: 1. To recognize and treat non-sustained ventricular tachycardia (NSVT). 2. To recognize the differential diagnosis of dizziness.

A 70 year-old male with a history of gout, hypertension, chronic renal insufficiency, and hypercholesterolemia presented to his primary care physician complaining of intermittent dizziness. He had approximately three episodes per week, each lasting ten minutes, and resolving spontaneously. He described feeling``lightheaded'' during each episode, and denied a positional component, vertigo, visual disturbances, tinnitus, history of seizures, aura, post-ictal state, loss of consciousness, palpitations, chest pain, and shortness of breath. An EKG shortly after the first episode showed no rhythm abnormalities, ischemia, or infarction. His chronic medications were simvastatin, allopurinol, and lisinopril. Physical examination revealed a blood pressure of 156/84mmHg, pulse 66, and respiratory rate 16. He did not have orthostatic hypotension. Cardiac exam revealed a non-displaced PMI, regular rate and rhythm, normal S1 and S2 with no murmurs, gallops, or rubs. Holter monitor testing revealed multiple episodes of multifocal ventricular ectopy including short runs of ventricular bigeminy, trigeminy, and quadrigeminy with a heart rate of 80 beats per minute. He was diagnosed with non-sustained ventricular tachycardia (NSVT). A review of the patient's log revealed that each tachyarrhythmic event correlated with an episode of dizziness. He underwent echocardiography, which showed a structurally normal heart and an ejection fraction of 55%. He was prescribed metoprolol 12.5mg po qam, and at a one-month follow-up visit reported improvement in his symptoms. IMPLICATIONS/DISCUSSION: Dizziness is a common complaint heard by primary care physicians, yet only a small percentage of patients receive a firm diagnosis and an effective treatment. In this patient, the discrete nature of these episodes hinted at the possibility of a cardiac arrhythmia. Clinical suspicion for a cardiac problem prompted an evaluation by Holter testing. The results showed a temporal relationship between NSVT and dizziness, and provided evidence for a firm diagnosis. Patients with NSVT and a structurally normal heart are not at risk for sudden death, and may be treated with daytime oral beta-blocker therapy to decrease symptoms. Conversely, large studies have shown that the combination of NSVT and a structurally abnormal heart is a risk factor for sudden death. Treatment of NSVT with a structurally abnormal heart requires the use of an Automatic Implantable Cardioverter-Defibrillator (AICD). Beyond cardiac arrhythmias, dizziness has many causes. A proper history of the dizzy patient should include questions about syncope, hyperventilation, anxiety, visual disturbances due to incorrect eyeglasses or diplopia, and concussion. Physical examination should evaluate orthostatic hypotension, hypertension, and peripheral neuropathy. Anemia and hypoxia should be evaluated by laboratory studies.

PUTTING IT ALL TOGETHER: A CASE OF PRIMARY HYPOGONADISM. E.J. Favus 1 , R.C. Brooks 2 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA; 2 Pittsburgh VA Healthcare System, Pittsburgh, PA (Tracking ID #73840) LEARNING OBJECTIVES: 1. To recognize the clinical presentation of male hypogonadism. 2. To recognize the differential diagnosis of acquired primary hypogonadism. CASE INFORMATION: A 66 year-old male presented with bilateral gynecomastia, osteoporosis, and erectile dysfunction. Three years ago he was seen by a urologist for erectile dysfunction and hesitency. He was diagnosed with a low testosterone state (laboratory values unavailable), and treated with testosterone. He had improvement of his erectile dysfunction but worsening of his hesitency and was switched to sildenafil. No cause was found for urinary hesitancy, but he was treated with tamsulosin without relief. Two years ago he fell and broke his left fourth metatarsal. Dual x-ray absorptiometry scan revealed a T-score of À2.7, and he was treated with alendronate. He denied a history of glucocorticoid use. One year ago he noticed increased breast tissue bilaterally and a mass in the right breast. A bilateral mammogram was negative and a breast biopsy was negative for malignant cells. His medical history is significant for tinea capitis, treated with 2% ketoconazole shampoo. His medications are sildenafil, alendronate, and ketoconazole shampoo. He has no history of alcohol, tobacco, or drug use. Physical examination reveals a normal thyroid, moderate bilateral gynecomastia without masses, no kyphosis, and normal size and shape of the penis, testicles, and prostate. Laboratory tests show total testosterone 239 ng/dL (241±827ng/dL), free testosterone 5.28 ng/dL (5±21ng/dL), FSH 32.1 mIU/mL (adult male normal range 1.55±9.70 mIU/mL), LH 14.7 mIU.mL (adult male normal range 0±9.0 mIU/mL), prolactin 13.0 ng/mL (adult male normal range 3.7± 17.9 ng/mL), TSH 4.13 uIU/mL (0.35±5.5 uIU/mL), PSA 1.68 ng/mL (0±4ng/mL). Given his low-normal testosterone and his clinical symptoms, he was re-started on testosterone therapy. IMPLICATIONS/DISCUSSION: The clinical presentation of osteoporosis, erectile dysfunction and gynecomastia should provoke a search for a unifying diagnosis of hypogonadism. The medical history of this patient is suggestive of a low testosterone state. His serum testosterone level is in the very low-normal range, and the FSH and LH levels needed to maintain this low-normal testosterone level are three times the upper limit of normal. High levels of FSH and LH exclude the diagnosis of secondary and tertiary hypogonadism. The low-normal level of testosterone has not been enough for this patient to avoid developing clinical disease. Male hypogonadism is defined as a failure of the testes to produce a sufficient amount of testosterone. Hypogonadism can be primary (testicular failure), secondary (pituitary failure), tertiary (hypothalamic failure), or combined primary and secondary. Primary hypogonadism can be either acquired or developmental. Our patient's laboratory values suggest primary hypogonadism. Since he had normal sexual development and fathered two children, he likely has acquired primary hypogonadism. Acquired primary hypogonadism may be the result of amyloidosis, autoimmune destruction, cryptorchidism, leprosy, leukemia, mumps, polyarteritis nodosa, radiation therapy, trauma, surgery (castration), or drugs such as cancer chemotherapy, ethanol, ketoconazole, marijuana, or spironolactone. In this patient, long term administration of ketoconazole shampoo for the treatment of tinea capitis may have resulted in acquired primary hypogonadism.

USING THE HEAD AND NECK EXAMINATION TO DIAGNOSE FOCAL NEUROLOGIC DEFICITS. D. Fotino 1 , N. Parekh 1 ; 1 Tulane University, New Orleans, LA (Tracking  ID #77089)   LEARNING OBJECTIVES: USE THE EXAM SKILLS TO DIAGNOSE FOCAL  NEUROLOGIC DEFICITS.  CASE INFORMATION: A 41 year-old diabetic man presented with a sudden onset of slurred speech and left-sided weakness. On examination, he had severe dental caries, slurred speech, and a left facial droop. His tongue deviated to left on protrusion, and he had left upper and lower extremity weakness. There was tenderness over the right mastoid process. His WBC was 27,000 with 14% bands. A CT showed subdural fluid collection in the right frontoparietal region. Vancomycin, ceftazidime and metronidzaol were empirically started for a presumptive diagnosis of subdural empyema. Shortly after admission, he deteriorated to persistent and refractory status epilepticus. The CSF protein was 149; WBC 630 (70% neutrophils); the gram stain was negative. A repeat CT showed an area of hypodensity and a midline shift, consistent with subdural empyema. He underwent drainage of the abscess; the cultures grew out pseudomonas aeruginosa. Ciprofloxacin was added to his regimen to double cover the pseudomonas. His seizure activity relented soon thereafter. IMPLICATIONS/DISCUSSION: Sinusitis is the leading cause of subdural empyema, and can present with focal neurological signs if intra-cerebral extension occurs. Diabetic patients are also at risk for malignant external otitis, and empiric coverage for pseudomonas is warranted at even the lowest level of suspicion. Although this patient's symptoms suggested a cerebrovascular accident, the finding of mastoid tenderness directed the diagnosis towards the infected mastoid sinus and the subdural abscess. In diabetic patients, empiric pseudomonas coverage should be initiated early; double coverage should be instituted when a pseudomonas infection is confirmed, as this reduces the mortality of deep tissue infections by 50% when compared to single coverage. A thorough examination of the oro and nasopharyngeal cavities can direct and expedite diagnostic testing and prevent grave sequelae of treatable diseases.

A ROCKY SITUATION. F. Francois 1 , J. Park 1 , C.T. Tenner 2 , S. Finkelstein 1 ; 1 New York University School of Medicine, Brooklyn, NY; 2 New York University School of Medicine, New York, NY (Tracking ID #74431) LEARNING OBJECTIVES: 1. Recognize the potential for bowel dysfunction in chronically ill patients 2. Consider the differential diagnosis of lower gastrointestinal bleeding in the elderly population 3. Review the management of stercoraceous masses. CASE INFORMATION: A 72-year-old HIV positive Hispanic male on highly active anti retroviral therapy (CD4 = 612 cells per cubic millimeter, viral load<50 copies per milliliter), was admitted for evaluation of hematochezia. The patient had a history of poorly controlled hypertension and had been hospitalized three weeks prior to this presentation with an acute change in mental status during which he was found to have a basal ganglia infarct. The family reported that the patient had been mainly bed bound since the stroke, and had intermittently complained of difficulty moving his bowels without any associated abdominal pain, nausea, or vomiting. On physical exam the patient was noted to have a right facial droop, right-sided hemiparesis, and normal active bowel sounds without abdominal distention, tenderness, or guarding. On rectal examination a freely mobile mass was palpated in the vault and bright red blood was seen on the glove. Laboratory evaluation was significant for a seven-point hematocrit drop from his baseline. On colonoscopy the patient was found to have 3 discontinuous areas of ulceration in the rectosigmoid region, with the largest measuring 6cm  2cm. The ulcers were associated with 3 large (4cm in diameter) hard fecal masses (fecalomas). The fecalomas were manually evacuated and the patient was started on a bowel regimen consisting of stool softeners and hydration. The patient's hematocrit remained stable with no further episodes of rectal bleeding and he was discharged to to the care of his family. IMPLICATIONS/DISCUSSION: Elderly patients may develop bowel dysfunction due to diabetes mellitus, hypothyroidism, renal failure, dementia, immobilization, cerebrovascular accidents, and medications. Once chronic constipation occurs the patients are at risk for fecal impaction and stercoral ulcers (a.k.a. Huntley syndrome). These ulcers result from pressure necrosis on the colonic mucosa by the rock-like fecal mass. Patients may present with rectal bleeding or colonic perforation with peritonitis. In the elderly population, the differential of hematochezia as a presenting sign in the setting of a change in bowel habits includes, malignancy, infectious colitis, and ischemic colitis. Initial management of a stercoral lesion involves manual evacuation of the stecoraceous mass followed by a bowel regimen with stool softeners along with adequate hydration. Patients with recurrent ulcer bleeding or perforation may require surgery as definitive therapy.

SEA-BLUE HISTIOCYTOSIS: A NEWLY REPORTED COMPLICATION OF PARENTERAL NUTRITION. S. Frost 1 ; 1 Cleveland Clinic Foundation, Cleveland, OH (Tracking ID #73897) LEARNING OBJECTIVES: 1) Diagnose sea-blue histiocytosis syndrome as a complication of total parenteral nutrition (TPN). 2) Recognize that bone marrow sea-blue histiocytes are associated with many diseases in which the degradation of lipids and cellular lipid products is exaggerated. CASE INFORMATION: A 40 year-old man receiving chronic TPN with lipid emulsion after esophagogastrectomy following caustic ingestion was admitted to the hospital with fever for 5 days, jaundice, hepatitis, and pancytopenia. The patient did not appear ill. The physical exam was notable for a clean subclavian Hickman catheter site without erythema or tenderness, hepatomegaly, no heart murmur, and no peripheral stigmata of endocarditis. Laboratory revealed WBC = 3.8 K/uL, hemoglobin = 10 g/dL, platelet = 70 K/uL, AST = 223 U/L, ALT=160 U/L, alkaline phosphatase = 339 U/L, and bilirubin = 9.4mg/dL. Investigation for bacterial, fungal, mycobacterial, and viral infection was negative. Abdominal sonogram and CT scan revealed hepatomegaly without other abnormality. Echocardiogram revealed no vegetations. Upper extremity ultrasound was negative for catheter associated thrombosis. The Hickman catheter was removed and catheter culture specimens were sterile. Fever persisted despite therapy with piperacillin/tazobactam, vancomycin, fluconazole, and amphotericin B. Bone marrow biopsy revealed sea-blue histiocytes. TPN was held and improvement in liver function abnormalities and cell counts began on hospital day (HD) 6 and 7 respectively. Fever dissipated on HD 8, and antimicrobials were discontinued. TPN was restarted without lipid emulsion, and the patient has remained well with resolution of hepatitis and cytopenias. IMPLICATIONS/DISCUSSION: Sea-blue histiocytes (SBHs) are macrophages with lysosomal lipid accumulations that appear blue with Giesma staining. The sea blue histiocytosis syndrome is a typically benign idiopathic disorder characterized by hepatosplenomegaly, purpura, thrombocytopenia, and pulmonary infiltrates. SBHs have also been noted in association with hematologic disorders such as chronic myeloid leukemia, and metabolic illnesses such as Niemann Pick disease. SBHs in the bone marrow of patients with hepatosplenomegaly, jaundice, and pancytopenia receiving TPN containing lipid emulsions was first reported in 1996. Lowering the TPN lipid content has been shown to improve pancytopenia. Lipid induced hematopoetic cell membrane alterations triggering macrophage phagocytosis is one postulated mechanism accounting for TPN related sea-blue histiocytosis (TPN-SBH). This patient's illness is consistent with prior descriptions of TPN-SBH, except for fever, which has not been previously reported. However, the resolution of fever coincident with the improvement in pancytopenia and hepatitis after the discontinuation of parenteral lipids suggests an association with TPN-SBH.

IT'S BLACK, IT'S HAIRY . . . BUT IS IT A PROBLEM? C.C. Fu 1 , G. Applebaum 1 ; 1 University of California, Los Angeles, Los Angeles, CA (Tracking ID #74949) LEARNING OBJECTIVES: 1. Recognize the presentation of black hairy tongue. 2. Review possible predisposing conditions. 3. Emphasize benign nature of this phenomenon. CASE INFORMATION: A 53-year-old Mexican man with no significant medical history presented with one month of easy bruising and gum bleeding. The patient's only medicines were occasional aspirin for pain and bayberry extract. Lab results were significant for 2.2 WBCs, Hb 8.2, and 4 platelets. Bone marrow biopsy revealed a hypocellular and fatty marrow consistent with aplastic anemia. The patient's three-week hospital stay was complicated. He had extraction of an infected tooth and was started on a peroxide-based swish and spit regimen. Treatment for aplastic anemia was begun with anti-thymocyte globulin and cyclosporine. The patient experienced prolonged neutropenic fevers for which he was treated with ceftriaxone, tobramycin, metronidazole, and vancomycin. During this period, the patient's tongue was noted to develop a dark gray,``hairy'' appearance, the surface of which could actually be brushed with the end of a cotton swab. IMPLICATIONS/DISCUSSION: Black hairy tongue is a rare condition caused by the elongation of the filiform papillae associated with oral bacterial overgrowth. Black hairy tongue is idiopathic and has been associated with various predisposing factors including alcoholism, systemic illness, immunosuppression, cancer therapy, coffee, antibiotic use, and use of peroxide-based mouthwash. Our patient was a likely candidate to develop black hairy tongue as he had been given broad-spectrum antibiotics and used peroxide based mouthwash during immunosuppressive therapy. Treatments for black hairy tongue have included topical retinoin gel, podophyllum, and attempts at repeated tongue brushing. However, in consideration of our patient's underlying immunosuppression and profound thrombocytopenia, we chose not to treat the patient's tongue. It is important not to complicate the treatment of an ill patient with the unnecessary treatment of a benign, albeit strange, condition. A 45 year old Mexican female with a history of diabetes mellitus was brought to the emergency room by her family for increasing abdominal pain and a four day history of nausea, vomiting and diarrhea. There was no recent history of fevers, chills, or dysuria. Initial examination revealed an ill-appearing woman, moaning in response to painful stimuli, but not following commands. Although she was afebrile and normotensive, her resting heart rate of 119 beats per minute established systemic illness. Her other examination was remarkable for right lower quadrant tenderness in a soft abdomen, but no peritoneal signs. There was evidence of costovertebral angle tenderness bilaterally. Initial laboratory results were consistent with diabetic ketoacidsosis (DKA). Leukocytosis and pyuria led to the additional admitting diagnosis of pyelonephritis. Declining mentation led to rapid transfer to the intensive care unit on the day of admission. Computed tomography (CT) of the abdomen showed bilateral emphysematous pyelonephritis, emphysematous cystitis, bilateral perinephric abscesses, and air surrounding the inferior vena cava (IVC). Broad spectrum antibiotics were initiated. Emergent urology consultation recommended medical management due to high perioperative mortality risk. Bilateral percutaneous drains were placed under CT guidance. Nevertheless, the patient's condition rapidly deteriorated with development of thrombocytopenia and septic shock, requiring intubation and pressor support. She died the following hospital day. Blood, urine and perinephric fluid cultures grew Klebsiella pneumoniae. IMPLICATIONS/DISCUSSION: Emphysematous pyelonephritis (EPN) is a rare condition that causes an acute necrotizing parenchymal and perirenal infection due to gas-forming uropathogens. Bilateral disease is exceedingly rare. EPN occurs predominantly in diabetic patients and in patients with urinary tract obstruction. E.coli, Klebsiella and Proteus are the most frequently identified organisms. Computed tomography is used for diagnosis and evaluation of the extent of disease. Antibiotics and percutaneous drains can lead to successful outcomes in patients with limited disease. However, nephrectomy is often considered the treatment of choice, especially in patients with extensive disease or multiple poor prognostic factors. Bilateral disease makes the surgical decision even more difficult. Understanding the indications for surgical versus medical management may mean the difference between life and death in patients with EPN.

J.A. Garcia 1 ; 1 Wayne State University, Troy, MI (Tracking ID #74175) LEARNING OBJECTIVES: Physicians should be able to recognize early adverse events of commonly prescribed drugs. CASE INFORMATION: 56 y/o male, previously heatlhy presented to ER with fever, left calf pain and swelling which started after a brief hospitalization for a febrile illness. Lower extremity dupplex revealed thrombosis involving the Left popliteal and lesser saphenous veins. He was started on unfractionated heparin. Labs: WBC 10.2, Hemoglobin 11.7 and Platelets, 386k. Infectious work up was negative and he was eventually switched to coumadin and discharged. On the 4th day, he presented with fever and worsening left calf pain. A Lower extremity dupplex showed progression of the thrombus involving the posterior tibial vein. Heparin was restarted. WBC count 16.1, Hemoglobin 9.7 and platelets 240k . The fourth day of this admission Hb dropped to 6.5 with plts of 150k. On the 9th day, patient developed chest pain. EKG showed ST elevations and he had increased cardiac biomarkers compatible with acute lateral Myocardial Infarction. Cardiac catheterization revealed clean coronary arteries. On the 12th day, he complained of constipation, abdominal distension and pain. Abdominal Series showed ileus. Amylase 136, Lipase 73, ALT 21, AST 29, Alkaline Phosphatase 131, Tbili 0.9. WBC 27.2 Hemoglobin 11.7 and Platelets 72k. Because of the dropping platelets and the multiple thrombotic events, heparin was held, antibodies drawn, and liperudine was started. Heparin induced platelet aggregating antibodies were positive with ELISA. Abdominal CT showed focal areas of low attenuation with peripancreatic fat stranding compatible with necrotizing pancreatitis. IMPLICATIONS/DISCUSSION: Heparin is a widely used medication. Uncommon presentation of HITT should be early recognized to prevent unwarranted management. LEARNING OBJECTIVES: 1. Recognize the common toxicities of ecstasy 2. Diagnose water intoxication and its complications. CASE INFORMATION: KD is a 20-year old woman brought into the UCSF ED because she developed altered mental status after taking ecstasy. Seven hours prior to admission, she took 1.5 tablets of ecstasy, while her companion took 2 tablets of the same preparation. They remained at home and``drank lots of water.'' One hour prior to admission, KD complained of severe headache and multiple episodes of vomiting. She then``stopped making sense.'' In the ED, KD was alert and oriented to person and place but appeared agitated and confused. She then had a generalized tonic-clonic seizure, became apneic, and was intubated. A NCHCT showed bilateral uncal herniation with diffuse effacement of the sulci. Significant laboratory abnormalities included leukocytosis, serum sodium of 124, rhabdomyolysis, and evidence of SIADH. A urine toxicology screen was positive only for amphetamines. An ECG showed sinus tachycardia with diffuse ST elevations, and a chest radiograph showed bilateral patchy infiltrates consistent with pulmonary edema. Repeat physical exam three hours after admission documented the absence of brainstem reflexes. She expired 24 hours later, and her organs were harvested for transplantation. IMPLICATIONS/DISCUSSION: Ecstasy, or methylenedioxymethamphetamine (MDMA), is a recreational designer drug popular both for its pleasurable psychological effects and for its safe reputation. Acute adverse effects can range from nausea, headache, and myalgias to insomnia, paranoia, and depression. An ecstasy tablet often contains contaminants and other drugs. In addition, the dose of MDMA itself can range from 0 to 200 mg per tablet, and the toxic or even fatal dose range overlaps that of recreational use. The pattern of major physical toxicity is usually hepatic, cardiovascular, hyperpyrexic, or cerebral, although DIC, rhabdomyolysis, and acute renal failure also contribute to morbidity. Cerebral toxicity is manifested as seizures or cerebral edema, thought to result from hyponatremia. In most cases, the low sodium level is hemodilutional; users often sweat profusely and then drink large amounts of free water to rehydrate and to prevent overheating. Occasionally, SIADH contributes to hyponatremia in this setting. In addition to the physical toxicity, ecstasy can also lead to increased risk-taking behavior. Despite the widespread use of ecstasy and the range of potential toxicity, fatalities attributable to the drug are uncommon. KD's demise likely began with ingestion of MDMA, which led to water intoxication and SIADH. Hyponatremia followed, precipitating cerebral edema, increased intracranial pressure, and then uncal herniation. Respiratory arrest occurred with compression of the brain stem. The immediate cause of death was hypoxic encephalopathy. Several case reports suggest young women, such as KD, and children appear to be at the highest risk of poor outcomes associated with hyponatremia. This unfortunate case emphasizes the often overlooked and unpredictable morbidity and mortality associated with casual use of ecstasy.

GET YOUR COLONOSCOPY, GET YOUR CURE. D. Garrow 1 ; 1 New Hanover Regional Medical Center, Wilmington, NC (Tracking ID #74301) LEARNING OBJECTIVES: 1. Present a case of metastatic colon cancer. 2. Provide screening recommendations with colon cancer in a first-degree relative. 3. Discuss genetic factors implicated in colon cancer. CASE INFORMATION: The patient is a 57 year-old female who presented with dysequilbrium and hand tremor for one month. Head MRI revealed multiple intracranial lesions. ( fig. 1 ) Biopsy revealed poorly-differentiated adenocarcinoma. A colonoscopy was performed because of the above histology and a family history of colon cancer involving two brothers and a son. A near-obstructing mass was discovered in the right colon. Patient also had liver, spleen and multiple lymph node involvement via PET scan.

IMPLICATIONS/DISCUSSION: The majority of studies have shown a two-to four-fold increase in the incidence of colon cancer in patients with similarly afflicted first-degree relatives. Screening for colon cancer with a positive history in a first-degree relative is advised ten years prior to the index case. Hereditary nonpolyposis colon cancer (HNPCC) is a consideration in this patient. The genetic basis for HNPCC is heterogeneous involving chromosomes 2, 3, and 7. With the multiple genetic focus of HNPCC, genetic testing is seldom employed. The family is clinically positive for HNPCC as there are more than two cases of colon cancer spanning at least two generations. HNPCC is caused by defective DNA mismatch repair genes. Afflicted patients develop polyps at a rate similar to the normal population. However, because of genetic defects, precursor adenoma lesions undergo a more rapid progression to carcinomas than usual adenomas. HNPCC typically presents during the fourth and fifth decades of life. Affected patients are predisposed to a higher frequency of proximal colonic lesions with more advanced pathology, as seen in this case.

A. George 1 , R.D. Hobbs 1 ; 1 Oakwood Healthcare System, Dearborn, MI (Tracking ID #76605) LEARNING OBJECTIVES: To recognize that shingles, although most commonly thought of as a sensory problem with a characteristic rash, can cause diaphragmatic paralysis. CASE INFORMATION: A 71 year-old white male with stable hypertension, CHF and COPD, presented to the emergency room with severe dyspnea. He had a 12-year history of chronic elevation of the left hemidiaphragm and had been well except for recent right-sided neck pain. There was no rash. He was intubated. The following day he developed a classic shingles rash involving the right side of the neck. An EMG revealed a right-sided C3-C4 motor neuropathy. Phrenic nerve function did not return. He died six weeks later when he extubated himself at a nursing facility. Autopsy revealed that the chronic elevation of the left hemidiaphragm was due to a benign angiolipoma and unrelated to the viral infection. IMPLICATIONS/DISCUSSION: Sir William Broadbent first described muscular paralysis in association with zoster in 1866. In 1949, Halpern and Covner published the first description of zoster induced diagphragmatic paralysis. Since then, anecdotal cases have been reported although complete historical data is frequently missing and it has been difficult to elucidate the natural history of the condition. Based upon cumulative data from 10 well-documented cases, several tentative conclusions can be made. The average patient is 69 years of age (range 54±79). The time from rash to paralysis can vary widely from almost immediately to 210 days. In 7/10 cases phrenic nerve function did not recover. In the remaining cases, recovery occurred between 30 and 540 days later. The right side was affected in 7/10 cases although this is not statistically significant. The ratio between male and female patients is 7/3 but not statistically significant in this series. Pathologically, zoster induces a myelitis that involves the dorsal root ganglia. Why certain individual develop this rare complication is unknown and will require many further observations. At present, though, the point is clear±herpes zoster can cause diaphragmatic paralysis in the elderly. In such cases the paralysis may develop as a late complication with a poor chance of recovery. CASE INFORMATION: A 63-year-old woman was referred to our center for evaluation of tinnitus in her right ear for 9 months. She described the sensation as,`like the sounds of a steam engine pumping in my ear,' and that it coincided with her heart beat. She noted that applying pressure with fingers over an area in the right retroauricular area would reduce this abnormal noise. Work-up at an outside hospital was negative including, carotid ultrasound, CT scan of mastoid and temporal bone, audiometry and MRI of the head and internal auditory canal. Examination was significant only for a loud continuos bruit over the retro-mastoid area. Complete blood counts, serum chemistry, and electrocardiogram was normal. Cerebral angiogram showed an extensive dural arteriovenous fistula (AVF) affecting the distal transverse and sigmoid sinuses with supply through both internal and external carotid arteries as well as right vertebral artery. There was no evidence of cortical venous thrombosis. Thrombophilia work-up was normal. She underwent a combined transarterial embolization and stereotactic radiosurgery using gamma knife. Tinnitus resolved completely after intervention. She remains asymptomatic at the 3-month follow-up visit. IMPLICATIONS/DISCUSSION: Pulsatile tinnitus resulting in audible retro-auricular bruit could result either from systemic diseases, causing alteration in hemodynamic, or due to local disorders within or close to the petrous bone. The most common causes of pulsatile tinnitus includes benign intracranial hypertension, atherosclerotic disease, and glomus tumor. Dural AVF is a rare cause of pulsatile tinnitus (2%).However, 90% of patients with dural AVF present with pulsatile tinnitus. Dural AVF has been reported following trauma, infection, pregnancy related thrombophlebitis, surgery on the sigmoid and ethmoid sinuses. Cerebral angiogram remains the diagnostic modality of choice. If untreated, a third of dural AVF's develop intracranial bleeding or infarction. Treatment of dural AVF involves transarterial particulate embolization and radiosurgery using a gamma knife .High index of suspicion and thorough physical examination remains crucial in the early recognition of dural AVF. 2) Recognize principles of management of diabetes mellitus during Ramadan. CASE INFORMATION: A 40-year old female immigrant from Somalia with the history of poorly controlled type II diabetes for the past seven years was enrolled in our continuity clinic. She had been on numerous oral hypoglycemic agents without adequate benefit. Her blood glucose ranged from 200±380 mg/dl and glycosylated hemoglobin was 10.7%. She was started on insulin 70/30, 100 units in the morning and 70 units in the evening with addition of oral thiaglitazone agent. During the month of Ramadan her insulin dose was decreased to 50 units in the morning and evening and she was advised to take her oral medication in the evening as most of her meals were spread over night till dawn. While accompanying her daughter for routine checkup she complained of feeling of generalized``shakiness'' which was new to her. We obtained a random blood glucose level, which revealed a blood glucose of 37mg/dl. She was treated with supplemental glucose with complete resolution of her symptoms. Her insulin regimen was subsequently adjusted further and dietary education and hypoglycemia education was given. Frequent telephone calls were made to adjust her insulin doses and monitor her blood sugars. IMPLICATIONS/DISCUSSION: Fasting in the month of Ramadan represents a recurring annual event in the life of a Muslim patient. Patients with brittle type I diabetes and poorly controlled type II diabetes could develop complications during month long fasting with change in dietary habits. Physicians should monitor their diabetic patients closely and adjustment in the insulin regimen should be made to prevent hypoglycemia. Long acting oral hypoglycemics and premixed insulin should be avoided. Dietary principles should be reinforced. Education regarding home monitoring of blood glucose, hypoglycemia episodes is recommended. After Ramadan, patient's therapeutic regimen will need to be changed back with repeat overall education. Obtaining detailed history could help in ascertaining additional cultural factors which could interfere with management of chronic illnesses.

ADULT ONSET RECALCITRANT PRURITIS Ð TIME FOR A SERIOUS LOOK. P. Chahal 1 , A.K. Ghosh 1 ; 1 Mayo Clinic, Rochester, MN (Tracking ID #74142) LEARNING OBJECTIVES: 1) Recognize the differential diagnosis of worsening chronic pruritus.

2) Recognize that patients with adult-onset recalcitrant eczema may have underlying noncutaneous lymphoproliferative disorder. CASE INFORMATION: A 38-year old male presented with history of two and a half years of insidious onset of severe itching involving his feet and gradually spreading and becoming generalized in few months. Subsequently, he developed a rash, which consisted of hard bumps', intensely pruritic in nature. He was seen by several physicians and had multiple skin biopsies demonstrating folliculitis and wound cultures growing Staphylococcus species. Numerous treatment attempts were unsuccessful. Examination revealed hundreds of equally spaced excoriated crusted pink papules measuring up to 1 cm diameters. Rest of his systemic examination was normal. Investigations revealed a normal complete blood count, hepatitis profile, and complement levels. HIV and fungal serology and PPD test were negative. Skin biopsies showed chronic dermatitis and the direct immunofluorescence was negative. Chest radiograph revealed multiple lung masses and subsequent CT scan of chest revealed extensive anterior mediastinal, bilateral hilar, right paratracheal, and subcarinal adenopathy and multiple bilateral pulmonary nodules. CT abdomen was normal. He underwent mediastinoscopy and lymph node biopsy, which revealed the diagnosis of Hodgkin's Lymphoma, Nodular Sclerosing type. He was started on combination chemotherapy with ABVD. IMPLICATIONS/DISCUSSION: Chronic unexplained eczema and pruritus of adult onset might be associated with underlying lymphoproliferative malignancy. Although pruritus has been associated with Hodgkin's disease, the reports of prurigo nodularis' association with Hodgkin's lymphoma are rare. Prurigo nodularis is also associated with other malignancies like transitional cell bladder cancer, leukemia and HIV. When an obvious cause like drugs or atopy year old Asian male presented with complaint of inability to move his arms and legs. His symptoms began one day prior to admission after walking a significant amount while shopping at a local mall. After leaving the mall, he started to experience numbness and tingling of his arms, legs and abdomen. Later that day, he started to experience generalized weakness and went to sleep early due to fatigue. When he awoke the morning of admission, he could not walk or move his body. He had to be assisted out of bed and brought to the emergency room. He had no prior medical problems and was not taking any medications, drugs or supplements. Upon further questioning, he revealed that his mother has had problems with low potassium levels. His review of symptoms prior to this episode was completely negative. Physical exam was unremarkable except for neurological exam. He was alert and oriented. His cranial nerves and sensory exam were intact. Motor strength was 0/5 in upper extremities and 1/5 in lower extremities. The patient was areflexive. Labs: Na 145, K 2.0, Cl 106, CO2 16, creatinine .7, CPK 519, Ca 7.9, Phos 1.3, Mg 1.5, TSH 0.0, T4 total 13.8, T3 total 236.4. His urinary potassium excretion was normal. EKG: low voltage t waves and u waves. Patient was diagnosed with hypokalemic periodic paralysis and treated with oral and intravenous potassium chloride. Within a few hours, his potassium improved to 5.0 and his strength was 5/5. The next day, he was discharged and told to follow up with endocrinology for his hyperthyroidism IMPLICATIONS/DISCUSSION: The diagnosis of hypokalemic periodic paralysis is made most easily when hypokalemia is documented during an attack of weakness and other secondary causes are excluded. Attacks begin during the first three decades of life and occur during the rest period following exercise, stress or high carbohydrate meal. The condition can develop in patients with a familial predisposition (autosomal dominant inheritance) or in those with thyrotoxicosis. The latter form is more common in Asian males. Although, the mechanism is not entirely understood, it is thought to be related to sudden shift of potassium into cells. Patients have normal potassium values between episodes and may have decreased magnesium and phosphorus during episodes. Treatment includes oral potassium chloride and correction of thyrotoxicosis. Prevention may include beta blockers, oral supplements, potassium sparing drugs and low carbohydrate meals. Recognition is important because the condition can lead to respiratory muscle paralysis and subsequent death. LEARNING OBJECTIVES: 1. Emphasize the importance of draining an infected galactocele and describe a less-invasive modality to achieve this. 2. Highlight follow-up measures in women with a recurrent galactocele. CASE INFORMATION: A 37 year-old lady presented with a non-tender lump in her left breast 4 weeks after birth of her fourth child. She was lactating without difficulty and denied redness of the overlying skin or fever. Following clinical examination, she had an ultrasound of the breast revealing a 3.7cm cystic mass with internal echoes. Ultrasound-guided aspiration was performed and 30cc of milky fluid aspirated with complete resolution of the mass. However, the galactocele recurred within 24 hours but remained asymptomatic otherwise. Three weeks later, the patient presented with evidence of mastitis, was started on antibiotics, and the galactocele re-aspirated. With persistent signs of infection, galactocele-fluid cultures revealing Streptococcus viridans, and re-accumulation of the milk in the galactocele, incision and drainage was contemplated. This was subverted with a less invasive means by inserting an 8 french multiple side-hole pigtail catheter into the galactocele enabling complete drainage and healing of the underlying infection. The catheter was removed in 10 days and antibiotics given for a total of 2 weeks. To prevent development of a milk fistula through the drain site, fluid reaccumulation was monitored with ultrasound and re-aspiration performed at 4 and 16 days after drain removal. The patient recovered with complete healing of the catheter tract. The galactocele persisted even after cessation of breast-feeding. A mammogram was then performed which revealed no findings of underlying malignancy. IMPLICATIONS/DISCUSSION: A galactocele most commonly presents as a breast mass soon after the cessation of lactation, and an ultrasound evaluation is usually confirmatory. These masses usually disappear in few weeks to months. However, the persistence of a galactocele, particularly after repeated aspirations, necessitates further work-up to rule out ductal obstruction from an underlying malignant process. Our patient had another infrequent complication Ð an infected galactocele. The concern of incision and drainage of a galactocele was that of a high likelihood of milk fistula. On the other hand, if not drained, infection was likely to persist and progress to a breast abscess. An alternative was therefore considered of introducing a pigtail catheter into the galactocele to enable complete drainage while instituting appropriate antibiotic coverage. Catheter drainage of breast abscess has been described in the literature, but this is the first report, to our knowledge, of catheter drainage of an infected galactocele. A 78 year-old lady reported a``whitehead like'', non-irritating lesion on her right nipple. Watchful waiting was recommended and over the course of the next 3 weeks, this lesion progressed into a rash involving the nipple and areola with a painful central abrasion and crusting. With the use of antibiotic cream, the rash improved in 3±4 days but mild flaking of the skin persisted. Three months later, the patient presented to the Breast Clinic for evaluation of a mild, but persistent nipple rash. She denied breast lumps, pain or nipple discharge. Breast cancer risks included nulliparity, and use of hormone replacement therapy for nearly 40 years. On examination, there was mild scaling of the skin over the right nipple with no associated induration, erythema or excoriation. On palpation, no dominant mass, nipple discharge, axillary or supraclavicular lymphadenopathy was identified. Mammograms revealed increasing microcalcifications in the sub-areolar region of the right breast. Stereotactic biopsy of these calcifications was performed and demonstrated high-grade ductal carcinoma in situ (DCIS). Skin biopsy of the scaly region revealed Paget disease of the nipple characterized by tumor cells with large nucleoli distributed singly in the superficial epidermal layers with clusters in the basal portion of the epidermis. These tumor cells were immunoreactive to anti-cytokeratin 7 and carcinoembryonic antigen (CEA) antibodies confirming the diagnosis of Paget disease. In compliance with the patient's wishes, right mastectomy was performed and on pathologic evaluation, residual DCIS was noted around the biopsy site along with Paget disease of the nipple. IMPLICATIONS/DISCUSSION: Paget disease, with an incidence ranging from 0.5 to 2.6%, presents as a scaly persistent rash, and often mimics eczema, or contact dermatitis of the nippleareolar complex. It may or may not be associated with a breast mass. Diagnosis is established by a skin biopsy, revealing characteristic Paget cells. Delay in diagnosis may result when the rash is mild in intensity and if unassociated with a breast mass. Clinical management of a patient with a nipple, or areolar rash mandates continued follow-up. If the rash fails to resolve, a high index of suspicion for Paget disease of the nipple will enable appropriate work-up and optimal outcome.

BREAST NODULE AFTER PROPHYLACTIC MASTECTOMY. K. Ghosh 1 , K.R. Brandt 1 ; 1 Mayo Clinic, Rochester, MN (Tracking ID #75726) LEARNING OBJECTIVES: 1. Build awareness among physicians that prophylactic mastectomy does not completely eradicate the possibility of breast cancer. 2. Emphasize that any breast lump after prophylactic mastectomy warrants complete work-up to rule out breast cancer. CASE INFORMATION: A 56 year-old lady with fibrocystic changes in the breast had undergone several benign right breast biopsies for mammographically detected abnormalities, and finally decided to have bilateral prophylactic mastectomy to prevent the anxiety associated with these biopsies. Following the mastectomies, she had bilateral pedicle transverse-rectusabdominis-myocutaneous (TRAM) flap reconstruction of the breasts with a smooth postoperative recovery. She was very satisfied with the outcome of the procedure. Four months after the surgery, the patient incidentally felt a lump in the left upper breast and when it persisted for about a month, the patient sought further evaluation. Examination revealed a firm, non-tender, fixed mass with ill-defined margins in the left upper breast. Ultrasound evaluation of the palpable mass revealed a heterogenic echotexture with no evidence of malignancy. Diagnostic left mammogram revealed no evidence of malignancy. Magnetic resonance imaging of the breast with dynamic gadolinium enhancement was then recommended and showed benign appearing localized collection of fat lobules and postoperative changes. The patient continues to do well on follow-up. IMPLICATIONS/DISCUSSION: The management of women at high-risk of breast cancer includes the options of surveillance, chemoprevention, prophylactic mastectomy and/or prophylactic oophorectomy. Prophylactic mastectomy is an option for risk reduction of breast cancer, and in women with a strong family history, has been associated with a 90% relative risk reduction. The procedure does not however, eradicate the risk of breast cancer as residual breast tissue may be left behind depending on the surgical technique. Therefore, any breast lump after PM must be evaluated to rule out breast cancer. In general, breast lumps after PM are often benign and related to fat necrosis as was the case in our patient, but the possibility of malignancy must be borne in mind when evaluating these patients.

A MAN NEWLY DIAGNOSED WITH HIV REFUSES TO INFORM HIS SPOUSE. C. Gibbs 1 , J. Tsui 1 ; 1 Emory University, Atlanta, GA (Tracking ID #74714) LEARNING OBJECTIVES: 1.) To appreciate a care giver's ethical and legal responsibilities when partner notification is refused by a newly diagnosed patient; 2.) To identify various partner notification strategies and weigh their advantages and disadvantages. CASE INFORMATION: A 36 year-old man presented to the emergency room complaining of fatigue, shortness of breath, severe dyspnea on exertion, and cough worsening over several weeks. The patient had no significant past medical history and denied tobacco, alcohol, or IV drug use. He denied any previous history of blood-product transfusions.He stated he had been in a monogamous marriage for the ten years and had had no other sexual partners. Further, the patient reported a negative HIV test three years ago. Chest X-ray revealed bilateral patchy opacifications without any focal consolidation. Laboratory results were significant for a WBC of 5.1, an LDH of 514, and an ABG of 7.46/39/55. The patient was admitted for communityacquired pneumonia and started on ceftriaxone and doxycycline; however, given his clinical picture, the patient's sputum was sent for silver stain. It returned positive for pneumocystis carinii. The patient's medications were changed to trimethoprim/sulfamethoxazole and prednisone, and he was counseled about the likelihood of immunocompromise. At this point, the patient agreed to HIV testing. He subsequently tested positive for HIV and had a CD4 count of 26. Patient education regarding HIV infection and AIDS was initiated. The patient acknowledged the possibility that his wife may have been infected and agreed that she should be notified. Initially, he wished to talk with her himself (self-referral). After a few days, it was discovered that the patient had not disclosed his HIV status to his wife. With much encouragement and further education, he agreed to a dual referral approach involving a healthcare provider being present when he notified his wife. However, when the appointed meeting day arrived, the patient once again refused. Patient education and support continued. As the patient's discharge approached, the medicine team feared that the patient's wife would never be informed of his seropositive status and her potential risk. These concerns were discussed with the patient and he was informed that if he did not notify his wife, the medicine team would act according to state and federal laws and notify her of her HIV exposure and need for testing. The patient informed his wife within 24 hours. IMPLICATIONS/DISCUSSION: This case demonstrates various approaches to partner notification and deals with the ethical and legal decisions physicians are forced to make when newly diagnosed HIV patients refuse to participate. Partner notification strategies can be classified into three basic categories: self-referral, dual referral, and provider referral. Each approach has its own advantages and disadvantages. Regardless of the strategy chosen, the patient's rights to autonomy, trust, confidentiality, and safety must be respected while balancing the physician's moral and legal responsibility to patients' partner(s), children, and community. Healthcare providers must recognize their responsibilities, know their federal and state laws, and act according to individual cases. A 50 year old African American man with no significant past medical history presented to the office with malaise, weakness, anorexia, watery diarrhea and mild headache of 2 days duration. He was treated conservatively for presumed viral gastroenteritis, until he presented to the emergency room 2 days later with increasingly severe frontal headache and fevers. Physical examination was remarkable for a temperature of 39.6 deg C and nuchal rigidity, but no focal neurological signs or impaired sensorium. Laboratory studies included a WBC count of 8800, and cerebrospinal fluid analysis which demonstrated a CSF WBC count of 150/mm3 with a differential of 11% neutrophils, 88% lymphocytes, 1% monocytes, and a CSF-protein level of 117 mg/dl. CSF gram stain was negative. The patient was admitted and placed on empiric ampicillin and cefrtriaxone. Blood cultures and CSF bacterial, fungal and protozoal studies remained negative. The patient slowly defervesced and his headache improved, and he was discharged to home. Notably, this case occurred at a time when public awareness of West Nile Virus infection in Allegheny County, Pennsylvania was just emerging; the virus had been isolated in several dead birds in the area, although there had been no reported cases of human infection. During the hospitalization, serum was therefore sent for West Nile Virus serologic testing. Following discharge, results of IgM and IgG antibody ELISA assays subsequently returned positive, and were later confirmed by plaque reduction neutralization test (PRNT). The patient gradually improved, although notably after developing a transient morbilliform rash on his chest, back and arms, observed during outpatient follow-up approximately one week after discharge. IMPLICATIONS/DISCUSSION: West Nile Virus infection is a mosquito-borne arboviral illness that is commonest in the United States in late summer and early fall. One of the early clues to an epidemic is the presence of dead birds in the surroundings. Infection is most often asymptomatic, and clinical illness is generally mild, presenting with constitutional symptoms much like those of other viral syndromes. Among patients with more serious CNS illness, isolated meningitis Ð such as occurred in our patient Ð is relatively less common than encephalitis or meningoencephalitis. Treatment is supportive, and advanced age is the biggest risk factor for severe neurologic disease. This case illustrates the need to consider West Nile Virus infection, however, in cases of aseptic meningitis occurring in endemic areas.Diagnosis is by serum or CSF IgM antibodies to West Nile Virus; first-line testing is by ELISA assay, and positive results are generally confirmed by the more specific PRNT.

AN UNEXPECTED CAUSE OF FEVER, HEADACHE AND ELEVATED ERYTHROCYTE SEDIMENTATION RATE. A.N. Githaiga 1 , E. Anish 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #76143) LEARNING OBJECTIVES: 1) To recognize sarcoid as a cause of central nervous system dysfunction in a patient without other systemic evidence of sarcoidosis. 2) To appreciate the value of performing a brain biopsy to establish a diagnosis of neurosarcoidosis when CSF analysis and neuroimaging are nondiagnostic. CASE INFORMATION: A hypertensive 50-year-old African American woman presented to the hospital with a one-month history of retro-orbital headache, recurrent fevers, chills, sweats and weight loss. Temperature on admission was 38 deg and her neurologic exam was non-focal. Initial labs were significant for WBC-11,800,PLT-610, 000 and ESR-148. A brain CT scan showed old lacunar infarcts. Lumbar puncture showed protein of 111mg/dl, white cell count of 3 and 79% lymphocytes. Viral, bacterial and fungal cultures were negative. Autoimmune serological markers were negative. A bone marrow biopsy was negative for malignancy and granulomatous disease. Serum ACE level was normal ( 29 Units/L.). Chest CT scan was normal, and abdominal CT scan revealed numerous small mesenteric and retroperitoneal lymph nodes that were not accessible for biopsy. The patient was started on empiric prednisone therapy for temporal arteritis at 60 mg per day despite negative bilateral temporal artery biopsies. She noted rapid improvement of her headache and resolution of her fevers and was discharged home. Over the next 8 weeks her ESR dropped to 22 and she remained asymptomatic. However, as the steroid dose was being tapered, the patient began to experience recurrence of headache and fevers, as well as gait and cognitive dysfunction. An MRI was performed that revealed multiple subcortical areas with increased signal. Repeat CSF analysis showed a white cell count of 28 with 89% lymphocytes and increased protein (79 mg/dl). Brain biopsy performed revealed focal perivascular lymphocytic infiltrates with non-necrotizing granulomas. Special stains for AFB and fungus were negative. A diagnosis of neurosarcoidosis was made. Her symptoms steadily improved with high dose solumedrol and subsequent oral prednisone. IMPLICATIONS/DISCUSSION: This case illustrates the importance of considering a diagnosis of neurosarcoidosis as a cause of fevers and CNS dysfunction in an individual who does not have other overt manifestations of sarcoid. In 5% of cases, neurosarcoid is the initial presentation of the disease. CNS presentations typically include cranial nerve palsies, meningitis, optic nerve dysfunction and neuroendocrine disorders (e.g. diabetes insipidus and central hypothyroidism). CSF findings are nonspecific and include elevated protein and mononuclear pleocytosis. Contrast enhanced MRI may reveal meningeal/cortical masses or hydrocephalus. As demonstrated in the case presented, neural tissue biopsy may be useful, revealing perivascular non-caseating granulomas, which while not diagnostic, will be highly suggestive in the appropriate clinical context. FOOLED BY FAT/PERPLEXED BY PROPOFOL. E. Gjersvik Cichowski 1 , H. Sakowski 1 , H. Hashish 1 , R. Baltaro 1 ; 1 Creighton University, Omaha, NE (Tracking ID #74955) LEARNING OBJECTIVES: 1) Recognize laboratory error in the measurement of serum bicarbonate.

2) Utilize the Henderson-Hasselbach equation to indentify blood gas analysis errors.

3) Recognize interfering substances as potential causes of laboratory errors. CASE INFORMATION: A 72 year-old male was admitted for respiratory distress and confusion, and found to have a right upper lobe lung mass and hypercalcemia. He was intubated on the second hospital day due to worsening of his respiratory status. Propofol was initiated for sedation and methylprednisolone and levofloxacin were given for a presumed postobstructive pneumonia. His initial arterial blood gas after intubation showed a pH 7.38 pCO2 38 pO2 143 on an Fio2 of .60. His measured HCO3 was 26 meq/l. Over the next 4 days, his measured bicarbonate progressively dropped to 8 meq/l despite no change in his arterial blood gas (pH 7.38 pCO2 36 pO2 103 on an FiO2 of .45). His anion gap was calculated at 19. Serum lactate was normal, and serum ketones were absent. Consultation with the pathology department revealed the patient's serum to be grossly lipemic. A review of the chart revealed the patient did receive lipid infusions with TPN 36 and 18 hours prior to this discovery. A lipid panel was obtained and revealed marked hypertriglyceridemia at 4426 mg/dl. The lipid infusions were discontinued, and the propofol was weaned off. The bicarbonate level dropped to a low of 3 meq/l approximately 7 hours after the medication was discontinued. Four hours later, the bicarbonate had corrected to 21 meq/l. The serum, however, remained grossly lipemic. The patient's condition continued to decline with the development of septic shock, multi-organ failure and ventricular arrythmias. Results of a previous bronchoscopy demonstrated small cell carcinoma. The patient's family requested no further aggressive treatment and he expired later that day. IMPLICATIONS/DISCUSSION: This patient developed marked derangement in his measured bicarbonate levels that did not correspond to his arterial blood gas analysis. A laboratory error was hypothesized as the cause. Due to the finding of lipemic serum, the hypertriglyceridemia was initially suspected as the interfering substance. Upon discontinuing the propofol, the serum bicarbonate level normalized, the serum, however remained lipemic. In a review of the literature, neither propofol nor hypertriglyceridemia have been reported as potential causes of this lab error. Further testing is needed to determine the role of propofol as an interfering substance in bicarbonate laboratory analysis.

DYING TO BE THIN. R.E. Graham 1 ; 1 Lenox Hill Hospital, New York, NY (Tracking ID #75181) LEARNING OBJECTIVES: This case demonstrates the limitations of our current knowledge about herbal products, particularly in dose-related toxicities, and calls attention to the need for further studies. This case highlights the need for health care providers to be knowledgeable about the herbal products their patients may be using, and to be able to identify potential herbassociated adverse effects. I hope this case illustrates CAM's prevalence, benefits, and potential dangers but most importantly highlights the importance of obtaining a complete medical history; including asking our patients if they are using and/or incorporating alternative therapies into their general healthcare. CASE INFORMATION: 26 year old thin female presented to the ED at about 5:15 PM complaining of a frontal headache, nausea, and feeling weak after fainting. The patient stated to the triage nurse that she had eaten Mexican food at about 3:30 PM, went home and took``a fat burner pill'' at about 4PM. She has been on fat burner pills and herbal teas for about one year. Suddenly she began to feel nauseous, developed a worsening headache, then fainted which prompted her to seek medical attention. Initially, the patient was taken to the back of the ED. While awaiting physician examination, the patient syncopized and began to have a seizure. The patient was wheeled into trauma and found to be in Ventricular fibrillation with a potassium of 2.4. She was defibrillated and then became hypotensive and progressed into asystole, she was resuscitated and then intubated. She began posturing without corneal reflexes. After stabilization the patient was taken to CT; which revealed±Extensive subarachnoid hemorrhage with the presence of intraventricular hemorrhage. Saddly, over the next 48 hours she was placed on life support and an organ donation referral was made. Soon after she expired. IMPLICATIONS/DISCUSSION: Complementary and Alternative medicine (CAM) is one of the fastest growing sectors in health care today. In 1997 , Eisenberg & et al JAMA, 1998 :280:1569±1575, revealed that 42.1% of Americans (83million) used CAM over the past year. In the same article Eisenberg, showed that only 38% of patients disclose to their physicians their use of alternative therapies when not asked directly. As we continue to see an increase in the rate of obesity in the United States, our patients will incorporate both prescription and nonprescription products in hopes of obtaining their desired weight loss. This current vignette exemplifies the need for the health care provider to first, ask the unasked question, secondly, to have a basic understanding and knowledge regarding CAM, and finally to provide an important role in educating, advising and discussing the potential risks and benefits of CAM, and the need to closely monitor any use of them. CXR showed R mediastinal mass. CT showed diffuse LAN (mediastinal, peritoneal, retroperitoneal) and numerous liver metastases. HIV and hepatitis panel were negative. FNA of neck revealed atypical lymphoid cells. Excisional biopsy showed anaplastic carcinoma, no melanin but HMB-45 and melan A (melanocyte markers) were immunostain positive. IMPLICATIONS/DISCUSSION: Distinguishing between localized and generalized LAN helps guide the appropriate differential diagnosis. Diffuse LAN suggests HIV, mycobacterial infection, infectious mononucleosis, SLE, medications (i.e., phenytoin), metastatic carcinoma and lymphoma. The history and physical exam become crucial in the diagnostic work up of generalized LAN. The history should include signs and symptoms suggestive of infection or malignancy, exposures (cats±cat scratch disease; raw meat±toxoplasmosis; tick bite±lyme disease; unprotected sex or injection drug use-HIV), constitutional symptoms and medications. A complete physical exam should guide the appropriate diagnostic work-up. Patients with generalized LAN should have a CBC and CXR. If these are normal, consider PPD, HIV test, RPR, ANA, and heterophile test, although these tend to be low yield if not specifically indicated. An FNA for cytology is generally the first step due to ease and safety, especially for granulomatous versus malignancy and lymphoma versus carcinoma, yet an FNA fails to provide enough material to examine architectural detail or to perform immunostains. This is especially relevant with younger patients where hematologic malignancies or uncommon solid tumors are a consideration. Metastatic melanoma without a known skin primary accounts for around 3% of melanomas. Prior to melanocyte-specific immunostains, these cases were considered carcinoma of unkown primary. Cases of metastatic melanoma lacking primary skin lesion include primaries of mucosal surfaces (sinuses, oral mucosa, vulva, vagina and anorectum), occular and primary skin lesion which have regressed. Thus, the lack of skin lesion does not rule out metastatic melanoma.

No effective systemic therapy exists at this time for metastatic melanoma. Biotherapeutic approaches combining immunomodulators such as IL-2, INF, and vaccines with conventional cytotoxic chemotherapy are currenlty under active investigation.

A COURAGOUS CALL: SALINE FOR HEART FAILURE? M. Guidry 1 , J. Wiese 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77054) LEARNING OBJECTIVES: 1. Recognize the perils of over-diuresis in bi-ventricular heart failure. 2. Use disciplined methods of diagnosis to prevent errors in pattern recognition diagnosis. 3. Use the physical examination to predict cardiovascular function. CASE INFORMATION: An 80 year-old woman presented with two days of shortness of breath and orthopnea. Her blood pressure was 132/65 with a heart rate of 116. She had bibasilar crackles and 3+ pitting bipedal edema. There was an S3, S4, and an inferiorly displaced PMI. Her room-air ABG at presentation was pH: 7.44; pCO2:35; pO2:58. She was diuresed with a total of 320 mg of furosemide over one day. Her symptoms improved. On the third hospital day, she had a sudden worsening of her shortness of breath. Her neck veins were flat and there were no crackles. A repeat ABG was pH: 7.28; pC02: 57; p02: 81; HCO3:42 Her BUN tocreatinine ratio increased from 23/1.4 at presentation to 41/2.3 on the third hospital day. Diuresis was stopped, and hydration with normal saline was initiated. Her shortness of breath improved, with normalization of her acid base values. IMPLICATIONS/DISCUSSION: Dyspnea can result from hypoxia or hypercarbia. This patient initially presented with dyspnea due to congestive heart failure; she was appropriately managed with preload reduction via diuresis. Continuing diuresis was excessive however. In the setting of bi-ventricular heart failure, the over-diuresis resulted in an inadequate right ventricular preload, and a subsequent drop in her pulmonary artery pressure. With the alveolar pressure unchanged and the pulmonary artery pressure lowered, the percentage of dead space increased. This resulted in a ventilation to perfusion mismatch resulting in hypercarbia. The physical examination was the tell-tale sign, revealing that her volume status was low, instead of high. The ABG confirmed the diagnosis; the rehydration increased the pulmonary artery pressure, resolving the mismatch, and eliminating the dyspnea. In caring for patients with biventricular heart failure who are sensitive to preload reduction, it is important to remember that hypercarbia from dead space ventilation can result from aggressive lowering of the pulmonary artery pressure.

COLCHICINE±INDUCED MYOPATHY. K. Gupta 1 , T.A. Townley 1 ; 1 Creighton University, Omaha, NE (Tracking ID #76577) LEARNING OBJECTIVES: 1) Review the differential diagnosis of proximal muscle weakness in an elderly male 2) Review symptoms and signs of colchicine-myopathy 3) Review the risks factors for colchicine myopathy. CASE INFORMATION: INTRODUCTION: Colchicine has been used for 200 + years, but there are few reports of myopathy associated with its use. We present such a case. CASE: Patient is a 70-year-old male who was hospitalized for abdominal pain/diarrhea. He had fallen on his hip at home 1 week prior to his admission and became increasingly weak with considerable reductions in his ADL such as inability to get in and out of bed, stand from sitting and walk. His PMH includes COPD on home O2, CHF, HTN, DM, CRI (baseline Cr 2.2), obesity and gout. Medications include Oxycodone 5/325mg prn, metoprolol 50mg qd, colchicine 0.6mg qd, allopurinol 100mg qd, furosemide 80mg qd, glipizide 30mg qd, isosorbide dinitrate 30mg qd, fosinopril 40mg qd, ASA 325mg qd, KCl 20mEq qd, Insulin 70/30, MVI qd. His initial physical exam was normal except for reduced reflexes in upper limbs 2+/4 and lower limbs 1+/4 with no sensory deficits. Lab work revealed acute renal insufficiency on CRI (BUN 69/Cr 2.6), in addition LFT's were twice normal. CK was 1059 with MB fraction <5%. CXR and abdominal series were clear and EKG was unchanged. His abdominal pain resolved, and ARI improved with hydration and discontinuation of ACE-I. Initially his weakness was felt to be secondary to intercurrent illness superimposed on chronic illness. However weakness failed to improve and a repeat CK was 1825 with ESR of 36. His weakness localized to proximal muscles of upper and lower extremities, with strength 3/5. Distal muscle strength was 5/5. Colchicine was suspected as the cause of his myopathy and discontinued. He noticed a significant improvement in his proximal muscle of 4/5 on the following day. EMG showed myositis with predominantly proximal muscle irritability. Repeat labs 5 days after discontinuing colchicine, showed BUN 44/ Cr 1.4, and CK 958. There was a noticeable improvement in strength, with ability to stand from sitting, ambulate across room and get into and out of bed alone. IMPLICATIONS/DISCUSSION: DISCUSSION: Patients taking colchicine over an extended period of time have been reported to develop a subacute, often severe myopathy in conjunction with a relatively mild polyneuropathy. Chronic renal failure is a risk factor for this syndrome. Our patient had been on colchicine for more than a year. In this case an untreated myopathy may have resulted in nursing home placement versus a trial of steroids for polymyositis. In our patient, who had pre-existing renal insufficiency worsened by the dehydration, the clinical presentation and the improvement on discontinuation of colchicine strongly supports the diagnosis of Colchicine induced myopathy.

MANAGEMENT OF RAMSAY±HUNT SYNDROME. S. Gupta 1 , O. Melamed 2 ; 1 UCLA School of Medicine, Los Angeles, CA; 2 Olive View±UCLA Medical Center, Sylmar, CA (Tracking ID #75744) LEARNING OBJECTIVES: 1. Clinical presentation and pathophysiology of Ramsay±Hunt Syndrome 2. Lack of outcome benefit from head imaging, IV therapy, and surgery for RHS 3. Improved outcome with early treatment. CASE INFORMATION: A 30-year-old female presented to the urgent care clinic for evaluation of left ear pain, vertigo, left facial paralysis and small vesicles over the left pinna. The patient's past medical history was significant for chickenpox at the age of eight. On physical examination the patient had left ear swelling and erythema with multiple 0.5±1.0 mm vesicles around the pinna and marked erythema involving the external auditory canal. There was a positive Bell's phenomenon (the eyeball rolling up and outward on attempting to close the affected eye). A facial paralysis involved the left levator labii and left frontalis muscles. A left sensorineural deficit was observed with Weber test lateralizing to the right and a positive (normal) Rinne test bilaterally. The diagnosis of Ramsay±Hunt Syndrome was made. The patient was discharged from the clinic on a regimen of Acyclovir and Prednisone. She was instructed to avoid pregnancy, contact with pregnant women or neonates. IMPLICATIONS/DISCUSSION: Clinical presentation of unilateral facial paralysis and a vesicular rash on the ear (zoster oticus), often accompanied with hearing loss, tinnitus, nausea, vomiting, vertigo and nystagmus was first described by J Ramsay Hunt in 1907. Vestibulocochlear symptoms were explained by the anatomical proximity of the eighth nerve and the geniculate ganglion within the temporal bone. The pathophysiology of RHS involves the reactivation of varicella-zoster virus (VZV) within the geniculate ganglion and secondary edema in the facial nerve resulting in facial nerve palsy. VZV is considered a major etiologic agent of Bell's palsy. Use of contrast enhanced MRI in diagnosis of RHS does not appear to provide much information as enhancement of the geniculate ganglion, meatal fundus, and facial nerve is observed independent of etiology. Most patients with Bell's palsy tend to recover to complete or near normal function even without treatment. One prospective study found that 85% of patients showed signs of remission within the first 3 weeks, with 71% recovering complete function, 13% left with insignificant sequelae, and 16% left with permanently diminished function. Although most patients with RHS improve, many patients are left with functional and cosmetic deficits. Treatment of RHS with oral acyclovir and prednisone (AS therapy) may improve outcome. Two separate studies showed complete recovery in 75% of patients with RHS treated with AS. There has been no evidence of improvement in outcome with intravenous administration of either acyclovir or prednisone, though many patients are still admitted to the hospital for IV therapy. There is also insufficient evidence for efficacy of surgical facial nerve decompression. Evidence for improved outcomes with earlier administration of therapy have been observed. In one study 75% of patients beginning AS treatment within 3 days of onset of facial paralysis had complete recovery, compared with 30% of patients beginning therapy after 7 days. Earlier therapy decreased nerve degeneration and improved recovery of hearing.

SEIZURES ON POSTPARTUM DAY SEVEN. K. Gustafson 1 , R. Khurana 1 ; 1 University of Alberta, Edmonton, Alberta. (Tracking ID #76917) LEARNING OBJECTIVES: 1) To recognize that preeclampsia and eclampsia may occur in the postpartum period. 2) Diagnose eclampsia even when it presents without the typical signs of preeclampsia. We describe a case of postpartum eclampsia that was initially misdiagnosed. CASE INFORMATION: A 28 year old woman G2P2 was transferred to our tertiary case hospital on postpartum day 7 because of seizures. Her pregnancy had been uncomplicated and she had a vaginal delivery at term for a healthy 3515g female infant. Her past medical history was unremarkable and her blood pressure had remained normal throughout the pregnancy. She presented to a local hospital on postpartum day 7 complaining of severe headache, nausea and vomiting. Her blood pressure was 176/100. She was given analgesia, but then had two generalized seizures. She was given magnesium sulfate 5 g intravenously and transferred. When assessed, her blood pressure was 150/90. She had no focal neurologic findings, right upper quadrant tenderness, edema or hyperreflexia. Her liver enzymes and platelet count were normal. Urinalysis was negative for protein. Urate was slightly elevated. CT scan of the head was normal. EEG was normal. She was seen by the services of Neurology, Internal Medicine and the Intensive Care Unit. She was diagnosed with seizures of unknown origin and admitted for observation. The magnesium sulfate was discontinued. Her blood pressure varied over the next two days from 124/81 to 200/103. On postpartum day 10, she had another generalized seizure. MRI of her brain was consistent with hypertensive encephalopathy. She was given a diagnosis of postpartum eclampsia and treated with intravenous magnesium sulfate and antihypertensive therapy. She improved over the next few days and all therapy was discontinued. She remains well with no further seizure activity. IMPLICATIONS/DISCUSSION: Preeclampsia/eclampsia may worsen or even initially present in the postpartum period. Postpartum eclampsia represents 25% of all cases of eclampsia. The majority of these events occur in the first 24±48 hours postpartum, but have been reported to occur as late as 4 weeks postpartum. Eclampsia does not always occur in patients who have the classic triad of preeclampsia (hypertension, proteinuria and edema). About 20% of patients with eclampsia have no proteinuria. Computed tomography and EEG are often unremarkable, but should be performed to rule out other causes of seizure. When MRI abnormalities are present, hyperintense signals in cortical and subcortical areas on T2 weighted images may be seen. These are usually in the posterior parietal or occipital lobes. Management of eclampsia includes delivery of the fetus (if diagnosed antepartum), magnesium sulfate to prevent recurrent seizures and control of severe hypertension. A high index of suspicion is necessary to appropriately diagnose the woman with postpartum eclampsia and prevent further morbidity. LEARNING OBJECTIVES: To recognize focal muscle infarction as an unusual, and sometimes bilateral, cause of severe limb pain in patients with diabetes. CASE INFORMATION: A 55 year-old diabetic woman developed disabling pain in both upper legs, with thickening and tenderness of the soft tissues of the right lateral thigh. There was no evidence of infection. She had neuropathy but sensation in the thighs was normal. There was a history of disc disease but an MRI examination of the spine was unimpressive. She had arterial disease but ankle/brachial indices were only in the claudication range. There was a history of venous thrombosis but she was taking warfarin and duplex studies showed no clots. Plain films and a bone scan were negative. MRI examination showed diffuse edematous infiltration of the subcutaneous fat of both thighs, with increased signal in the right vastus lateralis muscle. These findings were consistent with infarction of the vastus lateralis, and conservative treatment was recommended. IMPLICATIONS/DISCUSSION: Diabetic muscle infarction causes pain, swelling, and tenderness, most commonly in the thigh, but sometimes in the calf. The opposite limb may be involved, either sequentially, or concurrently, as in this case. The MRI appearance is characteristic and allows the diagnosis to be made without the risks of biopsy. Treatment is supportive. This rare but important entity must be considered when diabetic patients suffer severe limb pain.

A CASE OF SPONTANEOUS BILATERAL CAROTID CAVERNOUS FISTULAS. S. Habib 1 , P.K. Han 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #76354) LEARNING OBJECTIVES: 1) To recognize the clinical symptoms and signs of carotid cavernous fistula. 2) To describe an unusual presentation of carotid cavernous fistula. CASE INFORMATION: An 85-year-old woman presented with a 3±4 week history of progressive difficulty with eye opening, poor vision, and tinnitus. She denied headaches, ocular or orbital pain, diplopia, worsening of symptoms with activity, dizziness, focal weakness, or other recent illnesses. She had a history of recent falls, but no head trauma. Her past medical history was significant for hypertension, primary hyperparathyroidism, normocytic anemia, Paget's disease of bone, and a fifty pack-year smoking history. She was on ferrous sulfate but no other medications Physical examination revealed a blood pressure of 168/74 without orthostatic changes, mild conjunctival pallor, and bilateral complete ptosis. There was chemosis of the right eye and opthalmoplegia, with bilateral palsies of cranial nerves III, IV, and IV. Both pupils were mid-dilated and non-reactive to light. No other neurological deficits were noted. Diagnostic evaluation included a normal CT scan of the brain, while brain MRI demonstrated changes suggestive of bilateral carotid cavernous fistulas. Cerebral angiography was performed, which confirmed the presence of bilateral type A carotid cavernous fistulas. The patient then underwent trans-carotid endovascular embolization, which was unsuccessful. Unfortunately the patient developed right-sided hemiparesis a few days later, and subsequently declined further intervention. IMPLICATIONS/DISCUSSION: Carotid cavernous fistula is an unusual problem caused by an abnormal communication between the internal and/external carotid artery and the cavernous sinus. It is classically characterized by the triad of pulsating exophthalmos, ocular chemosis and an orbital bruit. Other features include orbital pain or tightness, pulsatile tinnitis, visual loss due to ischemia of optic nerve and retina, retinal vein congestion, and glaucoma. Ophthalmoplegia often results from pressure upon local cranial nerves; CN VI is affected most often, and CN III and IV are involved less frequently. Our patient did not present with the classic clinical triad, but with bilateral complete ophthalmoplegia and pulsatile tinnitis. Trauma is the most common cause of carotid cavernous fistula although 20 percent of cases are non-traumatic. Spontaneous bilateral carotid cavernous fistula, as observed in our patient, is a very rare entity. Risk factors for carotid cavernous fistulas include older women, mothers during childbirth, hypertension, atherosclerosis and collagen vascular diseases. A four-type classification of carotid cavernous fistulas based on the anatomy of the lesion has been proposed. Our patient had type A fistulas, presumably due to a rupture of an intra-cavernous carotid artery aneurysm. Early recognition and intervention is important to prevent permanent visual loss and ophthalmoplegia. Endovascular interventions (embolization and balloon occlusion) represent a successful treatment option although stroke is a well-recognized complication in 5±15 % of cases. LEARNING OBJECTIVES: 1, To recognize that autoimmune hepatitis is a rare complication following allogeneic stem cell transplantation. 2, To understand the pathophysiology of auto immune hepatitis folllowing stem cell transplantation. CASE INFORMATION: A 43 year-old white female developed Ph-chromosome positive chronic myeloid leukemia. She received cytoreductive therapy, followed by a 6/6 HLA matched allogeneic peripheral stem cell transplant (SCT). Tacrolimus and prednisone were continued for 18 months. One month after tacrolimus dose reduction, her serum AST and ALT levels were 723 and 965 respectively, but bilirubin and alkaline phosphatase were normal. An abdominal sonogram was normal. After the tacrolimus dose was increased to its baseline level, serum AST and ALT levels decreased to 45 and 60. Tacrolimus was then gradually reduced and eventually discontinued, which caused a rise in AST and ALT levels. She had no risk factors for viral hepatitis. Physical examination was normal except for Cushingoid appearance. CBC with differential were normal. Biochemical tests showed total bilirubin 0.7, AST 88, ALT 128, ALP 96, GGT 74, albumin 3.7, and total protein 9.8. Other biochemical profile including TSH, iron studies, ceruloplasmin, a 1 anti-trypsin and a feto protein were all within normal limits. ANA and anti thyroglobulin antibodies were positive whereas anti LKM, anti mitochondrial, anti smooth muscle antibodies were all negative. She had negative serology for EBV, CMV, HZV and hepatitis A, B, and C viruses. The histology was most consistent with autoimmune hepatitis. In situ hybridization study for Y chromosome established that immune reactive cells were exclusively of donor origin. There was no evidence of recurrent chronic myelogenous leukemia. Serum transaminase levels normalized with prednisone 20 mg a day but relapsed on dose reduction. Azathioprine was therefore added. Her transaminase levels have been normal for 28 months. IMPLICATIONS/DISCUSSION: This report documents a case of liver dysfunction, following SCT, which was indistinguishable from`definite' autoimmune hepatitis (baseline diagnostic score > 15) as defined by the modified criteria of International Autoimmune Hepatitis Group. To our knowledge, the present case represents the first report of this complication after allogeneic peripheral SCT. One intriguing feature of this case is that the target liver cells and immune reactive cells are of different origins. The donor origin of immune reactive cells was clearly established in our female patient by in-situ hybridization labeling of the Y chromosome. As the term`autoimmune hepatitis' does not accurately reflect the disease process, we propose the term`alloimmune hepatitis' for this syndrome. A 50 year old white male was admitted to our hospital in July with three days of fever, chills, headache, and neck stiffness. He worked as an air-conditioner repairman and spent a considerable amount of time shirtless, outdoors in East Texas. Physical examination was significant for fever of 102.4 degrees Fahrenheit, meningismus, and Kernig's sign. The patient was awake, alert, and oriented to person, place, and time. Initial CSF analysis revealed WBC 91 with 92% neutrophils and 8% monocytes; protein 81, glucose 68; gram stain revealed few WBCs, and was negative for bacteria; latex agglutination screen was negative for H. influenzae, S. pneumoniae, N. meningitis A, B, C and group B streptococcus. CBC revealed a WBC count of 10.6 with 70% neutrophils, 20% lymphocytes, and 10% monocytes. Within two days of admission, the patient became progressively more lethargic and delirious and was oriented only to person, month, and year. Repeat CSF analysis revealed WBC of 223 with 15% neutrophils, 59% lymphocytes, and 26% monocytes; glucose of 66 and protein of 81. CSF bacterial cultures remained negative. CSF studies for syphilis, tuberculosis, and herpes simplex virus were negative. CSF IgM was positive for West Nile virus. IMPLICATIONS/DISCUSSION: Until 1999, West Nile virus was found only in Africa, Asia, and the Middle East. Since that time, West Nile virus has infected over 3852 individuals in the U.S. in at least 39 states. West Nile virus is a single-stranded RNA Flavivirus virus that belongs to the Japanese encephalitis complex. Birds are the natural hosts of West Nile virus and mosquitoes, particularly of the culex species, act as vectors. Infection in humans typically occurs in late summer through early fall when mosquitoes are most predominant. Severe neurologic disease accompanying West Nile virus infection is rare. One out of every 150 infected patients develops meningitis or encephalitis. Age greater than 50, is the major risk factor for developing life-threatening neurologic disease. West Nile viral encephalitis is similar to other viral encephalitities and is characterized by fever, headache and an altered level of consciousness. CSF studies typically show a lymphocytic pleocytosis with elevated protein.

Early viral encephalitis, however, may demonstrate CSF with a predominantly neutrophilic CSF pleocytosis, as in our patient. Lymphopenia is a common feature of West Nile virus encephalitis and thus it may aid in distinguishing this disease from other forms of viral encephalitis. Definitive diagnosis is obtained through confirmation of blood or CSF IgM to West Nile virus. Treatment is supportive. The main intervention is prevention by promoting the use of mosquito repellant and protective clothing. year old white male presented to our hospital with complaints of fever, diarrhea, and fatigue. His admission was preceded by two days of watery, non-bloody stools, fever to 102, fatigue, malaise, and generalized weakness. The patient denied any sick contacts or travel, although he noted living in a mosquito-infested area of East Texas. On admission, the patient's temperature was 102.2, pulse 69, blood pressure 117/61 and respiratory rate 24. The patient appeared fatigued and exhibited a diffuse, erythematous rash and injected conjunctivae. The neurologic examination revealed normal tone and 5/5 strength throughout. Sensation was intact and reflexes were 2+ and symmetrical in all extremities. The rest of the physical examination was unremarkable. Within days, the patient developed severe generalized weakness with areflexia and ultimately, respiratory failure requiring mechanical ventilation. Analysis of CSF revealed a WBC count of 78 with 55% lymphocytes, 30% neutrophils, and 5% monocytes; glucose 154, and protein 116. Electrophysiologic studies were performed and were consistent with a diffuse axonal polyneuropathy. Serologic studies were positive for the West Nile virus. IMPLICATIONS/DISCUSSION: Before 1999, West Nile virus, a single-stranded RNA virus belonging to the Japanese encephalitis complex, was found only outside the western hemisphere. Since then, West Nile virus has infected over 3852 individuals in the U.S. in at least 39 states. Many clinicians are aware that West Nile virus is associated with encephalitis and meningitis, however, the association between West Nile virus infection and acute flaccid paralysis is less well known. CDC surveillance during the most recent outbreak of West Nile Virus in Louisiana revealed that almost 20% of patients described as having severe neurologic disease presented with acute flaccid paralysis. Early reports of patients with West Nile virus acute flaccid paralysis often confused the condition with Guillain-Barre syndrome. Clinicians should be aware that unlike most patients with Guillain-Barre syndrome, patients with West Nile associated acute flaccid paralysis typically have fever, CSF pleocytosis, and electrodiagnostic studies consistent with a predominantly axonal neuropathy. Most patients with Guillain-Barre syndrome are afebrile, have an elevated CSF protein, few if any WBCs in the CSF, and electrodiagnostic studies consistent with a demyelinating neuropathy. The presence of a maculopapular or morbilliform rash, such as our patient had, may also suggest the presence of West Nile virus infection. LEARNING OBJECTIVES: 1. Develop a differential diagnosis for thrombocytopenia in a well-appearing adult. 2. Learn to diagnose and treat ITP in adults using the best available evidence. CASE INFORMATION: A well-appearing 72 year-old Chinese-American man being treated with glipizide for type II diabetes presented to clinic with a petechial rash on his trunk, arms, and legs. A CBC revealed isolated thrombocytopenia (platelet count 23,000). Glipizide was discontinued but thrombocytopenia persisted. His platelet count normalized with a prednisone taper but in the ensuing months, despite splenectomy, he continued to require 5 mg of daily prednisone to maintain a normal platelet count. His diabetes became poorly controlled while on prednisone, and he had one episode of pneumonia requiring antibiotics. The decision was made to stop prednisone. After the initial petechiae he has had no further evidence of bleeding, but his platelet count remains between 10,000 and 40,000. IMPLICATIONS/DISCUSSION: Medications and ITP are common causes of isolated thrombocytopenia in well-appearing adults. Glipizide is among the many medications with published case reports of thrombocytopenia as a side effect. ITP is a clinical diagnosis made in the setting of isolated thrombocytopenia with a normal peripheral smear and no other identifiable cause of low platelets. Experts recommend a bone marrow biopsy in patients over age 60 to rule out myelodysplasia. Anti-platelet antibodies are not specific for ITP. Case series suggest that in adults spontaneous remission occurs less than 10% of the time. Splenectomy is curative in 50±65% of all cases, with better results in patients less than 40 years old. Lifethreatening bleeding rarely occurs with a platelet count of greater than 10,000. Prednisone is not curative and is most helpful as a supportive measure in patients with platelets under 10,000 or other high bleeding risks (ie: surgery). Asymptomatic patients with platelet counts above 10,000 and no other risks for bleeding can most likely be safely managed without steroids. Develop an approach for the evaluation of dyspepsia through review of the current evidence and recommendations 3. Review diagnostic testing and treatment for H. pylori. CASE INFORMATION: 46 y/o woman presented with epigastric discomfort and nausea 1±2 months after she ran out of her cimetidine. Symptoms were similar to ones she experienced 2 years prior when she may have had a``stomach bug'' for which she thought she was given antibiotics. The patient did endorse drinking 2 beers/day but denied dysphagia, anorexia, weight loss or melena. Physical exam was benign. Symptoms initially improved with reinstituting cimetidine and decreasing alcohol intake. Initial labs demonstrated a normal CBC, LFTs, amylase and lipase, but was impressive for an H. pylori titer 1:87 U/mL. Despite continued cimetidine, the patient's symptoms recurred within months and lansoprazole was initiated. An H. pylori breath test was not pursued due to the patient's reluctance to discontinue medications prior to the test. Subsequent endoscopy revealed 2 small, linear, cleanbased ulcers biopsy positive for H. pylori. Symptoms resolved after treatment with amoxicillin, clarithromycin and lansoprozole. IMPLICATIONS/DISCUSSION: Dyspepsia, or chronic and/or recurrent pain or discomfort of the upper abdomen, is a common complaint accounting for 5% of all PCP visits. H. pylori is implicated in several of the etiologies of dyspepsia, thus the management of dyspepsia must involve strategies to appropriately diagnose and treat H. pylori. Testing for H. pylori is recommended only if treatment is intended; however, guidelines regarding the indications for treatment of H. pylori put forth by the American College of Gastroenterology (1998) and the Maastricht 2±2000 (European) are conflicting. Both agree on the need to treat in cases of active ulcer disease or gastric/MALT lymphoma, but the Europeans are more aggressive in their recommendations advising treatment in entities such as non-ulcer dyspepsia or concurrent NSAID use. A recent meta-analysis (Laine, et. al. 2001) helps to clarify the issue of non-ulcer dyspepsia Ð which accounts for the majority of dyspepsia Ð suggesting that eradication of H. pylori does not improve symptoms in non-ulcer dyspepsia. Yet the uncertainty regarding the utility of eradication of H. pylori makes the appropriate work up of uninvestigated dyspepsia somewhat unclear. We will review several algorithms for the evaluation of dyspepsia and discuss the current data supporting the most often recommended``test and treat'' approach with regards to H. pylori and dyspepsia. In addition, we will discuss the range of diagnostic testing available for H. pylori and the appropriate use of these tests during the evaluation of dyspepsia. The topics of treatment and treatment failures will also be addressed. spells of altered mental status and syncope. The patient's behavior ranged from combative and agitated to lethargic. These variations in behavior usually occurred early in the morning, lasted one to three hours, and were associated with diaphoresis, marked confusion, and generalized weakness. The patient often had no recollection of these events and returned to baseline between episodes. This pattern increased in frequency and severity prior to admission. The spells were associated with blood sugar measurements in the low forties. The patient was hospitalized for further work up and underwent a monitored fast. Serial lab values were consistent with insulinoma. Imaging studies to locate a tumor included body CT, ultrasound, endoscopic ultrasound, and nuclear imaging, which were non-diagnostic. Initially the patient's glucose was maintained at normal levels with intravenous 10% dextrose and frequent snacking. Diazoxide therapy was initiated which allowed the intravenous dextrose to be discontinued; however, even with frequent snacks the patient still had occasional low sugars. With failure of medical management the patient underwent exploratory laparotomy with intraoperative ultrasound which did not detect a distinct mass. A distal pancreatectomy was performed, which demonstrated hyperplasia of islet cells. Post-operatively the patient was able to maintain normal blood sugars without diazoxide. IMPLICATIONS/DISCUSSION: Nesidioblastosis is a rare cause of hyperinsulinemic hypoglycemia that is differentiated by an insulinoma only by pathology. In this case, the patient's hypoglycemia was associated with syncope and altered mental status. LEARNING OBJECTIVES: 1) to review neutropenia as a presentation of SLE 2) to discuss strategies to avoid misdiagnoses and how to manage lupus neutropenia. CASE INFORMATION: A 53 y/o Egyptian woman presented with two weeks of fevers reaching 102±103 degrees F. She denied cough, headache, dysuria, diarrhea, abdominal pain, joint pain, oral lesions, rash, weight loss, sexual promiscuity, recent travel, or drug use. She last visited Egypt four years ago and worked as an apartment manager. She took occasional Tylenol, no other medication. On examination she had a temperature of 103 degrees F and appropriate tachycardia. No lymphadenopathy, breast masses, abdominal masses/pain, lung crackles, cardiac murmurs, or neurological findings were found. She had a WBC 1.7, 64% PMNs and mild anemia Hgb 11.1. LFT's, TSH, Fe/Ferritin, and chemistry normal. An extensive infectious workup was negative including blood and fungal cultures, AFB cultures, urinalysis, CXR, visceral leishmaniasis, malaria, brucellosis, EBV, CMV, HIV, RPR, PPD. CT of the chest, abdomen, pelvis, and head found only mild splenomegaly. Transesophogeal echo revealed no valvular vegetations. The patient continued with daily fevers to 102±103 degrees F, anemia worsened to a Hgb 8.4, WBC decreased over ten days to a nadir of 0.7 (ANC 60). GCSF was started for neutropenia and empiric Ceftazidime and Tobramycin were begun. Bone marrow biopsy showed normal cell elements and myeloid to erythroid ratio 1:1. Her mammogram was normal. At this point ANA returned +1:320 as well as Coombs positive. Antids DNA and Anti-Smith was sent. On second day of GCSF patient developed polyarthritis in hands, wrists, elbows, knees, ankles as well as faint malar rash. Follow up CXR revealed small left pleural effusion. GCSF was stopped and patient was started on Prednisone with subsequent resolution of fevers, rash, and arthralgias. Anti-ds DNA returned +1:80. IMPLICATIONS/DISCUSSION: Lupus can present in a variety of ways. In this case, the initial presentation was neutropenic fever. Only after receiving GCSF did the diagnosis become apparent as it precipitated a lupus flare. The diagnostic criteria for Lupus developed by the ACR are 96% sensitive and specific. Non-specific symptoms such as fever, fatigue, and weight loss are common presenting complaints and are often attributed to causes other than lupus leading to misdiagnoses. Leukopenia occurs in more than 50% of lupus patients with either granulocytopenia or lymphopenia. GCSF has been used in the treatment of lupus induced neutropenia resulting in a rise in neutrophils within 48 hours, however the elevation is transient with return to pretreatment levels within days after withdrawal of therapy. In addition treatment with GCSF has been associated with flares in lupus that resolve when the drug is stopped. A 63 year old male with hypertension, chronic renal insufficiency, and peripheral vascular disease presented to the Emergency Department with acute onset of bilateral lower extremity numbness and weakness. Six weeks prior, he had received an arteriovenous fistula in preparation for hemodialysis and was feeling well until the morning of admission, when, upon rising from bed, he fell to the ground because of numbness and weakness of his legs. Review of systems was positive for urinary incontinence,``sharp'' back pain, and shortness of breath which had developed at the same time as the paresthesia. Upon reviewing his medical records, it was discovered that his prostate specific antigen had been elevated at 24.9, but the patient had not followed up with the urologist for further evaluation. Physical exam showed a well-developed male, alert and oriented, in moderate respiratory distress. His respiratory rate was 24, blood pressure 142/90, heart rate 82, and temperature 36 C. Other significant physical findings included bilateral crackles, a pericardial friction rub, absent sensation to light touch at an L3 level, 2/5 bilateral lower extremity strength, absent ankle and patellar reflexes, absent pedal pulses (previously documented), diminished but equal femoral pulses, and an enlarged prostate. Labs showed BUN of 71mg/dl and creatinine of 9.3 mg/dl. Chest radiograph demonstrated mild pulmonary edema. Thorax and abdomen CT without contrast showed a normal aorta. A vascular catheter was placed, and emergent hemodialysis started. The neurology and neurosurgery services were consulted, and plans were made to get an emergent MRI of the lumbosacral spine to rule out cord compression after the patient was stabilized. An hour after dialysis had begun, the patient lost consciousness, and ACLS for pulseless electrical activity was initiated. After 25 minutes of unsuccessful resuscitation, the patient was declared deceased. An autopsy was performed which showed hemopericardium from type A aortic dissection which descended to the bifurcation of the aorta. IMPLICATIONS/DISCUSSION: In this case, aortic dissection caused peripheral arterial ischemia which presented as paresthesia and weakness. Stroke is the most common neurologic presentation of aortic dissection, although 10% of patients present with ischemic peripheral neuropathies. Although pain describing dissection has classically been taught to be``ripping or tearing'', most patients classify the pain as``sharp.'' Given the high mortality associated with aortic dissection, a high index of suspicion should be maintained for patients presenting with paresthesia and back pain. year-old white male with unremarkable medical history presented with acholic stools, dark urine, and constitutional symptoms. Physical examination revealed a diffuse erythematous, maculo-papular rash of trunk and legs, profound jaundice, liver span of 14cm with a firm edge, no splenomegally and no stigmata of chronic liver disease. His initial outpatient laboratory tests revealed: alkaline phosphatase 413 U/L, total bilirubin 3 mg/dl, SGOT 510 U/L, and SGPT 515 U/L. Viral hepatitis serologies, an abdominal ultrasound and CT, and an endoscopic retrograde cholangiopancreatography were unremarkable. Three weeks later, the patient underwent a percutaneous liver biopsy at which time his laboratory values were: WBC 1.9 Â 103/ 3 , Hgb 12.6 g/dl, Platelets 62,000, alkaline phosphatase 706 U/L, total bilirubin 26.9 U/L (direct 21.8 U/L), SGOT 190 U/L, and SGPT173 U/L. The liver biopsy showed a high-grade malignant leukemic infiltrate. Bone marrow biopsy confirmed the diagnosis of B cell/ Burkitt's type acute lymphoblastic leukemia with flow cytometry showing CD19+/CD10+/CD20-/CD34-/CD13+/HLA DR+ cells. IMPLICATIONS/DISCUSSION: Acute lymphoblastic leukemia is primarily a disease of children; adults only account for approximately 20% of cases and Burkitt's B cell ALL, in turn, makes up only 5% of the cases of ALL. Unfortunately, over 60% of adults with ALL are not cured of their disease. The clinical features of ALL are often nonspecific and primarily constitutional as well as manifestations of cytopenias secondary to the bone marrow infiltration. Also, ALL has a predilection for the CNS and symptoms of meningeal leukemia or hyperleukocytosis are not uncommon at presentation. Cholestatic jaundice, however, is a much less common presenting feature with a limited number of case reports in the literature. As demonstrated in this case, one should entertain the diagnosis of acute lymphoblastic leukemia in those presenting with acute cholestatic jaundice. He also had intermittent episodes of gum bleeding, anorexia and shortness of breath. His medications included Atenolol. On physical exam, his vital signs were stable and he was noted to have pale conjunctiva, minimal gum bleeding and a non-radiating systolic murmur. His white blood cell count was 1,600 with a normal differential. He had a hematocrit of 14.9 and a platelet count of 7,000, and lactate dehydrogenase of 794. His remaining lab findings were normal. His peripheral smear showed decrease red blood cells and platelets with normal morphology and no immature white blood cells. Two bone marrow biopsies were both dry taps and confirmed a diagnosis of Acute Myelogenous Leukemia (AML) of the Megakaryocyte subtype (FAB classification M7). His course was complicated early on by neutropenic fever and broadspectrum antibiotics were initiated. Chemotherapy was started after a 48-hour period feverfree period with Idarubicin for 3 days and Cytosine-arabinoside for seven days. He tolerated the treatment well, but remained pancytopenic. Two days after completing induction, he became febrile and complained of severe abdominal pain and diarrhea. Broad-spectrum antibiotics for both bacterial and fungal pathogens were started. Imaging of his abdomen showed bowel wall thickening consistent with neutropenic colitis (typhlitis). Treatment initially consisted of broad-spectrum antibiotic coverage and supportive care. His condition progressively worsened, and both he and family did not want any aggressive intervention. The patient passed away shortly thereafter. IMPLICATIONS/DISCUSSION: Acute leukemia accounts for about 10% of human cancers and is the leading cause of death in adults younger than 35 years of age. In our case, the patient had poor prognostic factors of age greater than 60 years old and poor functional status. The treatment of AML consists of supportive care and chemotherapy with induction therapy conducted with an anthracycline and Cytosine-arabinoside (except for subtype M3). Complications from leukemia include those related to immunosuppression and pancytopenia. Typhlitis represents inflammation and/or necrosis of the cecum, appendix, and/or ileum and is a frequent complication of the treatment of AML. Patients usually present with abdominal pain, diarrhea and fever. The etiology of typhlitis is unknown, but profound neutropenia and mucosal injury from cytotoxic drugs play important roles in the pathogenesis. The mortality rate from typhlitis in leukemic patients can be high and the treatment consists of broad antibiotic coverage, nasogastric suction and supportive care. Surgical intervention is indicated if there is bowel perforation or persistent bleeding. CASE INFORMATION: A 74-year-old female, who was previously independent and ambulating well, presented with a four day history of progressively worsening bilateral knee pain and swelling. Her past medical history is significant for degenerative joint disease with chronic pain in her knees. Her medications included Rofecoxib, Oxycontin, Oxycodone, and Calcium with vitamin D. The patient had received an injection of Hylan G-F 20 in both knees four days prior to presentation for chronic knee pain. A similar injection had been performed one year previously with relief of pain. The next day she developed fever, chills and the knees became warm, erythematous, and swollen, with worsening pain, 10/10 in severity. Upon presentation, the patient was afebrile and both knees were swollen and tender. The patient was unable to bear weight, range of motion of the knees was limited to about 30 degrees bilaterally, and there was tenderness in the lateral joint line bilaterally. Laboratory results showed a normal white blood cell count, ESR 70, and C Reactive Protein 20.6. Venous doppler ultrasound was negative for DVT. Knee x-rays revealed bilateral effusions and evidence of severe osteoarthritis. Bilateral knee arthrocentesis showed (left/right) white blood cell count, 11300/10500 with a normal differential, red blood cells 475/38000, and no crystals. Gram stain and cultures were negative. The patient was admitted to the hospital for pain management and transferred to sub-acute rehabilitation for 3 weeks where she responded well to corticosteroid injections and physical therapy. IMPLICATIONS/DISCUSSION: Visculosupplementation involves using intra-articular injections of high elastoviscous solutions of hyaluronan and hylans in an attempt to restore the natural mechanical properties of synovial fluid. Complications of intra-articular injections with visculosupplementation occur in 2±4% of injections. Local reactions include joint pain, effusion, and rarely, warmth. Acute pseudogout, granulomatous inflammation, and severe systemic reactions have also been reported. Rest, analgesics, corticosteroid injections, cold packs, and therapeutic arthrocentesis may help relieve symptoms. The presence of fever, debilitating pain, and joint effusions in our patient suggested both a systemic and local reaction to the supplementation. This impacted her functional status as she became bedridden and she required a prolonged rehabilitation to regain her independent ambulatory status. LEARNING OBJECTIVES: 1. Recognize myxedema coma as rare, but important diagnosis in differential for obtunded patient 2. Recognize emergent need for treatment of myxedema 3. Recognize mortality due to the condition and its therapy. CASE INFORMATION: 80 year old Caucasian female with history of congestive heart failure, chronic obstructive pulmonary disease, hypothyroidism was found by neighbors to be in obtunded state. In emergency room, her temperature was 95.9 F, blood pressure 108/56, pulse 50, respiratory rate 11, glasgow coma scale score 3. Her skin was cool to touch, with induration and 1+ non-pitting edema of the lower extremities. She had peri-orbital swelling. Labs: Na 142, K 4.3, Glc 142, creatinine 2.9, Hgb 9.3, CPK 286, CPK MB 5, troponin I .1, TSH 309, T4 total < 1, T4 free .1. ABG (after intubation, 100% FIO2) pH 7.26 pCO2 52 pO2 624. EKG:sinus bradycardia at 50 beats/minute, low voltage. CT head was normal. Blood cultures were negative. After labs were drawn, patient was started on nasogastric levothyroxine but continued to deteriorate. The next day, she was switched to intravenous therapy and started on steroids. Her mental status improved markedly and she was extubated. However, a few days later, she was found in asystole and expired. IMPLICATIONS/DISCUSSION: Myxedema coma is a rare, deadly condition. It should be suspected in patients who present with hypothermia and altered mental status. They may also have hypotension, hypoventilation, hyponatremia, hypoglycemia, and cardiovascular abnormalities. It may be caused by severe longstanding hypothyroidism or precipitated by infection, infarction, cold weather, narcotics/sedatives. Elderly females are most commonly affected. Therapy should be based on clinical suspicion and started right after drawing TSH, free T4 and cortisol levels. Glucocorticoid therapy prevents adrenal crisis in cases with associated adrenal insufficiency. Type of thyroid therapy is controversial. Some prefer T3 because of its rapid onset and greater biologic activity. Others prefer T4, which should be given intravenously to avoid malabsorption. Careful dosing based on age and weight may prevent cardiac complications of thyroid therapy. The mortality rate is 30±40% despite adequate therapy. Even though intravenous therapy was delayed in this patient, she showed significant improvement prior to her demise. Thus, her death may have been due to cardiac complications of therapy rather than the delay in intravenous therapy. However, definitive cause of death was not determined. Since therapy is controversial and associated with complications, an additional lesson is to focus on prevention via recognition and treatment of hypothyroidism. In this tragic case, the patient had been lost to follow up.

INTESTINAL T-CELL LYMPHOMA PRESENTING AS SMALL BOWEL PERFORATION. P. Hulick 1 , H. Tun 1 ; 1 Mayo Clinic, Jacksonville, FL (Tracking ID #74266) LEARNING OBJECTIVES: 1. Recognize the association of primary gastrointestinal T-cell lymphoma and celiac disease 2. Recognize the poor prognosis, especially with +CD56 marker 3. Treatment must include systemic chemotherapy. CASE INFORMATION: A 73-year-old white female presented to the emergency department following an acute exacerbation of abdominal pain that had progressed over the past two months. The pain was originally diffuse in nature but became sharp in character with the acute presentation. The patient denied radiation to the back while movement exacerbated the pain. The patient reported decreased appetite with a fifteen-pound weight loss over the preceding six months, nausea but no vomiting, and intermittent fevers to a maximum of 105F over the preceding two months. The patient denied other constitutional symptoms. On admission, the patient was afebrile with normal vital signs. Physical exam was notable for diffuse abdominal discomfort on palpation, decreased bowel sounds of normal pitch, and the absence of generalized lymphadenopathy Laboratory studies were Hgb 11.1g/dL, MCV 85 fL, and platelet count of 385,000. Electrolytes, creatinine and liver profile were unremarkable. LDH was 185 u/L. Computed tomography (CT) scan of the abdomen/pelvis revealed a pneumoperitoneum without identification of a specific site of perforation. Exploratory laparotomy revealed a perforated small bowel mass (7.0 Â 4.0 Â 1.0 cm) with infiltrating neoplastic lymphocytes positive for CD 3, 43, and 56 staining. Flow cytometry showed a T-cell phenotype with anomalous expression of CD 103 (T-cell mucosal homing antigen receptor). Staging evaluation did not reveal evidence of metastatic disease. The pathology findings in our case are consistent with enteropathy associated T-cell lymphoma. Our patient presented with the rarer T-cell CD56 positive variant which has a poorer overall prognosis and aggressive course. IMPLICATIONS/DISCUSSION: Primary gastrointestinal lymphomas account for 30±40% of extranodal lymphomas, but they are usually of B-cell lineage. Celiac disease, a malabsorption disorder related to gluten intolerance, is thought to be a risk factor for developing primary intestinal T-cell lymphoma. Intestinal T-cell lymphoma continues to have a poor prognosis. CD56 (neuronal cell-adhesion molecule) positive tumors have been associated with a more aggressive course. Additional poor predictors include nutritional status at presentation and presence of a bowel perforation. Survival data for cases presenting with bowel perforation has been estimated at 28% and 0% six months and one year post diagnosis. Treatment consists of surgical resection of the tumor and adjuvant chemotherapy which consists of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) which our patient received. Systemic chemotherapy is necessary, regardless of stage, because of the malignant clonal population of T-cells that exists in the normal gastrointestinal mucosa. Relapse rate is thus high, even in patients with initial response to chemotherapy. year-old woman with recurrent ovarian cancer was hospitalized and conservatively managed for a partial small bowel obstruction. After a second unsuccessful attempt to anti-coagulate her right su-bclavian central venous catheter, the patient developed acute left-sided weakness associated with slurred speech. She denied chest pain but stated she was increasing short of breath overnight. Vital signs included a heart rate of 117 beats per minute and a respiratory rate of 26 breaths per minute. Physical exam was remarkable only for a left facial droop, left arm and leg weakness, and dysarthria. An emergent CT scan revealed an acute, non-hemorrhagic right-sided cerebral infarct. ECG, duplex scan of the carotid arteries and chest radiograph were normal. Cardiac isoenzymes were negative for myocardial infarction. An arterial blood gas analysis revealed severe hypoxia and an alveolar-arterial oxygen gradient of 42. A ventilation-perfusion scan showed high probability for pulmonary embolism and a transesophageal echocardiogram revealed a patent foramen ovale. IMPLICATIONS/DISCUSSION: Indwelling catheters can serve as a nidus for thrombus formation. Emboli may produce pulmonary sequela with concomitant increased right sided circulatory pressures. This results in paradoxical emboli entering the arterial circulation though a right to left shunt, such as a patent foramen ovale, with resultant cerebral ischemia. Patients who demonstrate symptoms of both a cerebral infarct and a pulmonary embolism should be evaluated with a CT scan, carotid duplex, ventilation-perfusion scan and transesophageal echocardiogram to identify the source and location of the embolus. Treatment involves immediate evaluation for emergent anticoagulation if not contraindicated. Operative closure of a patent foramen is not indicated if the elevation of right sided pressure is related to an acute event. year old Asian female without significant medical history presented with ten days of rash, fever, joint pains and stiffness. Rash, which was erythematous and non-pruritic, began on her thighs and spread to her back and chest. Joint pains spread from her hands and wrists to her shoulders, ankles and knees. Her course of illness included high fevers and a sore throat. Physical exam revealed temperature of 103.9 F and erythematous, salmon colored maculo-papules on her trunk and proximal extremities. Palms and soles were spared. The rash was exacerbated by fever spikes, which usually occurred in the afternoon. Koebner's phenomenon occurred when rubbing caused the rash to appear on previously uninvolved skin. Metacarpophalangial joints, wrists and left shoulder were tender, but without erythema, warmth or effusions. There was no lymphadenopathy or splenomegaly. Labs: WBC 22,000 (85% neutrophils, 5% bands). Blood cultures and tests for HIV, enterovirus, cytomegalovirus, Ebstein-Barr virus, hepatitis, parvovirus were negative. Anti-streptolysin O titers were negative. LFT, ANA, RF, chest xray, CT chest/abdomen/pelvis, echocardiogram were normal. Skin biopsy showed perivascular infiltrate, no vascultis. Patient was started on nonsteroidal anti-inflammatory medications and gradually responded to therapy. IMPLICATIONS/DISCUSSION: Adult Still's disease, although uncommon, should be considered in adults with fever, joint pains and rash. The diagnosis requires atleast 5 criteria, including atleast 2 major ones. The major criteria are temperature of > 39 C for atleast 1 week, arthralgias for atleast 2 weeks, typical rash (salmon, maculopapular, evanescent, koebners phenomenon), WBC > 10,000 (> 80% neutrophils). Minor criteria are sore throat, lymphadenopathy and/or splenomegaly, elevated transaminases or LDH, negative ANA and RF. Diagnosis also requires exclusion of infection, malignancy and other rheumatic diseases. Treatment is aimed at joint symptoms because extent and chronicity of arthritis is best predictor of long term consequences. Nonsteroidals, corticosteroids and immunomodulating drugs are therapeutic options. Choice of therapy depends upon organ involvement and severity of disease. LEARNING OBJECTIVES: 1) To recognize intussusception as a cause of intestinal obstruction, 2) To recognize that the treatment of adult intussusception differs from pediatric cases, 3) To recognize that adult intussusception is often a presentation of underlying pathology. CASE INFORMATION: A 53 year old male with a past history of small cell lymphoma treated three years prior with CHOP chemotherapy and radiation therapy presented to the emergency department with several days of diffuse, unremitting periumbilical abdominal pain. He denied melena or hematochezia, and, until recent constipation, his bowel habits were unchanged. His intake of food was reduced due to bloating, but he denied nausea or vomiting. He did not experience fatigue, night sweats, fevers, or weight loss. On examination, his abdomen was soft and non-distended. He had normal bowel sounds. Despite diffuse nonspecific tenderness, he did not exhibit guarding or rebound. The spleen and liver were normal size, and no masses were palpated. A rectal exam was normal, and stool hemoccult was negative. Because of his medical history, a CT scan of the abdomen was performed which revealed ileocecal intussusception and resulting obstruction. A barium enema confirmed an intussusception but was unable to reduce it. He was taken to the operating room where the surgeons found intra-abdominal lymphadenopathy and ischemia of the proximal colon requiring hemicolectomy. Pathology of the resected tissue revealed follicular B-cell lymphoma within the terminal ileum and cecum. IMPLICATIONS/DISCUSSION: Intussusception is a process of gastrointestinal invagination in which a proximal segment telescopes into a distal portion. While common in children as the second leading cause for acute abdomen, adult intussusception occurs in only 5±10% of all cases. Presentation may be either acute or of a chronic indolent nature. It is rarely idiopathic in adults as it is in children, and underlying pathology is readily identifiable in up to 90% of all cases. Common causes include polyps, Meckel's diverticulum, endometriosis, and inflammatory bowel disease, but 54%±69% of identified pathology are malignancies including lymphomas. The process of intussusception causes gastrointestinal circulatory obstruction which can lead to ischemia and bowel infarct. Avoiding delay in surgical intervention preserves tissue. While barium enema is both diagnostic and therapeutic in children, it is less efficacious in adults, and its role in adult therapy is actually controversial. Because of the likelihood of underlying pathology, primary resection is often the treatment of choice. Whether or not to attempt reduction before resection is arguable; some authors have suggested that time spent on barium enemas compromises the integrity of bowel tissue. While uncommon, intussusception should be readily recognized when it occurs. Treatment of the disease requires timely surgical intervention to preserve bowel tissue. It is paramount to recognize that treatment in adults differs from pediatric cases where barium enemas are often successful. Discovery of adult intussusception must arouse clinical suspicion of underlying pathology which should be addressed. He was taken to the local emergency department, which was unable to run ethylene glycol level assays. At the outside hospital, he had an anion gap of 25, but an osmolar gap was not measured. He was placed on an ethanol drip and transferred to a tertiary care center. A stat ethylene glycol level returned elevated at 432 mg/dL, and the osmolar gap was 140 mOsm/kg. At this time, although stuporous, he was arousable and conversed appropriately. Unfortunately, urine was not sent for analysis, but serum creatinine was 1.2 mg/dL. Instead of initiating hemodialysis, the patient was placed on intravenous fluids with dextrose and saline and given fomepizole every 12 hours. Treatment continued for the next 60 hours until his ethylene glycol level fell within a non-toxic range. Clinically, his mental status returned to baseline, and his serum creatinine improved to 0.8 mg/dL. The patient underwent psychiatric evaluation and after medical clearance was transferred to an inpatient psychiatric facility for treatment of his depression. IMPLICATIONS/DISCUSSION: Ethylene glycol is a sweet liquid found in antifreeze. The taste has led to accidental intoxication in young children, but ingestion also occurs during suicide attempts. It is metabolized into oxalate, which is excreted by the kidneys, through several enzymatic steps beginning with alcohol dehydrogenase. Early toxicity is manifested by mental status changes ranging from stupor to coma. Renal damage from direct toxicity to the kidneys develops later although the rate of occurrence depends on the severity of intoxication. Presumptive diagnosis, based on a history of ingesting solutions likely to contain ethylene glycol, such as antifreeze, is the first critical step in diagnosis. While ethylene glycol can be measured directly, the laboratory equipment may not be available readily in all emergency departments. However, diagnosis can be confirmed indirectly with basic laboratory tests. Ethylene glycol itself causes an increased osmolar gap, and its metabolite glycolic acid creates the anion gap metabolic acidosis. The end product of metabolism, oxalate, can precipitate in urine, and urinalysis may reveal calcium oxalate crystals. Treatment must occur expediently to preserve renal and neurological function. This should involve adequate hydration and inhibition of alcohol dehydrogenase to prevent breakdown of ethylene glycol into its toxic metabolites. Ethylene glycol is dialyzable, and severe intoxication may require hemodialysis. However, in most cases, fomepizole, a more efficacious inhibitor of alcohol dehydrogenase than ethanol, can be used alone without need for dialysis. If both methods are used the dose of fomepizole needs to be increased since it is a dialyzable agent. Fomepizole can preserve renal function without invasive vascular access required for hemodialysis. Recovery without permanent sequelae is possible but requires timely recognition of ethylene glycol intoxication and familiarity with the treatment methods. A 24 year old man with severe hemophilia A and AIDS was admitted to the medical service with new neurological deficits. Eight weeks prior to admission he was started on highly active retroviral therapy (HAART). Six weeks prior to admission he developed left facial droop and left upper extremity weakness. The patient's family described behavioral changes including mood disturbances and aggressive behavior. On the day of admission the patient experienced two witnessed generalized seizures. On physical examination he appeared chronically ill. Neurological examination revealed a left cranial nerve VII upper motor neuron palsy and left upper extremity weakness. There was no papilledema. An MRI of the brain revealed multifocal hyperintense signals in the right frontal, left frontal, and right parietal areas predominately affecting the white matter without enhancement or mass effect. A subsequent spinal tap revealed a normal opening pressure with 1 white blood cell, 0 red blood cells, total protein of 74, and glucose of 54. Evaluation of the cerebrospinal fluid for tuberculosis, bacteria, fungus, toxoplasmosis, syphilis, herpes, CMV, and cryptococcus were negative. JC virus DNA was detected by PCR from the CSF. Based on the clinical presentation, radiographic findings and positive JC virus DNA in the CSF, the diagnosis of progressive multifocal leukoencepholapthy (PML) was made. IMPLICATIONS/DISCUSSION: PML is a disorder characterized by multiple rapidly progressive focal neurological deficits. Hemiparesis, visual field defects, cognitive impairment, and cranial nerve deficits are most common. Intracranial pressure usually remains normal. Ninety-five percent of all patients with PML have an underlying immunosuppressive disorder such as HIV. Conversely, 1±3% of AIDS patients will develop PML. CT or MRI of the brain reveals multiple bilateral, usually asymmetric areas of demyelination. The lesions are usually localized to the periventricular area and subcortical white matter. There is no contrast enhancement or mass effect. The diagnosis is made based on the clinical picture of multiple neurologic deficits, characteristic radiographic findings, and isolation of the JC virus from the CSF. Detection of JC virus from the CSF has a sensitivity of 74±95% and a specificity of 92±100%. There is currently no proven effective therapy for PML. HAART therapy has been shown to slow the progression of the disease. However, most patients deteriorate rapidly within 6 months. LEARNING OBJECTIVES: 1. Recognize the importance of opthomologic exam in the differential diagnosis of aseptic meningitis 2. Understand the role of steroid therapy in Vogt-Koyanagi-Harada Syndrome. CASE INFORMATION: A 24-year-old previously healthy man was admitted to the medical service with progressively worsening generalized headaches, decreased visual acuity, and hearing loss for two weeks. The patient reported malaise, but denied nausea, vomiting and fevers. He had never traveled outside the United States and did not use drugs or alcohol. The patient was afebrile. HEENT examination revealed bilateral papilledema and decreased visual acuity and hearing. Neck examination was remarkable for nuchal rigidity. The neurological exam was otherwise normal. CT scan of the head and orbits confirmed the papilledema but did not reveal any mass effect. A subsequent spinal tap revealed normal opening pressure, 727 white blood cells with 70% lymphocytes, a protein = 81, and glucose = 53. The patient was begun on broad-spectrum antibiotics and anti-tuberculous therapy without significant improvement. RPR, HIV, ESR, and cryptococcal antigen were negative. Ophthalmologic consultation was obtained. Slit lamp examination revealed cells in the anterior chamber consistent with uveitis, choroidal inflammation, and depigmentation. The patient was diagnosed with Vogt-Koyanagi-Harada (VKH) syndrome based on the ophthalmologic findings, aseptic meningitis and hearing loss. The patient was started on high dose steroids with relatively rapid resolution of the headaches and visual and hearing loss. IMPLICATIONS/DISCUSSION: VKH is a uveomeningoencephaltic syndrome and appears to be an autoimmune reaction to melanocytes thus making it more common in Asians, Middle-Easterners, and Hispanics than whites. Melanocytes are located in the skin, uvea, retinal choriod, membrane of the inner ear, and leptomeninges, accounting for the particular pattern of involvement seen in this syndrome. The ocular findings may include cataracts, glucoma, and globe atrophy. Meningeal involvement may lead to encephalopathy, seizures, myelopathy, or other focal signs. CSF findings include a lymphocytic pleocytosis, elevated total protein, and normal opening pressure. Other manifestations of VKH include dysacousia, alopecia, poliosis, and vitiligo. Although the optimal steroid dosage for treating VKH has not yet been defined it is generally accepted to begin therapy with high-dose systemic steroids followed by oral steroids for at least 6 months. Patients typically have a rapid decrease in symptoms. In about half of the patients, disease recurs within six months of discontinuation of steroids.

NONSTEROIDAL ANTI-INFLAMMATORY DRUG ASSOCIATE D LOWER GASTROINTESTINAL TOXICITY. J.T. Jacob 1 , A.K. Jaffer 1 ; 1 Cleveland Clinic Foundation, Cleveland, OH (Tracking ID #74333) LEARNING OBJECTIVES: 1) Recognize the lower gastrointestinal (GI) adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs). 2) Examine the differential diagnosis of multiple gastrointestinal ulcers. 3) Implement appropriate testing and treatment of NSAIDinduced lower GI pathology. CASE INFORMATION: An 80-year-old female with coronary artery disease, hypertension, dyslipidemia and osteoarthritis was admitted to the hospital with chest pain and two episodes of syncope. Each episode of syncope was preceded by use of sublingual nitroglycerin. Review of systems was positive for chronic fatigue, but negative for weight loss, nausea, vomiting, abdominal pain or GI blood loss. Medications were metoprolol, omeprazole, hydrochlorothiazide, indomethacin, and gemfibrozil. Exam revealed a BP = 113/60 without orthostasis, a Pulse = 95 and 97% O2 sat. The exam of the abdomen was normal except for guaiac positive stool on rectal exam. A CBC showed a hemoglobin of 8.9 g/dl with a normal MCV and RDW. An iron panel, B12, folate, LDH, bilirubin, and haptoglobin were also normal. A dipyridamole thallium stress test was negative. The syncope was felt to be related to transient hypotension from nitroglycerin in the setting of anemia. She was therefore transfused blood and underwent upper and lower endoscopies. Multiple ulcers were noted in the stomach, terminal ileum, ileocecal valve, transverse colon and descending colon. Biopsies demonstrated acute nonspecific inflammation. Gastrin levels were normal. Indomethacin was discontinued, acetaminophen was initiated and omeprazole continued. She was discharged home in stable condition with a two-month follow up endoscopy. IMPLICATIONS/DISCUSSION: Adverse gastrointestinal (GI) effects of NSAIDs are not limited to the stomach and duodenum. Although these sites are most commonly affected, adverse effects related to the large bowel and the distal small intestine are increasingly being recognized in practice. NSAIDs can cause a variety of pathology in the lower GI tract including erosions, ulcers, diaphragms, strictures, small bowel enteropathy, diverticular bleeding and colitis resembling or exacerbating inflammatory bowel disease (IBD). The pathophysiology of these changes has not been elucidated. Other etiologies of multiple GI ulcers include: viral and bacterial infections, vasculitides, IBD and Zollinger-Ellison syndrome. Treatment consists of discontinuation and avoidance of all NSAIDs. Gastrin levels should be checked to rule out a gastrinoma. A repeat endoscopy in 6±8 weeks is needed to confirm healing otherwise other etiologies need to be considered. An increase in reporting of these adverse effects will lead to a better understanding of NSAID induced lower gastrointestinal toxicity amongst physicians. -old male with a history of DM1, inflammatory bowel disease (IBD) and PG was admitted for ileostomy closure. The patient discontinued his insulin pump the night prior to surgery. The preoperative glucose was 500 and the surgery was canceled. He was well until three weeks prior when his shin lesions started to get worse after minor trauma. Review of systems was otherwise negative. On exam, he appeared lethargic, T = 38.3 8C, Pulse = 145, and BP = 110/50 mmHg. The patient had four necrotic shin and ankle ulcers with exposed bone and tendon. Labs revealed a serum bicarbonate of 9 mg/dl, potassium of 4.6 mg/dl, glucose of 527 mg/dl, anion gap of 26 and elevated serum ketones. A blood gas revealed a pH of 7.24, pCO2 of 17 mmHg, pO2 of 123 mm Hg and HCO3 of 7 mg/dl. Culture of the ulcers grew gram positive and negative bacteria. The patient was treated with intravenous (IV) Insulin, fluids and antibiotics. After the DKA resolved, therapy for PG was begun using infliximab, topical cromolyn, clobetasol and whirlpool therapy. During infliximab infusion the patient developed transient hypotensive and shortness of breath. He was treated with diphenhydamine and hydrocortisone with resolution of his symptoms. He was switched to oral cyclosporine and discharged home. IMPLICATIONS/DISCUSSION: There are two accepted alternatives in the preoperative management of DM1. Patients can hold short-acting insulin on the morning of surgery and take one-half to two-thirds of their normal long-acting insulin dose or omit their morning insulin regimen entirely and be administered regular insulin on arrival to the hospital based on their glucose level. Patients with insulin pumps should continue their pumps at a basal rate until the morning of surgery. PG is an idiopathic dermatosis associated with epidermal and/or dermal inflammation. It is most commonly associated with systemic diseases such as IBD, rheumatoid arthritis and lymphoproliferative disorders. These lesions typically involve the lower extremities and are painful. Treatment is directed at the underlying systemic disease. Systemic steroids were avoided in this patient's case due to concerns for recurrent hyperglycemia. Alternatives include infliximab, dapsone, thalidomide, azathioprine, cyclophosphamide, 6-mercatopurine, tacrolimus and cyclosporine. Adjunctive therapies include antimicrobials, topical cromolyn, clobetasol and whirlpool therapy. female with Crohn's disease on long term TPN presented with shallow breathing, paresthesias involving the extremities and progressive motor weakness over a period of 2 days. Two weeks prior to presentation she was diagnosed with linerelated candidemia; the port was removed and she was treated with intravenous fluconazole. Exam revealed a cachectic female who was afebrile, BP = 110/80, HR = 90, RR=22, O2 sat = 97%. Neurological exam revealed a right facial droop, dysarthria, motor strength was 2/5 in the upper extremities (UE) and 0/5 in the lower extremities (LE) bilaterally. All reflexes were absent. Brain and spine MRI were unremarkable. The CSF cell count and glucose were normal while the protein was elevated. Blood, urine and CSF cultures were negative. The initial vital capacity (VC) was decreased to 0.89 L and the negative inspiratory force (NIF) was unobtainable. EMG revealed features of generalized sensorimotor polyneuropathy with demyelination and axonal loss. Recurrent asymptomatic episodes of non-sustained ventricular tachyarrhythmia were observed on telemetry but cardiac evaluation revealed no structural heart disease. The patient was diagnosed with GBS with cranial nerve involvement, a GBS variant called Miller-Fisher syndrome. Plasmapheresis was instituted and after a couple exchanges improvement was noted in her motor strength, VC and NIF. She was discharged after completing five session of plasmapheresis. 6-weeks post-discharge, her neurological examination was remarkable only for mild residual diplegia. IMPLICATIONS/DISCUSSION: GBS is an acute ascending inflammatory demyelinating polyradiculoneuropathy. The management of GBS requires early recognition because the respiratory muscles can be involved. Elective intubation should be considered when the forced VC falls below 15 mL/kg or when the patient is unable to generate more than 20 cm H2O of maximal NIF. Initial symptoms include parasthesias with rapid progressive muscle weakness and areflexia. The Miller-Fisher syndrome is a variant of GBS in which the cranial nerves are affected. Autonomic dysfunction with cardiac dysrythmias occurs in one half to two thirds of patients. The disease generally has a good prognosis with close cardiopulmonary monitoring. Plasmapheresis and IVIG have been shown to alter the natural history of GBS if treatment is instituted quickly. year old male presented for further workup after suffering a seizure episode on two separate occasions. 10 days prior to his presentation at the university hospital, the patient experienced a witnessed tonic-clonic event and was taken to a local hospital. The patient was admitted to that hospital and found to have a normal CT, MRI, and EEG. While preparing for discharge home, he had another tonic-clonic event which was witnessed by hospital personnel, and he was transferred to the university hospital for further evaluation. He complained of feelings of mild generalized weakness over the past few months as well as some tingling and numbness in his hands and feet. He denied any recent trauma or seizure history. He also denied any chills, fevers, nausea, vomiting, or weight loss. Past medical history was noncontributory. He denied the use of illicit or prescription drugs, tobacco, ethanol, or herbals. On examination, his vital signs were pulse 101, blood pressure 146/90, and temp 35.4C. Physical exam was unremarkable including normal neurological exam. Labs on admission were significant for K of 3.1 meq/L (nl 3.5±5.0), Cl of 96 meq/L (nl 100±110), CO2 33 meq/l (nl 20±32), Ca 9.0 mg/dl (nl 8.5±10.5), and Mg 1.0 meq/l (nl 1.5± 2.4). Records received from the outside hospital showed low Mg and K levels during the time of both wintessed seizures. Patient was repleted with IV Mg and K and placed on phenytoin. Repeat MRI and EEG were negative. The patient continued to have low serum magnesium levels in spite of aggressive IV and PO repletion. 24 hour urine studies revealed a significantly elevated urine magnesium excretion of 25 MEq/24hr (nl 6±10 MEq/24hr), as well as a decreased urine calcium excretion of 94 mg/24hr (nl100±300 mg/24hr). Urine diuretic screen was negative. Renin and aldosterone were both elevated at 15.8 ng/ml/hr (nl 0.2±1.6 ng/ml/hr) and 38.4 ng/dl (nl 1.6±16) respectively. The patient was diagnosed with Gitelman's Syndrome and discharged home on magnesium oxide, amiloride, aldactone and potassium supplements. He suffered no further episodes of seizure activity and his weakness improved. IMPLICATIONS/DISCUSSION: Seizures presenting with normal MRIs and EEGs can present a diagnostic dilemma for internists. This case emphasizes the importance of considering metabolic disorders as a cause of seizures especially in the setting of normal MRIs and EEGs. Gitelman's Syndrome, an autosomal recessive disorder which usually presents in early adulthood, is a rare variant of Bartter's syndrome resulting from defects in renal tubular function. Unlike Bartter's, Gitelman's patients present with hypomagnesemia and hypocalciuria, along with complaints of severe fatigue, cramps, muscle spasms, and polyuria. with progressive failure to thrive. Three exploratory laparotomies over that time for acute abdomen revealed no pathologic diagnosis. PMH includes asthma, G1P1. P.E. reveals a cachectic, female, 4ft. 11in., 36.1 kg. Evidence of hypotelorism, bilateral ptosis, decreased lateral gaze with nystagmus at end gaze. Abdominal exam reveals distended and tympanic epigastrum. Neurological exam reveals normal visual acuity, decreased C.N. 8 bilaterally, strength of proximal muscle groups 4/5 with atrophy, while distal muscle groups 5/5 bilaterally. DTR's brisk through out. Laboratory studies included CBC, basic metabolic panel, thyroid function tests, Vitamin B12, folate, and lactic acid which were normal except hemoglobin 9.9g/dl, low iron saturation 11%, ferritin 51. She underwent EGD which was normal including duodenal biopsies, aspirates and electronmicroscopy of duodenal biopsies. Her esophageal manometry revealed hypotensive LES, gastric emptying scan showed prolonged liquid gastric emptying with T 1/2 = 136 minutes (mean is 90 minutes). SBFT showed slow emptying of barium. In consultation with neurology, work up included urine porphyrin studies that were negative, while MRI of brain showed diffuse leukoencephalopathy. LP was recommended but nondiagnostic. Fatty acid levels were normal. Ophthalmology evaluation revealed retinal pigmented degeneration while audiometry revealed bilateral moderate sensorineural hearing loss. Muscle biopsy would be indicated if genetic testing were not available. Pt. had chromosomal karyotyping, as well as mitochondrial DNA and thymidine phosphorylase levels, which are absent in specific mitochondrial disorders. These confirmed the diagnosis of a mitochondrial disorder, subtype called mitochondrial neurogastrointestinal leukoencephalopathy(MNGIE). IMPLICATIONS/DISCUSSION: Mitochondrial disorders certainly accounts for <0.1% of causes of nausea and vomiting. On review of the patient's history and physical exam she also had salient findings of proximal muscle weakness, hearing and eye abnormalities.

Gastrointestinal involvement is an unusual presentation for mitochondrial disorders with only 21 reported cases. More typical findings of mitochondrial myopathies are progressive ptosis, ophthalmoplegia and proximal muscle weakness in young patients. All these findings can be found on an internists thorough physical exam, as this case illustrates.`I CAN'T TIE MY SHOES. '' ADENOCARCINOMA OF THE LUNG AND PARANEOPLASTIC ANTIBODY ENCEPHALOPATHY: FOLLOW UP 2 YEARS LATER. K.S. Jorn 1 ; 1 Mayo Community Internal Medicine, Jacksonville, FL (Tracking ID #74452) LEARNING OBJECTIVES: 1. To describe symptoms that may be seen in primary care that should prompt evaluation for paraneoplastic limbic encephalopathy 2. To describe the clinical course of and paraneoplastic antibody levels in this patient over time 3. To present the concept that paraneoplastic antibody levels may not be cost-effective for surveillance after cancer is treated, but additonal study is needed. CASE INFORMATION: A 47 yo nurse presented for primary care in May 2000 after recovering from a massive pulmonary embolus in February 2000. Previous medical history was significant only for tobacco abuse and history of depression and anxiety, stable with medical therapy. Evaluation for causes of the embolus revealed only a 1cm coin lesion in her right lung, stable on follow-up CT through June 2001. In Fall-Winter of 2000, the patient, co-workers, and her supervisors noted a decline in the patient's concentrating ability and documentation efficiency. An accusation of diversion of narcotics triggered severe depression and anxiety in December 2000. The patient was receiving medical and psychological therapy for depression and anxiety when apraxic symptoms such as inability to tie her shoes, loss of direction sense, fecal and urinary incontinence, and absence-seizure type episodes were noted in the spring of 2001. She was felt to have symptoms of limbic encephalopathy. A paraneoplastic antibody panel revealed an elevated P/Q calcium channel antibody. Thoracotomy with removal of the coin lesion July 2001 revealed it to be bronchoalveolar cell carcinoma. Patient's cognitive function has gradually improved to near-normal levels. Though the elevated P/Q antibody led to her cancer diagnosis, the antibody levels have not paralleled her clinical course. IMPLICATIONS/DISCUSSION: Neurologic paraneoplastic antibody syndromes are more typically associated with small cell lung carcinoma and often involve brain stem, cerebellar, or neuromuscular junction dysfunction. There is little literature to guide the follow-up use of paraneoplastic antibody testing after cancer has been treated. This unusual case is characterized by cognitive dysfunction in the presence of lung adenocarcinoma and suggests that follow-up paraneoplastic antibody testing does not add much to clinical assessment after treatment of cancer. Additional studies are needed to determine if there is prognostic information to be gained by surveillance with paraneoplastic antibody testing.

EVALUATION AND SIGNIFICANCE OF PERSISTENT ASYMPTOMATIC ELEVATED BONE ALKALINE PHOSPHATASE. K.S. Jorn 1 ; 1 Mayo Community Internal Medicine, Jacksonville, FL (Tracking ID #74454) LEARNING OBJECTIVES: 1. To review a series of cases in which asymptomatic elevated bone alkaline phosphatase was discovered, evaluated, and followed. 2. To propose an algorithm for evaluation of asymptomatic elevated bone alkaline phosphatase. 3. To suggest that additional study is needed to determine if this algorithm is cost-effective. CASE INFORMATION: Asymptomatic elevated liver enzymes are commonly encountered in primary care and are well documented in medical literature. Asymptomatic elevated alkaline phosphatase (bone subtype) also appears to be common in primary care but there is a lack of guidance in the literature for further evaluation of the abnormality once it is discovered. The cases presented provide examples of persistently elevated bone alkaline phosphatase and the outcome of the evaluation and followup over three to five years. Diagnoses revealed during evaluation of asymptomatic elevated bone alkaline phosphatase include metastatic lung cancer, male osteoporosis, and an apparently benign elevation of the enzyme. An algorithm for evaluation of an asymptomatic elevated bone alkaline phosphatase is proposed. IMPLICATIONS/DISCUSSION: The author hopes that this limited case series will help to focus additional attention on this relatively common clinical problem, ultimately providing more robust guidance to the clinician in its evaluation and management. -old female with a history of fibromyalgia and penicillin allergy presented several weeks after rectal abscess drainage with malaise, generalized myalgias and subjective low grade fever. On the first visit to her physician, the patient was sent home with the presumptive diagnosis of fibromyalgia exacerbation. Having continued to experience symptoms that she described as different from her usual``fibromyalgia pain'', she returned to the office to seek additional medical care. She was afebrile and her physical exam was notable for a diastolic murmur and generalized muscle tenderness. Pertinent labs included H/H of 11/ 39, WBC 14 and ESR 66. Blood cultures were drawn and returned 24±48 hours later, being positive for Enterococcus faecalis in 3 out of 3 bottles. TEE demonstrated an aortic valve vegetation with regurgitation. The diagnosis of IE was made and she was treated initially with vancomycin and gentamicin. She was successfully desensitized to penicillin and her treatment course with IV penicillin and gentamicin continued for 6 weeks. The patient had gradual resolution of her presenting symptoms during her treatment course. IMPLICATIONS/DISCUSSION: Patients with fibromyalgia or chronic pain syndrome can be challenging as they present frequently with multiple nonspecific complaints. It can be tempting to attribute all of their symptoms to these underlying disorders. However, physicians should objectively evaluate the patient and entertain other diagnoses when these patients present with new or worsening symptoms. In our case, this finally led to the diagnosis of IE.

The symptoms and signs of IE often are constitutional and, when localized, result from a complication of IE. Consequently, if physicians are to avoid overlooking the diagnosis of IE, a high index of suspicion must be maintained. This is especially true in cases of IE that have a subacute course. Subacute endocarditis is characterized by an insidious onset and by nonspecific signs and symptoms of chronic illness, such as low grade fever, fatigability, and malaise. Immunologic phenomena occur when the disease is protracted. Musculoskeletal symptoms, as was described in this patient, are common. Although fever is the most common sign in patients with IE, it is typically low grade. Heart murmurs are noted in 80 to 85 percent of patients with native value endocarditis (NVE) and are emblematic of the lesion predisposing to IE. Enterococci, which comprise normal gut flora, account for 5 to 15 percent of cases of NVE. There are no specific clinical manifestations nor is there a single lab test that establishes the diagnosis of IE unequivocally. A combination of major and minor clinical findings, outlined in the Duke criteria, makes the diagnosis highly probable. In the absence of surgical indication, optimal therapy for enterococcal endocarditis requires synergistic bactericidal interaction of antimicrobial agents targeted against the bacterial cell wall (penicillin, ampicillin, or vancomycin) and an aminoglycoside. Because of her overall clinical and laboratory presentation, the pituitary-adrenal axis was evaluated. The AM Cortisol was level 1.4 and ACTH was 5. Brain MRI and CT abdomen were unremarkable. The diagnosis of secondary adrenal insufficiency, potentially secondary to Megace 1 , was made. Patient was started on hydrocortisone 20 mg PO qAM, and 10 mg PO qPM. She had marked improvement in her symptoms. Megace 1 was discontinued and hydrocortisone was ultimately tapered. IMPLICATIONS/DISCUSSION: Findings in adrenal failure are nonspecific, and, without a high index of suspicion, the diagnosis of this potentially lethal but readily treatable disease is missed easily. Symptoms due to cortisol deficiency include anorexia, nausea, vomiting, weight loss, weakness, and fatigue. Although orthostatic hypotension is more marked in primary than secondary adrenal insufficiency because of aldosterone deficiency, it does occur in the latter. Hyperpigmentation (due to increase ACTH), hyperkalemia and volume depletion (due to aldosterone deficiency) occur only in primary adrenal failure. Hyponatremia is seen in both. In patients in whom adrenal insufficiency is merely to be ruled out, plasma cortisol is measured between 8 and 9 AM. Concentrations of <3 Ag/dl are indicative of adrenal insufficiency and obviate the need for other tests. Concentrations greater than 19 Ag/dl rule out the disorder. The short cosyntropin stimulation test is the most commonly used test for the diagnosis of primary adrenal insufficiency. Secondary adrenal insufficiency is characterized by low blood cortisol and ACTH levels, a low baseline rate of steroid excretion, and abnormal ACTH and metyrapone responses. Megace 1 is a progestational agent with activity in advanced breast and endometrial cancer and AIDS-related cachexia. Long-standing Megace 1 therapy can result in marked suppression of serum cortisol levels and decreased ACTH .The depressing effect of megestrol acetate on the pituitary-adrenal axis does not cause clinically evident problems in the overwhelming majority of cancer patients. However physicians should be aware of the possibility of adrenal insufficiency while taking or upon withdrawal of this drug. This is especially important in severely ill patients, in whom the subtle signs and symptoms of adrenal insufficiency can be attributed to their primary disease. LEARNING OBJECTIVES: 1) To recognize some causes of gait disorder in the elderly 2) To recognize the importance of a detailed history and 3) To recognize the role of genetic testing in appropriate elderly patients with gait disorders. CASE INFORMATION: 64-year-old female patient with past medical history of diabetes, mild osteoarthritis, and hypercholesterolemia developed gait problems over the last year and a half. She started losing balance around that time and her gait had become slow. She denied headaches, seizures, swallowing problems, memory disturbances or any sensory involvement. Her family history is significant for one sister and all male members in her father's family who developed gait disorders in their sixties. On examination, slurring of speech was present. Extraocular movements were intact. Strength in all extremities was normal and there was no pronator drift. Sensory examination was intact. Reflexes were symmetric and brisk. Gait was wide-based and she could not walk on her heels or toes. Her handwriting was small and she had difficulty with rapid alternating movements. An MRI showed mild cerebellar atrophy. Tests for Lyme disease, rheumatoid factor and anti-nuclear antibody were negative. Vitamin B12 level and sedimentation rate were normal. Genetic testing revealed that she possessed the CAG/ CAA repeat expansion mutation associated with spinocerebellar ataxia 17. Genetic counseling has been offered to her family members. IMPLICATIONS/DISCUSSION: There are many potential causes for gait disorders in the elderly. The most common are related to the presence of a sensory-motor polyneuropathy such as seen with diabetes, or strokes related to cerebrovascular disease. Also common are disorders secondary to compressive myelopathy. In this patient the presence of slurred speech made myelopathy and neuropathy unlikely and the absence of structural lesions on MRI suggested a progressive degenerative disorder. Spino-cerebellar ataxia(SCA) type 17 is a rare autosomal dominant neurodegenerative disease caused by an abnormal CAG expansion in the TATAbinding protein (TBP) gene. SCA 17 was identified in 4 Japanese pedigrees and first reported in 2001. Most individuals present between the ages of 20 and 30 with gait ataxia and dementia, progressing over several decades to include bradykinesia, dysmetria, dysdiadokokinesis, hyperreflexia, and paucity of movement. Neuroimaging shows cortical and cerebellar atrophy. Even the small number of SCA 17 patients identified so far suggests that there would be substantial phenotypic variability, probably secondary to incomplete penetrance. This case emphasizes the details of the differential diagnosis of gait disorders in the elderly and the importance of the family history even in the elderly patient. This has become especially important with the greater availability of genetic testing that will provide the basis for genetic counseling. 2) The importance of a complete history in pinpointing a rare diagnosis; CASE INFORMATION: A 37 yo white female with no significant PMH presented to the ER with a chief complaint of constant, progressive weakness over the past ten days. The patient initially noted swelling, paresthesias, and muscle tenderness in her legs, followed by progressive weakness from the ankles to the hips. She described difficulty in standing from a seated position, climbing stairs, and ambulating. She denied any alleviating or exacerbating factors or similar past symptoms. She had taken only acetaminophen as needed and had no known drug allergies. She denied any ingestions, exposures, or recent travel. On ROS, she denied fever, changes in appetite, weight, urine output or color, any GI upset, recent illness, or rashes. She was a smoker, but denied any alcohol or drug use. Exam revealed a thin, well-developed female laying in bed in no apparent distress. Her temperature was 98.28F, pulse was 100, BP was 139/ 82, RR was 20, weight was 115 lbs., and height was 5 H 7 HH . HEENT exam revealed poor dentition, otherwise normal. Cardiac, lung, neck, and abdominal exams were normal. Musculoskeletal exam showed strength to be 5/5 in the upper extremities, 3/5 in the proximal lower extremities, 4/5 in distal lower extremities. A positive Trousseau's sign (carpopedal spasm) was noted upon inflation of BP cuff. DTRs were slightly brisk in all 4 extremities but no spasticity was noted. Otherwise, neurologic exam was normal. Skin exam showed no rashes. Laboratory evaluation revealed significant hypokalemia of 1.7 mmol/L (normal 3.5±5.0), plasma chloride of 94, plasma CO2 of 31, serum calcium of 7.4, serum magnesium of 1.3, and serum phosphorus of 3.3. Other electrolytes, BUN/Cr, and glucose were normal. Serum CPK was significantly elevated at 5,098 U/L (normal 24±170). Urine sodium was 177 mmol/L, urine potassium was 8 mmol/L, and 24 hour urine potassium was 14 mmol/L. MCV was 104 fL, folate level 3.3 ng/mL, and albumin 3.7 g/dL. Toxicology and diuretic screens were negative. The profound hypokalemia, hypokaliuria, macrocytic anemia, and hypoalbuminemia were consistent with the suspicion of a 18 dietary disorder; i.e, low intake vs. eating disorder. The patient consistently denied an eating disorder or distorted body image. Upon obtaining further dietary history, the patient's daily consumption of 5±6 L of Pepsi 1 stood out as an apparent etiology. The patient stated that she had been drinking caffeinated colas heavily for several years. Upon cessation of cola consumption and replacement with a total of over 820 meq of KCL, the patient's weakness improved. IMPLICATIONS/DISCUSSION: Colas and other caffeinated beverages have been reported to be causes of significant hypokalemia, likely due to caffeine toxicity and/or phosphatepotassium binding. Although a rare diagnosis, this case of cola induced myopathy was made by using fairly simple, bedside physician-patient discussion.

PAINFUL RASH. K. Kamjoo 1 ; 1 University of California, Los Angeles, Sylmar, CA (Tracking ID #76685) LEARNING OBJECTIVES: 1-To recognize the clinical presentation of sarcoidosis and Lo È fgren's syndrome. 2-To understand that sarcoid is a systemic disease with multi-organ involvement and 3-To discuss treatment modalities for sarcoid and sarcoid arthritis. CASE INFORMATION: A 24 year old male without significant past medical history presented to Emergency Department (ED) with complaint of painful rash over both legs for 2±3 weeks. Patient is an Argentinean exchange student who traveled to the US approx. six months prior to this presentation. Patient was seen at an outside clinic for the same complaint and was treated with Keflex and Ibuprofen without improvement. Patient reported that few days after appearance of rash; both of his ankles became swollen and painful. Although patient reported that walking was very painful, he denied any weakness or limitation of movement. In addition to the rash, patient admitted that he has been having night sweats and subjective fevers for the past couple of weeks. Patient also reported a slight dry cough. Initial vitals in ED were: temp of 38.2, blood pressure of 132/70, pulse of 95, and respiratory rate of 16. On physical exam patient appeared alert but in mild distress due to leg pain. Heart exam was regular sinus without any murmurs and lungs were clear to auscultation bilaterally. Abdomen was benign. Examination of skin revealed large nodules that were raised, red and tender to touch. Nodules were warm to touch and distributed randomly all over both legs. Both ankles had non-pitting edema but they had full range of motion. Ankles were tender to touch and passive range of motion was painful. Initial lab results showed a serum calcium level of 9.4 and a sedimentation rate of 47. Chest x-ray examination revealed bilateral hilar lymphadenopathy and EKG showed a normal sinus rhythm without any conduction abnormalities. Patient was subsequently admitted to hospital and placed in respiratory isolation. Patient had negative coccidiomycosis titers and ruled out for pulmonary Tuberculosis. HIV test was also negative. Patient remained clinically stable but continued to have a low-grade fever. CT scan of chest showed bilateral hilar and sub-carinal lymphadenopathy as well as multiple 1 cm nodules within lung fields. Subsequently, patient had bronchoscopy with biopsy and pathology report confirmed presence of non-caseating granulomatous lesions. Patient was started on 40 mg of prednisone per day and made a remarkable recovery. IMPLICATIONS/DISCUSSION: Sarcoidosis is a multi-system disorder of unknown cause characterized by a non-caseating granulomatous reaction in affected organs. Lo È fgren's syndrome is a variant of sarcoidosis in which acute sarcoidosis often presents with constitutional symptoms, polyarthritis, and erythema nodosum. The diagnosis of sarcoidosis should be based on a tissue biopsy, but a patient with typical Lo È fgren's syndrome may not need biopsy proof. Non-steroidal anti-inflammatory agents usually effectively alleviate sarcoid arthritis and joint symptoms associated with erythema nodosum. In severe acute arthritis and in chronic arthritis, corticosteroids may be required to control the symptoms. with a productive cough of white sputum and intermittent fevers, chills and night sweats for 1 month. She also complained of dizziness, weakness, a decreased appetite and a 5 pound weight loss over 4 weeks. She had been treated with antibiotics for 14 days which provided no relief. She denied visual changes, head pain, neck stiffness, chest pain, shortness of breath, dyspnea on exertion, nausea, vomiting, dysphagia, abdominal pain, diarrhea, urgency, dysuria, arthralgias or myalgias. Her medications included hydrochlorothiazide (HCTZ) and lisinopril. On physical exam, she appeared cachectic with dry mucous membranes and decreased skin turgor. Temperature was 38.4. Lung exam was clear bilaterally. Cardiac exam revealed a II/VI systolic murmur. There was no lymphadenopathy or skin rash. Abdominal exam revealed no masses or tenderness. She was hydrated and her HCTZ was held. She had multiple episodes of fever of up to 39.1. At the end of 7 days, her diagnostic testing revealed the following: normal CBC with differential; normal LFT's; 6 blood and 2 urine cultures were negative; Legionella antigen was negative; non-reactive PPD and a TSH of 2.6. Chest x-ray revealed biapical pleural thickening. ESR was 85. ANA, Rheumatoid factor (RF) and Anti-ds DNA were negative. Transthoracic echocardiogram (TTE) was negative for vegetation. Chest and abdominal CT scans revealed no significant findings. Bone marrow biopsy, aspirate and culture were negative. Bilateral temporal artery biopsies revealed severe temporal arteritis (TA). She was discharged on prednisone and her symptoms resolved after 1 week of therapy. IMPLICATIONS/DISCUSSION: FUO is defined as a temperature greater than 38.3 on several occasions for more than 3 weeks or after 1 week of thorough diagnostic testing performed in the out-or inpatient setting. Earlier studies reported that infections represented 41% of all cases. Collagen vascular diseases represented 30% and tumors represented 13%. Miscellaneous causes represented 2% and in 13% of cases the etiology was not identified. More recent studies reveal that infections are less common than multisystem disease and this trend was even more pronounced in patients over 70 years of age. A cost-effect approach in the elderly consists of confirmation of fever and a thorough history and physical exam. Laboratory analysis should consist of a CBC with differential, ESR, TSH, chemistry and liver panel, urine analysis and multiple blood and urine cultures. HIV, EBV, CMV, ANA and RF should be considered in certain cases. Stop all nonessential drugs. Imagining should include a TTE, chest and abdominal CT scans. A temporal artery biopsy should be considered if the ESR is more than 40 mm/hr, even in the absence of symptoms. Gallium scan for hidden abscesses and liver and bone marrow biopsies should be considered only in certain cases. Explorative laparotomy is a final resort. LEARNING OBJECTIVES: Introduction: Typhoid fever is a common disease in the developing countries.

Step-wise rising fever, bacteremia, diarrhea associated with abdominal pain and hepatosplenomegaly are the usual manifestations. We report a case of typhoid fever with sore throat as an integral part of the clinical picture. CASE INFORMATION: A 21-year-old immigrant male from Ecuador presented with a seven-day history of sore throat associated with a foreign body sensation and dysphagia for solid foods. Three days prior to presentation, in addition to his sorethroat, the patient complained of vomiting, diarrhea, mild abdominal discomfort, myalgias, fatigue and subjective fevers. On examination, his temperature was 94.68F with a pulse rate of 66 beats/minute. The oropharynx was markedly erythematous. The monospot test and rapid streptococcal screen were non-reactive. A diagnosis of acute viral syndrome with pharyngitis was made and he was treated symptomatically with Ibuprofen. He returned to the emergency department two days later with worsening sore throat, fever, new onset of low back pain, and mild abdominal discomfort with nausea. Physical examination revealed a temperature of 103.28F, pulse rate of 60 beats/minute, mild peri-umbilical tenderness and splenomegaly. The patient was hospitalized and started on intravenous fluids and oral Ciprofloxacin 750 mg twice daily. His fever subsided and he showed significant symptomatic improvement on antibiotic therapy. On the fourth day of hospitalization, blood cultures yielded Salmonella Typhi. He was discharged home on day five with two weeks of ciprofloxacin. IMPLICATIONS/DISCUSSION: Conclusion: Once considered an integral part of the symptomatology of typhoid fever, sore throat is infrequently reported, perhaps due to differences in causative strains, less emphasis on documentation of all symptoms and early and effective treatment in the antibiotic era. Physicians should be aware that typhoid fever could present as pharyngitis and should be considered especially in immigrants, to aid in early diagnosis and treatment. 

A 27 year old African American female with a past history of the human papilloma virus, gonorrhea, and chlamydia presented with two weeks of diffuse joint pains. The pain started in her knees and progressed sequentially to include her elbows, shoulders, back, and hips. Her associated symptoms were nausea, fever, and a sallow complexion. She denied any history of intravenous drug use, but did endorse a history of multiple sexual partners in the past. Physical exam was remarkable for a temperature of 38.3 C, scleral icterus, and jaundiced skin; However, there was no cardiac murmur or hepatosplenomegaly. Musculoskeletal exam revealed no joint effusions, warmth, erythma, or tenderness. A pelvic exam was normal with negative gonorrhea and chlamydia testing. Labs demonstrated a normal CBC with differential, and an erythrocyte sedimentation rate was 11; An antinuclear antibody was less than 1:40; Rhuematoid factor, hetrophile antibody, cytomegalovirus (CMV) IgM, and rapid plasma reagin tests were all negative; AST and ALT were elevated at 605 and 1303, respectively; Bilirubin was 3.3, alkaline phosphatase 204, and albumin 3.3. At this point, work up was initiated for acute hepatitis. While hepatitis A and C serologies were negative, hepatitis B surface antigen and anti-hepatitis B core antigen were positive. HIV testing was negative. A diagnosis of acute hepatitis B was made. It was presumed that the aquisition of hepatitis B in this patient was from sexual contact. Over the next 10 days her AST and ALT peaked at 4500 and 5500 respectively, bilirubin at 10, albumin decreased to 2.0, and INR was 1.9. Treatment was supportive in nature including fluids and pain control. At time of discharge her AST and ALT were trending down toward normal levels and her symptoms were resolving. She was educated about transmission of hepatitis B with attention to safe sex practices. IMPLICATIONS/DISCUSSION: Migratory polyarthralgia has a challenging and broad differential diagnosis. Infectious causes are many and include gonorrhea, syphilis, CMV, Epstein-Barr virus, Lyme disease, and bacterial endocarditis. Viral hepatits is a possible but uncommon infectious cause. Inflammatory causes are a major category and include rhuematoid arthritis, systemic lupus erythematosis, scleroderma, and polymyositis. Postinfectious causes include rheumatic fever and Reiter's syndrome. Crystalline diseases namely gout and psuedogout can also cause polyarthralgias. Joint aspiration and analysis is the key to diagnosis, however our patient had no joint effusions. With the advent of vaccination, acute hepatitis B virus (HBV) infection is now much less common in the United States. However, it remains a major global problem, particularly in developing countries. Signs and symptoms include malaise, fatigue, myalgias, anorexia, nausea, vomiting, abdominal pain, fever, and jaundice. Migratory polyarthralgia, particularly with a benign joint examination, constitutes an atypical presentation of acute hepatitis B. The incubation period for HBV is 1 to 6 months. While 30% of patients who acquire HBV present with acute symptoms, the majority of patients remain asymptomatic with anicteric hepatitis. Ninety percent of cases of acute hepatitis B clear infection and resolve symptoms within 6 months. They remain asymptomatic carriers of HBV. This is demonstrated by disappearance of the heptitis B surface antigen and appearance of the hepatitis B surface antibody. Less than 1% of patients develop acute fulminant hepatitis. The potential outcome of this subgroup is poor and therefore close follow up of synthetic function is warranted during the initial period. Approximately 5 to 10% progress to eventually develop symptomatic chronic HBV infection. Sequelae can include cirrhosis, hepatic decompensation, and hepatocellular carcinoma. Diagnosis of acute HBV is confirmed with serology, and quantification can be done with the polymerase chain reaction. Treatment is mainly supportive in nature, and patients should be educated about disease transmission. Antiviral therapy is not currently recommended or approved for the treatment of acute HBV.

A. Kapoor 1 , J. Hefner 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #76642) LEARNING OBJECTIVES: 1.) Recognize an unusual cause of persistent hypokalemia; 2.) Diagnose an atypical presentation of Cushing syndrome; 3.) Recognize the clinical presentation of an ectopic ACTH-producing tumor. CASE INFORMATION: A 77-year-old male with hypertension and Type II diabetes mellitus presented with a 2 month history of fatigue and weakness. He subsequently developed a gait dysfunction and had frequent falls. Outpatient potassium (K) was 1.9 and he was admitted for management of hypokalemia. Physical exam revealed a BP of 180/90, facial plethora and bilateral diffuse rales at the bases of the lungs. Proximal muscle strength was 4/5 in the upper and 3/5 in the lower extremities. Distal strength was 5/5. No moon facies, buffalo hump or abdominal striae were found. His K remained low despite aggressive replacement and secondary causes were investigated. Results of diagnostic testing included a urinary Na 17, K 52, pH 6 (4.8±8), serum Na 140, Cl 95, HCO3 40, BUN 28, Cr 1.4, renin 0.6 (<5 mcg/ml) and aldosterone 5.7 (2±9 mcg/ml). Urinary metanephrines were normal. Cortisol at 8 am was 100 (7±20 mcg/ml) and ACTH 380 (9±52 pg/ml). Post high-dose (8mg) dexamethasone suppression test (DST) cortisol was 118 and ACTH was 126 (2±8 pg/ml). FSH, LH, prolactin and IGF-1 were normal. Brain MRI revealed a normal sized pituitary. Chest CT showed pleural effusions, no masses or lymphadenopathy. Abdominal CT revealed a 3 cm renal mass and bilateral adrenal hypertrophy. Biopsy of the renal mass showed poorly differentiated small cell carcinoma (SCC). Treatment with ketoconazole failed to suppress his cortisol. The patient decompensated and expired. Autopsy revealed numerous nodules in the liver, the right renal mass with focal hemorrhage and no lung masses. Pathology revealed SCC of renal origin with metastasis to the liver. IMPLICATIONS/DISCUSSION: Cushing syndrome is an unusual cause of hypokalemia. Other causes include primary or secondary hyperaldosteronism, Type 2 renal tubular acidosis, Bartter syndrome, Liddle syndrome, diuretic use and VIPoma. Patients with ectopic Cushing secondary to carcinomas often lack the clinical manifestations associated with classic Cushing syndrome±the centripetal fat distribution, moon facies and striae. The metabolic abnormalities, however, are more common in ectopic ACTH syndrome namely hypokalemia, metabolic alkalosis, excessively high cortisol and elevated ACTH levels. Differentiation of ectopic from pituitary dependent Cushing is made by non-suppression of cortisol with the 8 mg DST. There have been reported cases of ectopic ACTH with lung SCC, bronchial carcinoid, medullary carcinoma of the thyroid, gastrointestinal and prostatic adenocarcinoma and pheochromocytoma. However, there are no reported cases of SCC of renal origin causing ectopic ACTH production as was present in our patient.

A CATASTROPHIC COMPLICATION OF GIANT CELL ARTERITIS. P. Kapoor 1 , S. Parikh 1 , P. Radhakrishnan 1 , M. Yungbluth 1 , D. John 1 ; 1 St. Francis Hospital, Evanston, IL (Tracking ID #75985) LEARNING OBJECTIVES: 1. Awareness of the association of aortic aneurysm (AA) with giant cell arteritis (GCA) will aid prompt recognition and therapy. 2. To highlight the significance of using Chest XRay (CXR) as a screening modality in patients of GCA for timely detection of thoracic AA.

A 75-year-old male presented with acute, severe right upper quadrant (RUQ) pain, radiating to the right shoulder and associated with nausea and vomiting. He denied any fever, chest pain, shortness of breath, change in bowel habits or similar episodes in the past. He had a history of coronary artery disease, well-controlled hypertension and biopsy-proven GCA, diagnosed 15 months ago. Physical examination: afebrile;pulses: 86/min, regular and symmetric; BP: 170/108 mm;tenderness in the RUQ with palpable gall bladder 4 cm below the right costal margin; an ejection systolic murmur in the aortic area. The rest of the physical examination was essentially unremarkable. Laboratory data: WBC-10000, Hb-13.8 and platelets-251,000. The CT scan of abdomen was suggestive of acute cholecystitis. A dissection of the superior mesenteric artery (SMA) was also noted. CXR showed aneurysm of ascending aorta. CT scan of thorax showed a Stanford Type A aortic dissection (AD) with aneursymal dilation of 7 cm. Communication of the true and false lumen suggested chronicity (see figure) . After stabilization of BP, he underwent an emergency laparoscopic cholecystectomy which led to a resolution of his abdominal pain. Subsequently, he was referred for an elective repair of his asymptomatic, chronic aortic dissection. IMPLICATIONS/DISCUSSION: Horton's syndrome or GCA is the commonest primary systemic vasculitis in the United States, associated with diverse manifestations and outcomes. The true incidence of aortic involvement is unknown, but is estimated to be 3±15 %. Patients with giant cell aortitis may be asymptomatic or may present with aortic arch syndrome, dilation of aorta, aortic aneurysm, AD or aortic incompetence. Although, in this patient AD may well be attributed to atherosclerosis,the history of GCA and segmental involvement of ascending aorta and SMA implicate GCA as a predisposing condition.A high incidence of thoracic aortic aneurysm has led Evans et al to recommend annual CXR, including lateral views in patients of GCA. Since the diagnosis of GCA is commonly made by the internists, awareness of it's possible complications helps us manage these patients better. A 37 year old Mandarin speaking woman with no known PMH presented with chest palpitations for 6 months. Her history was obtained in a crowded, noisy ER through a telephone translator, with her husband as a middle translator. She states having symptoms for over 6 months with acute decompensation over the last 2 months involving constant fast heart rate, swelling in her face, abdomen, and extremities for 2 months, dyspnea when walking 2±3 blocks, a 20 lb unintentional weight loss, poor concentration, and constipation. She went to a doctor 1 month ago and was told she has a thyroid problem, but has not been taking the prescribed medications. More than 10 years ago in China, she had problems with her thyroid and was given Western medications for 6 months with improvements. Otherwise, review of systems was unremarkable. On exam, her pulse was irregular, atrial fibrillation, at 125±145, BP 98/64. She was anicteric with swollen eyelids, no proptosis. She had an enlarged thyroid, JVD, a hyperdynamic precordium, no heart murmurs, a distended abdomen, and non-pitting edema in all extremities. Lab studies showed a mild transaminitis, negative hepatitis serologies, and positive thyroid stimulating antibodies. She was diagnosed with Graves disease. Echocardiography showed severe tricuspid regurgitation and right heart failure without evidence of left sided dysfunction, pulmonary artery hypertension or septal defects. Her atrial fibrillation was treated with beta blockers and anticoagulation, and she was scheduled for repeat echocardiogram in 2 months to evaluate for valve disease that may be contributing to her right sided failure. She would like more children, so she opted for medical therapy with propythiouracil to treat her hyperthyroidism and would consider radioactive iodide or surgical therapy after her thyroid disease is under control. IMPLICATIONS/DISCUSSION: 1. Obtaining a complete history in non-English speaking patients can be difficult. Despite seeing a private doctor, this patient came to the ER without her primary doctor's support, without her medications, and without the ability to communicate with hospital doctors. Studies have shown that intepreter services increase cost-effectiveness and quality of care as well as patient understanding and participation in healthcare, despite potential increases in the time and resources to provide such services. 2. Recurrent hyperthyroidism, most commonly due to Grave's disease, is treated similarly to the initial episode. Anti-thyroid medications are the drug of choice in pregnant women and are not known to effect reproductivity. Radioactive iodide is contraindicated in pregnancy, although has been shown to have no effect on reproductivity in the long term. Surgery is effective, although has no advantages and has been associated with increased fetal losses if done during pregnancies. A 74 year old male was brought by his friend to the emergency room with a four week history of gradually progressive shortness of breath that began 2±3 days after dual-chamber pacemaker placement for Mobitz II heart block and symptomatic bradycardia. The procedure was without any immediate complications. CXR post-precodure was negative for pneumothorax. He currently denied chest pain, cough, fevers, chills, sweats, lightheadedness, or dizziness. PMH was significant for, in addition to Mobitz II heart block, coronary artery disease, severe aortic stenosis and hypertension. Medications included felodipine 10 mg PO qd, simvastatin 10 mg PO qd, and lisinopril 20 mg PO qd. He had a remote history of tobacco use and was a former steel mill worker. On physical examination, VS: HR 105, RR 26, BP 150/90, pulse ox 92% (on room air). Pertinent findings included no JVD, a II/VI SEM at the right upper sternal border radiating to carotid arteries, laterally displaced PMI, decreased breath sounds on the left 2/3 up the lung fields, no organomegaly and 1+ pretibial edema. CXR showed a free flowing large left pleural effusion. The patient was admitted to the hospital and a thoracentesis was performed from which serosanguinous fluid was obtained. CT of the chest demonstrated a perforated right ventricle from the pacer wire. Surgical repair was successful but the patient had a very complicated postoperative course and expired. IMPLICATIONS/DISCUSSION: Pacemaker insertion is a relatively common and safe procedure and can be lifesaving. Ventricular rupture is a rare, albeit potentially serious, complication. The elderly, in whom most pacemakers are inserted, are at increased risk of complications. The Pacemaker Selection in the Elderly (PASE) study, a prospective multicenter trial involving 407 patients age 65 years and older, documented a 6.1% complication rate; 4.4% of patients required a repeat procedure. The most common complications were lead dislodgement (2.2%), pneumothorax (2.0%and observed only in those with subclavian venous access) and cardiac perforations (0.98%). Most perforations occur intraoperatively and rarely cause symptoms. However, as in our patient, serious complications, including death, have been reported postoperatively. Complications of pacemaker insertion may masquerade as other less serious entities with symptoms of dyspnea, chest pain, fever and weakness. It is paramount that internists be alert to the potential serious complications of cardiac rupture and pneumothorax in the patient presenting with these symptoms postprocedure. Symptomatic patients require surgical intervention. A 53 year-old Puerto Rican male presents with a chief complaint of two years of increasing dyspnea on exertion. Past medical history was notable for multiple episodes of pneumonia. Although the patient had been successfully treated as an outpatient during these episodes with oral antibiotics, his chronic baseline dyspnea and decreasing exercise tolerance continued to worsen. For one of these exacerbations, the patient was admitted to the hospital, where physical exam revealed nystagmus, poor visual acuity, oculocutaneous albinism, and a bleeding diathesis. Radiological studies revealed bilateral lower lobe infiltrates and diffuse pulmonary honeycombing fibrosis. The patient improved following a ten-day course of IV cefotaxime, gentamycin, and chest physical therapy. IMPLICATIONS/DISCUSSION: The combination of oculocutaneous albinism, a bleeding diathesis, and pulmonary fibrosis in this Puerto Rican patient raised the suspicion for Hermansky-Pudlak Syndrome. HPS is an inherited disease which results in a platelet storage pool defect and lysosomal accumulation of a substance called ceroid lipfuscin. HPS is an autosomal recessive syndrome found primarily in individuals from the northwestern quadrant of Puerto Rico. Patients have legal blindness, nystagmus, iris transillumination, foveal hypoplasia, decreased number of melanocytes, pulmonary fibrosis, renal disease and granulomatous enteropathic disease. Lab studies in patients with HPS may show an increased bleeding time with a therapeutic response to desmopressin, decreased bone density, and genetic testing showing a mutation on the HPS1 gene on chromosome 10q23. The most accurate diagnosis, however, is made by a pathognomic platelet morphology diagnosed only by electron microscopy. Management consists of recognizing the disease, having a lower threshold for admitting individuals for inpatient management, and administration of immunosuppressants and steroids. Current trials of a test drug called pirfenidone are being conducted and offer patients some hope for a treatment. Back to our patient: A careful history taking revealed that the patient presented above had all of the above manifestations, even decades prior to his official diagnosis being made. Management of this patient's disease ultimately consisted of various trials of steroids, interferon, and methotrexate. While the inpatient stay focused primarily on his pulmonary pathology, outpatient management consisted of patient education to minimize complications of the disease and carefully orchestrated care with numerous specialists. week history of progressive pain and swelling in his left index finger after an attempt to straighten an iron pipe with this left hand. Past medical history was significant for a similar episode involving his right index finger after trauma that resolved with symptomatic treatment. Patient had a 50pack year history of smoking. The rest of his review of systems was unremarkable. Physical examination was unremarkable except for a swollen and tender left index finger with a gangrenous tip. The left ulnar pulse was absent. His radial pulses were intact in both extremities. Laboratory data including ANA and sedimentation rate were within normal limits. An arteriogram of the left upper extremity revealed thrombosis of the distal ulnar artery and occlusion of digital arteries of the second digit that were thought to be secondary to embolic events from the ulnar artery thrombus. Duplex ultrasound also revealed a thrombosed pseudoaneurysm in the left ulnar artery at the hypothenar eminence. Diagnosis of Hypothenar Hammer Syndrome (HHS) was made. IMPLICATIONS/DISCUSSION: HHS is a rare clinical entity that results from repetitive palmar trauma leading to damage of the ulnar artery as it passes over the hammate bone. The syndrome usually manifests as unilateral digital ischemia caused by embolic digital artery occlusion from the thrombosed palmar ulnar artery. It is predominantly seen in males around the age of 40. In a small study of 21 patients, 12 out of 13 who had arteriography of both upper extremities had bilateral palmar ulnar disease (1). Diagnosis is made on clinical features and confirmed by angiography that shows a palmar ulnar artery abnormality and digital artery occlusion. Treatment may include surgery involving excision of abnormal palmar ulnar artery segment. LEARNING OBJECTIVES: To recognize and manage pustular psoriasis and to differentiate it from other causes of erythroderma. CASE INFORMATION: DP is a 58-year-old African American male who presented with an exfoliative erythroderma and pustules in the palmar-plantar areas that had coalesced to form`l akes of pus.'' The patient noted a similar but milder eruption 3 months earlier in which he was treated at another facility with oral prednisone with some improvement. He reported that the pustules had started on his hands, progressing rapidly over several days to affect the entire body. Erosions later appeared in the mouth. He complained of an intense pruritus and burning sensation along with a fetid odor. At the time of presentation he was noted to be febrile with a leukocytosis. A skin biopsy showed spongiform pustules in the upper epidermis with numerous PMNs present. Inpatient management included a combination of actretin, IV vancomycin, and topical mid-potency steroids, with rapid improvement in the patient's condition. IMPLICATIONS/DISCUSSION: A presentation of erythroderma should prompt the physician to consider pustular psoriasis, pemphigus foliaceus, pityriasis rubra pilaris, underlying leukemia/lymphoma, severe atopic dermatitis, ichthyoses, drug induced erythroderma, diffuse seborrheic dermatitis, scabies, and staphylococcal scalded skin. Pustular psoriasis can be differentiated by sudden onset of acral pustular lesions, fever, intense pruritis, and occasionally, hypocalcemia and mucous membrane lesions. Patients will often have a personal or family history of plaque psoriasis and/or psoriatic arthritis. Treatment of choice is acitretin (a second generation retinoid). Topical steroids are often helpful, but systemic steroids should be avoided.

WITH KLIPPEL-TRENAUNAY-WEBER SYNDROME. M. Kennedy 1 , C.V. Mueller 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #77195) LEARNING OBJECTIVES: 1) Learn about the vascular malformations seen in Klippel-Trenaunay-Weber Syndrome. CASE INFORMATION: A 25 yo Caucasian male originally presented to an outside hospital with bright red blood per rectum. He denied associated abdominal pain, nausea, vomiting, fever or prior history of rectal bleeding. Initial systolic blood pressures were in the 80-90's with a heart rate in the 130's. Work up at the outside hospital included flexible sigmoidoscopy that revealed nonbleeding internal hemorrhoids, a negative tagged RBC scan and an unremarkable CT of the abdomen. Upon transfer to our facility, he was hemodynamically stable, but found to have a hemoglobin of 7.5 with a baseline of 13.5. The morning after admission, the patient developed massive hematochezia associated with diaphoresis and tachycardia. He was urgently sent for tagged RBC scan that showed distal ileal bleeding. Subsequent mesenteric angiography did not identify any active bleeding or vascular malformation. The patient again decompensated and was taken for exploratory laparotomy that revealed bleeding ileal and colonic varices. He underwent ileocecectomy without complications and had no further episodes of bleeding. He required a total of 20 units of PRBC's during his hospitalization. IMPLICATIONS/DISCUSSION: KTWS is classically described as a venous monoangiodysplasia, but is actually associated with a variety of vascular malformations including: subcutaneous hemangiomas, cavernous hemangiomas, AV fistulas, deep vein malformations and/or aplasias, varices and a variety of lymphatic abnormalities. Vascular malformations may involve visceral organs such as the bowel, liver, kidneys, and lungs and can, uncommonly, cause complications in those organs. Treatment of KTWS is supportive and/or cosmetic unless orthopedic or bleeding complications arise, at which point surgery is generally indicated.

LEARNING OBJECTIVES: 1) Consider the potential for a fatal overdose of Metformin when treating diabetic patients who are at risk of commiting suicide. 2) Recognize the constellation of signs that are consistent with a Metformin overdose.

3) Recognize the need to quickly and aggressively treat a Metformin overdose and its medical consequences. CASE INFORMATION: A 42 year-old woman with a history of diabetes, hypertension and schizoaffective disorder was found obtunded in her apartment and admitted to the MICU. She had recently been hospitalized for suicidal ideation. Empty pill bottles of a benzodiazepene, an atypical antipsychotic, a SSRI and Metformin were found. Six hours after admission, the patient developed lactic acidosisand a severe sepsis-like syndrome consistent with Metformin overdose. She subsequently became critically-ill, and had a clinical course which included severe ARDS and anuric renal failure. Support was withdrawn at the request of her family following a prolonged course of aggressive treatment. IMPLICATIONS/DISCUSSION: Metformin is commonly used in primary care and its potential for lethal side effects is well known in the setting of medical illness. This case demonstrates how Metformin also has potential for great harm in the setting of an overdose. Physicians should be aware of the risks of prescribing Metformin to diabetic patients with depression or a history of impulsive behavior. A 49 year old female with recent diagnosis of pulmonary embolism due to oral contraceptive use presented with acute onset of left sided abdominal pain associated with nausea but no vomiting, diarrhea or constipation or changes in urinary habits. Patient's medications were warfarin, ibuprofen prn, home O2 and amitryptiline. Had 25 pack year smoking history. On examination, she seemed to be in moderate distress with severe tenderness on left side of midline from epigastrium to suprapubic region, worse with any movement associated with mild fever. Vital signs were stable otherwise. Stools hemoccult negative. Lab studies revealed a wbc count of 12,700, Hb of 10.7, noted to be reduced from previous admission. Creatinine 0.7 mg/dl, lipase 94 mg/dl, PT 23.1, INR 3.73 with normal liver function tests and normal UA. Contrast enhanced CT revealed acute hematoma of left rectus sheath, 20cm  6cm with active bleeding. Patient's Hb further dropped so eventually transfused, coumadin stopped and surgery consulted. They suggested conservative treatment with analgesia and rest and later on, IVC filter placement. Repeat CT Scan showed stable hematoma. Patient clinically better with stable Hb. So, again started on low dose coumadin and sent home with caution not to smoke and avoid trauma as on further questioning, eventually, patient provided history of fall. IMPLICATIONS/DISCUSSION: Left sided abdominal pain and fever can be mistaken for number of causes of acute diseases of abdomen. But, due to advent of CT, an unusual diagnosis is relatively easy to make. But, since rectus sheath hematoma is one of the reported complications of anticoagulation therapy, this diagnosis should always be kept in mind. Once diagnosis is established and if this hematoma is not causing severe symptoms, the condition can be managed nonoperatively with bed rest and analgesics. Ideally, anticoagulation should be discontinued. It is rarely necessary to reverse the coagulation defect if operation is not undertaken. As in our case, patient was clinically improved so it was decided to manage her conservatively and avoid surgery. She was restarted on anticoagulation because risk of pulmonary embolism is greater than hematoma. It was made sure to counsel her about any trauma as it increases risk of hematomas in future. Patient continued to do well on further follow ups.

M. Khalil 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73745) LEARNING OBJECTIVES: 1. To recognize ascites as a complication of eosinophilic gastroenteritis (EG) 2. To diagnose and treat EG. CASE INFORMATION: A 50 year-old female with no significant PMH presented with a 2 month history of epigastric pain that was associated with nausea and decreased appetite. She reported the pain to be constant and exacerbated with food, but mildly relieved with a bowel movement. She denied any vomiting, melena, hematochezia, fever, chills, recent travel, change in diet or alcohol abuse. Two weeks prior to admission, she developed non-bloody, watery diarrhea, increased abdominal girth, and 12 lb. weight gain, despite the poor appetite. Outpatient evaluation with abdominal ultrasound was unremarkable and an upper GI series revealed dysmotility of the lower esophagus with tertiary contractions. Treatment with rabeprazole provided minimal relief. Physical examination upon admission was remarkable for a mildly distended and diffusely tender abdomen with positive shifting dullness but no rebound, guarding or organomegaly. The remainder of physical exam was normal including heme negative stool. Lab work was significant for WBC of 14,000 with 30% eosinophils. Liver function tests were normal. Serum albumin was 2.4 and ascitic fluid analysis showed: pH 7.31, albumin 1.8, negative cytology, and WBC of 4700 with 96% eosinophils. Stool culture and sensitivity, ova and parasites were negative. Further workup with abdominal ultrasound with Doppler showed patent vessel and normal direction of flow. Upper endoscopy revealed erythema of the antrum. Colonoscopy was normal. CT scan of the abdomen and pelvis showed diffusè`L akes of pus'' small bowel thickening without fat stranding and moderate ascites. Trans-vaginal ultrasound was negative for ovarian mass. Bone marrow biopsy was normal. The patient refused surgical bowel biopsy and diagnosis of EG was established on the basis of exclusion. She was started on oral dose of prednisone for 6 weeks and discharged to home. Follow up visit and blood work showed 0% eosinophils, resolution of ascites, resolution ofabdominal pain, and good appetite. IMPLICATIONS/DISCUSSION: EG is an uncommon disorder characterized by gastrointestinal symptoms, blood eosinophilia, and eosinophilic infiltration of the gastrointestinal wall. The signs and symptoms of EG are related to the layer and extent of the bowel involved with eosinophilic infiltration. Patients with subserosal infiltration may develop eosinophilc ascites. The diagnosis of EG is confirmed by a full thickness biopsy of the bowel in the absence of intestinal parasitic infection. Treatment of EG is empiric because no prospective, randomized clinical trials are available to guide treatment. Prednisone (20 to 40 mg/day) is recommended for two weeks and should be tapered over the next two weeks. Improvement usually occurs within two weeks of therapy. Despite the rarity of EG, it should be suspected in a patient with any GI symptoms associated with peripheral eosinophilia because this treatable disease can disguise itself as the irritable bowel syndrome. LEARNING OBJECTIVES: 1) Recognize that pulmonary hypertension is not uncommon patients with SLE; 2) Recognize that primary pulmonary hypertension in SLE patients often presents earlier than pulmonary hypertension from a secondary cause. CASE INFORMATION: A 21-year-old woman was transferred to our hospital for management of her pulmonary hypertension (PHT) and systemic lupus erythematosus (SLE). She initially presented a year ago with progressive cough and pleuritic-type chest pain. 8 months prior to admission, she underwent an echocardiogram which revealed a pulmonary artery pressure (PAP) of 27 mm Hg. Four months later, she was admitted to a community hospital for congestive heart failure and was found to have positive anti-Smith, antiphospholipidand anti-nuclear antibodies, and was diagnosed with SLE. Her symptoms gradually progressed to dyspnea on exertion, paroxysmal nocturnal dyspnea and Raynaud's phenomenon. She was subsequently readmitted to that hospital 2 weeks prior to transfer to us for worsening of her symptoms. There, she had a generalized seizure and was initiated on plasmapheresis treatment. Examination revealed a thin, anxious lady in mild dyspnea and an obvious malar rash. Cardiac auscultation revealed a loud and palpable P2, and a II/VI systolic murmur at the tricuspid area. She had a non-tender hepatomegaly and mild bilateral pedal edema. Echocardiogram revealed a PAP of 76 mm Hg, with evidence of right heart enlargement and mild tricuspid regurgitation. A chest CT scan with angiography and a ventilation-perfusion scan showed no signs of a pulmonary embolism. A right heart catheterization was done as well showing moderate PHT and a moderate response to epoprostenol challenge. Workup for lupus cerebritis was negative. She was initiated on prednisone and Cytoxan for SLE. Plasmapheresis was discontinued. Diltiazem, Valsartan and Warfarin were initiated to control her pulmonary hypertension. She tolerated the medications well and was discharged with outpatient follow-up, with the consideration of using epoprostenol in the future should her condition worsen. IMPLICATIONS/DISCUSSION: Prevalence of PHT in SLE ranges from 5% to 14%. A third of SLE patients have positive antiphospholipid antibodies, although the significance of this in the development of PHT is unknown. In one study of SLE patients, 5.9% were found to have pulmonary hypertension, of which 48% of them had no identifiable cause, the rest found to have a secondary cause. For the subgroup with secondary hypertension, 50% of them were due to valvular abnormalities. The primary pulmonary hypertension tended to present far earlier after diagnosis of the SLE compared to secondary PHT, 8.8 versus 43.2 months. Raynaud's phenomenon in secondary hypertension is associated with a more severe pulmonary artery pressure. These patients seem to respond to epoprostenol therapy although there have been documented cases of fatal thrombocytopenia. year-old female with rheumatoid arthritis, hypertension, and seizure disorder presented with two days of hematuria. She denied fevers, dysuria, urinary frequency, headaches, visual changes, or cough. Her last seizure was two weeks prior to presentation. Medications included gabapentin, phenytoin, methotrexate, and amlodipine. There was no fever and her physical examination was otherwise negative for lymphadenopathy, hepatosplenomegaly or petechiae/purpura. Initial workup revealed a platelet count of 7,000, H/H of 7.3/24, WBC of 8.2, LDH of 900, and Cr of 3.5. Peripheral smear demonstrated schistocytosis. The patient was diagnosed with TTP-HUS and began daily plasmapheresis and prednisone, during which her platelet count improved to 130,000 and her LDH normalized. She was discharged to continue outpatient pheresis but was readmitted one week later with fever (1038 F) and a platelet count of 78,000. She was begun on plasmapheresis with cryoprecipitate-poor plasma, vincristine, and steroids. She responded well; her pheresis was decreased to every other day and prednisone was tapered. She was discharged with a platelet count of 398,000 to continue outpatient pheresis and vincristine, which were discontinued after one month. One month later, the patient had a platelet count of 70,000, LDH of 1,186, and schistocytes on peripheral smear. Plasmapheresis and prednisone were restarted, and a splenectomy was performed. Discharge platelet count was 199,000. Two weeks later, her platelet count was 57,000. Pheresis and vincristine were restarted with good response. IMPLICATIONS/DISCUSSION: TTP and HUS are diseases with abnormalities in multiple systems. Classically, TTP is described as having more severe neurologic disease, whereas HUS has more of a renal component. Clinically, however, patients are described as having TTP-HUS because most present with the same symptoms, have identical pathologic changes, and receive the same treatment. The classic pentad of thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, renal abnormalities and fever is present in few patients. The diagnosis is made primarily by the presence of thrombocytopenia and microangiopathic hemolytic anemia. The etiology is a deficiency of von Willebrand factor (vWF) cleaving protease, which results in the accumulation of unusually large vWF multimers, causing platelet aggregation. Causes of TTP-HUS include E. coli 0157:H7 and medications such as ticlopidine, cyclosporine, and quinine. Most adult cases, however, are idiopathic. Treatment is plasmapheresis, the mechanism of which is not completely understood. 10 to 20% of patients have an incomplete response; steroids, vincristine or IVIG can be added in these cases, but are not alternatives to pheresis. Some studies show improvement with splenectomy, especially in conjunction with pheresis and steroids. 30 to 50% of patients have exacerbations of thrombocytopenia and hemolysis when pheresis is tapered. Relapse is defined as recurrence after 30 symptom-free days without treatment. Both are treated with reinstitution of daily pheresis. It is essential that physicians involved in the care of the patient with TTP-HUS recognize that many patients may have worsening disease with tapering of pheresis and to be aware of alternate life-saving treatments if this occurs. year-old female presented with 4 weeks of malaise, a dry cough, and recent high fevers. She also had night sweats for the 6 months since she started hormone replacement therapy. She had no pets and no recent travel history. Though exposed to tuberculosis as a child, she had never been tested or treated for it. She had begun minocycline just over a month earlier for rosacea and was on loratidine for seasonal allergies. She did not drink alcohol and quit smoking 5 years prior. Physical exam was notable for high fever, tachypnea, pulse oximetry of 96% on room air, inspiratory crackles at the right base and dullness at the left base. Labwork: WBC 15.2 with 84% neutrophils; blood eosinophilia increased over several days to 15%. ESR was 70. Chest radiograph showed small bilateral effusions, no cardiomegaly, and bilateral, peripheral, apical alveolar infiltrates. PPD was negative. Her fevers persisted and the left pleural effusion increased on intial therapy for community-acquired pneumonia. The effusion was transudative, with 1755 WBCs, 12% neutrophils and 10% eosinophils. A bronchoalveolar lavage (BAL) and transbronchial biopsies were performed; BAL fluid contained 63% eosinophils and biopsies revealed focal aggregates of eosinophils around the airways, consistent with eosinophilic pneumonia. Oral prednisone was started and both symptoms and eosinophilia resolved 48 hours after her first steroid dose. IMPLICATIONS/DISCUSSION: EP is characterized by eosinophilic pulmonary infiltrates. It presents as an acute febrile illness with dyspnea, night sweats, weight loss, dry cough, crackles or wheezing on lung exam, increasing blood eosinophilia and bilateral, peripheral patchy infiltrates on chest radiograph. The ESR is often elevated. Etiologies include common medications, including minocycline, parasitic infections, HIV, and fungal infections. A high index of suspicion, confirmed by BAL fluid eosinophilia and diffuse eosinophilic infiltration of the lung on biopsy, leads to the diagnosis. The response to steroids is dramatic, as was seen in our patient, with symptoms, eosinophilia, and lung infiltrates decreasing within 48 hours. Treatment is continued for 3 months to prevent relapses, which respond to re-intitiation of steroids.

A POTENTIAL BLOOD DONOR. J. Kimberly 1 , R. Watkins 2 ; 1 Wake Forest University Baptist Medical Center, Winston-Salem, NC; 2 Wake Forest University, Winston-Salem, NC (Tracking ID #76222) LEARNING OBJECTIVES: 1) Be able to counsel patients with evidence of infection with HTLV-I and 2) appreciate associated diseases. CASE INFORMATION: A 43 year old African American female with a history of hypertension, diabetes, and treated syphillis presents to clinic reporting that she fears she may have contracted HIV disease. She recently donated blood and subsequently received a letter stating she could no longer donate blood``because of an infection like AIDS.'' The patient presented the letter which notified her of the presence of HTLV-I/II antibodies with Western Blot confirming HTLV-I infection. ELISA for HIV 1 and 2 was performed and was negative. The patient was initially fearful and had many questions regarding HTLV-I infection: How did she get infected and was it sexually transmissible or contagious via other routes? Would she develop immunosuppression similar to that seen with HIV disease? Were there any other possible adverse effects on her health? IMPLICATIONS/DISCUSSION: HTLV-I is a retrovirus endemic in parts of Japan with other clusters of high prevalence including the southeastern US. The virus is transmitted by three known routes: 1) from mother to child, especially through breast feeding, 2) through sexual activity, and 3) through blood, either from contaminated needles or transfusion. In areas where HTLV-I is endemic, many inflammatory and autoimmune diseases have been attributed to the virus though causation has only been shown for two diseases. HTLV-I is clearly linked to adult T-cell leukemia/lymphoma (ATL), classically an aggressive, usually deadly, hematogenous malignancy characterized by rapid progression of skin lesions, pneumonitis, hypercalcemia, and lymphocytosis. The second disease with a clear association with HTLV-I infection is tropic spastic parapesis or HTLV-I-associated myelopathy (HAM) which, unlike ATL, is characterized by an insidious onset with symptoms often including stiffness or weakness in one or both legs, back pain, urinary incontinence, and mild sensory changes. Onethird of patients are bedridden by ten years. Both ATL and HAM occur in 2-5% of HTLVinfected patients. ATL is slightly more common in infected males and usually occurs after 20-30 years of infection whereas HAM is more prevalent among females and can occur just a few years after infection. More than 95% of patients with ATL and HAM have evidence of HTLV-I infection. The patient under discussion was educated about the nature of HTLV-1 and how it differed from HIV, and counselled to practice``safer sex'', avoid donating blood, and, should she become pregnant, avoid breast feeding. She was also informed of the risk, albeit a fairly low one, of ATL and HAM. 2) Identify the diagnostic criteria for eosinophilic gastroenteritis.

3) Understand the management and prognosis of eosinophilic gastroenteritis. CASE INFORMATION: A 38 year-old woman presented to the ER with vomiting and diarrhea for four weeks. She experienced 6-8 watery, non-bloody stools per day; vomiting after consuming any food or liquid; and a``pulling sensation'' across the lower abdomen. One week after the onset of symptoms the patient was admitted to the hospital, rehydrated, and discharged with a diagnosis of acute gastroenteritis. The symptoms worsened soon after discharge, and the patient was readmitted to the hospital. Evaluation included routine stool cultures and ova and parasites. The patient was treated empirically with levofloxacin and metronidazole and was discharged home. Stool cultures were later found to be negative. The patient's symptoms quickly worsened and she presented again to the ER. Past medical history was remarkable for asthma and lactose intolerance. On physical examination, BP = 115/62, P = 110, and T = 99.18F. Abdominal examination revealed a moderately distended abdomen with shifting dullness and mild tenderness to palpation in the upper abdomen. The remainder of the examination was unremarkable. The white blood cell count was 15,600 with 55.3% eosinophils; the hemoglobin was 8.9. CT of the chest, abdomen, and pelvis revealed a thickened terminal ileum and cecum, ascites, and bilateral small pleural effusions. Paracentesis was performed. The peritoneal fluid revealed 1,920 white blood cells with 3 neutrophils, 12 lymphocytes, and 85 eosinophils. Ascites fluid albumin was 3.3; the serum-ascites albumin gradient was 1.2. Upper and lower endoscopy revealed only melanosis coli. Biopsy of the duodenal mucosa revealed lymphocytic and eosinophilic infiltration. The patient was treated with prednisone. Her symptoms improved and she was discharged home. IMPLICATIONS/DISCUSSION: Eosinophilic Gastroenteritis (EG) is a rare disease whose etiology is unknown, though it may be a Type I hypersensitivity reaction. Patients with EG present a range of symptoms from nausea, vomiting, and diarrhea, to ascites and bowel obstruction. The symptom complex is determined by the degree of eosinophilic infiltration of the gastrointestinal tract. The diagnosis of eosinophilic gastroenteritis requires the presence of gastrointestinal symptoms, eosinophilic infiltration of one or more areas of the gastrointestinal tract on biopsy, absence of eosinophilic involvement of multiple organs outside the gastrointestinal tract, and absence of parasitic infection. Eosinophilic gastroenteritis without ascites is treated with cromolyn; the presence of ascites requires glucocorticoid treatment. More than 90% of patients respond quickly to treatment. The relapse rate is high with cessation of treatment (>33%). Those who relapse often require maintenance therapy with glucocorticoids.

A CURIOUS CASE OF CYANOSIS. C.T. Ko 1 , N. Spell 1 ; 1 Emory University, Atlanta, GA (Tracking ID #76425) LEARNING OBJECTIVES: 1. Recognize methemoglobinemia as a cause of cyanosis, even without G6PD deficiency. 2. Diagnose and treat methemoglobinemia by understanding its mechanism of action. 3. Recognize the drugs that can cause methemoglobinemia. CASE INFORMATION: A 26-year-old African-American female with HIV presented complaining of worsening shortness of breath, headaches, and generalized weakness. Her CD4 count was 11/mm3. She had been discharged from the hospital one week prior with treatment for presumptive Pneumocystis carinii pneumonia. Her discharge medications included clindamycin and primaquine. On physical exam, she was a thin, cachetic, pleasant female in mild respiratory distress. Vital signs included a temperature of 102.5F (39.2C), blood pressure 90/50 mm Hg, pulse 124 beats/minute, and respiratory rate 24 breaths/minute. Her pulse oximeter reading was 85% saturation on room air and 89% saturation with a 100% nonbreathing oxygen mask. She had conjunctival and mucosal pallor as well as cyanosis of her nail beds, diffuse shoddy lymphadenopathy, and tachycardia with no associated murmurs/rubs/ gallops. Lung fields were clear to auscultation with adequate airflow. Laboratory evaluation revealed white blood cells 3400/mm3 (47N, 46L, 6M), hemoglobin 7.0 g/dl, hematocrit 20.2%, platelets 130,000/mm3, and reticulocytes 1.4%. Her hematocrit one week prior was 35.5%. Chemistry profile showed total bilirubin 1.0 mg/dl, LDH 1374 U/L, and G6PD 10.6. All other chemistry values were within normal limits. Chest X-ray was unchanged from her previous films with minimal bilateral reticular prominence likely secondary to mild interstitial scarring. Arterial blood gas on room air showed pH 7.40, pCO2 28 mm Hg, pO2 73 mm Hg, oxyhemoglobin 73%, carboxyhemoglobin 0.2%, and methemoglobin 25%. Primaquine was discontinued, and methylene blue was administered. Methemoglobin level was 13.6% within one hour. One week later in outpatient follow-up, methemoglobin level was 2.6%. IMPLICATIONS/DISCUSSION: Methemoglobinemia causes cyanosis that is unresponsive to oxygen therapy. In addition, pulse oximeter readings are not accurate when there is methemoglobin in the blood. Etiologies of methemoglobinemia include medications, chemical agents, and hereditary causes. The goal of therapy in methemoglobinemia is to reduce heme iron in order to restore normal oxygen transport. year-old Asian-American woman presented with three weeks of progressive muscle weakness. She had difficulty combing her hair, lifting her arms or getting out of a chair. At presentation she could not walk. She had a dusky, almost dirty appearing rash on her chest and around her eyes. An erythematous rash was noted on the dorsal surface of the MCP and PIP joints of her hands. She could not lift either thigh off the bed. Laboratory values: CK 14,245, RF 273, ANA + >1:640 (speckled pattern), AST 605, ALT 207, ALK PHOS 95, LDH 150. Hepatitis B CAb +, Hep Sab +. Anti-RNP, Anti-Jo, Anti-SSA, Anti-SSB and anti-DS DNA were all negative. A presumptive diagnosis of dermatomyositis was made, a confirmatory muscle biopsy performed and prednisone begun. Malignancy workup was negative. She improved slightly and was discharged to a rehabilitation facility. IMPLICATIONS/DISCUSSION: Dermatomyositis (DM) is a rare idiopathic inflammatory myopathy that has a 2:1 female preponderance and presents most commonly in the fifth decade. The incidence of DM is 1:100,000. Pathogenetically, DM is associated with immune complex deposition in a perivascular and perifasicular distribution. The etiology is unknown although viruses have been implicated. The typical presentation of DM is proximal muscle weakness in association with classic dermatological findings. Gottren's papules, as seen in our patient, are the most commonly seen skin rash. The classic heliotrope rash is the most specific manifestation of DM but is only rarely seen. Other findings include acanthosis nigricans,`m echanics hands,'' diffuse flat erythema in a shawl like distribution, and periungual erythema. The elevated liver enzymes in this patient are problematic since DM alone can raise parenchymal liver enzymes. The hepatitis B profile is not suggestive of an acute infection and unlikely to be causing the elevated liver enzymes. Hepatitis B, however, has been implicated in the pathogenesis of some cases of DM and raises the question of a delayed slowly progressive humorally mediated immune reaction. The relationship between the two conditions is unknown although a few select reported cases suggest it may be more than coincidental. There was no history of smoking, travel, or prolonged immobilization. His ROS was otherwise negative. His medications were aspirin, metaprolol, lisinopril, and sulfasalazine. After initial treatment for pulmonary edema at an outside hospital, he was transferred to our institution. He was intubated due to worsening hypoxia. A bronchoscopy was performed: bronchoalveolar lavage (BAL) was bloody. VS: Temp -378C, BP -124/60 mmHg, HR -110/min, SaO2 -98% on assist control ventilation. Exam was notable for bilateral rales and absence of S3 or JVD. Initial labs revealed Na-127, creatinine -1.0, CK-MB -15, Troponin I -10.2. EKG was normal; CXR showed interstitial pulmonary edema. Echocardiogram showed EF of 35%. A highresolution chest CT showed ground glass appearance consistent with ARDS. He was treated with ceftriaxone and azithromycin. His hospital course was complicated by right middle and anterior cerebral artery ischemic stroke, ARF (BUN/Cr 118/3.3), anemia and ultimately shock. He expired on the ninth hospital day. Autopsy reports confirmed thrombotic microangiopathy consistent with HUS. BAL culture subsequently grew influenza A. IMPLICATIONS/DISCUSSION: Influenza, occurring as outbreaks in winter seasons, is usually self-limited; but causes increased morbidity and mortality in high-risk populations. Such high-risk group includes patients with underlying cardiac, pulmonary, and immunosuppressive diseases, nursing home residents and older than 65. Primary viral pneumonia is the most severe pulmonary complication that tends to occur in individuals with elevated left atrial filling pressures, and pulmonary diseases. Systemic complications include rhabdomyolysis, Reye syndrome, transverse myelitis, and myocarditis. Other rare complications, such as hemolytic uremic syndrome and toxic shock syndrome worsen the clinical outcome. Apart from the tissue culture, the virus can be detected in throat swabs and by serologic methods. This high-risk patient presented with acute severe respiratory failure from primary influenza A pneumonia complicated by HUS leading to renal failure and anemia. Increasing the pretest probability by clinical evaluation will be helpful in initiating treatment earlier in the course rather than be fooled by the flu. LEARNING OBJECTIVES: 1. To recognize the clinical and pathologic presentation of talcosis, also known as foreign body granulomatosis. To recognize the sequelae of talcosis, specifically panlobular emphysema, acute pulmonary hypertension, ARDS, and spontaneous pneumothorax. 2. To recognize signs and symptoms of factitious disorders (Munchausen's). 3. To discuss differences between factitious disorders, somatoform disorders and malingering. CASE INFORMATION: A 50 year-old Oregon man with an extensive past medical history including chronic pain syndrome involving his hip, knee, and groin, total hip replacement surgery with multiple revisions and post-surgical complications presented with a recent history of hypertensive episodes and syncope. He was referred to VMMC for evaluation of a possible pheochromocytoma. In addition to syncope, the history and physical revealed an antecubital abscess and fevers. The patient was admitted and an Infectious Disease consult ordered. He reported that In March, 2002, he developed increasing frequency of attacks characterized by chill, abrupt fever, hypertensive episodes, and syncope. In mid-March, he noted swelling, redness and warmth in his right antecubital fossa and continued to have fever every few days. The patient's hospital course was complicated by multiple episodes of fever >39 oC, witnessed and unwitnessed syncopal episodes, frequently infliltrated intravenous lines, polymicrobial blood cultures, increasing oxygen needs, infected PICC, and atrial fibrillation. His medical work-up was extensive. He ultimately underwent a chest CT which showed multiple 2-3mm, bilateral pulmonary nodules. The patient had thoracoscopic lung biopsy of several nodules. The pathology revealed near complete occlusion of small and medium vessels by extracellular refracticle material. The patient was confronted with these findings and confessed to having crushed and injected oxycontin on several hundred occasions.

Occurs when tablets are pulverized and injected. The most common fillers used in tablets are talc, cornstarch, cellulose. These fillers cause an initial arteritis which is associated with rapid influx of neutrophils around the intravascular foreign body. The influx of neutrophils is followed shortly thereafter by granuloma formation as talc particles migrate through the vessel wall to the surrounding perivascular and interstitial tissue. The most common radiographic finding is widespread, 2-3mm well defined nodules typically in the mid lung. The clinical presentation is typically non-specific and may mimic URI with: cough, dyspnea, increased sputum. Sequelae of talcosis includes: panlobular emphysema, acute pulmonary hypertension, ARDS, and spontaneous pneumothorax. Treatment options are limited but include: Dexamethasone and D-penicillamine. Steroids appear to have a limited (if any) role. Vasodilatation with hydralazine may help those with pulmonary hypertension. FACTITIOUS DISORDER-A form of feigned illness which differs from malingering (which has a external incentive-avoiding work, financial gain) in that it has no other incentive other than to be a patient and experience the sick role. Both factitious disorder and malingering differ from somatoform disorders in that they are voluntarily produced. Munchausen's Syndrome is the most extreme (and highly publicized) form of factitious disorder. Patients with factitious disorder often appear more comfortable than their condition would warrant. They may be pleasant, cooperative and receptive to ANY intervention-even if painful and risky. Nurses often note that they often have no visitors/phone calls suggesting anti-social or isolating behaviors. They may also give a medical history that is unbelievable or``too good to be true''. Be suspicious when pt's deny you the right to access old records or speak with previous providers. Yesterday she had been seen in the clinic and diagnosed with trichomonas vaginitis. The resident had dutifully told her that this was a sexually transmitted disease and that both she and her husband needed to be treated simultaneously. Unfortunately, because of her husband's health they had not had sex in over ten years. Now her husband was accusing her of infidelity, a fact she denied vehemently. The Case: The patient is a 59 year old white woman with a 1 week history of burning on urination and a mild vaginal discharge, described as thin and clear. She denied fever or flank pain. Her social history was significant for part-time work as a housekeeper which took her out of the house periodically. Her husband had been disabled for 10 years with a back injury and there had been no sexual activity since the injury. The pelvic examination was remarkable only for a thin watery discharge with a mild odor. Cervix and adnexa were benign. A wet prep revealed numerous trichomonads. IMPLICATIONS/DISCUSSION: Trichomonas vaginalis infection classically presents as a vaginitis/cervicitis with a thin, yellow, frothy, foul smelling discharge often times associated with dysuria. Nevertheless, up to 40% of infections are asymptomatic. The association with sexual activity is well documented. As an illustration of this, the incidence of infection in the general population has been reported as high as 5-10%, while in venereal disease clinics the incidence jumps to 25% and up to 70% among prostitutes. However, unlike other sexually transmitted diseases, the age distribution of of trichomonas infection is bimodal. For example, most women with gonorrhea are in their early 20's, with less than 2% over the age of 40. Trichomonas infections also peak during years of maximal sexual activity but there appears to be a second peak around the time of menopause. Indeed, >30% of patients are over the age of 40. It has been hypothesized that this represents women infected at an early age who harbored the trichomonas asymptomatically but present with symptoms at a time when the vaginal milieu changes (eg. menopause) allowing the trichomonas to propagate. There are several reported cases of newborns and apparent virgins with trichomonas. These likely represent either transmission from infected mothers at the time of birth or a nonsexual source. Studies from the British literature (Burgess,1963; Whittington 1957) establish that trichomonas can survive for up to 45 minutes on a toilet seat, although transmission by this route has never been proven. Has she been faithful? Clearly there is valid justification to believe that she is telling the truth. year-old man presented with a five weeks of bowel and bladder incontinence and parethesias of the lower extremities. He had a history of diabetes mellitus and HIV. Two weeks prior he had presented for evaluation of urinary hesitancy and paresthesias of the lower extremities. He was diagnosed with diabetic peripheral neuropathy and released. On this admission, his neurological examination revealed decreased sensation in the lower extremities, absent ankle reflexes, an ataxic gait, saddle anesthesia, and decreased anal sphincter tone. An MRI of the spine revealed an extradural mass extending from L4 to S4. Biopsy confirmed the neoplasm to be Burkitt's lymphoma. IMPLICATIONS/DISCUSSION: Although spinal cord compression is a medical emergency, access to an MRI may be limited. The physical examination is instrumental in establishing the diagnosis and expediting appropriate therapy. Although diabetes and HIV are common causes of peripheral neuropathy, they are not causes of the cauda equine syndrome (CES). A methodical physical examination detected saddle anesthesia and sphincter impairment, establishing the diagnosis of CES. Compression of the roots can be caused by a ruptured disk, infection, fracture, or tumor. HIV patients are at increased risk for tumors associated with co-sexually transmited viral infections such as HHV6 and HHV8. CES is a neurosurgical emergency, requiring immediately operative decompression of the spinal canal. A timely diagnosis of this syndrome is essential, as patients with paraneoplastic impingement may not regain function beyond the deficit at presentation.

CORONARY DISEASE. E.J. Lee 1 , K. Barnard 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #75596) LEARNING OBJECTIVES: Recognize gender differences in the presentation of myocardial ischemia and consider microvascular spasm as a cause for chest pain in women with angiographically normal coronary arteries. CASE INFORMATION: A 54 year-old Asian-American woman with history of chronic back pain presented with retrosternal chest pain. The pain was sharp, radiated to her left arm, awoke her from sleep, and lasted for one hour. She had had similar pain the previous day, lasting an hour before spontaneously resolving. Neither episode was associated with nausea, vomiting, diaphoresis, or exertion. Another similar episode occurred one year ago. Echocardiogram at that time showed mild hypertrophy and normal overall function, while coronary catheterization revealed normal coronary arteries and an ejection fraction of 65%. The patient had no history of diabetes, hypertension, hyperlipidemia, smoking or family history of coronary artery disease. On initial evaluation in the Emergency Department, the patient was without chest pain. Her electrocardiograph showed normal sinus rhythm with no ischemic changes. Chest radiograph was normal. Total CPK was 71 and troponin was less than 0.2. She was admitted to rule out myocardial infarction. Shortly after being admitted, the medicine house staff were called to evaluate the patient for``seizure-like activity.'' The patient was found in severe emotional distress with taut extension of her upper and lower extremities, and clawing of her hands bilaterally. She was alert, oriented, and able to follow commands throughout this episode which resolved within minutes. Electrolytes showed a calcium of 9.7, magnesium of 1.7, phosphate of 3.3, and potassium of 3.8. An electrocardiograph at this time showed ST depression in leads II, III, and AVF. Repeat electrocardiograph showed a similar pattern of ST depressions. The patient was transferred to the cardiac step-down unit with a presumptive diagnosis of unstable angina and started on anticoagulation therapy. Aspirin and beta-blockers were held due to reported allergies. Subsequent electrocardiographs showed normal ST segments in all leads. Second and third sets of cardiac enzymes were negative. Cardiac catheterization the following day revealed normal coronary arteries and an ejection fraction of 60%. The patient was discharged home the following day in good condition. IMPLICATIONS/DISCUSSION: There is abundant data to suggest there are gender differences in the risk factors, presentation, and management of cardiac disease. It has been shown that negative affect and emotional distress may increase risk of ischemic heart disease and interfere with effective cardiac rehabilitation. Mental stress has been known to cause ischemic changes on electrocardiograph and abnormalities in regional and global left ventricular function. These effects have been associated with microvascular spasm. A mental stress-induced ischemic episode may have occurred in this patient. A coronary catheterization that showed normal coronary flow would not be uncommon in such a case. It is important to realize that despite angiographically normal coronary arteries, this may be an atypical presentation of true underlying coronary disease.

THROMBOTIC THROMBOCYTOPENIC PURPURA-HEMOLYTIC UREMIC SYNDROME (TTP-HUS) AFTER A SINGLE DOSE OF QUININE. J. Lee 1 , M. Krasnoff 1 ; 1 Dartmouth Hitchcock Medical Center, Lebanon, NH (Tracking ID #74449) LEARNING OBJECTIVES: 1. Identify a potentially fatal complication of a commonly prescribed therapy for nocturnal leg cramps. 2. Recognize quinine as the most common cause of drug-associated TTP-HUS. CASE INFORMATION: The patient is a 66 year old previously healthy female who presented to the emergency department with the acute onset of nausea, vomiting, abdominal pain, diarrhea, and disorientation 2.5 hours after taking a single dose of 260 mg of quinine for nocturnal leg cramps. Over the next few hours, she developed severe hypotension, requiring pressors. Labs were notable for WBC 3.6 Plt 123,000 Bun 25 Cr 1.9 T bili 1.7 PTT 75 PT > 100. A CT scan of the abdomen and pelvis was unremarkable. The patient was admitted to the ICU with a presumed diagnosis of sepsis of unclear etiology; she was started empirically on IV ampicillin/sulbactam. Over the next few days, the patient developed microangiopathic hemolytic anemia, severe thrombocytopenia (Plt 12,000), and acute renal failure (Cr 8.4). Cultures of sputum, urine and blood showed no growth. Her clinical diagnosis was felt to be TTP-HUS; her antibiotics were stopped and she was begun on daily plasmapheresis. Dialysis was instituted. After two weeks of therapy, the patient's anemia, thrombocytopenia, renal failure, disorientation, and coagulopathy were all improving or resolved. An adverse event report was sent to FDA MedWatch. IMPLICATIONS/DISCUSSION: Nocturnal leg cramping is a common complaint encountered in the primary care setting. Despite quinine being frequently prescribed, its potential for severe adverse reactions is largely underrecognized. Quinine is the most common cause of drug-associated TTP-HUS. Common presenting symptoms include the acute onset of abdominal pain, nausea, vomiting, diarrhea, fevers and chills. The symptoms usually begin abruptly, several hours after the ingestion of quinine. A single tablet is sufficient to cause TTP-HUS. In addition to the expected findings of TTP-HUS, low-grade DIC and leukopenia can also be seen. The mechanism of quinine-associated TTP-HUS is presumed to be caused by drug-dependent antibodies. Treatment involves avoidance of quinine exposure, plasmapheresis and supportive therapy. While available by prescription, quinine is also found in beverages, such as quinine water, tonic water, and gin and tonic. In addition, there is an extensive list of herbal remedies containing quinine including cinchona tree, peruvian bark, and china bark. Physicians should carefully question any patient with TTP-HUS for quinine exposure, especially since patients may not report it among their medications. In addition, physicians need to counsel patients regarding future avoidance of all quinine-containing compounds, since repeat ingestion of quinine may cause relapse of TTP-HUS.

PATIENT. D. Lehman 1 , J. Mills 1 , C. Sorensen 1 , J. Whitesel 1 , R. Reves 1 ; 1 Denver Health and Hospital Authority, Denver, CO (Tracking ID #75102) LEARNING OBJECTIVES: To recognize that tuberculosis can present with unusual clinical manifestations, often sub-acute or chronic, especially in the immunocompromised context, such as HIV infection. CASE INFORMATION: 48 y/o male with heterosexually acquired HIV infection and a CD4 count of 306, presented with a 1-month history of penile and rectal pain and 1 week of no urethral voiding. He noted urine coming from the rectum with feces. Voiding cystourethrogram showed a prostatic-rectal fistula and a Foley catheter was placed. He was born in Mexico and had a negative PPD 10 years earlier. Four months earlier he had presented with dysuria, an enlarged prostate, pyuria and microscopic hematuria. CT scanning then showed a 2.7 by 3.0 cm hypodensity within an enlarged prostate that, in the absence of fever and toxicity, appeared clinically not consistent with a prostatic abscess. No urine culture was done, but he received 10 days of levofloxacin. Fistula evaluation by GI with colonoscopic biopsy showed chronic inflammation and necrosis. Transrectal ultrasound showed a large prostate with prostatic calculi with no cyst or abscess. Granulomas and acid-fast bacilli (AFB) were found in biopsies obtained during an unsuccessful surgical attempt to repair the fistula. Bilateral infiltrates were found on a post-operative chest X-ray. AFB were found in urine and sputum and cultures grew Mycobacterium tuberculosis (TB). Standard 4-drug therapy for TB was successful and the fistula closed without further surgery after 6 months of directly observed treatment and Foley drainage. IMPLICATIONS/DISCUSSION: Delayed and missed diagnoses of active pulmonary and extrapulmonary TB are common due to the relative rarity of the disease and a lack of familiarity with its protean manifestations. TB of the genitourinary tract accounts for about 1% of reported cases of TB in the US. Extrapulmonary forms (27% of US cases) are more common among children and patients with HIV-infection or other disorders of immunity. The keys to earlier recognition of active TB are awareness of: 1) the manifestations of the disease, 2) risk factors for previous exposure and latent TB infection, and 3) risk factors for progression from latent TB infection to active disease. In retrospect this patient had all three of these features. The clinical features of active TB, both pulmonary and extrapulmonary are variable, but chronic and sub-acute presentations are common. Signs of systemic toxicity are helpful if present but are commonly absent. TB of the urinary tract should be suspected in patients with unexplained``sterile'' pyuria and/or hematuria and in those with unexplained chronic inflammation and fibrosis. This patient had a common risk factor for infection, having been born in Mexico, and had HIV infection as a risk factor for progression to active TB. Although the GU tract is a relatively common extra-pulmonary site for TB, there is little mention in the literature of fistula as a complication of TB prostatitis. The most likely etiology of a prostaticrectal fistula is surgery, rarely by infection. Radiological studies revealed what appeared to be a solid posterior occipital mass consistent with a malignant lesion and surgical intervention was pursued. At craniotomy he was found to have an abscess; smears revealed yeast forms and cultures grew Cryptococcus neoformans. CSF results were WBC 255, protein 112, glucose 27 and cryptococcal antigen 1:64. Serum cryptococcal antigen was 1:128. He disclosed no risk factors for immunodeficiency which was confirmed by negative studies for HIV-1 and 2 antibody, HIV-1 and 2 PCR, HTLV-1 and 2 antibody and HTLV-1 and 2 PCR. Of note, his CD4 count was 79 and his total IgG, IgG1 subclass and IgG2 subclass levels were low. IgA and IgM levels were at the lower limits of the normal range. He received two weeks of amphotericin B and improved appropriately. Lumbar puncture at that time revealed: WBC 440, protein 111, glucose 30 and cryptococcal antigen 1:2. Repeat CD4 count was 191 and serum cryptococcal antigen was 1:64. His therapy was changed to fluconazole and he continued to improve. IMPLICATIONS/DISCUSSION: Although possible in immunocompetent hosts, cryptococcal meningoencephalitis presents most commonly in patients with HIV infection, drugassociated immunosuppression, leukemia and complement deficiency. This infection has rarely been reported in cases of hypogammaglobulinemia. Cryptococcus neoformans infects through aerosolization producing a primary respiratory infection that spreads hematogenously to distant sites. In hypogammaglobulinemia of the type shown in this patient, the proposed host defect stems from dysfunctional T-cell activity resulting in fundamental difficulties with complement fixation, opsonization and reduction of circulating antigens. We propose the possibility that the hypogammaglobulinemia facilitated the development of this patient's CNS disease. These immunosuppressed patients present with fever, headache and malaise similar to, but typically more intense and shorter in duration than infections in the immunocompetent host. Response to treatment with amphotericin B and fluconazole are similar to those in immunocompetent hosts.Close monitoring and medication adjustments per clinical response are essential. Thus, this case provided an unusual initial presentation of hypogammaglobulinemia as cryptococcal meningoencephalitis. LEARNING OBJECTIVES: To recognize filariasis in the differential diagnosis of nephrotic syndrome. CASE INFORMATION: A 46 year old man who had recently emigrated from West Africa presented with a three month history of lower extremity pitting edema. His physical examination was significant for anasarca. Laboratory data revealed a white blood cell count of 9900 with 58% eosinophils, an albumin level of 1.2 g/dl as well as a BUN and creatinine of 16 and 1.0 respectively. An initial urinalysis revealed protein level of greater than 300 mg/dl and microhematuria. A subsequent 24-hour urine collection revealed 7.6 grams of protein confirming a diagnosis of nephrotic syndrome. The differential diagnosis of nephrotic syndrome with eosinophilia includes lymphoma and various parasite infections. While parasitic serologies were pending, chest and abdominal CT scans were normal ruling out a diagnosis of lymphoma. A renal biopsy showed membranous glomerulonephritis with diffuse IgG deposits in the subepithelium. Subsequent peripheral blood smears showed obvious microfilariae of the Loa loa species, indicating active infection. Further laboratory studies revealed the absence of other conditions associated with membranous glomerulopathy. Therefore, it was concluded that the nephrotic syndrome and the membranous glomerulonephritis were most likely caused by the filarial infection. The patient was treated with metolazone and lisinopril to treat the anasarca/ nephrotic syndrome and given ivermectin to treat the filariasis. At follow-up two months later, the edema had resolved and his urinalysis had almost normalized. IMPLICATIONS/DISCUSSION: Loa loa is one of eight filarial species and occurs mainly in the rain forests of Africa. Adult worms develop and mate to form microfilariae, which appear in the blood. Whereas other filarial species cause the classic symptoms of lymphedema, the loaisis species is more commonly associated with pruritus and localizd areas of subcutaneous swelling. Various nephropathies, including nephrotic syndrome, are rare and likely result from immune complex deposition within the glomerulus. In tropical countries, infectious diseases are common causes of the nephrotic syndrome. As demonstrated in this case, one should consider the diagnosis of filariasis in patients that present with anasarca and/or nephrotic syndrome and who have a history of travel to endemic countries for filariasis. year-old white female with a history of von Willebrand disease presented with 3 weeks of severe fatigue. She denied history of trauma or abnormal bleeding although she reported easy skin bruising. On physical examination, her temperature was 37.4 degrees Centigrade and BP 102/72 mmHg. She appeared thin and pale. Neck was supple, without thyromegaly. Lungs were clear. Heart was regular, without murmurs or gallops. Abdomen was benign without masses, tenderness or hepatosplenomegaly. Extremities had no cyanosis, clubbing or edema. Neurological examination was non-focal. CBC revealed a hemoglobin of 10g/dl, platelet of 33,000/mm3, and WBC of 3500/mm3 with 13% blasts. Bone marrow biopsy found 40% blasts with positive CD33 and CD34. She was diagnosed with acute myeloid leukemia. Chemotherapy with cytarabine was started. Five hours later, she developed severe stabbing left upper quadrant abdominal pain radiating to the back and left shoulder, aggravated by body movement, only slightly relieved by intravenous hydromorphone. One hour later she became hypotensive with a BP of 90/50 mmHg. Hemoglobin dropped from 9.0 to 7.1g/dl in 4 hours. Electrocardiogram showed sinus tachycardia and no acute ischemic changes. Abdominal series was unremarkable. An abdominal CT scan was reported unremarkable initially, but further review demonstrated blood surrounding the spleen. Emergent laparotomy found acute rupture of a normal sized spleen (8.0 Â 5.5 Â 2.3 cm). Splenectomy was performed. She was transfused a total of 6 units of packed red blood cells. Hemoglobin remained stable after the surgery. She developed acute respiratory distress syndrome and died of respiratory failure and cardiac arrest within a week. IMPLICATIONS/DISCUSSION: The spleen is an immunologic organ commonly involved in hematologic diseases. Splenic rupture can be classified into 1) traumatic; 2) spontaneous; and 3) pathologic. Pathologic splenic rupture occurs in a spleen affected by a disease without previous trauma. The presentations of splenic rupture are the result of intra-abdominal hemorrhage, hypotension, tachycardia, peritoneal irritation signs, and fever. The abdominal pain could radiate to the left shoulder (Kehr's sign). Pathologic rupture of a spleen affected by a hematologic malignancy is a rare event and it is especially unusual for a normal sized spleen to rupture. The risk of splenic rupture increases with age and size of the spleen. The release of the enzymatic content of cells shortly after induction chemotherapy may lead to splenic damage, followed by rupture of the spleen. The present patient had received cytarabine just 5 hours before the abrupt onset of abdominal pain. Other risk factors of bleeding such as thrombocytopenia and von Willebrand disease might also have contributed to her catastrophic event. The diagnosis of pathologic splenic rupture begins with a high index of suspicion. A patient with risk factors presenting with left upper abdominal pain should be observed closely and investigated. Plain abdominal X-ray, ultrasound and CT scan are valuable tests. Aspiration of blood by abdominal puncture could confirm the diagnosis. For insidious rupture, liverspleen scintigraphy is of value. The only therapy is splenectomy. A 67-year-old male was well until 6 weeks prior to presentation, when he developed diffuse extremity deep aching pain and difficulty with walking, maintaining his balance and doing buttons. He denied diplopia, but had trouble looking to the left. He denied weakness, numbness, sensory loss, trouble with speech or articulation, or bowel or bladder dysfunction. On physical examination, he had normal vital signs. He was alert, cooperative, but somewhat slow. A 2 Â 2 cm non-tender supraclavicular lymph node was palpable. Heart, lungs and abdomen were unremarkable. Extremities had no cyanosis, clubbing or edema. Eyes could not move past the midline on leftward gaze. Motor strength was 5/5 in all muscle groups tested. Vibratory sense was diminished distally in the right lower extremity. A heel-to-shin testing was ataxic. He could not sit nor stand unaided. Romberg's sign was noninterpretable even with the eyes open. Plantar responses were flexor bilaterally. Cerebral spinal fluid reveaked glucose 93, lymphocyte 4, IgG 15.1, and protein 100. Anti-Hu antibody was positive. Brain MRI showed a small old lacunar infarct. Chest CT scan identified a 1 ± 2 cm right suprahilar pulmonary nodule, 3 right upper lobe nodular densities less than 1 cm each, and a prominent 3.5 cm nodule in the right pretracheal area. EMG and nerve conduction studies demonstrated a sensory motor polyneuropathy. Lymph node biopsy showed neoplastic cells staining with synaptophysin and chromogranin, supporting the diagnosis of large cell neuroendocrine carcinoma. The patient was treated with carboplatin and etoposide for three doses and IVIgG for five doses. The symptoms were stabilized. IMPLICATIONS/DISCUSSION: Paraneoplastic encephalomyelitis (PEM) is a frequent remote effect of cancer characterized by neuronal loss and inflammatory infiltrates in the nervous system. The onset is usually subacute and causes severe neurological dysfunction which antedates the diagnosis of cancer. The presenting neurological syndrome is usually sensory neuropathy, cerebellar dysfunction and cortical encephalitis. Diagnosis of the primary cancer remains challenging and requires a high index of suspicion. Usually, it is made by the demonstration of specific paraneoplastic antibodies. Anti-Hu antibody recognizes a family of RNA-binding proteins expressed in the nuclei of neurons and cancer cells. It has been used as a diagnostic marker, but no evidence suggests it causes neuronal damage. Effective treatment of the tumor with chemotherapy is an independent predictor for stabilization of PEM. Large cell neuroendocrine carcinoma is a highly aggressive tumor that usually occurs in smokers, and may be either central or peripheral. It has been suggested that surgically resectable tumors be excised and that advanced stage lesions be treated with combination chemotherapy. Immunotherapy has been proven effective in some patients in tumor regression and PEM stabilization or improvement. The prognosis is poor, with a median survival of 11 months. LEARNING OBJECTIVES: Recognize that the clinical manifestations and radiologic findings of peritoneal tuberculosis (TB) may mimic ovarian carcinoma. Recognize that an elevated CA-125 level may be more suggestive of tuberculous peritonitis than ovarian carcinoma in certain populations such as young women, HIV-infected women and women from areas endemic for tuberculosis. CASE INFORMATION: A 29 year-old Vietnamese woman with no significant past medical history presented to the emergency department with a 10 day history of fever, non-productive cough, abdominal pain, and increasing abdominal girth. A PPD placed as an outpatient was reactive to 16mm. She emigrated from Vietnam ten years prior, had no recent travel history, and had no recent sick or TB contacts. Family history was negative for cancer. On physical examination, the patient was febrile to 102.6F with a pulse of 111 BPM. Pulmonary exam was clear to auscultation. Abdominal exam was significant for mild distention, and tenderness in the epigastric and right upper quadrant regions without rebound or guarding. Gynecologic exam was normal. Chest x-ray was normal. A CT scan of the abdomen and pelvis showed diffuse intraabdominal ascites with omental caking, strongly suggestive of metastatic disease from ovarian carcinoma. Pelvic ultrasound was negative for adnexal masses. Ascitic fluid analysis showed a predominantly lymphocytic exudate. There were no malignant cells, acid-fast bacilli (AFB) or other organisms detected in the fluid. Fluid culture yielded no growth. Multiple sputum smears were negative for AFB. A CA-125 level was elevated to 546 U/ml. A CT guided biopsy of the omentum revealed granulomatous inflammation and well-defined granulomas with central necrosis ± histology consistent with tuberculous peritonitis. The patient was started on a regimen of isoniazid, rifampin, ethambutol and pyrazinamide. On follow-up two weeks after discharge, the patient reported feeling well with complete resolution of the fever and abdominal pain. IMPLICATIONS/DISCUSSION: Peritoneal tuberculosis is an uncommon entity. The common clinical presentation is ascites or an abdominal mass. The elevated CA-125 and radiologic appearance of the omentum, as in the case of our patient, can be highly suggestive of ovarian carcinoma. However, it is well established that many other conditions, including peritonitis can elevate the CA-125. When these features are present in a patient who is at high risk for developing tuberculosis and who is at low risk for developing ovarian cancer then the diagnosis of tuberculosis must be considered. Establishing the diagnosis of peritoneal tuberculosis can be difficult as ascitic fluid is rarely positive for AFB and even culture of biopsy specimens may be negative. Diagnosis is often made on the basis of suggestive histopathology and clinical features. Clinicians must maintain a high index of suspicion for tuberculous peritonitis in patients presenting with ascites and abdominal masses, especially in young women (in whom ovarian carcinoma is uncommon), HIV-infected patients and patients from areas endemic for tuberculosis. In these cases, empiric antituberculosis therapy can be considered while further workup is pending. CA-125, while nonspecific for peritoneal tuberculosis, can be useful in monitoring response to therapy and would be expected to return to normal levels.

CHRONIC SINUSITIS AND BEYOND. A. Loewen 1 ; 1 University of Calgary, Calgary, Alberta, Canada (Tracking ID #77075) LEARNING OBJECTIVES: To review an approach to the patient with chronic infection. To discuss the manifestations of Wegener's Granulomatosis. CASE INFORMATION: A 33 year old male with a 4 month history of chronic sinusitis which is refractory to antibiotics, and an episode of suppurative otitis media, presents with left sided Bell's palsy and multiple boils. There is microscopic hematuria with normal renal function. Drainage and biopsy of sinuses demonstrates necrotizing granulomatous inflammation. Anti PR3 level is 18.5 kEu/L. A diagnosis of Wegener's granulomatosis is made. The patient later develops hemoptysis while on therapy with prednisone and cyclophosphamide. IMPLICATIONS/DISCUSSION: An approach to the patient with apparently chronic infection must include infectious causes, underlying immunosuppressed states and noninfectious causes. Wegener's granulomatosis is a vasculitis of small arteries and veins and usually presents as a pulmonary-renal syndrome. In this case it presented with upper airway involvement, pyoderma gangrenosum and cranial nerve palsy, butpulmonary and renal symptoms were minimal. A broad differential diagnosis can lead to the correct diagnosis, avoiding unnecessary interventions, and hasten administration of appropriate therapy.

G. Loukatous 1 , J. Wiese 1 , J. Aliota 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77080) LEARNING OBJECTIVES: 1. Identification of the clinical signs and symptoms of Vibrio Vulnificus infection 2. Recognition that early and aggressive intervention is essential to optimal patient outcome CASE INFORMATION: A 42-year-old Vietnamese man presented with a two-day history of fever and a painful left leg. He denied trauma or stasis involving the leg. His pulse was 110; blood pressure 110/50; temperature 38.0 C. There was a 10 cm eccyhmotic lesion on his left lower leg. Despite therapy with cefazolin his condition deteriorated. Over 12 hours, the ecchymosis extended as the skin lesion rapidly developed multiple fluid-filled bullae. General surgery was consulted for surgical debridement. Upon further questioning, the patient noted a recent history of raw oyster ingestion. Wound and blood cultures returned positive for Vibrio vulnificus. He was started on tetracycline. Although he subsequently developed multi-organ failure, he recovered after 22 days of aggressive medical treatment and continued surgical debridement. IMPLICATIONS/DISCUSSION: Early diagnosis and treatment is the critical component of a successful outcome from a Vibrio vulnificus infection. The key to diagnosis is combining an astute history with an observant physical examination. In sea-side cities, the consumption of oysters or exposure to the water may be so common as to preclude the patient from thinking to offer this historical clue unless prompted. Recognizing the appearance of Vibrio, then, is the key to diagnosis. Erythematous and ecchymotic skin lesions that rapidly evolve to hemorrhagic vesicles and bullae should alert the physician to the possibility of a Vibrio infection. Like necrotizing faciitis, vibrio invades the deep fascia, destroying the facial structures as it rapidly extends. Ecchymosis, bullae and anesthesia reflect the loss of vessels, skin partitions and nerves. Early intervention with appropriate antibiotic therapy and aggressive wound debridement is essential in such cases. Even with early intervention, bacteremia from V. vulnificus carries a 50% mortality that increases to 90±100% in the presence of hypotension. A 34 year old non-smoking, HIV-negative Hispanic male, who received his last dose of chemotherapy for lymphoma 1 week prior, presented with 3 days of increasing cough, dyspnea on exertion, and fever. He denied any sick contacts, TB exposure, recent travel, or pet exposures. His vital signs were:T 99.6 F, BP 115/78, P 100, R 20, and Pulse Ox 96% on room air. Respiratory exam showed unlabored breathing and clear lungs. His studies showed: WBC 1.9 (N 51%, L 12%, M 35%), Hb 9, Hct 25.9, Plt 44, and LDH 1461. Chest xray showed bilateral hilar fullness not seen on prior films. Differential diagnosis on admission was pulmonary infection (community acquired, atypical, and fungal pneumonia; TB; PCP) versus recurrence of lymphoma. Hospital course:Ceftriaxone and azithromycin were empirically started on Day 1. By Day 2, the patient remained febrile and showed signs of decompensation with decreasing BP and increasing oxygen need to 4 liters. A room air ABG at that time showed: pH 7.49, pCO2 36, PO2 43, saturation 83%. Chest CT showed progression to diffuse bilateral alveolar infiltrates without adenopathy. Trimethoprim/sulfamethoxazole was added empirically for PCP. The patient was then transferred to the ICU for prophylactic intubation and diagnostic bronchoscopy showing positive Pneumocystis carinii direct fluorescent antibody on lavage. All other studies (biopsy, brush, and sputum/blood samples) were negative for bacterial, fungal, and malignant processes. Prednisone was subsequently added. The patient improved dramatically with extubation on Day 3 and discharge within the week. IMPLICATIONS/DISCUSSION: PCP is usually seen in AIDS patients with CD4 counts <200 without chemoprophylaxis. Unfortunately, it may not be readily considered in the differential in immunosuppressed, non-HIVpatients. The above vignette serves to remind us to not exclude PCP in the differential because a delay in evaluation could be fatal. Our patient fared well because we recognized his predispositions (hematologic malignancy and immunosuppression from chemotherapy) early in his hospital course which led to prompt treatment. The calculated absolute lymphocyte count was 228, making the CD4 count likely <200. LEARNING OBJECTIVES: Formulate a differential diagnosis of facial swelling using clinical and laboratory data. Initiate early and aggressive treatment based on the presumed diagnosis of facial swelling. Recognize that individuals with recurrent severe infection should be tested for immunodeficiencies. CASE INFORMATION: A 19 year old male was admitted in August, 2001 with face and lip swelling and pain. He has no significant past medical history or family history. He smokes cigarettes, drinks alcohol, and uses cocaine and marijuana. On physical exam he is afebrile, with a pulse of 132, respirations of 20 and a BP of 110/70. Oxygen saturation initially was 100% on room air. His left face, mouth, and neck are swollen and firm, his left eye was swollen shut and his tongue was swollen. He had no cervical adenopathy and clear lung fields. Initial impression was angioedema and treatment involved epinephrine, solumedrol, and with worsening respiratory status, intubation. Fever climbed to 103.3, treatment was started with ampicillinsulbactim and clindamycin. With positive blood cultures the diagnosis was now thought to be necrotizing fasciitis. Supportive care including TPN continued until he was extubated and discharged after 3 weeks. Patient never followed up and was readmitted in May, 2002 with a similar presentation and was found to have common variable immunodeficiency. Upon discharge, he still has not followed up and is not being treated. IMPLICATIONS/DISCUSSION: Necrotizing infections of the skin and fascia involve tissue destruction, systemic toxicity, and a high mortality rate. There is a tendency to underestimate the severity and extent of infection. We now see more angioedema and might miss this clinical presentation. Normal complement studies make hereditary angioedema unlikely and normal tryptase makes angioedema from other causes unlikely. Treatment of necrotizing fasciitis involves airway control, IV antibiotics, and early, aggressive surgical debridement. Individuals with common variable immunodeficiency frequently present with recurrent infections with encapsulated bacterial pathogens as in our patient. Those with recurrent infections should be checked for the disorder and treated with IV immunoglobulin. LEARNING OBJECTIVES: This case report illustrates a rare diagnosis and an often overlooked complication of a benign therapy. Prompt diagnosis is essential to preventing long term sequelae. CASE INFORMATION: A fifty-four-year-old man presented with nausea and vomiting for one month. He was having more than five non-bloody emeses per day, often within 10 minutes of eating. Emesis was not always associated with eating. He stated that he was unable to keep down any food. He denied fevers, chills, rigors, or night sweats. He described low-grade headaches with associated tinnitus, an 18-pound weight loss and generalized weakness with increased somnolence as well as new onset erectile dysfunction. He complained of intermittent epigastric abdominal pain, and had had a previous laparotomy for abdominal pain approximately five years ago. He is a lifetime non-smoker and denied taking any medications. Evaluation revealed total calcium of 16.6 with ionized calcium of 7.7 and a creatinine of 4.9. Unenhanced CT revealed a band of calcification in the midline of the anterior abdominal wall measuring approximately 6 cm in length and 1.4 cm in diameter. In addition, there were numerous small mesenteric and retroperitoneal lymph nodes along with a 1cm node in the suprapubic anterior abdominal tissue. He had a tiny stone in the left kidney and all the bones were noted to be hyperdense. His hemoglobin was 11.7 with a normal peripheral smear, erythrocyte sedimentation elevated at 38. B12/folate, LDH and T-and B cell surface markers were normal. PTH-RP was non-detectable and PTH was appropriately suppressed. He was treated with IV fluids, furosemide and pamidronate, with normalization of his calcium at time of dismissal. Upon further questioning, discovered that he was ingesting 6 to 7 grams of calcium per day for the last 20 years. IMPLICATIONS/DISCUSSION: These findings were consistent with milk-alkali syndrome. The recent emphasis on calcium therapy for prevention of osteoporosis and the availability of calcium carbonate has made milk-alkali syndrome the third leading cause of hypercalcemia.

This presentation is consistent with the subacute form of milk-alkali syndrome referred to as Cope's Syndrome. These patients are exposed intermittently for many years and present with symptoms of both acute and chronic hypercalcemia. This patient responded to therapy and his creatinine remained minimally elevated at 1.8 at a six-month follow-up visit.

A FIFTY-SEVEN YEAR OLD FEMALE PRESENTING WITH AGRAPHIA FROM CEREBRAL EMBOLISM OF UNUSUAL ETIOLOGY. E. Martorell 1 , P. Abraham 1 ; 1 Mayo Clinic, Jacksonville, FL (Tracking ID #75540)

LEARNING OBJECTIVES: 1) To describe an unique presentation of a cardiac myxoma.

2) To recognize cardiac myxomas in the differential diagnosis of acute embolic cerebrovascular accident in adult patients. 3) To assess, diagnose and manage cardiac myxomas early in order to prevent potential mortality and morbidity. CASE INFORMATION: A 57-year-old right-handed woman presented to the emergency department with a three-hour history of new onset writing difficulty without additional symptoms. On physical exam her vitals were normal except for an elevated blood pressure of 156/73. Her head, eye, mouth, neck, skin, cardiovascular and pulmonary examinations were unremarkable. Her neurological examination was completely unremarkable with the exception of a mild impairment of finger to thumb movements (apraxia) on the right hand. She was able to write her own thoughts, but had difficulty due to significant agraphia. MRI demonstrated multiple acute and sub-acute ischemic as well as hemorrhagic lesions without surrounding edema. Electrocardiogram and chest films were normal. Baseline CBC, coagulation studies, chemistry studies and rheumatologic serologies were within normal limits. Carotid duplex showed mild stenosis of the carotid arteries bilaterally. A tranesophageal echocardiogram revealed a large multilobulated, motile left atrial mass affixed via a stalk to the left interatrial septum consistent with atrial myxoma. The patient subsequently underwent urgent thoracotomy. A mucinous dark red polypoidgelatinous 5cm  2cm  1cm mass was resected from the left atrium. Biopsy revealed a benign cardiac atrial myxoma. The patient remained neurologically stable and was discharged home on day #10. IMPLICATIONS/DISCUSSION: Myxomas are twice as common in women as in men and most frequently develop between the third and sixth decades of life. About 1% of ischemic strokes in young people are caused by atrial myxomas. Although embolic complications from myxoma most often affect the brain in more than two third of cases, our patient is unique because of her mild, single neurological deficit and absence of the typical presenting signs and symptoms characteristic of this tumor such as obstructive cardiac signs (54±95%) and constitutional symptoms (90%). Systemic emboli occurs in 10±45% of myxoma patients. Cardiac myxoma should always be considered in the differential diagnosis of embolic stroke in adult patients because rapid diagnosis allows curative surgical resection and prevents further morbidity and mortality. heparin. An IVC filter was placed on day #2 because of large clot burden and concern for further pulmonary emboli. Given his right ventricular hypertrophy and likelihood of future pulmonary emboli, the patient was discharged on life-long therapy with coumadin. IMPLICATIONS/DISCUSSION: The incidence of pulmonary emboli in the US approximates 400,000 cases a year, with another 800,000 cases remaining undiagnosed. In one large series of patients with no pre-existing pulmonary disease, the incidence of dyspnea was 73%, pleuritic chest pain 66%, cough 37%, tachypnea 70%, tachycardia 30% and rales 51%. Laboratory, EKG and CXR findings are routinely nonspecific. The untreated mortality for PE is~30%, while the mortality in treated cases ranges from 2 to 8%. It is imperative that clinicians maintain a high index of suspicion for pulmonary emboli when evaluating the patient with dyspnea. Cerebral aneurysms are an extrarenal complication of APKD, with rupture causing 11% of deaths in theses patients. The prevalence of cerebral aneurysms increases with age, averaging around 10% in this population. Patients with a family history of subarachnoid hemorrhage or cerebral aneurysm are at greatest risk. In one study, asymptomatic cerebral aneurysms were found in 22% of patients with a family history, versus 5% of patients with no family history. Risk of rupture increases with size of the aneurysm and with location in the posterior circulation, with values ranging from 0.5 to 4% per year. As the size of the aneurysm is directly related to age, it is rare to detect an aneurysm in patients younger than age 30. Magnetic Resonance angiography is the recommended method of screening. APKD should be considered in patients with a strong family history of renal disease. Screening for cerebral aneurysms in patients with APKD is controversial. Many investigators recommend screening after the age of 30. Other authors recommend screening only for patients with a family history of cerebral aneurysms. Recommended screening intervals vary from every 3 to every 10 years. LEARNING OBJECTIVES: 1. Transient myocardial dysfunction has been described in many non-cardiac illnesses, including sepsis, subarachnoid hemmorhage (SAH), Acute Respiratory Distress Syndrome (ARDS), and and post operatively in non cardiac patients. 2. Mechanisms include oxygen supply and demand mismatch, circulating myocardial depressants, and calcium overload secondary to catecholamine surges. 3. Resolution is usually complete over ten to fourteen days, but elevated troponins may be a predictor of imcomplete recovery. CASE INFORMATION: The patient is a 20 year old previously healthy college student who presented to the emergency department with a three day history of increasing myalgias, sore throat, and diffuse erythematous rash with desquamation of her finger tips. She rapidly developed multi system organ failure, and required temporary mechanical ventilation, continuous veno-venous hemodialysis, and high doses of three pressors for blood pressure support. We had high clinical suspicion for toxic shock syndrome, which was later confirmed by positive TSST-1 antigen. On hospital day #3, she developed a wide complex tachycardia. Her ejection fraction was estimated at 15±20% by echocardiogram. Serial troponins peaked at 33.3. By the time of discharge, 2 1/2 weeks later, her ejection fraction had increased to 34±40%. Her ejection fraction was 30% at four weeks, and 30% at 4 months after initial presentation. She is maintained on a beta blocker, and an agiotensin converting enzyme inhibitor. IMPLICATIONS/DISCUSSION: Transient myocardial dysfunction has been described in a multitude of non-cardiac illnesses, including subarachnoid hemmorage (SAH), Acute Respiratory Distress Syndrome (ARDS), trauma, sepsis, and post operatively in non-cardiac surgical patients. It is a common complication of sepsis. A variety of non-coronary artery related mechanisms have been proposed, icluding oxygen supply and demand mismatch, circulation of various myocardial depressants such as cytokines, and high catecholamine surges leading to calcium overload. While transient myocardial dysfunction has been described in both ARDS and severe sepsis, there is only one other case report in the literature specifically related to toxic shock syndrome. The usual course of sepsis-related myocardial dysfunction is complete resolution over ten to fourteen days. The fact that this patient had an elevation in troponin, and that she still had a depressed ejection fraction four months after presentation, suggests that she may have experienced some degree of ischemic myocardial injury. The magnitude of the persistence of the myocardial insult attests to thd dangers of toxic shock syndrome, even in patients who recover from the acute sepsis and respiratory failure. A 52 year old homeless male presents with multiple complaints. He last saw a doctor ten years ago. His main complaints include right hand numbness and weakness, particularly while he's working. Additionally, he reports occasional dizziness and headaches. On further review of systems, he describes claudication symptoms, difficulty swallowing, especially solid foods, but denies weight loss. His past medical history includes diabetes and hypertension. However, he last received medications over ten years ago. He does drink alcohol daily and smokes cigarettes. On exam, his blood pressure reads 150/100 in the left arm and 130/70 in the right arm. His heart rate is 76, respiratory rate is 6, and he is afebrile. Significant findings on exam include right carotid, right subclavian, and right and left femoral bruits. He also has diminished pulses in the right radial and right brachial arteries, as well as decreased pulses in his feet. An EKG suggests enlarged left ventricle hypertrophy. He eventually received an angiogram, specifically to see if his subclavian bruits and right hand symptoms were significant. His right subclavian artery was aberrant and appeared to wrap behind his esophagus. He also had a severe stenosis of his right subclavian artery proximal to the right vertebral take-off. Furthermore, an exam of the lower extremities revealed severe stenosis in his right iliac artery that received angioplasty. Given the stenosis on angiogram and evidence of flow-reversal, it appeared that subclavian steal syndrome accounted for several of his symptoms, such as the dizziness, headaches, right hand claudication, and exam findings. Coincidentally, the aberrant subclavian seemed to explain his symptoms of dysphagia. Although the diagnosis of subclavian steal syndrome can be deduced by his history and exam, the aberrant subclavian was unexpected, but along with his stenosis, accounts for many of his symptoms. IMPLICATIONS/DISCUSSION: DISCUSSION: Subclavian stenosis can cause symptoms related to subclavian steal. The vertebral artery on the side of the stenosis creates retrograde blood flow from the brain stem by essentially stealing blood from the contralateral vertebral artery. The prevalence of an aberrant right subclavian has been reported as 0.5%-2.9%. The finding of dysphagia has also been reported. This is termed dysphagia lusoria, and was originally described in the 18th century. It translates as jest of nature. The treatment is surgical resection if it causes significant symptoms. He admitted to intravenous drug use, using his right thigh for access. His temperature was 101 F, pulse 110, blood pressure 90/60. His right thigh was erythmatous, edematous and tender, with 10  8 centimeter posterolateral area of fluctulance. The rest of the exam was unremarkable. Labs: WBC 50,000 (93% neutrophils), hemoglobin 7.1, CPK 104, creatinine 5.9. Blood and wound cultures were drawn. MRI showed necrotizing fascittis of posterior/lateral thigh with overlying cellulits, no osteomylelitis. Surgical exploration revealed necrotic skin and subcutaneous tissue extending down to muscle and fascial level, involving half the circumference of thigh. Wide excisional debridement of thigh was performed. Blood and wound cultures grew group A streptococcus sensitive to cefazolin. After antibiotic treatment and two subsequent debridements, the patient improved. Upon discharge, his WBC and creatinine were normal. IMPLICATIONS/DISCUSSION: There are two types of necrotizing fascittis. Type one, which is caused by mixed aerobic and anaerobic bacteria, is associated with diabetes mellitus, cervical necrotizing fasciitis, and fournier's gangrene of perianal area. Type two necrotizing fasciitis, due to group A streptococcus, is associated with history of blunt trauma, varicella, intravenous drug use, penetrating injury and possably with nonsteroidal antiinflammatory drugs. Necrotizing fasciitis should be suspected in patients with severe unexplained pain increasing over time, skin changes (erythema, red-purple discoloration, blisters, bullae), fever, systemic toxicity, myalgias, diarrhea and anorexia. Lab tests show leukocytosis with marked left shift and elevated CPK and creatinine. Imaging studies are most helpful in type one, where gas formation occurs. MRI may overestimate deep tissue involvement. Thus, the only way to make a definitive diagnosis is via surgical exploration. Surgery is indicated for severe pain, toxicity, fever and elevated CPK. Early surgery may improve the outcome, but mortality rates are high even in cases of optimal therapy. Repeat explorations and debridement should be performed until all necrotic tissue has been removed. Additional therapies include antibiotics and intravenous immune globulin.

NON-HODGKIN'S LYMPHOMA PRESENTING AS FLANK PAIN. K.Y. Miskel 1 ; 1 Hospital of the University of Pennsylvania, Philadelphia, PA (Tracking ID #73961)

LEARNING OBJECTIVES: 1) Recognize an atypical presentation of lymphoma 2) Recognize that systemic non-Hodgkin's lymphoma is a common HIV-related malignancy CASE INFORMATION: A 33 year old healthy male with no significant past medical history presented with three weeks of bilateral flank pain. His flank pain was intermittent but had progressively worsened, with radiation to his groin. The pain was associated with movement. He denied fevers/chills, nausea/vomiting, dysuria, or hematuria. Social history was negative for tobacco, alcohol, or illicit drugs. He was homosexual and involved in a long-term monogamous relationship. He had a family history of nephrolithiasis. On initial exam, he was afebrile with a benign abdominal exam, no costovertebral angle tenderness, a normal rectal exam, and guiac negative stool. A urinalysis was significant for +++blood and no leukocyte esterase or protein.

An abdominal xray showed a normal bowel gas pattern with no renal calculi. He was presumed to have radiolucent nephrolithiasis and was advised to follow-up closely. Five days later, he presented to the emergency room with unremitting flank pain, new suprapubic pain, dysuria and fevers to 103±104 F. His only medications were ibuprofen and percocet (prescribed recently for his flank pain). On exam, he appeared uncomfortable, had a T 99.2 F, oral thrush, and bilateral cervical/axillary lymphadenopathy. His abdomen was soft, mildly distended, and diffusely tender to palpation, particularly in the suprapubic area. He had scattered papules with central umbilication on his face, buttocks, and thighs. Laboratory studies were significant for a WBC 5.6, hemoglobin 11.9, creatinine 2.6, AST 124, ALT 158, alkaline phosphatase 627, and total bilirubin 1.5. Abdominal CT scan showed bulky retroperitoneal and pelvic lymphadenopathy, bilateral hydronephrosis, and a circumferentially thickened bladder wall. Bone marrow biopsy and bladder wall biopsy confirmed the diagnosis of stage IV immunoblastic non-Hodgkin's lymphoma involving the bone marrow, GI tract, liver, spleen, and bladder. HIV was positive with a CD4 count of 138 and a viral load of >500,000. IMPLICATIONS/DISCUSSION: Non-Hodgkin's lymphoma occurs in 10-30% of AIDS patients, the most common type being high-grade diffuse large B cell (immunoblastic variant) or Burkitt's-like. Patients usually present with stage IV disease and frequently have involvement of the bone marrow, CNS, liver, and gastrointestinal tract. Although HIV associated systemic lymphoma frequently presents with rapid nodal enlargement and B symptoms, it has no pathognomonic features. This previously healthy male had HIV risk factors as well as molluscum contagiosum and oral thrush that suggested the diagnosis of HIV infection. In addition to chemotherapy, immune reconsitution with highly active anti-retroviral would be necessary for effective treatment.

ALPHA-INTERFERON THERAPY AND DELIRIUM. D. Misra 1 , S. Young 1 , C. Schleupner 1 ; 1 New Hanover Regional Medical Center, Wilmington, NC (Tracking ID #75477) LEARNING OBJECTIVES: Recognize delirium as one of the neuro-psychiatric adverse effects of alpha interferon therapy. We intend to share our experience because it may pose as a diagnostic challenge for clinicians. CASE INFORMATION: We present the case of a 57 yr old caucasian male who had previously been diagnosed with malignant melanoma. He had undergone local excision and was found to have positive lymph nodes. He was started on adjuvant alpha interferon therapy, initially at a dose of 40 million units a day which he could not tolerate primarily because of constitutional symptoms. His symptoms included severe arthralgias, myalgias and headaches. He received this dosage for only 4 days, which was then discontinued and subsequently started back on a reduced dose of 20 million units a day after a drug free interval of one week. He tolerated the lower dose without any side effects. The following week, he was started back on 40 million units a day of interferon which he received for five days. Within a couple of days, pt was experiencing severe headaches along with myalgias and arthralgias. This became worse and patient presented with delirium, agitation and combativeness. He required intravenous sedation and eventually endotracheal intubation for airway protection. His workup including blood counts, basic metabolic panel; urinalysis, drug screen, CT scan of the head and CSF examination were all within normal limits. Serum transaminases were mildly elevated but this was unchanged since the beginning of interferon treatment. His stay in the intensive care unit lasted 24 hours. The following day, he was back to his baseline cognitive level and was discharged home. IMPLICATIONS/DISCUSSION: Alpha interferon is a glycoprotein produced by leukocytes which has broad spectrum antiviral, immunologic and antiproliferative properties. Therefore, it is commonly used in treatment of hairy cell leukemia, hepatitis, renal cell carcinoma and malignant melanoma. The spectrum of side effects is wide and depends on various factors including the dose of the drug, age of the patient and the type of interferon. Our literature search revealed very few case reports of interferon induced delirium. Neuro-psychiatric adverse effects occur with doses higher than 30 million units per day. The temporal relationship of the onset of delirium with high dose interferon treatment in our patient stands out prominently. We believe that this occurrence should be brought to the notice of physicians prescribing interferon so that patients presenting with neuro-psychiatric manifestations are diagnosed and managed appropriately. A 51 year-old man with an ischemic cardiomyopathy presented to the emergency department after experiencing multiple shocks from his automatic implantable cardiac defibrillator (AICD). In the ED, the patient developed ventricular tachycardia at a rate of 162 bpm with a BP of 132/102. His AICD began antitachycardia pacing and DC countershocks without success. The patient was loaded with amiodarone and placed on a 2mg/ min infusion of amiodarone. Sinus rhythm was restored. Lab values included normal liver function tests and a creatinine of 2.1. The patient stabilized. After 24 hours, the amiodarone infusion was reduced to 1 mg/min. Twelve hours later, the patient developed confusion and severe dyspnea. Lasix was given without improvement. The patient developed fever, hypotension, and became lethargic. The exam showed a quiet, tender abdomen. The HCO3 had fallen to 6 meq/L, and the creatinine had risen to 3.2 mg/dl. The ALT was 1947 U/L, the AST was 2629 U/L, the bilirubin was 4.2, and the PT was 16.9s (INR 2.8) . The patient was diagnosed with fulminant hepatic failure. Dopamine and a bicarbonate infusion were begun. Antibiotics were started. The patient was intubated and vitamin K was given. Amiodarone was considered to be a possible cause of the fulminant liver failure. Thus, 72 hours after admission, the amiodarone infusion was stopped despite persistent ventricular ectopy. The patient's status declined and he died on the fifth day from complications from a liver biopsy. IMPLICATIONS/DISCUSSION: Fulminant hepatic failure develops in less than 2 weeks after an insult to the liver. The diagnosis of liver failure should be entertained in the presence of encephalopathy associated with jaundice, coagulopathy, acidosis, fever and hypotension. In this patient, clinical suspicion was confirmed by the rapid change in the liver function tests. The viral hepatidities and drug/toxin exposure are the most common etiologies of fulminant liver failure. In this patient, the leading considerations were ischemic and drug/toxin exposure. A review of the literature revealed at least twenty fatalities from acute hepatic failure following the administration of high dose parenteral amiodarone over the last twenty years. The chronology of exposure and onset of hepatic failure were consistent with amiodarone induced hepatotoxicity in this patient. Regardless of the cause, the treatment of acute liver failure requires removal of the exposure and supportive care for the expected complications. Despite aggressive support, mortality remains at 60-90% without transplantation. LEARNING OBJECTIVES: To recognize that brown recluse spider bites may cause pyoderma gangrenosum and pathergy due to persistent neutrophil mediated injury. CASE INFORMATION: A 47 year-old woman presented with a six month history of recurrent, painful, nonpruritic ulcers on the dorsa of both wrists and the right calf. Past history revealed that six months prior, while cleaning debris from an old tavern, she was bitten on the hand by a spider. The spider was captured and identified as a brown recluse spider. Within hours she was ill with nausea, vomiting, malaise and fever. She improved with supportive treatment. The lesion cleared but weeks later, began to reoccur following minor trauma such as that caused by mosquito bites. On physical examination we discovered pyoderma gangrenosum like lesions that were confirmed by biopsy. Long-term therapy with dapsone was started. IMPLICATIONS/DISCUSSION: Pyoderma Gangrenosum was first described by Brunsting et al in 1930. The etiology is unknown in fifty percent of the cases but associated with Ulcerative Colitis and Behcet's Disease. Spider bites rarely lead to pyoderma gangrenosum and even more rarely lead to recurrent lesions and pathergy. Brown recluse venom has been purified and studied and is known to persist in some wounds for a relatively long time. The precise mechanism of the lesions is not known although neutrophil inhibitors such as nitrogen mustard and dapsone can mitigate or prevent the reaction. The development of new lesions at distant sites from the inciting lesion is unexplainable and suggests an immune mediated response and not a local reaction. The observed clinical response to dapsone suggests an ongoing neutrophil mediated injury. Currently dapsone is being carefully tapered. It is unknown if the lesions will persist and argue for a permanent ongoing cell mediated injury or cease and suggest a self limited condition as remaining venom is cleared.

PLASMAPHERESIS FOR THE TREATMENT OF HYPERTRIGLYCERIDEMIA. C. Carosella 1 , C. Karmen 1 , S. Warshafsky 1 , Y. Murray 1 ; 1 New York Medical College, Valhalla, NY (Tracking ID #76460) LEARNING OBJECTIVES: To recognize the value of plasmapheresis in the treatment of triglyceride-induced acute pancreatitis. CASE INFORMATION: A 50-year-old Hispanic woman with a history of insulin-dependent diabetes mellitus, coronary artery disease and hypertriglyceridemia presented to the emergency room with severe abdominal pain, nausea, vomiting and poor oral intake all gradually worsening over the prior two weeks. She had been treated with a combination of atorvastatin, gemfibrozol, and niacin with only marginal success in controlling her lipid levels. Physical exam revealed an ill-appearing woman complaining of abdominal pain. Bowel sounds were hypoactive, and the abdomen was diffusely tender. The serum was grossly lipemic. Laboratory studies revealed a glucose of 1321 mg/dl, amylase of 1008 mg/dl, lipase 2001 mg/dl, and triglycerides 9198 mg/dl. CT scan of the abdomen was consistent with acute pancreatitis. Her condition rapidly deteriorated with respiratory failure, requiring ventilator support, and renal failure, requiring dialysis. She was transferred to the University Hospital for plasmapheresis. One plasmpheresis treatment with continuous infusion of heparin lead to a substantial and sustained reduction of triglyceride level to less than 150 mg/dl. The patient steadily improved with decreased dependence on the ventilator, increased urine output, and decreased swelling of the pancreas. Unfortunately, the patient suffered a cardiac arrest on the sixteenth hospital day. IMPLICATIONS/DISCUSSION: Plasmapheresis has been used to treat hypertriglyceridemia when adequate diet and drug therapy fail. In this case plasmapheresis was highly effective in removingthetriglyceridesand mayhave ledto thepatient'ssteady,albeit temporary,improvement. (1) to recognize hyperammonemia due to acute valproic acid intoxication (2) to manage hyperammonemia due to acute valproic acid intoxication by understanding its mechanism.

CASE INFORMATION: The patient is a 42 year-old male who ingested 90 500 mg tablets of valproic acid following an argument with his wife. The exact time of ingestion was unclear, but was felt to be 6 to 8 hours prior to presentation. The patient's wife assumed that he was sleeping, but when found to be unresponsive again several hours later, he was brought to the emergency department. On physical examination, the patient was unresponsive, hypotensive, and without hyperreflexia or clonus on neurological examination. Laboratory values revealed normal liver function tests, hypocalcemia, valproate level of 1157 (ref 50±150 ug/ml), and an ammonia level of 270 (ref 9±33 umol/L). The patient's electrocardiogram was notable for QT prolongation. CT scan of the head and lumbar puncture were unremarkable. Intravenous fluids were administered and dopamine was initiated for blood pressure support. The patient's respiratory status declined, he was unable to protect his airway and therefore intubated. Carnitine was administered for the hyperammonemia on a daily basis. The valproic acid and ammonia levels declined over the next 48 hours and his mental status improved. He was extubated after approximately 72 hours. The patient did well and was transferred to psychiatry. IMPLICATIONS/DISCUSSION: Hyperammonemia results when valproic acid is metabolized to propionic acid, which inhibits carbamyl phosphate synthetase, the first enzyme involved in the urea cycle. Valproic acid also binds to carnitine, a molecule important in the metabolism of long-chain fatty acids and ketoacid analogues of various amino acids, thereby depleting serum concentrations of carnitine. Valproic acid also causes increased renal production of ammonia by reducing the synthesis of glutamine. Administration of exogenous carnitine is thought to decrease ammonia levels by binding to valproic acid, and also by relieving the inhibition of carbamyl phosphate synthetase and thus urea synthesis. Management of valproic acid intoxication is largely supportive. Patients who present early may benefit from gastric lavage and a single dose of activated charcoal; however, multiple-dose activated charcoal does not increase the elimination of valproic acid. Other interventions may involve blood pressure support with intravenous fluids and vasopressors, correction of electrolyte abnormalities, and correction of acid/base disorders (commonly an anion gap metabolic acidosis). Mechanical ventilation may be necessary in patients who require airway protection. In the majority of cases, this management strategy results in favorable outcomes. Hemodialysis and charcoal hemoperfusion are additional treatment options. Typically, extracorporeal removal is employed in patients with renal abnormalities, hypotension refractory to all supportive measures, severe metabolic abnormalities, active seizure, or those who are persistently comatose. However there are no controlled trials that demonstrate an improvement in outcome with these measures. year old female initially presented to her primary physician 5 years ago with a blood pressure of 159/98. Repeat readings were similar and she was started on hydralazine 25 mg. There was a modest effect from hydralazine, but control was never acheived. Four months later hydralazine was changed to losartan 50 mg. No significant lowering was obtained. Losartan was increased one month later to 100mg and two months later hydrochlorothiazide 25 mg was added. Her blood pressure stabalized to 140/90 for 6 months. Then a gradual increase in her blood pressure was noticed, so diltiazem was added. Her physical exam and lab values were unremarkable. Due to failure of multiple antihypertensive medications,a magnetic resonance arteriogram of the renal artery was conducted which revealed renal artery stenosis. An angiogram was conducted showing segments of stenosis and dilatation of the right renal artery, consistent with the diagnosis of fibromuscular dysplasia. Renal artery angioplasty was performed, and follow up blood pressure normalized on two medications. IMPLICATIONS/DISCUSSION: This is an elderly female with hypertension refractory to medications. A secondary cause was sought out with an imaging study, which showed a unilateral fibromuscular dysplasia of the right renal artery. It is unusual for a women in this age group to present with this type of secondary hypertension. Patients with fibromuscular dysplasia respond well to angioplasty. LEARNING OBJECTIVES: 1. The reader should be able to list three common causes for hypophosphatemia. 2. The reader should be able to explain why phosphate repletion is typically not be necessary for hypophosphatemia from respiratory alkalosis. CASE INFORMATION: Hyperventilation can precipitate life-threatening alkalosis and severe hypophosphatemia that does not require phosphate repletion. A 36 yo female who was status post cadaveric tracheal transplant and multiple stent placements presented with suspected stent re-stenosis, complaining of dyspnea, increased work of breathing, and inability to clear secretions. Her respiratory rate was 30±34 with normal oxygenation. Emergent bronchoscopy revealed only minimally occlusive concretions, however peri-procedure labs revealed an arterial blood pH of 7.71 and a phosphate of 0.6 mg/dL. The patient reported weakness and paresthesias in all four extremities plus arthralgias in her hands. The patient was started on a NaPO4 infusion @ 0.6 mmol/kg over 6 hrs. She was given supportive care and reassurance for her hyperventilation. After only three hours, the PO4 was 3.3 mg/dL and the infusion was stopped. Repeat ABG showed a pH of 7.49, with improvement in pCO2 from 14 to 27 mmHg. The patient's symptoms resolved. IMPLICATIONS/DISCUSSION: Severe hypophosphatemia, defined as a serum PO4 <1.5 mg/dL, has been reported in 0.22±2.15% of adult hospital admissions. It occurs more commonly in alcoholics and malnourished patients and has a variety of causes, including respiratory alkalosis. In respiratory alkalosis, carbon dioxide readily diffuses from the intracellular space resulting in higher intracellular pH. This activates glycolysis and the formation of phosphatecontaining compounds. Phosphate is used from the circulating inorganic phosphate pool, depleting extracellular stores. This process induces relative hypophosphatemia. This contrasts with metabolic alkalosis where excess extracellular bicarbonate is only poorly diffusible and does not significantly raise intracellular pH. Severe hypophosphatemia can be a lifethreatening disturbance but may not represent total body phosphate depletion or require supplementation. An understanding of the basic physiology guides therapy. 67 year old male initially seen in the emergency room five days before admission for right lower extremity redness, pain and swelling. He was given pain medication and sent home. He returned the following day and two days later with persistent symptoms and was given appropriate oral antibiotics for presumed cellulitis. An ultrasound showed no thrombosis. After his fourth ER visit he was admitted for intravenous antibiotics. Additionally, over the past three months he had noted bilateral lower extremity pain with walking over one block. Work up to date included normal resting and exercise ankle/brachial indices a CT scan of the lumbar spine, which showed disc bulges at L3-4 and L4-5 with mild spinal stenosis. When we met him, he complained of severe pain despite oral narcotics and also endorsed difficulty with his gait over the past week. On physical exam, temperature was 98.60 and the right lower extremity had diffuse anterior erythema without distinct borders. There were no breaks in the skin but onychomycosis was present on bilateral toes. There was 2+ edema on the right and none on the left. Dorsalis pedis pulse was noted only by doppler on the right, but was intact on the left. Neurologic exam revealed significant difficulty with dorsiflexion of the right foot which was presumed to be secondary to pain or possibly related to his known spinal stenosis. Labs revealed a normal white blood cell count, elevated C-reactive protein, small blood in the urine with 0±5 red cells and a creatinine slightly above his baseline. Plain radiographs were normal. Broad spectrum intravenous antibiotics, elevation and pain control were initiated at admission. After two days, the redness and swelling improved but a foot drop and pain persisted. Neurology felt his foot drop could be consistent with his known disc disease but also suggested surgical evaluation. Anterior compartment syndrome was subsequently diagnosed based on a direct compartment pressure reading of 45 mmHg. Because of the delay in diagnosis, the fact that pulses were present and that there was no tissue necrosis or abscess seen on subsequent scanning, the decision was made not to operate. The patient's pain and swelling gradually resolved over weeks but he was left with a permanent foot drop. IMPLICATIONS/DISCUSSION: Compartment syndrome is a surgical emergency that must be detected early to avoid potential serious sequelae. Causes are many and include closed trauma (most commonly), vascular injury and reperfusion, burns, prolonged surgery or traction, overexertion/exercise, and infection. It occurs most commonly in the arm or leg but can be seen in the foot, abdomen, retroperitoneum and mediastinum. Recognition depends on clinical suspicion and can be remembered as the five P's: pain (severe and out of proportion to injury); pulselessness, paralysis (excluding concomitant nerve injury); paresthesia and pallor. Laboratory may show myoglobin in the urine or elevated creatine kinase. Imaging studies may help rule out other causes but direct measurement of compartment pressures are needed for diagnosis. Also well described is the syndrome of chronic compartment syndrome, which is typically thought of as an overuse injury in runners but remains as an interesting possible explanation for this patient's claudication history. LEARNING OBJECTIVES: Early recognition and treatment of Alcohol Withdrawal Syndrome (AWS) may reduce perioperative morbidity and mortality. Intravenous Ethanol (IVE) is still used for the peri-operative management AWS. This case illustrates the importance of 1) identifying patients who require AWS treatment and using evidence-based treatments early to prevent AWS peri-operative complications, 2) exploring the use of alcohol to treat perioperative AWS, and 3) discussing optimum treatments of AWS with patients and family prior to surgery. CASE INFORMATION: T.O. is a 65 year-old man with history of hypertension, congestive heart failure and peripheral vascular disease with bilateral thigh claudication admitted for aortobifemoral bypass. Initial documentation of alcohol use consisted of an admission nursing note stating that the patient drank alcohol. After an uncomplicated surgery, he was successfully extubated and on post-operative day (POD) 2 was transferred to a general surgical bed. On POD 3, he became increasingly agitated and combative. AWS was suspected and Lorazepam 1±2 mg PRN was ordered. Over the next three days he did not improve and was returned to the SICU for re-intubation for airway protection and IV benzodiazapine treatment. After being informed of his clinical condition, the patient's son requested his father receive alcohol to prevent delirium tremens since his father had not consented to``detoxification''. A 10% ethanol drip was begun to 100 cc/h on POD 8 and on POD 9 he was successfully extubated. Although he became more alert and interactive, attempts to wean his IVE caused increased agitation. On POD 11 he was transferred to a general surgical bed, his IVE was discontinued, and he was ordered 12 ounces beer PRN. On POD 12, he continued to be confrontational and was discharged to home. IMPLICATIONS/DISCUSSION: AWS is a complex constellation of signs and symptoms related to autonomic hyperactivity in alcohol dependent patients whose alcohol intake is decreased or discontinued. Severe AWS includes life-threatening delirium tremens that may be exacerbated by the stress of surgery. Pre-or peri-operative detoxification from alcohol may also increase surgical morbidity. Symptom triggered, appropriate dosing of benzodiazapines are effective first line treatment for AWS. However, intravenous and oral alcohol use continues to be used in the perioperative period. Although multiple case reports exist detailing the use of IVE or oral alcohol to prevent withdrawal symptoms, no clinical trials exist to demonstrate its efficacy in management of peri-operative AWS. The use of IVE in the perioperative period is complicated by electrolyte disturbances, pancreatic complications, and difficulty in objectively measuring treatment efficacy. Use of oral alcohol may also reinforce unhealthy outpatient alcohol drinking behavior. Insufficient evidence-based studies exists to guide clinicians regarding the optimum management of peri-operative AWS and until such time, alcohol treatments will continue to be used.

Center, San Jose, CA (Tracking ID #75786) LEARNING OBJECTIVES: To diagnose nephrotic syndrome in a diabetic. To assess the clinical complications of nephrotic syndrome. To recognize the clinical challenges of the obese patient. CASE INFORMATION: A 52 year old morbidly obese male presented to his primary care physician with four days of facial and upper extremity edema. He had developed orthopnea, paroxysmal nocturnal dyspnea, and dyspnea with exertion. His past medical history included poorly controlled diabetes, chronic lower extremity edema, and untreated obstructive sleep apnea. An initial chest CT demonstrated pleural effusions and a soft tissue mediastinal mass thought to be compressing the superior vena cava. Mediastinoscopy of the mass demonstrated no tissue findings; a repeat chest CT, with dye injected in both arms simultaneously, revealed the mass was likely lipomatosis. Further workup of the pleural effusion included an unremarkable echocardiogram and an ultrasound-guided thoracentesis. The pleural effusion was transudative and negative for cytology. The patient's urine revealed 3+ proteinuria and oval fat bodies, and a spot urine protein/creatinine ratio demonstrated over 4 grams of protein.

These findings, along with hypoalbuminemia, were consistent with nephrotic syndrome. The patient's symptoms improved with furosemide diuresis. However, the patient was rehospitalized a week later, complaining of acute shortness of breath. He was already known to be hypoxic, probably from obstructive sleep apnea. A ventilation perfusion scan was performed, and demonstrated a new lingular mismatch of intermediate probability for a pulmonary embolism. The patient stayed in the hospital until five days of oral coumadin overlapped with a heparin drip, as his obesity prevented accurate dosing of low-molecular-weight heparin. IMPLICATIONS/DISCUSSION: Diabetes is a common cause of nephrotic syndrome. The diagnosis can be made by quantification of urine protein excretion; oval fat bodies suggest hyperlipidemia from a fall in oncotic pressure and decreased clearance of very low density lipoproteins. Clinical symptoms include peripheral edema, pleural effusions, and hypercoagulable conditions like pulmonary embolism. The pathophysiology of these clinical symptoms may be due to sodium retention from renal disease and hemostatic abnormalities such as urinary loss of antithrombin III. The diagnostic workup was made more difficult for this patient due to complicating conditions related to his morbid obesity, such as the lipomatosis and obstructive sleep apnea. As obesity increasingly becomes a public health epidemic, generalists need to recognize the extensive clinical challenges for the obese patient. LEARNING OBJECTIVES: 1) To discuss the differential diagnosis of hypoglycemia.

2) To recognize that accidental sulfonylurea ingestion is a cause of hypoglycemia in adult nondiabetics.

3) To recognize that polypharmacy issues are common and are not limited to a patient's own prescriptions. CASE INFORMATION: An 80 year old male on multiple medications presented with severe hypoglycemia. He had no prior history of diabetes and never used alcohol. During his initial hospitalization, the patient was found to be hypogonadal and diagnosed with cholangitis. Diagnosis was based on hypothermia, choledocholithiasis and ductal dilatation although blood cultures were negative and initially there was no leukocytosis. Cortisol levels were normal and no abdominal tumors were found by CT. Insulin levels and c-peptide levels were elevated. The patient's medications did not include any associated with hyperinsulinism. The patient's glucose normalized after two days of treatment with a glucose drip, antibiotics, and stone extraction with sphincterotomy. Upon discharge, the leading diagnosis was sepsis-induced hypoglycemia. The patient was rehospitalized five months later with another episode of hypoglycemia. A sulfonylurea level was sent and returned positive for glipizide. It was then discovered that the patient was erroneously taking his wife's glipizide. The patient has had no further episodes of hypoglycemia. IMPLICATIONS/DISCUSSION: The differential diagnosis of hypoglycemia includes hormone deficiencies, enzyme defects, acquired liver disease, malnutrition, sepsis, malignancy, medications, and hyperinsulinism. Hyperinsulinism can be caused by sepsis, insulinoma, autoantibodies and medications. These medications include exogenous insulin, sulfonylureas and other sulfa drugs, and also quinine and pentamidine. Hypoglycemia due to accidental oral sulfonylurea ingestion in non-diabetics is more common in the pediatric rather than the internal medicine literature. Drug-induced hypoglycemia should be considered whenever the patient has potential access to hypoglycemia-inducing agents. Polypharmacy is a wellrecognized cause of adverse drug events among the elderly. However, estimates of polypharmacy are limited to an individual's medications obtained by prescription or overthe-counter. It should be recognized that individuals with multiple medications may inadvertently consume medications other than their own.

A CASE OF ASCITES AND UNILATERAL LEG SWELLING. B. Taqui 1 , D. Oxman 1 , L. Kaplan 1 ; 1 Temple University, Philadelphia, PA (Tracking ID #76436)

LEARNING OBJECTIVES: 1. Recognize iliac vein compression (May-Thurner) syndrome as rare cause of left leg swelling in patient with negative venous dopplers 2. Recognize potential for endovascular damage and thrombosis resulting from condition 3. Recognize endovascular stenting as potential cure CASE INFORMATION: 38 year old Caucasian male with history of alcohol abuse presented with three days of abdominal pain and increasing abdominal girth. Serum lipase was markedly elevated and paracentesis showed ascitic fluid consistent with pancreatic ascites. He was started on total parenteral nutrition. He subsequently developed left leg and scrotal swelling. Lower extremity venous duplex imaging was negative for deep venous thrombosis, but contrast venography revealed compression of the iliac vein by the right iliac artery. The patient underwent endovascular stenting of the femoral vein with complete resolution of leg and scrotal swelling. His swelling has not recurred since then. His pancreatitis and ascites also gradually resolved. IMPLICATIONS/DISCUSSION: The potential for obstruction of the left common iliac vein by the overlying right common iliac artery against the pelvic brim was first noted by Virchow. Later, May and Thurner described the``iliac compression syndrome.'' In this patient, it was believed that the ascites coupled with intravascular volume burden of parenteral nutrition led to the patients symptoms. The syndrome, which can be acute or chronic, predisposes patients to thrombosis. Thus, contrast venography should be considered in patients with unilateral left lower extremity swelling and negative duplex imaging. Therapy with endovascular stenting of femoral vein offers patients the chance of cure. angiogram showed a beaded segmental narrowing involving the right internal carotid artery from the bifurcation to the base of the skull. Fibromuscular dysplasia was considered, but a repeat angiogram 3 days later showed that the vessels had returned to normal. The patient was discharged on a calcium channel blocker and coumadin. IMPLICATIONS/DISCUSSION: Stroke in young adults is usually due to cardiac embolism, dissection of arteries, vasculitis, and conditions associated with hypercoagulable states. Reversible cerebral segmental vasoconstriction' also known as Call-Fleming syndrome is a rare cause of stroke or TIA and is characterized angiographically by multiple areas of reversible segmental arterial narrowing. Symptom onset can be spontaneous, but has also been associated with pregnancy, migraine, and use of sympathomimetic drugs. Most patients present with headache. Symptoms can last from few minutes to 6 months. The mechanism of vascular narrowing is not understood. Repeat angiogram may be needed to demonstrate the reversible nature of the angiographic changes. LEARNING OBJECTIVES: 1. Consider scurvy in the differential diagnosis when patients appear to have vasculitis, especially in populations at high risk. 2. Appreciate that early diagnosis, facilitated by taking a good dietary history, is important, as scurvy is potentially fatal. CASE INFORMATION: A 54-year-old schizophrenic man presented to rheumatology clinic with a vasculitis-like skin rash, joint swelling and tenderness, edema of a lower extremity and poor dentition. He was a chronic smoker and had a history of alcoholism. He was not on any medication other than haloperidol on a prn basis. An extensive work up for vasculitis was negative. The patient was referred for biopsy of his skin lesions and scurvy was clinically suspected and confirmed with a low vitamin-C level. Biopsy did not show evidence of vasculitis. The patient's symptoms and signs resolved rapidly with oral vitamin-C. IMPLICATIONS/DISCUSSION: Scurvy is a disorder caused by vitamin C deficiency. Its protean manifestations include petechiae, ecchymoses, hyperkeratoses, arthralgias, malaise, fatigue, impaired wound healing, hair with corkscrew deformity and swollen, red purple gums. Our case is unusual because our patient presented predominantly with joint symptoms and a vasculitic-appearing rash. The diagnosis was missed by the rheumatologist, but was later made based on a dermatologist's suspicion. Scurvy is rare in industrialized nations but can occur in certain high-risk groups because of poor intake of vegetables and fruits or an increased need for vitamin C. High-risk groups include the elderly, pregnant and lactating women, infants, the urban poor, the malnourished, food faddists, alcoholics and those with cancer. Scurvy has also been reported in psychiatric patients with depression, schizophrenia and anorexia nervosa. Schizophrenic patients are predisposed to abnormal dietary patterns, food fads and self neglect which subject them to a risk of scurvy. Our patient was at risk because of underlying schizophrenia, a history of alcoholism, and malnutrition, which predisposed him to poor intake. His smoking history probably contributed to his deficiency by increasing vitamin C needs. LEARNING OBJECTIVES: Recognize that pulmonary edema is one of the many causes of localized upper lobe infiltrates, especially when patients at risk for heart failure have been in dependent positions for prolonged periods of time. CASE INFORMATION: A 52-year old man with type-2 diabetes and severe atherosclerotic cardiovascular disease, who had had a toe amputated for an infected ulcer two days before, was admitted with a 3-day history of orthopnea and dyspnea on exertion. He had been on prolonged bed rest to facilitate healing of his foot. On admission he was hypoxic, with coarse crackles at the apices of the lungs and decreased breath sounds at the lung bases. There was no elevation of JVP and the rest of the cardiovascular exam was unremarkable. CXR showed upper lobe alveolar shadows bilaterally with bilateral pleural effusions and Kerley B lines. Spiral CT of the chest done to rule out pulmonary embolism showed bilateral pleural effusions and bilateral nodular upper lobe infiltrates without evidence of embolism. Atypical pulmonary edema was suspected and the patient was propped up in bed, and given furosemide. His symptoms and CXR abnormalities resolved in 2 days. Natriuretic peptide was found to be markedly elevated at 857 pg/ml and an echocardiogram confirmed LV dysfunction with an EF of 20%. The atypical presentation of this patients pulmonary edema was explained by a gravitational effect on the pulmonary circulation, caused by his prolonged assumption of the Trendelenberg position as part of the management of his diabetic foot problems. IMPLICATIONS/DISCUSSION: Pulmonary edema presents classically with bilateral parahilar alveolar shadows producing a bat wing appearance on CXR. In situations characterized by gravitational effects or alterations in lung perfusion, as in COPD or pulmonary embolism, pulmonary edema may present in less typical ways. Acute mitral regurgitation has been reported as causing right upper lobe pulmonary edema and unilateral pulmonary edema has been attributed to the gravitational effects of posture. These atypical presentations can be confused with pneumonia and aspiration. To make the correct diagnosis in patients with atypical CXR's, clinicians must rely on other clinical and radiologic signs of heart failure and take a careful history. Workup revealed pulmonary infiltrates, anemia with left-shift, and a sputum KOH preparation demonstrating round, non-staining elements felt to be consistent with blastomycosis. After four days of intravenous amphotericin, the patient developed progressive pulmonary infiltrates requiring ventilatory support. Subsequent evaluation with broncho-alveolar lavage revealed alveolar hemorrhage and red cell ghosts within macrophages; these findings were consistent with a vasculitic rather than an infectious disease process. Eleven years later, the patient presented with hemoptysis, fatigue and arthralgias leading to initiation of immunosuppresants for presumed autoimmune disease. After discharge, however, sputum cultures grew Blastomyces dermatitidis, and followup chest CT revealed bibasilar consolidation with cavitary changes prompting a reduction in steroid dose and initiation of anti-fungal therapy. IMPLICATIONS/DISCUSSION: The literature contains multiple cases of blastomycosis mimicking a variety of illnesses, from neoplastic to autoimmune disease. Certain confounding factors can limit the differential diagnosis: (i) the indolent course of blastomycosis with nonspecific presenting symptoms may catch the unwary off-guard, (ii) blastomycosis may present in a manner similar to a variety of disease processes, (iii) and finally, blastomycosis may be superimposed upon another illness, clouding both diagnosis and management.

ACUTE TUBULOINTERSTITIAL NEPHRITIS ASSOCIATED WITH CLOPIDOGREL. N. Palanichamy 1 , C. Kumar 1 ; 1 Oakwood Healthcare System, Dearborn, MI (Tracking  ID #76611) LEARNING OBJECTIVES: To describe clopidogrel induced acute renal failure, a previously unreported drug reaction. CASE INFORMATION: An 89 year-old white male presented with hematuria and acute renal failure. His Medications were aspirin, plavix, metaprolol, prinivil, lasix and flomax. He was placed on clopidogrel two weeks prior. He stopped the drug the day before admission. His creatinine level was 3.9 mg/dl (baseline creatinine 1.3 mg/dl). Urinalysis showed proteinuria, leukocytes and erythrocytes. 24-hour protein excretion was 756 mg. A renal ultrasound showed no obstruction. Over the course of the next week his renal function deteriorated (creat 8.9 mg/ dl). Renal biopsy showed a widened, edematous interstitium with moderate lymphocytosis, plasma cells and regenerative tubules and was compatible with tubulointerstitial nephritis (AIN). Dialysis was started and the patient was placed on steroids. With treatment the creatinine decreased to 2.6 mg/dl, the dialysis stopped and the steroids tapered. Based on the history and presentation clopidogrel was thought to be the etiology of the nephritis in this case. IMPLICATIONS/DISCUSSION: To our knowledge, this is the first case of clopidogrel induced acute tubulointerstitial nephritis. The rapid deterioration in the renal function two weeks after starting clopidogrel and the absence of confounding factors suggests the diagnosis in the presence of the biopsy findings. Clopidogrel affects platelet aggregation by inhibiting the ADP receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. The precise mechanism of the renal dysfunction is unknown but, like ticlopidine, a chemically similar drug with known adverse renal effects, may be caused by cell-mediated injury. Guerciolini et al. (1985) demonstrated a positive lymphocyte stimulation test in explaining agranulocytosis associated with ticlopidine. The other known mechanism of drug induced AIN, antibody mediated injury and circulating immune complexes are less likely causes insofar as the immunoflorescent studies in our case were nonspecific. In addition to the more commonly known side effects of clopidogrel physicians now need to realize that in rare instances it may cause renal dysfunction. LEARNING OBJECTIVES: Think about malignancy in the differential diagnosis of leukemoid reaction. CASE INFORMATION: A 68 year old Caucasian male with no significant past medical history presented with complaints of swelling of both legs, vague abdominal pain, watery diarrhea and increased urinary frequency of 6 weeks duration. He also reported a weight gain of 50 pounds over the past 6 months. On physical examination, he was afebrile, pulse was 81/min and blood pressure was 145/82 mm Hg. He had pallor and massive lower extremity edema extending upto the scrotum. There was no lymphadenopathy. Abdominal examination revealed a large hard mass extending anteriorly from the right lumbar region to the opposite flank and pelvis. Laboratory data-Hb 8.7gm/dl, Total WBC 74,800/cu mm, Differential±40% neutrophils, 56% bands and 4% monocytes, platelets 195 K/cu mm, LAP score 217. Urinalysis was normal. Alkaline phosphatase 144 IU/L, total serum protein 6.3 g/dl, C-reactive protein 13.3 mg/dl. Both blood and urine cultures were negative. Peripheral smear±leukocytosis, mature granulocytes and band forms, no blasts. CT scan of the abdomen showed a large, lobulated retroperitoneal mass extending to the posterior aspect of the right kidney, measuring 9Â8Â15 cm and another left sided pelvic mass, 14Â10Â17 cm, contiguous with the urinary bladder and pressing on the IVC. Multiple low-density lesions were also noted in the liver and spleen. Bone marrow biopsy revealed a myeloid predominant hypercellular marrow, no blast cells. A CT guided biopsy from the hypodense lesion in the liver revealed a metastatic, poorly differentiated malignant fibrous histiocytoma (MFH), pleomorphic type, positive for vimentin and negative for cytokeratin and alpha-fetoprotein on immunostaining. The IL-6 and IL-2 levels were normal. The patient was started on chemotherapy with cyclophosphamide, dexamethasone, adriamycin and dacarbazine. He developed disseminated intravascular coagulation on the 5th day of chemotherapy and expired. IMPLICATIONS/DISCUSSION: This case is unique because of the association of malignant fibrous histiocytoma with leukemoid reaction (LR). Several cases of soft tissue sarcomas with leukocytosis have been reported, but less than 15 cases of MFH with this phenomenon were found in the review of literature. The relationship between cytokine levels and LR has not been consistently demonstrated in the cases reported. Although, in our patient, serum cytokine levels were noninformative and histologically, the metastatic component of the tumor was not significantly different from the``non-inflammatory'' fibroxanthosarcomas, the absence of any other cause of leukocytosis highlights its association with MFH. The prognostic significance of leukocytosis with these tumors is yet to be defined, an added survival benefit of the inflammatory component is debatable. year-old male with a history of 30 pack-year tobacco use and positive tuberculin test, presented with nonproductive cough and night sweats for several months. Physical exam was normal. Serum immunofixation tests and acid fast stains of sputum were normal. Pulmonary function test (PFTs) showed moderate obstructive airway disease, and transthoracic echocardiogram was unremarkable. Chest x-ray (CXR) exam revealed a rounded opacity in the right lung apex. Computed tomography (CT) showed a 2.5 cm right apical mass and multiple small nodules seen in both lung fields. Transbronchial biopsy of the apical mass was consistent with pulmonary nodular amyloidosis. Follow-up CT imaging showed no significant change after one year. Case 2: A 73 year-old Caucasian male with a history of 40 pack-year tobacco use, had a CXR for preoperative evaluation for blepharoplasty. He denied cough, weight loss, and night sweats. Physical exam and laboratories were all within normal limits. PFTs were consistent with mild obstructive airway disease. CXR exam showed an incidental finding of a round density in the right middle lung field. CT revealed a 1.5 cm round opacity in the right middle lobe. Transbronchial lung biopsy of the mass was consistent with pulmonary nodular amyloidosis. Follow-up CT imaging showed no significant change after one year. IMPLICATIONS/DISCUSSION: Pulmonay amyloidosis may present in one of three ways:

(1) diffuse, interstitial process associated with primary, systemic amyloidosis and a median survival of 16 months after diagnosis; (2) Endobronchial amyloid causing obstruction that is usually amenable to treatment with laser therapy; and (3) isolated, pulmonary nodular amyloidosis that is not associated with systemic disease and follows a benign course. Our two cases are examples of pulmonary nodular amyloidosis. Pulmonary disease is uncovered as an incidental finding with one or more nodular opacities seen on chest imaging suggesting a malignant process. Transbronchial lung biopsy may establish the diagnosis with light microscopy showing amorphous, extracellular deposits that stain pink with hematoxylin and eosin. Under polarized light, amyloid produces apple-green birefringence. In our two cases of primary nodular amyloidosis, elevated monoclonal proteins were not found, consistent with the absence of systemic involvement in this presentation of disease. Further, follow-up chest imaging has revealed no change in the pulmonary nodular opacities, reflecting the benign course of this disease. year-old homeless male with a history of untreated Schizophrenia was brought in for evaluation of fatigue and altered mental status. On presentation, the patient was noted to be disheveled and confused with initial BP 128/61, P88, RR 17, and T99.9. Physical exam was remarkable for numerous nits on hair and clothing, and skin with innumerate number of excoriated, hemorrhagic papules. Rectal exam revealed no masses but guaiac negative brownish stool. Initial laboratories included: WBC 13.7, HGB 3.7, HCT 11.5, PLT 375, MCV 72, RDW 16, and 71% PMN. Gastric lavage was negative for occult blood. Computed tomography of head and a diagnostic lumbar puncture were normal. Serum anemia work-up was remarkable for low ferritin (11) and iron (76). Folate and vitamin B12 levels were normal. The remaining laboratories, imaging studies, and cultures were all within normal limits. He was treated for pediculosis with permethrin and received blood transfusion with an appropriate increase in blood counts. His mental status and leukocytosis significantly improved as pediculosis and anemia were treated. Blood counts has remained stable after treating pediculosis. IMPLICATIONS/DISCUSSION: The 3 most common arthropod exoparasites in humans are Pediculus capitis (head louse), Pediculus corporis (body louse), and Phthirus pubis (pubic louse). They belong to the order Anoplura, the sucking lice that feed on blood approximately 5 times per day for approximately 40 minutes each time. Hemorrhagic macules or papules develop at the sites of feeding lice, and vertical excoriations due to scratching and postinflammatory hyperpigmentation are common (aka, vagabond's disease). These lice can be transmitted directly from person to person. They are also a potential vector for transmission of diseases such as typhus, louse-borne relapsing fever, and endocarditis. Bacterial superinfection at the sites of infestation is also common. Zoonotic pediculosis (louse infestation) has been reported as a major cause of anemia in domestic animals. This possibility, however, has not been reported in humans. Our case presents a homeless male wtih severe iron-deficient anemia associated with chronic pediculosis. This case supports the hypothesis that louse infestation is an uncommon cause of anemia in humans. To our knowledge this is the first case report of its kind (Internet and Medline search from 1960 to present). year-old woman presented with chest pain and syncope after exertion. The chest tightness was associated with shortness of breath, nausea, and diaphoresis. She first experienced exertional angina at age 18 during military training. The episodes had increased in frequency since. Her vital signs were normal. The cardiac examination was normal with the exception of a a left-sided heave and a loud, persistently split S2 that widened with inspiration. An electrocardiogram demonstrated normal sinus rhythm, right axis deviation, and T-wave inversion in the inferior and anterior leads. Three troponin assays were negative. Echocardiography revealed right ventricular enlargement, dilated pulmonary arteries with pressures of 50 mm Hg, normal chamber sizes, normal valves, and no septal defects. A ventilation/perfusion scan, ANA and RF were normal. A right heart catheterization confirmed pulmonary artery hypertension with a systolic pressure of 70 mmHg and a normal wedge pressure. A bubble study looking for small septal defects was normal. Angiography confirmed the presence of dilated pulmonary arteries without evidence of thromboembolic disease. IMPLICATIONS/DISCUSSION: Primary pulmonary hypertension is a diagnosis of exclusion, with a prevalence of one to two people per million. Because of its low incidence and protean nature, the most cost effective strategy is to exclude common etiologies of pulmonary hypertension such as pulmonary embolism, valve disease, lupus, CREST and left heart failure. Right heart catheterization is the best diagnostic test. The median survival after diagnosis is 2.5 years. Intravenous epoprostenol is the drug of choice, but oral vasodilators are also used. Anticoagulation has been shown to prolong life; some patients may also respond to oral vasodilators. Anticoagulation improves mortality by decreasing thombosis and thromboembolism. This patient was started on a trial of oral bosentan and warfarin. Since primary pulmonary hypertension has no cure, an exhaustive search for secondary causes is warranted in any patient with this diagnosis. Other than these findings, her neurological examination was unremarkable. MRI of the head revealed multiple foci of hyperintensities in the white matter; bilateral enhancement of the tentorium and cranial nerves III, V, VII; and unremarkable orbits (Fig 1,2,3) . Cerebrospinal fluid (CSF) revealed a protein level of 600 mg/dl; WBC 210/uL (lymphocytes 95%) and glucose 91 mg/dl. Serum and CSF were positive for Lyme antibodies on ELISA. The result was confirmed by western blot assay on the CSF. The patient was started on intravenous ceftriaxone 2 gm every 24 hrs. On the 4th day of antibiotic therapy, she developed left sided LMN facial palsy. After 4 weeks, a repeat CSF study showed significant improvement: the protein level fell to 82 mg/dl and WBC count to 33/ul. Six weeks after ceftriaxone therapy, the diplopia, trigeminal neuralgia and facial palsy resolved completely. IMPLICATIONS/DISCUSSION: Though facial palsy is a relatively common presentation of Lyme disease, multiple cranial neuropathies may be the initial manifestation and must be borne in mind. The diagnosis can be easily missed in such cases without any antecedent history of tick bite or rash. A history of travel or residence in an endemic area is a useful clue. In addition, MRI may play an important role in the diagnosis. Our patient's MRI at admission revealed bilateral enhancement of meninges and cranial nerves III, V and VII indicating evidence of inflammation that preceded the full clinical expression. To our knowledge, multiple cranial neuropathies as the initial manifestation and evidence of gadolinium enhanced MRI lesions of the involved cranial nerves have been rarely reported. Recognizing these subtle imaging findings, combined with high clinical suspicion is the key to diagnosis and allows early treatment which can help prevent further complications.

WALDENSTROM'S MACROGLOBULINEMIA AND HEART FAILURE. R. Pearl 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77006)

LEARNING OBJECTIVES: 1. Use the physical examination to determine cost-effective use of echocardiography 2. Use an understanding of physiology to guide diagnostic procedures 3. Diagnose infiltrative cardiomyopathy. CASE INFORMATION: A 73 year-old man presented with right-sided chest pain and shortness of breath. The shortness of breath had worsened over two weeks, with new onset three-pillow orthopnea and lower extremity edema. His vital signs were normal. He had a soft S1, a normal S2, and an S4. Although he had bilateral crackles and an elevated JVP, there was no S3 or inferiorly displaced PMI. His edema was initially ascribed to hypo-albuminemia (Albumin = 2.) although his pit recovery time was greater than 90 seconds. Based upon a suspicion of a restrictive cardiomyopathy, an echocardiogram was obtained. This showed left ventricular hypertrophy and an E-to-A mitral-flow reversal consistent with diastolic dysfunction. His ejection fraction was 20% despite ventricular hypertrophy. A bone marrow biopsy was performed that confirmed the diagnosis of Waldenstrom's macroglobulinemia. IMPLICATIONS/DISCUSSION: The physical examination in concert with an understanding of the physiology underlying disease is the foundation for cost-effective identification of occult diagnoses. The silent S1 suggested a low ejection fraction, and while the S4 without an S3 or inferiorly displaced PMI suggested a non-compliant hypertrophic ventricle. Both of these conclusions were confirmed by echo. A low ejection fraction despite ventricular hypertrophy suggested an infiltration of the ventricular wall. LaPlace's law states that wall tension is a function of the pressure and radius of a chamber, divided by the thickness of the chamber's wall. Because wall tension is proportional to afterload (like a spring, the ventricle must overcome the weight that has stretched it) a thick ventricle wall should lower wall tension, thereby decreasing the ventricular afterload. The ejection fraction should increase proportional with the wall thickness. Failure to do so suggests that the thickness is due to infiltration with a non-contractile substance. The history of chronic renal insufficiency and anemia suggested the diagnosis of amyloidosis due to Waldenstrom's macroglobulinemia. This clue was instrumental in prompting the bone marrow biopsy that confirming the diagnosis. The finding of a speckled myocardium on echocardiogram is a classic, though late state finding of the disease. A 54-year-old male with a history of leukocytoclastic vasculitis was noted to have a diffuse erythematous rash while being admitted for an unrelated endoscopic procedure. The rash first developed two weeks prior in the patient's right groin and gradually spread to include both legs and his right arm. It had not responded to a course of levofloxacin or over the counter topical ointments. In the month prior to admission the patient had been tapered from 15 milligrams to 12.5 milligrams of prednisone. On admission the patient had warmth, erythema, and mild tenderness to the affected areas. Numerous 1 to 5 millimeter pustules also were present on the erythematous base. The patient was afebrile and had a mildly elevated white count of 11 thousand. Gram stain and culture of the pustules revealed no bacteria. Fungal elements were not seen. A punch biopsy was taken and returned consistent with pustular psoriasis. Acitretin therapy was initiated. IMPLICATIONS/DISCUSSION: Psoriasis is a relatively common dermatologic disorder that occurs in approximately 1% of the North American population. While generally benign, psoriasis can present in an atypical and potentially life threatening manner. Pustular psoriasis can occur in varying degrees of severity with distinct subtypes. These include the relatively limited form of palmoplantar pustulosis to the more severe generalized von Zumbush type. If untreated, disruption of the skin's barrier can lead to large amounts of volume loss and secondary bacterial infections. Systemic involvement including arthritis, heart, liver, and kidney failure has been associated with advanced cases. Triggering events are often unknown, but there has been an association with pregnancy, concurrent infections, and medications. Given the nonspecific somatic complaints and laboratory abnormalities, successful diagnosis requires recognition of the pustular areas on the erythematous base. Our patient had two associated medication risk factors of hydroxychloroquine therapy and corticosteroid withdrawal that likely acted as the inciting event. IMPLICATIONS/DISCUSSION: t is a challenge to manage pregnant patients who require anticoagulation for prosthetic valves. Coumadin is the drug of choice for anticoagulation, however because it freely crosses the placenta it is not considered safe to use in pregnant patients. The teratogenic effects of coumadin usually occur between the sixth and ninth weeks of gestation. The most common abnormalities occur in bone and cartilage development. In the second and third trimesters one can develop abnormalities of the fetal central nervous system, optic atrophy, microcephaly, mental retardation, spastisity and hypotonia. Unfractionated heparin does not cross the placenta because of its high molecular weight. Since it does not cross the transplacental barrier it lacks teratogenic effects and will not anticoagulate the fetus. Low molecular weight heparin is another anticoagulant that should be considered in these patients. However, its use in pregnancy is not well studied. The ideal treatment for a pregnant woman requiring anticoagulation would be to switch from coumadin to heparin prior to conception. The patient shold be hospitalized until she is therapeutic on heparin. The three approaches that are recommended include: 1. Dose adjusted unfractionated heparin throughout pregnancy. Heparin is given subcutaneously every 12 hours and then dose adjusted to maintain two times the normal PTT, or anti-Xa levels of 0.35 to 0.70 U/ml. 2. Dose adjusted low molecular weight heparin throughout the pregnancy so as to keep a four hour post injection anti-Xa level at 1.0 U/ml. 3. Unfractionated or low molecular weight heparin therapy until the thirteenth week, with a change to coumadin until the middle of the third trimester and then restarted on unfractionated or low molecular weight heparin until delivery. LEARNING OBJECTIVES: 1) Recognize the cutaneous manifestations of sarcoidosis 2) Review the differential diagnosis of a nodular cutaneous lesion in a immigrant from subsaharan africa 3)Review the pathophysiology of cutaneous sarcoidosis CASE INFORMATION: A healthy 21 year old South Sudanese woman, 4 weeks post-partum, who had spent 2 years in an Ethiopian refugee camp before immigrating to the U.S one year ago, presented with a rash on her left cheek of over 2 years duration. She had noticed the rash first back in Sudan and had persisted during her refugee camp stay. She reported that the rash had been non-pruritic, non-exudative, indolent and asymptomatic. She had no history of photosensitivity, exposure to chemicals or insect bite. A week's trial of anti-fungal topical application was unsuccessful. Her recent pregnancy was uneventful including negative HIV, Hep.BSAg and VDRL serology. Her PMH was negative for major medical illnesses and prior eruptive lesions. She did have a history of positive PPD 1 year ago with negative CXR following immigration to the U.S. She had not been treated with anti-tuberculous agents. Her ROS was otherwise unremarkable. Exam revealed a hyperpigmented nodular lesion approximately 1cm wide and 4 cms long in a semi-circular distribution over the left malar area. The rash was further noted to be non-tender, normothermic with mild induration. Physical exam revealed a healthy 21 year old woman with normal cardiac, pulmonary, gastrointestinal and neurological exam, with no evidence of lymphadenopathy and a similar rash elsewhere. Her CBC was within normal limits. Given the patient's ethnicity and travel history, leishmaniasis and cutaneous mycobacterial infections were included in the differential. Consideration was also given to Sarcoid and variant discoid lupus. (Syphilis was considered unlikely, given recent negative serology). A diagnostic excisional biopsy revealed sarcoid-like granulomas surrounded by mild chronic lymphocytic infiltration. Special stains (including AFB, giemsa, PAS, Fite, Giemza and warthin-starry) did not reveal pathogenic microorganisms. Patient was initiated on a local topical steroid application (clobetasol propionate) for two weeks with dramatic resolution of the rash. A diagnosis of Sarcoidosis was therefore made by exclusion and dramatic response to treatment. IMPLICATIONS/DISCUSSION: The protean manifestations of Sarcoidosis include a) Erythema nodosum (most common, although non-specific lesion). b)Lupus pernio (classically involving the rim of the nose and associated with infiltration of the nasal mucosa causing ulcerations or even fatal airway obstructions). c) Papules, nodules or plaques (as seen in the above patient). d) Psoriasis like rash. e) lesions in scars and tattoos. The learning objectives of this presentation are to review the cutaneous manifestations of Sarcoidosis, the differential diagnosis of nodular cutaneous lesions in an imigrant population and the pathophysiology of Cutaneous Sarcoidosis. Considering the growing immigrant population in the U.S, the differential of an indolent chronic rash should include parasitic infestations. However, in patients of African decent, the extremely variable masquerading rash of sarcoidosis should be considered as an important part of the differential. Hemochromatosis is the most common adult genetic disorder. Early diagnosis enables rapid treatment and an improved prognosis. The first clinical manifestation is represented by arthropathy in 45% of the cases. The articular features of are often nonspecific and associated with a delay in diagnosis that may compromise outcome. Treatment of the arthritis with analgesics is often disappointing, but identification of the underlying disease permits institution of life-saving phlebotomy therapy. The aim of this report is to highlight the fact that patients with premature osteoarthritis should alert the physician to screen for hemochromatosis in order to formulate the correct diagnosis before the development of severe internal organ involvement. MRI of the head was done to rule out pituitary masses and was normal. After extensive review it was found that she received an injection of Kenalog 40 mg to the right shoulder from another MD six weeks prior to presentation. Without any other exogenous sources of steroid, it was concluded the pt had experienced cushingoid symptoms from the Kenalog injection followed by secondary adrenocortical insufficiency at presentation. IMPLICATIONS/DISCUSSION: Therapy with pharmacological doses of glucocorticoids is the most frequent cause of secondary adrenocortical insufficiency. The usual presentation is similar to that of primary adrenocortical insufficiency, with two important exceptions. Since pituitary secretion of ACTH is deficient, the characteristic hyperpigmentation of Addisons disease is absent. The clinical features of mineralocorticoid deficiency are usually absent in the unstressed state, and therefore volume depletion, dehydration, and electrolyte abnormalities are usually absent. Hypotension is also less severe, except in acute presentations. Hyponatremia can be present, and is usually due to water retention and inability to excrete a water load rather than to sodium loss. The clinical features of ACTH and glucocorticoid deficiency are nonspecific and consist predominantly of weakness, lethargy, easy fatigue, anorexia, nausea, and occasionally, vomiting. Patients may also describe arthralgias, myalgias, and exacerbation of allergic responses. With acute decompensation, severe hypotension or shock may occur and be unresponsive to vasopressors unless glucocorticoids are administered. At that time he also described shortness of breath, insomnia, anorexia, and a sense of anxiety. The exam revealed an agitated but otherwise well-appearing man with tachycardia. Mr J had a positive urine cocaine screen. He was admitted and ruled-out for myocaridal infarction (MI) with serial troponins and electrocardiogram. Two months later, Mr J returned with similar complaints. Again his urine was positive for cocaine and his serum was negative for troponins. Over the next three months he returned to the ED four more times with a new resting tremor and a weight loss of over sixty pounds. Cocaine screens remained positive. The patient refused treatment for substance abuse and expressed dissatisfaction with the quality of care he received. Finally in September of 2002 a Thyroid work-up was performed, demonstrating a TSH <0.1 and a free thyroxine >6.5. A radioiodide uptake scan confirmed the diagnosis of Graves' disease. The patient had symptomatic relief with beta blockade and propylthiouracil. He is currently scheduled for thyroid ablation. IMPLICATIONS/DISCUSSION: An estimated 1.5 million Americans (0.7%) abuse cocaine chronically. In 1998, cocaine contributed to Emergency Department visits on 152,000 occasions (1). Cocaine abuse is a potentially life-long chronic disease. Acute cocaine intoxication may mimic other diseases, preventing or delaying their diagnosis. An easy explanation for Mr. J's tremor, weight loss and agitation were already available, thus a thyroid work-up was delayed. Cocaine abuse may draw the physician's attention to conditions caused by chronic abuse rather than unrelated medical problems. MI should be ruled out, but not without considering hyperthyroidism. In one study of 165 patients with cocaine intoxication and psychotic symptoms, only 18% were given the proper diagnosis of schizophrenia on the initial evaluation (2) . Finally, some physicians may perceive substance abuse as a primary and overriding health care problem. Mr. J did not wish to address his cocaine abuse and still rightly expected treatment of his other medical problems. In conclusion, many misperceptions may cloud the diagnostic process with patients who abuse cocaine: confusion of symptoms with drug effects, distraction from unrelated medical conditions and prioritizing abstinence above other medical care. LEARNING OBJECTIVES: Recognize the potential for endocarditis after an endometrial sampling procedure. CASE INFORMATION: Antibiotic prophylaxis is not recommended prior to endometrial sampling procedures or even dilation and curettage because of the very low risk of infectious complications. We report a case of acute bacterial endocarditis caused by Streptococcus agalactiae following endometrial sampling in a woman with no known valvular abnormalities. A 59-year-old woman with a history of abnormal uterine bleeding who had undergone office based endometrial biopsy about two weeks earlier was found unresponsive at home and was brought to the hospital. She was noted to have a temperature of 102.5 degrees Fahrenheit; she was awake, but did not speak and withdrew her left side more than her right side to painful stimuli. She also had petechiae in her conjunctiva, fingers and toes. Laboratory evaluation showed white blood cell count of 21,400 cells/mm3, normal electrolytes and glucose, and normal liver enzymes. CT scan of the head was normal at presentation. On hospital Day 3, blood cultures from admission grew beta-hemolytic Group B Streptococcus from all samples. Transthoracic and transesophageal echocardiograms demonstrated a 4Â3 cm lesion on the posterior leaflet of the mitral valve with moderate mitral regurgitation. Repeat CT of the head demonstrated a large left middle cerebral artery infarction, but no evidence of abscess. The patient responded to antibiotics, but died of complications before valve replacement surgery could be performed. IMPLICATIONS/DISCUSSION: Endometrial assessment by means of biopsy or sampling of endometrial cells is a minimally invasive alternative for dilation and curettage or hysteroscopy. Techniques using the Pipelle endometrial sampling device are the most popular due to high sensitivity and specificity compared to other office based procedures, and low rates of complications. In dilation and curettage, studies show transient bacteremia in 5% of patients and up to 0.34 in 100 patients have fever complicating their procedure. We hypothesize that our patient's endocarditis was caused by bacteremia resulting from her endometrial sampling, making this a very unusual complication of a common procedure. There is no data supporting the use of antibiotic prophylaxis for office based (i.e. Pipelle) or operating room (i.e. dilation and curettage) endometrial sampling. Unfortunately for our patient, mortality rates for Group B Streptococcus endocarditis approach 40%, similar to those associated with staphylococcal species.

WEIGHT fatigue, and night sweats. He denied using tobacco or intravenous drugs. On physical examination, he had orthostatic hypotension and a new 2/6 systolic ejection murmur. He did not demonstrate peripheral stigmata associated with endocarditis (Osler's nodes, Janeway lesions, or splinter hemorrhages). Pertinent labs for the hospitalization included a hemoglobin of 10.2 g/dL, hematocrit of 30.1%, and mean corpuscular volume of 81.9 fL (further labs confimed iron deficiency). An erythrocyte sedimentation rate (ESR) was 35; C-reactive protein was 12.5 and albumin was 2.0. WBC, BUN, creatinine, liver function tests, chest radiograph, and EKG were normal. PSA, TSH, and morning cortisol levels were normal. PPD and HIV screening were negative. Esophagogastroduodenoscopy and colonoscopy did not show any abnormal pathology. CT scans of the head, neck, chest, abdomen, and pelvis were unremarkable except for a small pericardial effusion and an old ischemic left cerebellar infarct. On day six of his hospital stay, the patient had a fever with a Tmax of 39.0 and a bandemia of 14% with a normal WBC count. Two sets of blood cultures were drawn and diphtheroids, identified as species other than Corynebacterium jeikeium, grew in all specimens. A transthoracic echocardiogram revealed an aortic valve vegetation, moderate aortic regurgitation, and an ejection fraction of 60 to 65%. A diagnosis of subacute bacterial endocarditis was made and the patient was treated with a four week course of intravenous ampicillin. Surveillance cultures drawn five days after starting antibiotics were negative and the patient remained afebrile for the rest of his hospital stay. IMPLICATIONS/DISCUSSION: Bacterial endocarditis is a common entity encountered in the hospital setting. The diagnosis may be missed as it can mimick a variety of conditions due its protean clinical manifestations and the diversity of pathogens associated with it. Recognition of these signs and symptoms can enable the clinician to make an early diagnosis and pave the way for intervention and further reduction in morbidity and mortality. These include constitutional symptoms such as fever, fatigue, and weight loss; new and/or changing murmurs; embolic phenomenon such as Janeway lesions, mycotic aneurysms, and peripheral emboli to multiple organs; and immune complex mediated phenomena such as glomerulonephritis, Osler's nodes, and arthritis. Elevated ESR and C-reactive protein, and a positive rheumatoid factor often accompany these presentations. Anemia is present in 70 to 90% of cases. Weight loss is found in up to 25% of cases and often leads to an exhaustive work up for malignancy, tuberculosis, and other chronic diseases. If there is a high index of suspicion, diagnosis can be made by positive serial blood cultures or the presence of valvular vegetations on echocardiogram. Streptococci, enterococci, and staphylococci are isolated in the vast majority of cases. Other pathogens are rather uncommon and include the HACEK group (Hemophilus, Actinobacilus, Cardiobacterium, Eikenella, and Kingella), Coxiella, Neisseria, Pseudomonas, Salmonella, Streptobacillus, Bacteroides, Corynebacterium and other anaerobic gram-negative bacilli. There are case reports of native and prosthetic valve endocarditis caused by diptheroids including C. jeikeium, C. urealyticum and C. striatum. Of the nondiphtheriae corynebacteria, C. jeikeium is the most worrisome as it is resistant to multiple antibiotics and warrants treatment with vancomycin. Diagnosis of the causative organism is imperative for initiation of therapy with appropriate antibiotics and possible surgical intervention. LEARNING OBJECTIVES: After listening to this vignette presentation the leaner will: 1. Recognize the importance of NSAID-induced adverse effects in the lower GI tract. 2. Add NSAIDs (including the selective COX-2 inhibitors) to the differential diagnosis of rectal bleeding and intestinal strictures. CASE INFORMATION: A 58 year old female with a history of GERD treated with a proton pump inhibitor, hypertension, hyperlipidemia, and hypothyroidism was prescribed celecoxib 200mg/day for mechanical low back pain. After approximately a month of therapy she presented with bloody diarrhea. She denied fever or chills. There was only minor abdominal cramping. The patient has a strong family history of colon cancer and had undergone a surveillance colonoscopy 2 years ago. This was normal except for a few small diverticula.

Abdominal examination was unremarkable. Rectal exam revealed a small external hemorrhoid and no masses, red blood was found on the exam glove. Stool culture, ova and parasites, and WBCs was negative. The patient discontinued the celecoxib and the bleeding diminished. A flexible sigmoidoscopy demonstrated a few 5 mm ulcers in the descending and transverse colon. Biopsies revealed nonspecific acute and chronic inflammation. No granulomas or crypt abscesses were seen. The bloody diarrhea completely resolved. The patient remains off of the celecoxib. Her back pain remains problematic. IMPLICATIONS/DISCUSSION: Upper GI tract ulceration with hemorrhage is a wellrecognized complication of NSAIDs. This serious side effect prompted the development of the selective COX-2 inhibitors which are touted as being safer in this regard. (However, this claim has recently been questioned.) Less known important GI adverse events attributed to NSAIDs include strictures and ulcerations of the small and large intestine. This case demonstrates symptomatic ulcerations of the colon attributed to celecoxib, a COX-2 specific NSAID. The patient's clinical presentation, and histology are consistent with that described with nonselective NSAIDS. Clinicians must consider NSAIDs in the differential diagnosis of lower GI tract bleeding, ulceration, or strictures. Studies are needed to determine if COX-2 specific inhibitors are safer than non-specific NSAIDs regarding the lower GI tract. This may become especially relevant in assessing the role of COX-2 inhibitors in the prevention of colon cancer. Although she had a family history of diabetes, a previous fasting glucose before beginning olanzapine was 85 mg/dL. Her exam was significant only for a non-obese, dehydrated appearing female who was orthostatic and tachycardic. Total glucose was 1122 mg/dL and measured serum osmolality was 320 mOsm/kg. A venous blood gas showed pH 7.38 and pCO2 41. Other labs included positive serum ACE test, trace urine ketones, and (in mEq/L) serum HCO3 23, sodium 122 and potassium 5.4 (anion gap of 19). IMPLICATIONS/DISCUSSION: As early as 1926, patients with schizophrenia have been known to have an increased risk of developing hyperglycemia, a process which was exacerbated with the introduction of phenothyiazines in 1956 and the atypical anti-psychotics in 1994. Increasingly, non-schizophrenic patients taking atypical anti-psychotics are demonstrating increased episodes of hyperglycemia and the complications thereof. One proposed mechanism for this hyperglycemia is through drug interference with cellular glucose transport proteins leading to increased insulin resistance and impaired glucose utilization in the periphery. This effect is not dose dependent and has its onset from 10 day to 18 months after the initiation of the drug. The literature is replete with examples of DKA in schizophrenic patients taking atypical anti-psychotics but does not specifically report the development of non-ketotic hyperosmolar syndrome. Additionally, patients taking atypical anti-psychotic medicines for diagnoses other than schizophrenia±including bipolar disorder and major depression with psychosis±risk developing hyperglycemia.

A CASE OF STAPHYLOCOCCAL COLITIS PRESENTING AS TOXIC SHOCK SYNDROME. T. Rutkoski 1 , C. Mueller 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #77132)

LEARNING OBJECTIVES: 1) Recognize the presentation of toxic shock syndrome.

2) Realize its occurrence in males and nonmenstrual females. CASE INFORMATION: MZ was an 18 y.o. caucasian female with a PMH of depression and PTSD who presented to the ER with complaints of fever, rash and abdominal pain. Outpatient medications included only quetiapine. The patient was currently living in a women's shelter b/c of reported sexual abuse and she denied tobacco, alcohol, and drugs. Initial PE was significant for fever, hypotension, conjunctival injection, rash, diffuse abdominal tenderness, and a negative pelvic exam. Labs revealed an elevated WBC count, a renal panel with elevated AG, mild LFT abnormalities, negative CSF tap, negative tox. screen, and a contaminated U/A with ketones. The patient was initially treated with ceftriaxone and aggressive fluid management. She did develop anemia and mild pulmonary edema. Her illness gradually improved. She was discharged home and follow up in the office 5 days later revealed desquamation of her hands. Her infectious w/u was negative except for a stool cx growing S. aureus. Toxic Shock Staphylococcal Toxin-1 was negative, but Staph aureus B toxin was positive. IMPLICATIONS/DISCUSSION: The initial cases of staphylococcal TSS were described in young menstruating females in the late 1970's. Much was learned about this disease in a short time. Soon an association was found between highly absorbent tampons and TSS. These tampons were removed from the market in the early 1980's. Since then the number of cases of TSS has declined greatly. Today, however the number of reported cases is relatively stable. These cases can be found in the menstruating and nonmenstruating female, the young and old, and the male and female patient. There are very few cases of Staph TSS secondary to colitis in the literature. Overall disease mortality has also improved throughout the years but remains as high as 15% in some studies (although more likely 2±5% by most accounts). It is therefore important to think of this disease in the differential diagnosis and treat it appropriately. The patient was started on a diltiazem drip for rate control and advanced to metoprolol for long term management. She was also started on aspirin for thrombus prophylaxis. No underlying etiology for her arrhythmia was identified. However, an extensive review of the patient's family history revealed that her father had been diagnosed with heart failure secondary to Chagas' disease back in El Salvador. A sample of the patient's blood was sent for serology for Chagas' disease and returned positive with a titer of 1:512. The patient was placed on nifurtimox. Although it was believed that she may have been in the subacute phase of her illness, treatment was initiated as a means of preventing advancement of her disease to chronic illness. IMPLICATIONS/DISCUSSION: Chagas' disease is a protozoan infection due to Trypanosoma cruzi and is primarily related to three problems: megaesophagus; megacolon; and cardiac disease. Chagas' myocarditis is the most common form of cardiomyopathy in Latin-American countries and therefore has become a considerable public health problem for many areas. It is estimated that over 750,000 years of productive life are lost annually because of premature deaths due to this disorder. The presentation of Chagas' disease consists of an acute and chronic phase, separated by an indeterminate phase. The latter describes a patient who has positive se-rology, but no symptoms, physical signs, or laboratory evidence of organ involvement. Biopsy was consistent with candida without evidence of aspergilus. IMPLICATIONS/DISCUSSION: Aspergillosis encompasses a variety of manifestations of infection. The major entities include invasive disease, acute bronchopulmonary aspergillosis (ABPA) and pulmonary aspergilloma. Disease due to aspergillus organisms is uncommon and usually occurs in the setting of immunosuppression for which neutropenia (ANC < 1500 TH/ MM3) and corticosteroids are the most common predisposing factors. The most common manifestation of invasive aspergillosis involve the lung and contiguous structures. The central nervous system and gastrointestinal system (especially esophagus and bowel) are the first and second most common target of dissemination respectively. Symptoms of aspergillus esophagitis are usually consistent with severe odynophagia similar to those of candidiasis. Isolated esophageal aspergillosis is very rare. There are two case reports published describing this unusual presentation, one involving a patient with acute leukemia and another occurred in a patient 25 days post bone marrow transplantation. This case is of interest because though our patient was steroid dependent she was not neutropenic prior to and at the time of presentation (ANC > 1500 TH/MM3). Further she was asymptomatic in regards to her fungal infection and did not have evidence of aspergillus involvement at other sites. In addition esophageal involvement usually occurs as a secondary complication of severe invasive lung disease. To our knowledge, this is the first case to describe isolated esophageal aspergillosis in a patient without the overt risk factors for invasive aspergillosis. Health is now moving forward in fostering high quality language programs that will help eliminate racial and ethnic disparities in healthcare and will promote access to optimal healthcare for all. Legislation has been introduced into the State legislature regarding cultural competency training and additional recommendations to the State are being drafted to expand this model program. Our hospital is now implementing an on-going training program for all interpreters and staff prior to enlisting their services, have hired bilingual greeters for the hospital, and a bilingual patient advocate. We have also initiated a cumulative and ongoing series of research projects in the field of cross-cultural -old Oriental man presented with complaints of cramping abdominal pain, tenesmus (immediately after eating) and constipation with pellet like stools of 3 weeks duration. His past history included Coronary Artery Disease and Radical Prostatectomy for Prostate Carcinoma 8 years ago with regular follow up. Physical examination was normal except for an irregular rectal mass partially occluding the lumen of the rectum. A preliminary clinical diagnosis of rectal carcinoma was made. Flexible sigmoidoscopy showed a cauliflower like ulcero-nodular mass occupying the lumen of the rectum. Biopsies of which were consistent with Adenocarcinoma. CT scan of the pelvis showed a mass adherent to the posterior wall of urinary bladder in the region of trigone, partially obstructing lumen of the rectum and also causing bilateral hydroureters and bilateral hydronephrosis. A subsequent serum PSA was 138 ng /ml, the previous value being 22 ng/ml. Based on this data a diagnosis of prostate carcinoma was made. Because of the extent of disease and underlying heart disease palliative measures were chosen for management including the stents in rectum and bladder to relieve obstruction. IMPLICATIONS/DISCUSSION: Finding a rectal mass on clinical examination is not uncommon. Our case is unusual in that the rectal mass was of prostatic origin, presenting 8 years after initial diagnosis. Though rectal involvement by prostatic carcinoma is present in 0.56% to 11.5% of cases on postmortem studies, the presence of Denonvillier's Fascia usually inhibits it. Commonest modes of involvement of rectum are a bulging prostate mass with intact rectal mucosa or an annular stricture, ulcerating masses being the rarest and accounting for less than 1% of these cases. Knowledge of this is important as it can avoid a misdiagnosis of primary rectal cancer, especially in patients who do not have a history of Prostate cancer or those with a history of prostate cancer who have received radiotherapy. LEARNING OBJECTIVES: 1. To recognise that superwarfarin causes prolonged coagulopathy needing high dose Vitamin K treatment for weeks to months 2. To suspect superwarfarin overdose as a cause of coagulopathy resistant to vitamin K and fresh frozen plasma treatment CASE INFORMATION: A 50 years old gentleman with a past medical history of depression and recurrent suicidal attempts presented to emergency room (ER) with history of hematuria, epistaxis and bruising of skin after suicidal attempt with anticoagulant ingestion. Physical examination revealed widespread ecchymosis of skin and heme positive stool but was otherwise unremarkable. Laboratory studies revealed hemoglobin (Hbg) 4.8 g/dl (13.7±16.5 g/dl), prothrombin time (PT) >50 sec (11.5±14.3 sec), INR too high to be reported, and activated partial thromboplastin time (APTT) >150 sec (21±37 sec). Patient was thought to have ingested warfarin, the most commonly available anticoagulant. His anemia was corrected with blood transfusion and coagulopathy treated by fresh frozen plasma (FFP) and Vitamin K. After 6 days of treatment his Hbg was12.2 g/dl, PT = 14.7sec, INR = 1.26, and APTT = 50 sec. Vitamin K was discontinued and he was discharged home after psychiatry consultation. His epistaxis and bruising of skin returned after 1 week resulting him to revisit ER. Patient denied any further intake of anticoagulant since discharge, however confirmed that the anticoagulant he had ingested 4 weeks ago with suicidal intent was infact superwarfarin (rodenticide) subsequently identified as brodifacoum. His blood studies revealed Hbg 7.9 g/dl, PT >200 sec, INR = 397.5 and APTT = 95.3 sec. He was again treated with FFP, blood transfusion and Vitamin K. This time he was discharged on long term high dose (100 mg/day) oral Vitamin K and out patient follow-up. IMPLICATIONS/DISCUSSION: Superwarfarins were developed in 1970's to overcome warfarin resistance in rats. They are long acting, fat-soluble anticoagulants, and 100 times more potent than warfarin. Their half-life varies from 16 to 69 days compared to 37 hours for warfarin. Brodifacoum is the most commonly used superwarfarin thus the commonest cause of superwarfarin poisoning. Its poisoning is mostly accidental however it can result from suicidal attempt, industrial exposure or deliberate self-poisoning with denial (Munchausen syndrome). Clinical features of brodifacoum poisoning are varied and include epistaxis, hematurea, gastrointestinal bleeding, ecchymosis, hemoptysis, spontaneous abortion and intracranial bleeding. PT, INR and PTT are usually severely prolonged but correct on mixing study. The diagnosis may be confirmed by detecting brodifacoum in blood however it is usually missed on the initial screening test for superwarfarin and may need a special assay. Physicians must have a high index of suspicion of superwarfarin exposure when patients have prolonged unexplained coagulopathy resistant to vitamin K replacement and FFP, along with undetectable warfarin levels and depletion of vitamin K dependent coagulation factors. After correction of initial life threatening coagulopathy by transfusion of blood products these patients should be placed on long-term high dose Vitamin K therapy and closely followed in outpatient clinic.

TRANSPLANT PATIENT. M. Schaeffer 1 , E. Warm 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #74228) LEARNING OBJECTIVES: 1) To understand that patients undergoing solid organ transplantation require immunosupressive medications and should undergo thorough evaluation for infectious diseases with consideration of subclinical parasitic infections. 2) To understand that patients taking glucocorticoids have compromised cell-mediated immunity and are susceptible to life-threatening infections by organisms that typically cause mild or no disease in healthy individuals. CASE INFORMATION: Solid organ transplant patients require immunosuppression and are susceptible to many life-threatening infections. We report a case of fatal fulminate infection with Strongyloides stercoralis 3 months following orthotopic heart transplantation. A 54-yearold male underwent orthotopic heart transplantation for ischemic cardiomyopathy. Over the next 6 weeks he required increasing doses of prednisone, tacrolimus and mycophenolate mofetil for graft rejection. 8 weeks after transplant he suffered a perforated colonic diverticulum, and underwent emergent surgery. On postoperative day 14 he developed hypotension, respiratory failure and decreased mental status. S. stercoralis was identified in stool and bronchoalveolar aspirate, and Gram negative bacteremia was found. LP revealed motile S. stercoralis larvae in CSF and Gram negative meningitis. Brain MRI revealed multiple areas of signal change consistent with extensive new infarcts. After 10 days of supportive care and antibiotics, treatment was withdrawn at the family's request and the patient died. IMPLICATIONS/DISCUSSION: Strongyloides Hyperinfection Syndrome (SHS) occurs when massive infestation by S. stercoralis occurs in the lungs, GI tract and rarely in the central nervous system (CNS). Strongyloides stercoralis is a helminthic parasite endemic to the southeastern region of the United States. S. stercoralis has a complex life cycle in the human involving the skin, circulatory system, lungs, and gastrointestinal tract. Compromised host defenses leads to susceptibility to SHS. Along with this massive invasion of S. stercoralis, secondary Gram-negative bacteremia and sepsis are common. CNS invasion is not common but has devastating consequences, as seen in our patient. Perhaps the most damaging aspect of CNS invasion by S. stercoralis occurs when bacteria cross the blood-brain barrier attached to the parasite or within the gut of the worm leading to secondary bacterial meningitis. Although pre-transplant patients infection screening occurs, thorough assessment for parasites is often lacking. In patients in endemic areas and with risk factors for subclinical parasitic infestation, consideration should be given to further evaluation prior to surgery and initiation of immunosupressive medications. Overall mortality of SHS is greater than 80%.

NEUROSYPHILIS PRESENTING AS FECAL INCONTINENCE. E. Schmidt 1 , B. Mathis 1 , E. Warm 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #74057) LEARNING OBJECTIVES: 1) Recognize various manifestations of tertiary syphilis. 2) Recognize treatment benefits of neurosyphilis. 3) Recognize that cases of tertiary syphilis may increase in prevalence in the clinic setting following the rise in cases of early syphilis seen in the past two decades. CASE INFORMATION: A 66 year-old African American male with history of treated syphilis at age 25 presented to an outpatient clinic following a hospital stay for recent subcortical stroke and non-Q wave myocardial infarction. He reported fecal and urinary incontinence and subjective memory deterioration for an undetermined amount of time. On exam he was found to have no anal sphincter tone and was unkempt. The patient was admitted to the hospital, and had a spine MRI that was negative for any lesions. He was found to have a SED rate of 117 mm/h, a positive RPR with a 1:1024 titer, and a positive serum FTA-Abs. Lumbar puncture revealed a pleocytosis with a predominance of lymphocytes, an elevated protein at 152 mg/dL, and a positive VDRL at 32 dilutions. The patient was treated for neurosyphilis with 14 days of intravenous penicillin G, 24 million units per day. He subsequently was found to be HIV positive. On clinic follow up, the patient had improved anal sphincter tone, improved physical appearance, and improved subjective cognition. His weight improved by 13 pounds and his RPR had decreased to a titer of 1:512. IMPLICATIONS/DISCUSSION: The patient described above had clear benefit of treatment with apparent reversal of some of the neurologic sequelae of his tertiary syphilis. There is lack of data in the literature supporting reversibility of the neurologic complications of this disease, especially the dementia, that is thought to be related to fibrosis, and therefore the thought of the RPR as a screening test for reversible causes of dementia has been questioned. It has been proposed that there may be an increase in the number of cases of tertiary syphilis in light of the increased number of primary syphilis cases seen in the past two decades, as well as an increase in the HIV population. There must be a heightened level of suspicion for this process in anyone with neurologic findings and history consistent with this diagnosis.

ENDOCARDITIS AS A RED-HERRING. N. Schmidt 1 , R. Witzig 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77065) LEARNING OBJECTIVES: 1. Develop a thorough diagnostic strategy for fever in patients who use intravenous drugs. 2. Diagnose splenic abcess. CASE INFORMATION: A 25 year-old woman presented with lethargy and fever. She reported a history of intravenous drug use and a recent forearm cellulitis. She had a temperature of 38.28C, a systolic murmur, diffuse abdominal pain, and a purulent pustule on the left leg. The WBC was 19,000. An Abdominal CT scan demonstrated several hypodense lesions in the spleen. Subsequent laparatomy confirmed splenic abscesses, and a splenectomy was performed. Blood and splenic tissue cultures grew methicillin-resistant Staphylococcus aureus. Transesophageal echocardiogram did not show evidence of endocarditis. The patient was diagnosed with impetigo and splenic abscesses with subsequent sepsis. IMPLICATIONS/DISCUSSION: Staphlococcal bacteremia is common in intravenous drug users due to unsterile injection techniques. Not all patients with bacteremia, however, will develop endocarditis. The evaluation of a fever in a patient who uses intravenous drugs should extend past the heart if the patient does not meet the Duke criteria for endocarditis. The local skin infection in this patient led to bacteremia and subsequent splenic abscess formation and sepsis. Spleenic abscesses with or without endocarditis are a frequent complication of patients who use intravenous drugs. Almost all patients have fever and abdominal discomfort, but signs and symptoms of a splenic abscess may be vague and overshadowed by underlying endocarditis. The careful attention to the historical complaint and a methodical and thorough physical examination led to the appropriate diagostic test. Treatment requires splenectomy and antibiotics directed against the involved pathogens. Patients with IVDU and fever require careful evaluation not only for endocarditis, but also for bacterial seeding of other organs. Abdominal signs should prompt the search for intraabdominal abscess formation. We present an unusual case of a patient with progressive and evolving postpartum neurologic changes thought secondary to a pregnancy related vasculitic process. A healthy 30 year-old female (G1 P0) underwent a Cesarean section after unsuccessful induction of labor. The pregnancy was uneventful without signs or symptoms of pre-eclampsia. Six hours postpartum she presented with right-sided hemiparesis and language difficulties. A head CT scan showed a hypodensity in the left caudate and anterior internal capsule. The patient was anticoagulated and evaluated for thromboembolic source. By hospital day 4, the patient's symptoms had nearly resolved. On day 5 she developed recurrence of symptoms and was found to have new areas of infarction including the left cerebellum and posterior frontal lobe. She was started on high dose steroids and cerebral angiogram was done which showed findings consistent with vasculitis. Subsequent imaging showed continuous evolving infarcts and intravenous cyclophosphamide was then added. A complete rheumatologic and hypercoagulable work up was performed and unremarkable except for an erythrocyte sedimentation rate (ESR) of 98 mm/hr on admission that decreased to 52 mm/hr prior to initiation of steroids. The patient was continued on steroids and cyclophosphamide, as repeat imaging 6 months postpartum showed new evolving infarcts. 9 months postpartum, no new areas of infarction were noted and repeat angiogram showed some resolution of changes. 18 months postpartum, the patient continues to improve and is slowly being tapered off of immunosuppressive therapy. The patient has never had any other manifestations of vasculitis other than the cerebral findings as above. IMPLICATIONS/DISCUSSION: The pathogenesis of postpartum cerebral vasculitis remains unclear. It is postulated that vasospasm of the vessels, as seen with migraine headaches, may be triggered by hormonal changes unique to the postpartum period possibly producing an autoimmune reaction resulting in a vasculitis. Contributing factors may also include altered hemodynamics, and the relative coagulopathy associated with pregnancy. Diagnosis of this rare but potentially neurologically devastating disease should be confirmed with angiogram as current therapy with high dose steroids and cyclophosphamide is not without risk. Recurrence of disease with subsequent births has been documented and women diagnosed with postpartum cerebral vasculitis should be counseled on potential risks with subsequent pregnancies. LEARNING OBJECTIVES: 1. Recognize the importance of eliciting a careful review of systems when evaluating patients with fever. 2. Consider prostatitis in the differential diagnosis of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia. CASE INFORMATION: A 53-year-old truck driver with diabetes presented with a three-day history of subjective fever and rigors. On review of systems the patient disclosed urinary urgency and dysuria. Physical examination was remarkable for a slightly enlarged, exquisitely tender prostate. Pertinent laboratory testing showed a mild microcytic anemia with a normal leukocyte count, glucose 275 mg/dl, hemoglobin A1C 11.7%, and a normal PSA. Urinalysis revealed no pyuria and urine cultures were negative. However, cultures of prostate secretions, and four blood cultures obtained before the initiation of antibiotics, were positive for MRSA. A transrectal ultrasound showed large, solid, nodules in the right and left prostate likely representing an infectious process. A biopsy of the prostate revealed severe acute and chronic prostatitis. Cultures of the prostate tissue grew MRSA. Notably, sensitivities from all MRSA cultures were identical. The patient was treated with intravenous vancomycin and his clinical status improved. IMPLICATIONS/DISCUSSION: Coagulase negative Staphylococcus is known to cause chronic prostatitis. Additionally, methicillin-sensitive Staphylococcus aures can cause chronic prostatitis, especially prostatic abscesses. However, we are unaware of prior cases of MRSA bacteremia resulting from MRSA prostatitis. The patient's prostate biopsy showing prostatitis, along with the identical antimicrobial sensitivities of MRSA from both the prostatic tissue and peripheral blood, implicate MRSA prostatitis with hematogenous spread. This is a unique case of MRSA bacteremia, which appears to have resulted from MRSA prostatitis. Furthermore, this case highlights the importance of eliciting a careful review of systems and performing a thorough physical examination when evaluating the source of a fever. LEARNING OBJECTIVES: To recognize Hypokalemic Thyrotoxic Periodic Paralysis and its precipitating factors, especially since it is a rare disorder that is treatable if diagnosed. We describe a case of HTPP likely precipitated by a test. CASE INFORMATION: The patient is a 59-year-old African-American female admitted for hypokalemia after a colonoscopy. The colonoscopy was for evaluation of her microcytic, hypochromic anemia and a recent history of a 30 lb. weight loss. The colonoscopy was negative, and a CT scan of the chest, abdomen, and pelvis was done for further evaluation of possible malignancy which was also negative. Review of systems was notable for bilateral lower extremity weakness in addition to the weight loss. Two months prior, she had a persantine thallium stress test for evaluation of chest pain which was positive and was followed by an angiogram which showed only moderate coronary artery disease requiring no intervention. Since the stress test, she had progressive lower extremity weakness associated with muscle cramps and had difficulty walking, standing at length, and had difficulty climbing stairs. Physical exam revealed tachycardia, thyromegaly, 3/5 motor strength of bilateral lower extremities, and areflexia. The remainder of the examination was unremarkable. Labs revealed a potassium level of 2.9 mg/dL, and oral and intravenous potassium replacement was given. ECG revealed a sinus tachycardia with left atrial enlargement. A thyroid workup revealed a TSH of <0.01 and a free T4 of 8.33. We diagnosed hypokalemic thyrotoxic periodic paralysis likely precipitated by iodine in the dye. The patient was started on propylthiouracil 150 mg three times daily and metoprolol. The patient was referred for radioactive thyroid scan and possible radioablation therapy. At discharge, the patient's hypokalemia and symptoms had resolved. IMPLICATIONS/DISCUSSION: HTPP is a rare, sporadic, acquired disorder usually seen in Asians. The incidence is <1% in Americans. The disease is associated with an underlying thyrotoxicosis (commonly Grave's disease or thyroiditis) and hypokalemia. The serum potassium level is low, but the total body potassium remains normal. Thyroid hormone mediates an increase in sodium-potassium ATPase activity and a transcellular potassium influx. This interferes with potassium's involvement in promoting muscle contraction Treatment of HTPP includes antithyroid drugs, beta-blockers, and cautious use of potassium. Definitive treatment involves radioablation therapy. The current vignette helps one to recognize the signs and symptoms of HTPP, and describes a case that was precipitated by dye used in an angiogram. LEARNING OBJECTIVES: 1) Review the differential diagnosis of an enlarged uterus in a non-pregnant woman.

2) Recognize intravenous leiomyomatosis as a rare cause of intracardiac tumors. CASE INFORMATION: A 56 year-old postmenopausal woman with a history of uterine fibroids presented with two days of exertional shortness of breath and constant retrosternal chest pressure, worse with exertion and lying flat. She denied orthopnea, paroxysmal nocturnal dyspnea or cough. Physical exam revealed normal vital signs, elevated JVD, clear lungs, regular rhythm with II/VI holosystolic murmur at the left lower sternal border, no extremity edema, and an enlarged uterus palpable 4 cm below the umbilicus. Basic labs, cardiac enzymes, and EKG were normal. Chest x-ray showed cardiomegaly and vascular prominence. An echocardiogram revealed normal left ventricular ejection fraction, dilated right atrium (RA) and right ventricle (RV), and tricuspid regurgitation. There were two linear mobile echodensities in the inferior vena cava (IVC) protruding into the right atrium and ventricle. Cardiac and abdominopelvic MRI showed multiple uterine leiomyomas, with a lobulated mass arising from the uterine fundus and extending up the right gonadal vein into the IVC, RA, and RV. The patient underwent total hysterectomy and total excision of the mass through the infrarenal IVC. Pathology of the mass showed intravenous leiomyomatosis. IMPLICATIONS/DISCUSSION: The differential diagnosis of an enlarged non-pregnant uterus includes endometrial and myometrial processes. Advanced endometrial carcinoma is the main endometrial cause. Myometrial causes are divided into benign and malignant. Benign conditions include leiomyomas (i.e. fibroids), adenomyosis, and stromal adenomyosis. Malignant causes include leiomyosarcoma and endometrial stromal sarcoma. Uterine conditions capable of extending into the IVC and heart are endometrial stromal sarcoma and intravenous leiomyomatosis. Intravenous leiomyomatosis is a rare benign condition in which nodules of benign smooth muscle tissue grow within the veins of the myometrium and may extend into the uterine and hypogastric veins. Rarely, these tumors extend up the IVC into the heart. Only 43 cases of intravenous leiomyomatosis with cardiac extension have been reported in the English literature. Symptoms of cardiac extension include venous obstruction, right-sided heart failure, and rarely, sudden death. Successful therapy entails total excision of the tumor, as residual tumor could result in recurrence. 3) Identify Salmonella as a rare infectious cause of spondylodiscitis. CASE INFORMATION: A 65-year-old woman presented with four days of low back pain and fever. The pain radiated down her left leg and was aggravated by movement. She denied trauma, weakness or numbness. She had a temperature of 104, blood pressure of 154/76, and heart rate of 115. Physical exam showed lumbar paraspinal spasm with no focal tenderness. Neurological exam was normal, including straight leg test. White cell count was 14000 with 90% neutrophils. ESR was 64. Blood and urine cultures were negative. Lumbar x-rays were normal. An indium scan done as part of the workup for fever and leucocytosis showed increased uptake at L4-L5. MRI of the spine revealed disc herniation at L4-L5, but no spondylodiscitis. Even though the source of fever was uncertain, the patient was treated empirically with vancomycin with resolution of fever. However, the pain persisted and she underwent discectomy. Pathological exam showed acute discitis, but cultures were not done. Despite the surgery, her back pain worsened, and repeat imaging showed destruction of L4 and L5 vertebral end plates, with prevertebral, epidural and paraspinal abscess. A CT-guided biopsy was done, and Salmonella javiana grew from the drained fluid. The patient had hemoglobin C trait but no immunocompromising conditions. She was treated with fluoroquinolones and slowly improved. IMPLICATIONS/DISCUSSION: Most cases of back pain are due to simple benign etiologies. However, certain red flags prompt the search for more serious causes. These include advanced age, malignancy, signs of infection, and progressive neurological symptoms. Spondylodiscitis is the simultaneous infection of the vertebral body and disc space. MRI is the most sensitive and specific imaging modality, with a sensitivity of 91% during the first two weeks of symptoms. Radionuclide scanning is done when MRI cannot be performed. It is very sensitive but not as specific. CT-guided biopsy should be pursued in cases of suspected spondylodiscitis, even with a normal MRI. Most cases of spondylodiscitis are due to Staphylococcus aureus. Other organisms include Streptococcus, E. coli and Salmonella, with the most frequent serotypes being Salmonella typhimurium and S. choleraesuis. Predisposing factors for salmonellosis include sickle cell disease, HIV, immunosuppressive therapies and previous trauma. Spondylodiscitis due to S. javiana has not been previously reported. Hemoglobin C disorders have not been associated with Salmonella osteomyelitis.

THE YOUNG WOMAN WITH NUMB FEET. J.J. Silverman 1 ; 1 University of Pennsylvania, Philadelphia, PA (Tracking ID #75939) LEARNING OBJECTIVES: 1) Recount the most common causes of a symmetric polyneuropathy; 2) Perform the initial evaluation of a polyneuropathy 3) Recognize an uncommon presentation of hypothyroidism. CASE INFORMATION: A 28 year-old female with no significant past medical history presents complaining of bilateral foot and hand numbness for the past six weeks. The sensation begins mid-foot, occurs intermittently throughout the day, and she specifically notes worsening symptoms walking on the treadmill at the gym. She reports similar but milder symptoms in her hands, which are not related to activity. Review of systems is otherwise notable for chronic constipation and longstanding irregular menses (since menarche at age 14). Family history is negative for polyneuropathies, cancer and thyroid disease. She smokes two packs of cigarettes per week, does not drink alcohol or use drugs, and denies toxic exposures. She has no history of blood transfusions, reports regular condom use with her two prior sexual partners, and is not presently sexually active. She takes fexofenadine as needed for seasonal allergies. Physical exam revealed a well-appearing young woman, who was afebrile, with a blood pressure of 130/80 and a heart rate of 74. Neurologic exam was notable for decreased sensation to light touch and pinprick in the plantar aspect of her right foot, as well as decreased vibratory sense in her right foot. The remainder of the physical exam was unremarkable. Labs were notable for a TSH of 109, FTI of 2.9, Thyroxine of 2.7 and T3U of 1.06. IMPLICATIONS/DISCUSSION: Polyneuropathy is not an uncommon problem in the primary care setting. The differential diagnosis is quite broad, but chronic systemic disorders, hereditary causes and inflammatory diseases account for the majority of cases. Chronic medical conditions commonly associated with polyneuropathies include diabetes mellitus, malignancy, collagen vascular disease, organ failure, B12 deficiency, alcoholism, AIDS, toxic exposures and plasma cell dyscrasias. Though the history can direct the initial evaluation, for most cases it will include a CBC, basic metabolic panel, liver panel, ANA, SED rate, B12, folate, lead level, RPR, HIV, hepatitis serologies and TSH. If this initial evaluation is inconclusive, an EMG and neurology consult are warranted. Finally, it is important to realize that hypothyroidism is protean in its manifestations, and can present without its most commonly recognized signs and symptoms.

SHORTNESS OF BREATH: A``NEGATIVE'' LOWER EXTREMITY DOPPLER STUDY. C.W. Simpkins 1 , C. Passaretti 1 , A. Zaas 1 , J. Cofrancesco 1 ; 1 Johns Hopkins University, Baltimore, MD (Tracking ID #76910) LEARNING OBJECTIVES: 1. Assess subacute progressive dyspnea in a young woman. 2. Recognize the presentation of pulmonary sarcoidosis. 3. Recognize the pathology and pathophysiology of early pulmonary sarcoid. CASE INFORMATION: A 48 year old African American female with hypertension, gastroesophageal reflux disease, bipolar disorder, a remote history of lithium therapy and history of total abdominal hysterectomy and bilateral salpingoophorectomy on hormone replacement therapy (HRT), presents with slowly progressive dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea for one year. Lower extremity duplex ultrasounds were negative for blood clot but did show inguinal adenopathy. Review of systems included loud snoring, possible apneic episodes during sleep, nonrestful sleep, intermittent lower extremity swelling, nonproductive cough for 1 week, but no daytime somnolence, fevers, chills, or sweats. She had an 18 pound intentional weight loss over the past year. No history of alcohol, tobacco, or illicit drug use. Physical exam: temperature 100.5 degrees F, blood pressure 146/57 mmHg, pulse 67 bpm, respiratory rate 20, pulse oximetry 95% on 2 liters supplemental oxygen. Patient was a mildly obese woman in no acute distress, with no palpable adenopathy, slightly elevated jugular venous pulse, normal air movement except for rare bibasilar crackles, a prominent P2 heart sound, and no peripheral edema, cyanosis, or clubbing. Arterial blood gas on room air: pH 7.44/PaCO2 35/PaO2 55/bicarb 23. Ventilation/perfusion (V/Q) scan was low probability for pulmonary embolism. Pulmonary function tests showed moderate combined obstructive and restrictive physiology with severe gas transfer defect. Computed tomography (CT) of the chest showed enlarged right atrium, bulky mediastinal adenopathy, and diffuse patchy ground glass infiltrates without effusion or consolidation. Echocardiogram showed normal left ventricular (LV) size and function, moderate dilatation of the right ventricle (RV) and right atrium (RA) with flattened septum. A diagnostic procedure was performed. IMPLICATIONS/DISCUSSION: Initial differential diagnosis included pulmonary embolus (young woman on hormones), sleep apnea (given the pulmonary hypertension), and hypertensive cardiomyopathy with heart failure. However, the negative V/Q and CT, and the bulky lymphadenopathy and patchy ground-glass infiltrates were suspicious for pulmonary sarcoid. Bronchoscopy with lavage and biopsy confirmed this diagnosis with negative cultures, peri-mucosal granuloma and reactive histiocytes. The patient was diuresed, started on high dose steroids with slow taper, and is doing well. The diagnosis, pathophysiology and treatment of pulmonary sarcoid will be discussed. LEARNING OBJECTIVES: 1) Review the differential diagnosis of normocytic anemia. 2) Recognize the cause of normocytic anemia by mixed processes of microcytic and macrocytic anemia.

3) Appreciate the wide and unusual manifestations of Vitamin B12 deficiency. CASE INFORMATION: A 56 year-old black male with history of hypertension presented to the outpatient clinic with six month history of intermittent low grade fever. On review of systems, he denied cough, chest pain or shortness of breath, palpitations, gastrointestinal bleed, urinary or bowel symptoms, arthritis, weight loss, numbness or weakness. Vital signs revealed temp 100.5, pulse 116, blood pressure 158/96, respirations 18. Physical exam was significant for pale conjunctiva, guaiac negative stool, and slight decreased sensation to light touch, pinprick, and vibration in the lower extremities. Labs showed Hgb 6.7, MCV 87 with normal WBC and platelet with blood smear displaying nucleated rbcs, anisocytosis, poikilocytosis, and isolated macrocytes. A work up including chemistries, cultures of blood and urine, ANA, ESR, and TSH was unremarkable. A vitamin B12 level was 108 pg/mL (normal 180±914 pg/mL) and hemoglobin electrophoresis showed beta thallasemia. With Vitamin B12 supplementation, the patient's fever resolved. IMPLICATIONS/DISCUSSION: The differential diagnosis of normocytic anemia includes chronic diseases, inflammation, endocrinopathies and renal diseases. In some cases, the simultaneous processes of microcytic and macrocytic anemia should also be in the differential diagnosis of normocytic anemia. The abnormal blood smear with size variation of erythrocytes and neuropathy led to the work up and concomitant diagnosis of beta thallasemia and Vitamin B12 deficiency. The clinical manifestations of Vitamin B12 deficiency include fatigue, glossitis, vomiting, diarrhea, dementia, and neuropathies, but fever is not considered a typical feature. From the literature, fever was found in approximately 40% of patients with megaloblastic anemia caused by folate and Vitamin B12 deficiencies in two case studies. The mechanism of the fever is uncertain, but one proposed theory is the increased activity and ineffective erythropoiesis in the bone marrow. Fever resolves rapidly with treatment and failure to do so should prompt a search for other causes. In summary, normocytic anemia can be caused by dual processes of microcytic and macrocytic anemia and fever should be recognized as an atypical feature of Vitamin B12 deficiency.`D LEARNING OBJECTIVES: 1) Differentiate between gynecomastia and breast cancer 2) Recognize the causes and treatment of gynecomastia. CASE INFORMATION: The patient is a 67 year-old male with alcoholic cirrhosis who presented with a painful lump in his right breast. Medications included spironolactone. Social history was significant for one year of sobriety and current tri-weekly use of marijuana. On physical exam, a 3 by 3 centimeter subareolar, tender, mobile, rubbery right breast mass was palpated. A smaller, similiar mass was palpated on the left. There was no nipple discharge or retraction, overlying skin changes, or lymphadenopathy. His testosterone was normal. A diagnosis of bilateral gynecomastia was made, felt to be due to his cirrhosis, compounded by his use of spironolactone and marijuana. The patient stopped both drugs. Two months later, the patient had significant improvement in his pain and decrease in breast tissue. IMPLICATIONS/DISCUSSION: Gynecomastia is common in adult males. The highest prevalence is between 50 to 80 years, with an incidence of 24 to 65 percent. Patients present with a unilateral or bilateral breast mass that may be painful. The most important differentiation is between gynecomastia and breast carcinoma. Carcinoma is less common, usually unilateral, and eccentric rather than symmetric to the nipple/areola. It is firm, fixed and may be associated with skin dimpling, nipple retraction or discharge, and lymphadenopathy. The conditions associated with gynecomastia are felt to represent an imbalance between estrogens and androgens. The most common causes in the adult male are as follows: idiopathic, drugs, cirrhosis, malnutrition, primary hypogonadism, testicular tumors, secondary hypogonadism, hyperthyroidism, and chronic renal insufficiency. Causal drugs include antiandrogens, antibiotics, antiulcers, chemotherapeutics, cardiovascular drugs, and drugs of abuse. The history, physical, and certain diagnostic tests can identify the cause in the majority of patients. Patients with a pain, acute onset, or without an obvious etiology should be evaluated with serum hCG, luteinizing hormone, testosterone, and estradiol levels. An asymptomatic patient found to have gynecomastia incidentally, deemed to be idiopathic, does not require further tests and should be reevaluated in six months. Otherwise, treatment should be directed at removing the underlying cause. Active treatment with androgens, antiestrogens, and aromatase inhibitors is indicated in persistent gynecomastia associated with severe pain, tenderness, or embarrassment. Surgical therapy, including liposuction or excision, is considered in patients who do not respond to medical therapy.

CAN'T WE JUST LET HER LEAVE? T. Spector 1 , P.P. Balingit 1 , A.G. Gomez 2 ; 1 UCLA San Fernando Valley Program, Sylmar, CA; 2 University of California, Los Angeles, Sepulveda, CA (Tracking ID #76525) LEARNING OBJECTIVES: 1. To recognize and avoid counter-transference with difficult patients. 2. To maintain a professional attitude in difficult circumstances. 3. To discuss when a patient has capacity to refuse treatment. CASE INFORMATION: A 36 year old female with a history of polysubstance abuse presented with 2 weeks of fevers and painful forearm lesions after skin-popping heroin. The patient was an ill-appearing, disheveled woman. Temperature was 38.4C, BP 114/68, heart rate 112. Multiple abscesses were noted on her forearms. A II/VI holosystolic cardiac murmur over the tricuspid area, not heard on previous exams, was also present. EKG and CXR were normal. The patient was admitted with the diagnosis of probable infective endocarditis. Within minutes of arriving to the monitored unit, she demanded to be moved to a room with a TV and swore at the nurses when they refused to give meperidine for her pain. She also demanded that the intern be paged until methadone was ordered for her heroin withdrawal. The intern arrived to the unit after the patient had ripped off her monitor leads, pulled out her IV line and was dressing to leave the hospital. A panicked intern told the resident that the patient was leaving because she felt her needs were being ignored. A psychiatrist was urgently called to determine her capacity to refuse treatment, but she left before the psychiatrist arrived. The resident found the patient outside the hospital. The patient was allowed to vent her frustrations with much vehemence and profanity. Satisfied that her grievances were heard, she allowed the resident to fully explain the benefits of treatment and the risks of refusing care, including death. The patient was alert, oriented, and able to repeat the risks clearly prior to leaving. IMPLICATIONS/DISCUSSION: Most internists are enthusiastic about finding solutions to difficult medical problems. However, a patient's psychological or social problem may not be greeted with the same enthusiasm. It is not uncommon for a patient's personality trait or attitude to invoke anger, disdain or frustration in health workers. Caring for such patients with compassion becomes a challenge. It is important to understand one's own response to difficult patients in order to recognize and prevent counter-transference from interfering with sound and appropriate medical decisions. One must also recognize that the patient's decision to leave without treatment, although a poor one by medical standards, was certainly within her rights. It was important to appease the patient's anger to assure that she made an informed decision to leave against medical advice rather than out of rash frustration and anger. By clearly repeating the risks and consequences, she demonstrated legal capacity to leave and was empowered with the knowledge to return or seek care elsewhere. Definitive guidelines exist that dictate when a physician can treat a patient against his will.

AN UNCOMMON CAUSE OF HYPOGLYCEMIA. S. Agresta 1 , B. Springgate 1 ; 1 Tulane, New Orleans, LA (Tracking ID #75148) LEARNING OBJECTIVES: 1. Recognize ethanol ingestion as an important cause of sustained hypoglycemia. 2. Provide appropriate treatment for ethanol-induce hypoglycemia. CASE INFORMATION: A 37 year-old man presented after a syncopal episode. Seven months earlier he was diagnosed with alcoholic liver disease. On presentation, he was tremulous and diaphoretic. The remainder of the physical exam was normal. An initial blood glucose was 30 mg/dL. He received one ampule of intravenously D50. Twenty minutes later the symptoms returned. His glucose was 28. Despite additional intravenous dextrose, his glucose continued to drop to between 30 and 40 mg/dl. His AST was 175 U/L, ALT 73 U/L, Hgb A1C 4.6%, and C peptide 15.5 ng/mL (nl). Drug and ethanol screens were negative. After two days of continuous dextrose-containing intravenous fluids, his blood glucose level returned to normal. IMPLICATIONS/DISCUSSION: Alcohol-induced hypoglycemia is an important but infrequently diagnosed sequella of ethanol ingestion. Symptoms are precipitated by a period of fasting followed by ingestion of alcohol. Ethanol inhibits the normal hepatic gluconeogenesis response to starvation-induced hepatic glycogen depletion. As this inhibition may be gradual, hypoglycemic symptoms may develop slowly. Patients may not demonstrate acute alcohol toxicity at the time of presentation. 1 Continuous intravenous glucose is required to prevent recurrent hypoglycemia and to replete hepatic glycogen stores. Chronic alcoholics may also have inhibition of pituitary ACTH, creating a hypo-cortisolemic state, exacerbating the hypoglycemia. surpassed those of the squamous cell type. The general locations of adenocarcinoma metastasis are lymph nodes and liver, and occasionally lung and bone. We report a case of adenocarcinoma of the esophagus with leptomeningeal carcinomatosis. A 56 year old thin white male presented with dysphagia, and a 40 pound weight loss over six months. He also had nausea, vomiting, abdominal pain, rectal bleeding, and diplopia during this period. On exam, he was alert and oriented. He had sluggish reaction of his left pupil, diplopia on downward gaze, guaiac positive stool, and a microcytic anemia (MCV 61). Esophagogastroduodenoscopy showed a mass that extended from the 28th cm of the esophagus to the 37th cm including the GE junction. Whole body CT scan showed an isodense mass in the foramen of Monro, midesophageal thickening, multiple hepatic lesions, and celiac lymphadenopathy. Brain MRI showed leptomeningeal carcinomatosis surrounding the pons and multiple cranial nerves. The patient received urgent whole brain radiation. Upon completion of radiation an Ommaya reservoir was suggested for intrathecal methotrexate. However, his overall quality of life deteriorated rapidly and he chose to receive hospice care. IMPLICATIONS/DISCUSSION: Metastatic sites for esophageal cancer typically involve the liver and lymph nodes and rarely lung and bone. Direct CNS involvement is an extremely rare occurrence. On identification of the leptomeningeal carcinomatosis our patient was able to undergo whole brain radiation to prevent any immediate risk of herniation, but given the extent of his disease his prognosis was extremely poor. The reasons why this adenocarcinoma spread to involve the CNS are unclear, and further study needs to be undertaken. As esophageal adenocarcinoma becomes more common, this type of presentation may be seen more frequently, and clinicians should be aware of this. week. The test took place at 6 AM with an ambient temperature of 75F. At the end of the test the patient collapsed complaining of``complete muscle failure''. He was found to be hypotensive and tachycardic. The patient's history was significant for the use of an herbal supplement called Energel. He had been taking this consistently for the past month to try improve his performance time. Laboratory results initially revealed severe rhabdomyolysis with a creatinine kinase (ck) of 11,000. Acute renal failure secondary to pigment-induced ATN was demonstrated by a serum creatinine (cr) of 2.4 mg/dl and urine positivity for myoglobin. The patient's ck peaked at 240,000 during his hospital course. After 8 days his ck was 45,000 and his cr returned to normal. IMPLICATIONS/DISCUSSION: Energel is a herbal supplement that contains Ma Huang. Ma Huang is the Chinese version of Ephedra which grows in many parts of the world and is used predominantly as a stimulant. Ephedra alkaloids are structurally similar to ephedrine and pseudoephedrine. They stimulate both alpha and beta-adrenergic receptors as well as release norepinephrine from storage sites. Each tablet of Energel contains 330 mg of Ma Huang extract, which is 6% (19.8 mg) of Ephedra. The dose is 2 gelcaps a day. Our patient took this dose. The FDA has banned the sale of Ephedra in large amounts (over 24 mg a day and does not recommend taking this product in small amounts for more than 7 consecutive days. Our patient was taking 40 mg a day for 30 days. Ephedra has caused 17 deaths and hundreds of serious side effects including stroke, myocardial infarction and seizures in previously healthy young adults. To this date there have been no reported cases of rhabdomyolysis associated with Ma Huang. This is an extremely important health concern since Ephedra, in its many forms, is readily available in unscrutinized and easily obtainable health supplements.

IATROGENIC STROKE AND UNDIAGNOSED DELIRIUM: OPPORTUNITIES TO IMPROVE CARE FOR HOSPITALIZED ELDERS. R. Sudore 1 , C. Landefeld 1 ; 1 University of California, San Francisco, San Francisco, CA (Tracking ID #73989) LEARNING OBJECTIVES: To describe the risk of stroke after cardiac catheterization and to recognize iatrogenic impediments to stroke rehabilitation in elderly patients. CASE INFORMATION: An independent 73 yr-old man with a history of NIDDM and HTN was transferred for cardiac catheterization (cath) after a recent non-Q-wave MI. An uneventful cath revealed 5 vessel disease and an ejection fraction of 30%. 90 minutes post cath he developed right hemiparesis and receptive and expressive aphasia. Head CT was negative and TPA was administered within 2 hours of symptom onset, but without clinical improvement. Two weeks later, neurologic function had not improved; agitation developed and hand restraints and diazepam were started. On consultation, we confirmed the sequelae of stroke, identified ischemic lesions in three toes, and diagnosed delirium. Serum sodium was 128, but other lab studies were normal. After discontinuing diazepam and restricting free water, his agitation resolved, and his dysphagia and receptive aphasia improved. Physical therapy was started. Once his restraints were discontinued his strength improved, though other than feeding, he remained dependent in all activities of daily living. IMPLICATIONS/DISCUSSION: This case highlights the importance of iatrogenic stroke and of undiagnosed delirium. Stroke occurs unpredictably in 0.1% of persons undergoing cath. Stroke is most often due to emboli, as evidenced by this man's cerebral and toe ischemia. His risk factors for stroke from cath included advanced age, extent of coronary artery disease, and depressed ejection fraction. In-hospital delirium incidence on medical wards varies from 11± 33%; the diagnosis is often missed in elderly patients. Delirium increases the risk of death 8fold and the frequency of nursing home placement 5-fold. Diazepam likely led to this man's delirium and slowed his rehabilitation. Also, restraints have been shown to exacerbate delirium, adding to deconditioning and slow recovery. In addition, the incidence of delirium is decreased from 15% to 10% by a multicomponent inter-vention including avoidance of benzodiazepines and restraints, but this intervention is not implemented in most hospitals, including ours. As more elders undergo cath, iatrogenic stroke may occur more often. Simple clinical strategies are indicated to prevent delirium, which is often missed and may slow or prevent rehabilitation from stroke.

A. Sura 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73858) LEARNING OBJECTIVES: 1. To recognize the impact of severely elevated triglycerides 2. To recognize the common causes of acute pancreatitis 3. To evaluate and manage the patient presenting with acute pancreatitis CASE INFORMATION: KD is a 17 year old female with a history of hypertriglyceridemia who presented to the emergency department with severe abdominal pain, nausea, and vomiting. She also complained of dizziness and lightheadedness. She denied alcohol use, medication use, family history of pancreatitis, history of gallstones or trauma. Although her symptoms were similar in character to her previous episodes of pancreatitis, they were much more severe. At the time of presentation, she was febrile to 103 degrees Fahrenheit and orthostatic. Her examination revealed significant abdominal distention, absent bowel sounds, and exquisite diffuse tenderness to palpation. There was no rebound tenderness. Her lab work revealed a hemoglobin of 6.8 (normal for her was 15), WBC 15.8, albumin 2.3, calcium 6.5 and triglyceride level of 11,000. Lab work also showed Na 133, K 3.3, Cl 100, CO2 22, BUN <2, Cr 0.4, glucose 217, lipase 1221, amylase 117, triglycerides >11,000, total cholesterol 245, HDL 14, Ca 7.4, albumin 2.3, Tbili 1.6, AST 25, ALT 22, GGT 83 and alkaline phosphatase 96. CT scan of the abdomen revealed severe necrotizing pancreatitis with necrosis of the pancreatic duct, large amount of ascites, and a large retroperitoneal phlegmon. She was started on imipenem, given blood transfusions, and maintained NPO. She was admitted to the ICU for severe necrotizing pancreatitis. IMPLICATIONS/DISCUSSION: Acute pancreatitis is an acute inflammatory process of the pancreas. It is associated with severe acute upper abdominal pain and elevated serum levels of pancreatic enzymes. Most cases are associated with gallstones or alcohol, but the precise pathogenetic mechanisms are not understood completely. Other causes of acute pancreatitis include biliary sludge, post-procedure, hypertriglyceridemia, hypercalcemia, drugs, trauma, HIV, and hereditary causes (pancreas divisum or a genetic mutation). The diagnosis is made via clinical exam, laboratory findings, and, if needed, imaging studies. CT scan is the most helpful imaging test for the diagnosis and its intrabdominal complications. Serum triglyceride concentrations above 1000 mg/dl can precipitate attacks of acute pancreatitis and may account for 1.3±3.8% of cases. The clinical manifestations of hypertriglyceridemia associated pancreatitis are similar to those seen with other causes with the exception that, for poorly understood reasons, the serum amylase may not be elevated substantially. Clinical assessment of severe pancreatitis is as accurate as most scoring systems. Treatment of acute pancreatitis is aimed at correcting predisposing factors and at the pancreatic inflammation itself. General management consists of supportive care with intravenous hydration, pain management, antibiotics, parenteral or enteral (jejunal) feeding, and in severe cases, necrosectomy.

ACUTE-ONSET ADULT TRACHEOBRONCHOMALACIA. A.C. Sura 1 , M. Ghajarnia 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #73859) LEARNING OBJECTIVES: 1) To recognize the clinical presentation and diagnostic workup of tracheobronchomalacia in adults. 2) To manage the patient with severe hypoxemia secondary to tracheobronchomalacia. CASE INFORMATION: A 74 year-old male with hypertension and degenerative joint disease presented for preoperative evaluation prior to hip replacement. He endorsed progressively worsening dyspnea with exertion in the past three weeks, orthopnea and lower extremity edema. His oxygen saturation was found to be 69% on room air. He denied fever, chills, chest pain, or chronic cough but endorsed occasional wheezing and cough productive of white sputum in the past two months. He had a distant history of 20 pack-years tobacco use as well as a 50 year history of work in a coal mine. On physical, blood pressure was 147/84, pulse of 69, and respiratory rate of 25; oxygen saturation improved to 91% on non-rebreather facemask. ABG revealed respiratory acidosis with metabolic compensation. The patient developed ventilatory failure with a drop in O2 saturation to 45% and PCO2 of 140. He was intubated, and chest CT revealed left lower lobe collapse. Bronchoscopy showed complete collapse of the left mainstem bronchus. The patient's subsequent hospital course consisted of intermittent respiratory failures requiring repeat intubations. Once extubated, he was maintained on supplemental oxygen and BiPAP. Repeat bronchoscopy found similar findings of flaccid airways. The patient was deemed ineligible for stent placement and high risk for distal collapse given extensive airway involvement. The patient was discharged on oxygen and BiPAP but subsequently weaned off of supplemental oxygen completely. IMPLICATIONS/DISCUSSION: Hypoxemia and hypercarbia refractory to standard treatments for obstructive pulmonary disease may result from airway collapse without any immediately identifiable causes. Well recognized in infants, tracheobronchomalacia (TBM) may also be present in 4.5±15% of all adult patients with respiratory complaints and can mimic chronic bronchitis. It is a disease of middle to late age, more common in males, and in those with a history of chronic respiratory irritation or inflammation but without a clear association to obstructive lung disease. Identified pathology has been limited to a decrease in the longitudinal elastic fibers of the trachea. Bronchoscopy under local anesthesia is the diagnostic gold standard, demonstrating airway narrowing greater than 50% during expiration. Also supportive are pulmonary function tests showing a low FEV1/EIV1 ratio and characteristic notching in the forced expiratory spirogram. Bronchodilators, antibiotics, and mucolytics may be beneficial in patients with concomitant obstructive airway disease or asthma; however, definitive treatment in TBM involves reversing the airway collapse. Avoidance of airway irritants and cough suppression are first line measures. Surgical stenting has been used with success in many cases, but in patients too frail to undergo such procedures or in those with extensive airway involvement, positive airway pressure appears to be the best means of medically managing patients with TBM. Moreover, airway inflammation may play a role in acute airway collapse, and the element of reversibility noted in our patient may point to a role for adjuvant anti-inflammatory medications.

YOUNG WOMAN. G. Szabo 1 , E. Warm 1 ; 1 University of Cincinnati, Cincinnati, OH (Tracking ID #74064) LEARNING OBJECTIVES: 1) Recognize the potential for lindane toxicity in adults.

2) Diagnose the signs and symptoms of lindane toxicity in adults. CASE INFORMATION: The toxicity of lindane is well known for the pediatric population, but is generally under appreciated among adults. Inappropriate application of lindane by adults can lead to significant neurologic changes and even death. A 22-year-old thin female without significant medical history was brought to the emergency room by her mother after one day of agitation, visual and tactile hallucinations, paranoia and a five-day history of rash. The rash consisted of pruritic erythematous macules on her abdomen and body. The patient was seen at an outlying emergency room, diagnosed with scabies and given lindane cream. Her rash persisted and she went to another emergency room for evaluation; again she was diagnosed with the scabies and prescribed lindane. 2 days later she presented with the above symptoms. Her exam showed numerous crusted, mildly erythematous erosions and excoriations throughout her body. No vesicles or burrows were noted. She was agitated with paranoia and visual hallucinations. An extensive workup was essentially negative and included a normal lumbar puncture, negative blood cultures and herpes simplex PCR, an unremarkable head CT, no vasculitic change on skin biopsy, and negative serologic studies for RMSF, varicella zoster, syphilis, cryptococcus and HIV. After her sensorium cleared she acknowledged that she left the lindane cream on for 12 to 16 hours, applied it all over her body and did not wash her sheets. She was discharged in stable condition without any neurologic deficits. IMPLICATIONS/DISCUSSION: Although lindane deposits in all lipid tissues, it has a high propensity for the white matter of the brain. Generally, children are at higher risk for toxicity because of their smaller size and lipid deposits. However, thin adults like the one described above, are also susceptible. Lindane absorption is enhanced by its contact with irritated skin, another risk factor also present in our case. Lindane toxicity is a clinical diagnosis and as such must be kept in mind especially in patients presenting with a history of ascabies-like rash and mental status changes.

S. Tadic 1 , J. Hefner 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #76487) LEARNING OBJECTIVES: 1.) Recognize an unusual presentation of a hypertensive emergency in a young person; 2.) Diagnose an atypical presentation of a pheochromocytoma; 3.) Evaluate and treat a catecholamine-producing tumor. CASE INFORMATION: A previously healthy 27-year-old Vietnamese male was brought to the emergency room with an acute onset of an expressive aphasia and left hemiparesis. He was unresponsive upon arrival and required intubation. A head CT revealed a large subcortical intracranial hemorrhage (ICH) involving the right basal ganglia. The patient underwent an emergent right craniotomy with evacuation of the intracerebral hemorrhage and placement of an extraventricular drain. Postoperatively, he was admitted to the Neuro Intensive Care Unit (NICU) for monitoring. Over the next 72 hours the patient was observed by nursing staff to have periods of intermittent hypertension, treated with prn IV medications and hypotension, treated with fluid boluses (SBP range 88±210). After 4 days in the NICU, the patient was observed to have facial and chest flushing. A pheochromocytoma was suspected. Abdominal MRI revealed bilateral large adrenal masses with increased T2-weighted signal. Results of a 24hour urine collection for metanephrines and catecholamines included: metanephrines 6,320 (26±230 mcg/24 hr); normetanephrines 24,760 (44±540 mcg/24 hr); VMA 16.5 (6 or less mg/ 24 hr); and total metanephrines 31,080 (90±690 mcg/24 hr). Urine dopamine 2,136 (80±440 mcg/24 hr); epinephrine 423 (0±25) and norepinephrine 3,071 (0±100). Calcitonin level was 5 (0-8) and genetic testing for von Hippel-Lindau (vHL) syndrome was negative. The patient developed a right femoral DVT and tested positive for the Lupus Anticoagulant. He underwent a bilateral adrenalectomy and was discharged to home 2 months later on Coumadin and Hydrocortisone. Pathology revealed malignant pheochromocytoma and a metastatic workup was negative. His post-surgical evaluation revealed normal levels of urine metanephrines and catecholamines. IMPLICATIONS/DISCUSSION: Although pheochromocytoma is a rare disease, this case represents the value of bedside evaluation by a physician. Paroxysmal symptoms (i.e. intermittent) can often be treated with prn interventions leading to misdiagnosis or delay in diagnosis. A rare presentation of pheochromocytoma is one of cyclic fluctuations of HTN and hypotension that occurs via an uncertain mechanism. While most pheochromocytomas are sporadic, bilateral tumors are often associated with 2 primary familial disorders: MEN-2 and VHL. Measurement of plasma or urine catecholamines and metabolites are diagnostic in 95% of patients with symptoms. MRI scans are sensitive (98±100%) but are only 70% specific. On T2-weighted images, however, pheochromocytomas appear hyperintense while other adrenal tumors appear isointense. While there is no universally accepted method of preparation for surgery, alpha-adrenergic blockade followed by beta-blockers with surgery 2 weeks later, is common practice. Recurrence rates are 14% at 10 years. LEARNING OBJECTIVES: This clinical vignette discusses the ethical implications of using medication and housing contracts in voluntary case management programs. The Medical High User Case Management Program provides intensive case management, assisting patients with medical adherence, entitlements and housing. When appropriate, case managers will draft housing and medication contracts for opiate pain medications Contracts are done in consultation with primary care providers and the program internist psychiatrist and nurse.

As part of these contracts, the program will assist with the refilling of opiates and provide temporary housing. Patients must agree to make scheduled medical and substance abuse appointments. CASE INFORMATION: The patient is a 47-year-old woman with a history of admissions for CHF secondary to cocaine dependence. Her care has been complicated by a history of borderline personality disorder, chronic back pain, a history of upper GI bleeds, major depression and homelessness. The patient's stated goals on enrollment include housing and sobriety. The patient signed a contract that included opiate pain medications, temporary housing, substance abuse treatment and money management. Over the course of the next few months the patient would repeatedly binge on cocaine after receiving her general assistance check at the beginning of each month. The case management program terminated the housing and medication contract and asked the patient to see her primary care physician for all opiate refills. While the patient continued to binge on cocaine, the case manager continued to assist the patient with non-opiate medication refills, appointments with her primary care physician and applications for both housing and a money management. The patient eventually enrolled herself in a residential drug treatment program. She was restarted on her pain medication contract after seeing her primary care provider and is awaiting housing. IMPLICATIONS/DISCUSSION: While we believe that contracts for housing and pain medication refills may be useful in providing external control for seriously medically ill patients, these contracts poses important ethical questions. These contracts may challenge the principle of patient autonomy in patients who retain the legal ability to make medical decisions. These contracts also use housing and pain medications as incentives, items that many feel should be viewed as rights. Therefore these contracts should never deny patients access to the usual standard of care. Instead they should be voluntary and provide additional services that are contingent on the patient's adherence to a care plan. It is also important that contracts be done as part of an ongoing patient provider relationship to insure patient safety. Finally these contracts have the potential to reduce morbidity and mortality, which remains an important ethical imperative. A 48 year old male presented with crushing chest pain of several hours duration and a worsening of his chronic headaches (which had started 8 months ago after a closed head injury). In the previous 30 hours, he had taken 14 tablets of clonidine to try to relieve the headache which he thought was due to his hypertension. On review of systems, he noted a 35 pound weight loss over the past 8 months and admitted to sexual activity with several prostitutes. The only other medication he takes is ibuprofen. His vitals revealed he was afebrile with a pulse of 42 and a blood pressure of 205/133. His exam showed some temporal wasting and grade III hypertensive retinopathy without papilledema. He had an S4 present, but the remainder of his initial cardiac, respiratory, abdominal, neurologic and musculoskeletal exam was unremarkable. Serial ECGs showed sinus bradycardia, left ventricular hypertrophy, and T-wave inversions in the lateral and inferior leads. Initial electrolytes, CBC and serial cardiac biomarkers were also unremarkable. A head CT without contrast showed grey-white matter changes consistent with hypertension. The patient was admitted to the cardiac care unit. A CT scan with IV contrast of the abdomen and thorax showed no evidence of an arotic dissection. His blood pressure was controlled with IV nitroglycerine initially, but then required fenoldopam and nicardipine drips, parenteral hydralazine, procardia, clonidine, and labetolol. He developed a third cranial nerve palsy on the right and his serum sodium dropped from 137 mmol/liter on admission to 121 mmol/liter three days later. CT scans of the head were repeated twice with and without contrast with no change from the initial CT scan. A lumbar puncture was performed and cryptococcal meningitis was diagnosed. A subsequent HIV test was positive. His CD4 count was 12. Amphotericin B was started. Elevated intracranial pressure was controlled by serial lumbar punctures. The patient's cranial nerve palsy showed minimal improvement, but his hypertension improved. IMPLICATIONS/DISCUSSION: The presence of intractable hypertension, bradycardia, and headache suggests increased intracranial pressure as a cause for his hypertension. It is a wellknown cause of hypertension but rarely considered. In this case, his bradycardia was initially thought to be secondary to clonidine. He also lacked any focal neurologic deficits or papilledema on initial presentation to suggest an intracranial pathology. A retrospective casecontrol study published in 1992 showed an increased incidence of diastolic hypertension in AIDS patients with cryptocccal meningitis.

SIADH. CAUSING OR CAUSED BY PSYCHOSIS? A. Tendler 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77076) LEARNING OBJECTIVES: 1. Recognize organic psychosis as a correctable cause of SIADH 2. Distinguish SIADH from from psychogenic polydypsia. 3. Know other causes of SIADH in the psychiatric patient. CASE INFORMATION: A 56 year-old woman with a history of schizophrenia was admitted to the inpatient psychiatry service with paranoid delusions of her brother trying to kill herself and all religious ministers. Her physical examination was normal, including normal neurologic and pulmonary examinations. Her serum sodium was 124 mmol/L and her measured osmolality was 261 mosm/kg. The urine osmolality was 522 mosm/kg. She was treated with risperidone and free water was restricted. She was allowed a liberal salt-containing diet. Her psychosis improved over the next week, with normalization of her serum sodium. IMPLICATIONS/DISCUSSION: Hyponatremia in the schizophrenic patient should not be reflexively attributed to psychogenic polydyspia. Because ADH is liberated from the hypothalamus through the posterior pituitary, anti-psychotic medications acting at surrounding structures may cause SIADH, as may primary psychosis. The urine osmolarity is the best test to distinguish SIADH from psychogenic water drinking, as the concentrating effects of ADH should increase the urine osmolarity. Hyponatremia may cause neurologic impairment, but this impairment is usually in the form of seizures as opposed to psychosis. Treatment of psychosis-induced SIADH is with neuroleptics designed to control the psychosis. Medical consultation for hyponatremia in the psychiatric ward is a common occurrence . Physicians should be aware of this underdiagnosed cause of hyponatremia, and of its successful resolution with anti-psychotic therapy. received no relief, however, and he re-presented with persistent back pain and fevers. Further questioning revealed he had a past history of mitral regurgitation and had had a tooth extraction six months prior. He had a 3/6 systolic murmur at the apex and point tenderness over the lumbar spine. His blood cultures grew Streptococcus viridans. An MRI of the lumbar spine showed edematous changes at T12-L1 with loss of disc space, consistent with discitis. An echocardiogram confirmed endocarditis. IMPLICATIONS/DISCUSSION: Although the diagnosis of urinary tract infection and lower back strain adequately explained his symptoms, each of the two diagnoses was insufficient in explaining all of the symptoms. William of Occam suggested that,``one should not increase, beyond what is necessary, the number of entities required to explain anything.'' Known as Occam's Razor, this principle guides physicians to search for one diagnosis to explain all symptoms, instead of invoking multiple diagnoses. The fever, bacteremia, discitis and immunemediated glomerulonephritis in a patient with valvular abnormality and poor dentition can all be attributed to infective endocarditis.

AN OIL PIPE CLEANER OUT OF BREATH. D. Tran 1 , J. Wallace 1 ; 1 UCLA±San Fernando Valley Program, Sylmar, CA (Tracking ID #75804) LEARNING OBJECTIVES: 1. Recognize silicosis as a cause of pulmonary fibrosis. 2. Discuss the differential diagnosis of silicosis CASE INFORMATION: 25 y/o Hispanic male presented to ER for increasing dyspnea on exertion. His symptoms began insidiously about a year prior to admission, and have gradually worsened to the point where he can walk less than 1 block. His clinical course, thus far, has been punctuated by periods of exacerbation for which he was treated with antibiotics and prednisone with moderate success. He denies fever, chills, weight loss. There is no history of wheezing, asthma, chest pain, orthopnea, PND, or edema. The patient emigrated from Mexico three years ago. He denies any current or past of tobacco, drug abuse, or alcohol. On further questioning, the patient states that he spent three years in Mexico working as an oil pipè`c leaner''±which involved sandblasting. Physical exam and labs are only significant for a respiratory rate of 32 and paO2 of 70 mmHg at rest. CXR showed diffused bilateral infiltrates. High Resolution CT showed extensive, bilateral, coalescing pulmonary nodules with an upper lobe predominance and non-calcified hilar adenopathy. Patient is PPD and HIV negative. ACE level was 73 (9±67). He underwent video assisted thoroscopic lung biopsy. The pathology showed non-casseating granulomas with bifringent spicules consistent with sicilosis. Fungal and AFB cultures were negative. IMPLICATIONS/DISCUSSION: Silicosis is a type of pneumoconiosis caused by the inhalation of silica dust leading to pulmonary fibrosis. Individuals who work in metal mining or cutting, polishing, or carving stone are at risk. Symptoms usually develop after 3 to 20 years, depending on exposure level. Silicosis can either be simple: asymptomatic and non-progressive, identified by small, round opacities on chest x-ray; or complicated: symptomatic with progression despite discontinuance of the insults. Differential diagnosis includes sarcoidosis, coal worker's pneumonconiosis, neoplasia, TB, and fungal pneumonia. The diagnosis of silicosis is based on careful occupational history, radiographical evidences and pathology. Radiographically, silicosis is characterized by small, round opacities with an upper lobe predominance that can form extensive coalescing masses in advanced cases. The presence of eggshell calcifications on hilar lymph nodes may help distinguish silicosis from other pneumoconiosis. ACE level is elevated in sarcoidosis but can also be elevated in miliary TB, berylliosis, asbestosis, and silicosis. When the diagnosis is in doubt, biopsy can help establish the diagnosis and exclude other causes. On pathology, hyalinized silicotic nodules can be seen. They are formed by macrophages engulfing the particles, releasing cytotoxic enzymes causing fibrosis. There is a high incidence of TB co-infection in individuals with silicosis. Co-infection can be confused with a progression of the silicosis and should be excluded first. There is no effective treatment aside from preventing further exposure.

A 92 YEAR-OLD WOMAN WHO TOOK A TURN FOR THE WORSE. V. Tsai 1 , R. Ziegelstein 1 ; 1 Johns Hopkins University, Baltimore, MD (Tracking ID #75756) LEARNING OBJECTIVES: To call attention to the possibility that moving a patient soon after a cardiac procedure can result in malposition and malfunction of a permanent pacemaker. CASE INFORMATION: A 92-year-old woman was found unresponsive in her nursing home bed. She was in complete heart block with a ventricular rate in the 20s±30s. Soon after arrival to the hospital, she sustained an asystolic arrest and required emergency temporary pacemaker therapy. The patient did not regain consciousness after electrical pacing at 60 beats per minute. The patient's health care agent consented to the implantation of a permanent pacemaker. After the procedure, a chest radiograph showed an appropriately placed dual chamber permanent pacemaker. The patient did not regain consciousness nor spontaneous movement. Nursing staff turned the patient every two hours to avoid pressure sores. Several days later, a chest radiograph showed that the pacemaker generator was rotated and in the opposite configuration from that noted on the original film. There was no evidence of electrode dislodgment or pacemaker malfunction. IMPLICATIONS/DISCUSSION: Pacemaker-twiddler's syndrome is an unusual complication of permanent pacemaker implantation, first described by Bayliss, et al. in 1968 . It is usually characterized by partial or total loss of pacemaker function secondary to rotation of the pulse generator in its subcutaneous pocket and subsequent electrode dislodgment. The rotation is related to manipulation of the generator by the patient, either consciously or unconsciously. The present report differs from previous cases, since the pacemaker generator rotation could not have been induced by the patient, but was likely the result of routine turning of the patient by the nursing staff in an effort to prevent pressure ulcers. The possibility that turning immobile patients soon after device implantation will result in malposition and malfunction of pacemaker or cardioverter-defibrillator generators is important to recognize, since these devices are being used in an increasing number of elderly patients. Caution should be exercised while moving elderly bedbound patients in the first few days after their cardiac procedure, in order to prevent a potentially life-threatening condition.

THE USUAL SUSPECT IN AN UNUSUAL SPOT. J.T. Tseng 1 , P.P. Balingit 1 ; 1 UCLA San Fernando Valley Program, Sylmar, CA (Tracking ID #76488) LEARNING OBJECTIVES: 1. Recognize the clinical presentation of liver abscess. 2. Consider mycobacterial and other atypical organisms as etiologies of liver abscess in the immunocompromised host. CASE INFORMATION: A 41 year old Mexican male with no significant past medical history presented to an urgent care clinic with 1 month of gradually worsening right upper quadrant abdominal pain associated with fevers and night sweats. He described the pain as a dull, constant discomfort without radiation, exacerbated with movement and without change with food intake. Several episodes of nausea and vomiting occurred in the last two days. Intermittent watery diarrhea was present over the past two weeks. He sought medical attention for his abdominal pain one week ago and was prescribed levofloxacin and metronidazole without relief of symptoms. The patient reported frequently visiting Mexico, his last trip being 2 months prior. He denied HIV risk factors including homosexual or promiscuous sexual behaviors, IV drug use, or transfusions. Exam was significant for temperature of 38.8 C and heart rate of 106. Tenderness was elicited upon palpation of the right upper abdominal quadrant. No hepatomegaly was apparent, and a Murphy's sign was not present. CBC was remarkable for lymphopenia. Liver transaminases were within normal limits. No organisms were identified from blood cultures, stool cultures, and studies for ova and parasites. HIV antibody test was positive. Abdominal CT scan revealed a 2 Â 2 cm low-density irregular lesion consistent an with abscess within the right hepatic lobe. Tissue obtained from percutaneous drainage of the liver lesion revealed necrosis and granulomatoid inflammation. AFB stain was positive, and TB was identified in culture. TB was also isolated from the patient's sputum, despite the absence of cough, dyspnea, or other pulmonary symptoms. Four-drug antitubercular therapy was initiated with resolution of the patient's presenting symptoms. IMPLICATIONS/DISCUSSION: Liver abscesses of varying etiologies tend to have similar clinical presentations. Patients typically present with fever, night sweats, and right upper quadrant abdominal pain. Identification of the causative agent becomes critical when patients fail to respond to empiric therapy against pyogenic or amebic abscesses. Serologies are often not helpful in identifying an organism as assays often lack sufficient sensitivity or specificity and blood cultures may not reveal the offending agent. While CT, MRI, or ultrasonography may help differentiate liver abscesses from neoplastic processes, they are unable to identify a specific organism. Drainage of the abscess remains the mainstay of diagnosis. For immunocompromised patients, laboratory analysis of drainage fluid should include evaluation for atypical organisms as well as Gram stain, culture, and ova and parasites. In these patients, mycobacterial and fungal organisms may form abscesses in addition to typical granulomatous lesions when they invade the liver. LEARNING OBJECTIVES: 1. Acromegaly can present in younger patients 2. The role of insulin-like growth factor 1 in diagnosis and therapy 3. The importance of early diagnosis CASE INFORMATION: 22 y/o latino male presented to our urgent care clinic with a history of headache for over 2 years. The headache was intermittent in nature, mostly frontal and without exacerbating, relieving factors or associated symptoms and with minimal relief from analgesics. On systems review he admitted to an increase in the size of his hands and feet. His family also reported a gradual change in his appearance. On examination, the patient was normotensive. He had prominent supraorbital ridges and a large lower jaw with poor occlusion of teeth and lower teeth overbite. His facial wrinkles were exaggerated and lips full. The nose tongue and ears were enlarged, the hands were large, doughy spade like and the skin over them thickened. Neurological exam showed grossly intact bitemporal visual fields. His appearance was consistant with the diagnosis of acromegaly. A work up consisting of growth hormone (GH), insulin-like growth factor 1 (IGF-1), TSH and random glucose was initiated with MRI imaging of the brain. The patient was also referred to ophthomology for visual field testing. IMPLICATIONS/DISCUSSION: Acromegaly is a disease caused by secretion of excessive amounts of growth hormone, almost always occurring as a result of a benign adenoma of the anterior pituitary gland. The disease occurs most frequently in middle age with an incidence of 3±4 per million. Somatotroph adenomas of the pituitary may be large enough to cause visual impairment or headaches as in our patient. Acromegaly leads to decreased life expectancy with a 2±3 fold increase in mortality from cardiovascular causes, cancer and all causes. The diagnosis is made clinically and confirmed by finding a high levels of GH and IGF-1. Growth hormone binds to receptors resulting in the stimulation of production of IGF-1 which mediates most of the actions of GH. Growth hormone release is pulsitile with concentrations varying throughout the day. Random GH is therefore not a reliable diagnostic marker and is only useful when correlated with the glucose tolerance test. IGF-I is present at more steady concentrations and is a reliable marker of disease and its control. Most patients are treated with transphenoidal surgery which usually results in clinical improvement with decreased GH and serum IGF-I concentrations. Other options include radiation therapy, medical therapy with dopamine agonists or somatostatin analogues. Pegvisomant is a newly developed GH receptor antagonist that leads to decreased IGF-I levels and clinical improvement. Reducing growth hormone levels improves symptoms and complications of the disease and increases life expectancy.

JUST ANOTHER CASE OF UNSTABLE ANGINA? G.J. Van Londen 1 , J. Hefner 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #76750) LEARNING OBJECTIVES: 1.) Distinguish between Type A and B aortic dissections; 2.) Recognize an uncommon clinical presentation of an aortic dissection; 3.) Manage and treat a dissecting aorta. CASE INFORMATION: A 56-year-old male with a history of a 3-vessel coronary artery bypass graft in 1991, HTN and hyperlipidemia presented to the Emergency Room (ER) with bilateral jaw and retrosternal chest pain accompanied by an occipital headache and dyspnea on exertion. The chest pain was waxing and waning in intensity, non-radiating with a maximum pain score of 5/10. There was diaphoresis but no nausea or vomiting. The night prior, he noted some parathesias in his fingers and blurred vision that resolved within two hours. On exam, the patient's pulse was 110 with a BP of 130/80 on the left and 124/70 on the right. Room air pulse ox was 96%. No pulsus paradoxus, JVD or bruit was appreciated. Lung exam revealed decreased breath sounds in the left lower lobe. Cardiac exam was regular rhythm with a 2/6 diastolic murmur. Exam of the upper and lower extremities revealed equal and symmetric pulses. EKG showed sinus tachycardia with no ischemic changes. His first set of cardiac enzymes was negative. Portable chest x-ray revealed a left pleural effusion and a widening of the mediastinum with the patient rotated to the right. The patient was diagnosed in the ER with unstable angina and admitted. Based on the diastolic murmur and left pleural effusion on chest x-ray, an aortic dissection was suspected and a stat MRI was performed. This revealed a Type A dissection. Emergent surgery with replacement of the ascending aorta, valve and evacuation of a left hemothorax was performed. Cardiac arrests and a CVA complicated the perioperative course. The patient expired nine days after admission. IMPLICATIONS/DISCUSSION: A dissecting aorta must be recognized quickly as an acute Type A dissection (involves the ascending aorta) is a surgical emergency, whereas an uncomplicated Type B dissection (all others) can be treated with pharmacotherapy. Acute management consists of blood pressure control while confirming the diagnosis and type. Aortic dissection is relatively common with over 2000 cases reported each year. A recent study showed that 100% of dissections were diagnosed when all of the following clinical features were present: 1.) Acute onset of tearing or ripping-like chest or back pain; 2.) Mediastinal widening on chest x-ray and 3.) Variation in pulse and/or pressure in the upper extremities. A diastolic murmur, EKG without ischemic changes and a left-sided pleural effusion (hemothorax) are uncommon presentations of a dissection. Transesophageal echocardiogram (TEE) is recommended for unstable patients with acute chest pain. MRI is preferred in stable patients with chronic chest pain. CT scan or aortography should be reserved for situations in which both TEE and MRI are unavailable.

A. Venditto 1 , J. Wiese 1 , M. Landry 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77081) LEARNING OBJECTIVES: 1) Utilize effective diagnostic methods in cases of encephalitis. 2) Recognize the importance of early diagnosis of West Nile virus to control disease outbreaks. CASE INFORMATION: A 58-year-old man presented with two days of fever, headache, unsteady gait, and a macular rash. Although initially lucid, he deteriorated into a state of delerium within the first day of hospitalization. His vital signs were normal. He had meningismus with passive and active neck flexion; he had an ataxia gait and a macular rash over his extremities. There were 6 white blood cells /mm3 in the CSF and a normal protein and glucose. Owing to the degree of impairment, a serum immunofluorescent assay for flavivirus IgM was ordered. The titer was 1:32, increasing to 1:64 over the next five days. An assay for West Nile virus was sent to the CDC for public health monitoring. IMPLICATIONS/DISCUSSION: Most non-herpetic viral encephalitities are due to arboviruses that cycle with the lifecyle of the tick or mosquito that is the primary vector. While all are endemic to warm climates, viruses such as the Eastern Equine Virus, West Nile and St. Louis encephalitis can become epidemic when the mosquito vector greatly exceeds its primary host. For all three viruses, there is little more than supportive care to be offered. Contrary to most medical interventions, however, testing for a definitive diagnosis has merit in providing community outbreaks. The best test for distinguishing St. Louis from West Nile is an enzyme-linked immunosorbent assay (ELISA). A positive serum ELISA indicates probable infection with West Nile virus, whereas a positive cerebrospinal fluid ELISA confirms the diagnosis. Early identification of West Nile virus is important for mosquito population control and public education to prevent further disease spread. LEARNING OBJECTIVES: To Illustrate potential clinical presentations that must be considered in a patient with sarcoidosis CASE INFORMATION: History: 49 year old African American female with history of obesity, asthma and possible fibromyalgia presented with worsening fatigue, SOB, DOE over 2 months. She has been tobacco-free for the past 4 years and compliant with her asthma regimen. Over the ensuing 6 months she continued to have worsening symptoms which required episodic reinstitution of systemic steroids for presumptive asthma exacerbation. Further review revealed a past medical history of a 2 cm right upper lobe nodule with bilateral hilar adenopathy and interstitial lung disease 2 years ago. CT guided-biopsy of the nodule yielded non-caseating granuloma. Serum labs, such as CBC, Chem 10 (including calcium), TSH, ESR and ACE levels, were normal. LFTs were mildly elevated. Subsequent viral hepatitis serologies were negative. PFTS were consistent with combined obstructive and restrictive lung disease with mildly reduced DLco. The patient returned for an urgent care visit complaining of worsening DOE, bilateral lower extremity edema, polyuria, nocturia, blurry vision and severe persistent daily headache and stiff neck for the past 2 months. Prednisone 60 mg was started empirically for pulmonary sarcoidosis exacerbation and possible sarcoidosis involvement of the eyes, CNS, liver and heart. Repeat of the above serum labs were normal. Fasting glucose level was not diagnostic for diabetes mellitus or glucose intolerance. Urinalysis and urine C&S were normal. Urine osmolality was ordered but not performed. A water deprivation test was deferred until other test results were known. PT (INR) and albumin did not suggest cirrhosis. PFTs were unchanged from the prior study. PPD test was <5 cm. Gallium scan showed no uptake in the lung, salivary and lacrimal glands (e.g.``panda bear'' sign) or any other part of the body. ECG and echocardiography were also normal. MRI of CNS showed dural enhancement but no pituitary or other parenchymal lesions. CSF fluid analysis revealed only a lymphocytic pleocytosis and negative cytology for malignancy. Ophthalmology referral showed no uveitis, cataracts or retinal abnormalities. The patient's symptoms improved but she complained of increasing weight, generalized edema, low back pain and bilateral knee pain after 6 months of Prednisone therapy. The patient reported no further polyuria, headaches, stiff neck, and blurry vision but still had residual DOE and fatigue. Repeat MRI showed no dural enhancement. Prednisone was tapered off and the resultant decrease in weight and edema lead to resolution of her low back and knee pain. IMPLICATIONS/DISCUSSION: Discussion: Sarcoidosis can have numerous extrapulmonary involvement. CNS and cardiac involvement portend worse prognosis than hepatic, pulmonary or arthritic involvement. SOB and DOE is most likely due to pulmonary involvement (i.e., due to endstage parenchymal fibrosis with or without acute inflammation) but concomitant restrictive cardiomyopathy due to sarcoidosis may exist synchronously. Echocardiography is essential in ruling out this possibility. Hepatic sarcoidosis involvement can progress from mild elevations in LFTs to frank cirrhosis, which fortunately was not present in this patient. The LFTs elevation may, however, be simply due to fatty liver of obesity. Uveitis due to sarcoidosis must be a consideration in patients with vision complaints, but retinitis, episcleritis, glaucoma and premature cataracts, as well as the sicca syndrome due to involvement of the lacrimal and salivary glands, can occur. Symptomatic CNS sarcoidosis classically manifests as diabetes insipidus due to posterior pituitary infiltration. Other CNS syndromes include aseptic meningitis and diffuse white matter disease. Diabetes insipidus is a distinct possibility in this patient. Although comparison of urine and serum osmolality and water deprivation test were not done to confirm diabetes insipidus, the patient's polyuria readily responded to glucocorticoids therapy. The MRI and CSF findings clearly support an aseptic meningitis picture and her headache symptoms responded to glucocorticoids therapy. LEARNING OBJECTIVES: To recognize a hypersensitivity reaction to dialyzers in a patient on hemodialysis CASE INFORMATION: A 67 year old female with end stage renal disease secondary to chronic uncontrolled hypertension was admitted to the hospital with fevers and chills. On admission, the potential etiologies of her fever were line sepsis or lower extremity cellulitis. She was begun on appropriate antibiotic therapy. Within 5 minutes on her routine hemodialysis, she suddenly became bradycardic, hypotensive and unresponsive. On examination before dialysis, vitals were HR-80/min, BP-215/110 mm Hg, and RR-16/min. Lungs were clear to auscultation. Cardiovascular exam revealed a normal S1 and S2 and a 3/6 holosystolic murmur at the apex. After 5 minutes on dialysis, her vitals were HR-48/min, BP-64 mm Hg systolic; respirations became agonal, followed by apnea. The patient became obtunded and unresponsive, with twitching of her lips. She sustained cardio-respiratory arrest and required CPR with endotracheal intubation and mechanical ventilation and oxygenation. Dialysis was aborted during this episode. Her EKG revealed pulseless electrical activity followed by junctional rhythm. Once dialysis was stopped, it converted to normal sinus rhythm with normalization of hemodynamic parameters. Her WBC was 8000, H/H 8.2/ 25.1, electrolytes were normal, BUN 72 and Cr 14.6, BNP-1300, CPK 20, Troponin I-0.21. Chest X-ray showed mild congestion and her subclavian catheter tip was in right atrium. Echocardiogram revealed concentric left verntricular hypertrophy with normal LV function. 72 hours later, at her next routine hemodialysis, a similar episode occurred. Heparin was discontinued from her dialysis regimen due to possibility of heparin sensitivity as she was thrombocytopenic with presence of heparin associated antibodies. However, a third episode occurred on the next dialysis. At this time, the patient's dialyzer was changed from B3-1.3 to F-8. Thereafter, no further episodes occurred and she tolerated subsequent hemodialysis without complication. IMPLICATIONS/DISCUSSION: Dialyzer-induced acute hypersensitivity reaction is a rare entity (5/100,000 dialysis cases), but is a potentially life threatening condition. Presentation varies from mild urticarial reaction to cardiorespiratory failure. The onset of symptoms due to dialyzer-induced hypersensitivity reaction is usually 5±30 minutes after initiation of hemodialysis. Possible causes are bio-incompatible membrane (i.e. cellulose), ethylene oxide use for sterilization, use of ANP69 membrane in patients on ACE inhibitors, bacterial contamination of dialysate in high flux dialyzer, heparin allergy, acetate bath (acetate is a vasodilator and myocardial depressant), and inappropriate cytokine and complement activation. Differential includes severe hypotension, acute MI, arrhythmias, air or pulmonary embolism, or severe pulmonary edema. A high index of suspicion is necessary to recognize this entity. Treatment is standard care for any anaphylactic reaction and includes intravenous steroids, antihistamines and supportive care. Removal and avoidance of the culprit inciting agent is of paramount importance. A 67 year-old Filipino male presented to the ED with right facial erythema, edema, and subjective fever. The lesion progressed from a pimple 2 days prior. His past medical history was significant for Lepromatous Leprosy diagnosed in 1998. He had been treated with rifampin and ofloxacin since then. In the ED, he was treated with amoxicillinclavulanate for presumed cellulitis. Nevertheless, his facial lesion worsened, and he developed diffuse lymphadenopathy and a reddish rash on his upper extremities. Upon admission, the patient was afebrile with normal vital signs. His exam demonstrated left facial erythema, edema, and induration with central ulcertation extending from the maxillary area to the left ear and mandible and exhibited normal sensation. He had diffuse lymphadenopathy of the head and neck, and erythematous plaques on both upper extremities. His chronic findings of a left hand claw deformity and decreased sensation in the lower extremities were unchanged. Lab studies were notable for a WBC of 13 and blood and wound cultures were negative. Antibiotics were changed to vancomycin and imipenem without improvement. Subsequent skin biopsy revealed numerous acid-fast rods within macrophages and a dense neutrophilic infiltrate. His clinical presentation and biopsy findings were consistent with a Type II lepromatous reaction, or Erythema Nodosum Leprosum (ENL). He was treated with prednisone and thalidomide with ultimate resolution of his symptoms within days of treatment. IMPLICATIONS/DISCUSSION: ENL is characterized by fever with multiple erythematous tender nodules, sometimes accompanied by neuritis, edema, arthralgias, leukocytosis, iridocyclitis, pretibial periostitis, orchitis, and/or nephritis. It is associated with Borderline and Lepromatous forms of Leprosy and occurs in up to 25% of patients. ENL is most common during treatment, but can also occur before or after therapy. It is thought to be an immunecomplex disorder with tumor necrosis factor alpha playing a role in its pathogenesis. Acute treatment consists of steroids and/or thalidomide; the latter is highly effective, generally controlling the reaction within 48 hours. Clofazimine may be effective for chronic reactions. Prompt detection and treatment of ENL has decreased the number of patients with resultant chronic disabilities. Our patient had a clinical picture consistent with ENL which was initially difficult to distinguish from cellulitis. He responded to treatment with prednisone and thalidomide. As international travel and immigration continue to increase, it is important to recognize the reactions associated with Mycobacterium Leprae. year-old man was admitted for elective T12-L2 posterior spinal fusion. His past medical history included CAD, s/p CABG, and idiopathic scoliosis with prior spinal surgeries. Six hours post-operatively, the patient developed hypotension, fever and hy-poxemic respiratory failure. Intra-operatively, he received multiple blood products including 6 units of whole blood, 5 units of PRBC, 12 units of FFP, and 3 6-packs of platelets. On exam in the ICU post-operatively, he had a temperature of 398C and a BP of 70/ 40. He had a normal cardiac exam including a normal JVP, lungs had coarse breath sounds, and his extremities were warm without a rash. Chest x-ray revealed diffuse bilateral infiltrates and a chest CT was negative for PE. Echo showed no focal wall motion abnormalities. Labs were notable for a new low WBC count (0.4). Successive blood and sputum cultures were negative. The blood bank was notified to investigate a possible transfusion reaction. There was no evidence of hemolysis and a direct Coombs' test was negative. The patient was treated with vasopressors, including epinephrine, and broad-spectrum antibiotics. On post-operative day 7, the patient suffered a cardiac arrest and expired despite full resuscitative efforts. Post-mortem analysis revealed that 1 of the 32 total blood product donors was a multiparous female who donated a platelet pheresis. She carried an HLA-I antibody against one of the patient's neutrophil antigens (Bw4 public antigen). This confirmed the cause of death as transfusionrelated acute lung injury (TRALI). IMPLICATIONS/DISCUSSION: TRALI is a clinical syndrome characterized by fever, severe hypoxemia, non-cardiogenic pulmonary edema, and hypotension occurring one to six hours post transfusion. Case reports have identified transient leukopenia as another manifestation. 80% of patients recover within 48-96 hours with little permanent sequelae. Despite being the third most common cause of death from transfusions in the developed world (estimated incidence of 1/5000 transfusions, with a mortality rate of 5±14%), it is probably significantly under diagnosed. The majority of cases are associated with transfused complement-activating antibodies, either HLA (class I or II) or granulocyte specific. All blood components containing plasma have been associated with the injury. Risk factors include multiparous donors, underlying recipient conditions such as recent surgery, cytokine treatments, massive blood transfusions, active infection, and prolonged storage of transfused products. Current treatment is limited to respiratory and hemodynamic supportive measures. Diuretics and steroids have been used with variable efficacy and have not been tested in clinical trials. Our patient had an unusual course for TRALI in that his symptoms developed relatively late post-operatively and he did not recover despite maximal support. TRALI should be considered in all patients with hypoxemia following transfusions. Previously, the patient was playing golf 3 times a week without difficulty. His hypoxia began post surgery to relieve a small bowel obstruction. He was treated with antibiotics for pneumonia and ruled out for PE with 2 low probability V/Q scans. The patient was discharged home on oxygen, but his symptoms worsened. He had increasing malaise with shortness of breath upon minimal exertion, such as sitting up in bed. Eventually, he was bed bound. He denied cough, fever, wheezing, chest pain, or leg swelling. Upon admission the patient was afebrile, BP 130/70, RR 18 and supine O2 saturation of 93% on 10 liters of oxygen. Upon sitting, the patient was dyspneic with RR 40 and O2 saturation 70% on 10 liters of oxygen. His exam was normal including a normal cardiac exam including JVP, slightly decreased breath sounds at the right base, and his extremities were warm without edema. Laboratory exam revealed a normal EKG, CXR with unchanged right opacity, chest CT negative for PEor A-V fistula, electrolytes, CBC, and cardiac enzymes were also normal. PA02 on 4 liters of oxygen was 54 mm Hg and on 100% oxygen 84 mm Hg. Transthoracic echo showed normal left ventricular size and function with an inter-atrial septum hypermobility and a large patent foramen ovale with normal right sided pressures. Injection of agitated saline revealed a large amount of immediate right to left shunting. Transesophageal echo confirmed the PFO with right to left shunting. The patient underwent transcateter closure of his defect. One day post procedure, the patient was markedly improved with O2 saturation on room air of 95% supine and sitting. The patient continued to improve as an outpatient and was playing golf within 2 weeks after discharge. IMPLICATIONS/DISCUSSION: Our patient exhibited the platypnea-orthodeoxia syndrome. This is defined as dyspnea and arterial desaturation in the upright position and improved by recumbency. This syndrome occurs with an intracardiac or intrapulmonary shunt. Our patient had the most common etiology, a patent foramen ovale, with a right-to-left shunt. Shunting in the face of normal right sided pressures, as in this case, is unusual but described in the literature. Diagnosis is made by visualization of the PFO with shunting on transesophageal echocardiogram with agitated saline (``bubble study''). Percutaneous closure of the PFO is safe and effective. Cardiac shunts should be suspected in all patients with persistent hypoxia, especially in those who exhibit worsening symptoms and hypoxia in an upright position.

SMOKING CHINESE BROCCOLI? J.L. Yuh 1 , E. Yee 2 , A.G. Gomez 3 ; 1 Olive View±UCLA SFVP, Sylmar, CA; 2 VA Albuquerque±University of New Mexico, Albuquerque, NM; 3 University of California, Los Angeles, Sepulveda, CA (Tracking ID #75461) LEARNING OBJECTIVES: 1. Recognize acute nicotine in toxication 2. Discuss the management and treatment of acute nicotine intoxication CASE INFORMATION: A 56 year old Thai nun, non-smoker, with no known medical history was brought in for an acute onset of confusion, lethargy, and diffuse body weakness. Following breakfast, the patient was found to be minimally responsive next to a bowl of soup. By report, this soup contained many leaves of Chinese broccoli self-grown at the temple. In the ED, the patient's presenting GCS was 9, T 37.1F, pulse 49, BP 91/39, respirations 16, and room air O2 sat 94%. She was minimally responsive and diffusely flaccid on motor exam. IV fluids, NG charcoal lavage, and sorbitol were administered. CBC, CHEM 10, LFTs, and UA were all normal; serum/urine toxicology screen, acetaminophen and alcohol levels were negative. CXR was clear, and head CT did not show any shifts, masses, or bleeds. EKG showed only sinus bradycardia at 50 bpm. On repeat exam, pt was slightly more responsive since presentation, with pupils dilated and sluggish, but not following commands in English or Thai. She was admitted to the ICU for monitoring. Several leaves of the Chinese broccoli used in the soup were brought in later. Upon calling poison control and researching botanical atlases, it was determined to be a tobacco plant. Her serum nicotine level was low, while her serum cotinine level was high, indicating the metabolism of nicotine to cotinine, and confirming an ingestion of 15+ tobacco leaves. The patient regained her strength and alertness gradually and was discharged in normal health on day 3. The temple members subsequently removed all remaining`Chinese broccoli' plants! IMPLICATIONS/DISCUSSION: Nicotine overdose can result from overuse of cigarettes, nicotine gum or patches, and plant ingestion. It is seen most commonly in patients smoking while on a patch. Patients can exhibit weakness, convulsions, coma, respiratory distress/apnea, pupillary dilatation, abdominal cramps, vomiting, initial tachycardia/hypertension, followed by bradycardia/hypotension. Diagnosis is by careful history and physical exam as there are no set serum toxicity levels. The half-life of nicotine is 0.5±2 hours while that of cotinine (a better marker due to its slower clearance) is 12±30 hours. Management includes airway protection, charcoal lavage, sorbitol, hydration, and circulatory support. Symptoms can last several hours, and survival after 4 hours of intoxication usually prognosticates complete recovery. Lethargy may remain for several days. Caution needs to be emphasized for patients ingesting unknown plants and to remind patients of the dangers of using nicotine replacements while continuing to smoke.

PREECLAMPSIA AND PSEUDO POSTPARTUM CARDIOMYOPATHY. H. Zakariya 1 , R.D. Hobbs 1 ; 1 Oakwood Healthcare System, Dearborn, MI (Tracking ID #76568) LEARNING OBJECTIVES: To recognize that volume overload in the preeclamptic patient can lead to pulmonary edema and the misdiagnosis of postpartum cardiomyopathy. CASE INFORMATION: A 29 year-old, G5P3AB2 woman presented with severe dyspnea, orthopnea and peripheral edema five days after delivering a baby. Her pregnancy had been complicated by preeclampsia but managed without difficulty. Vital signs were: BP 157/96, P 110, R 22, T afebrile. Oxygen saturation was 94% on 100% O2. Bilateral rales, jugular venous distention, an S3 and S4 with 3+ pitting edema and a mitral regurgitation murmur were noted on physical examination. Cardiac enzymes were normal. Hgb was 9.7 g/dl. An EKG showed sinus tachycardia. Spiral CT was negative for pulmonary embolus. She was admitted with a diagnosis of postpartum cardiomyopathy. An echocardiogram showed severe mitral regurgitation, trivial tricuspid regurgitation, a small pericardial effusion and an ejection fraction of 50-55%. She was treated with furosemide and rapidly improved. Repeat echocardiography, done two weeks later when she was asymptomatic and off medications, showed that the mitral regurgitation had cleared, there was no pericardial effusion and her ejection fraction was unchanged. Further history revealed that in the last months of pregnancy and immediately postpartum she had been advised to``drink a lot of fluids.'' IMPLICATIONS/DISCUSSION: In preeclampsia the expected fall in colloid oncotic pressure is greater than that seen in normal pregnancies. Cardiac output increases 40% during normal pregnancy and extravascular volume is expanded. Following delivery, significant amounts of extravascular fluid move into the intravascular space and are cleared. In our patient, increased fluid intake led to over expansion of the extravascular volume with pulmonary edema occurring as the fluid was mobilized. Notably, this is not a case of postpartum cardiomyopathy. Her ejection fraction was normal on both initial and repeat echocardiograms and does not show primary muscular dysfunction. The mitral regurgitation cleared with diuretics and is not suggestive of a structural lesion. Small pericardial effusions may occur as a normal variant during pregnancy. Instead, her condition is explained by extreme fluid shifts in a preeclamptic woman. Diagnostic confusion occurs if the physician interprets the findings in terms of the non-pregnant state. year old female with no PMH except appendectomy, admitted with a five days of abdominal pain. It began as``indigestion'' in the epigastrum for several days but progressed to a sharp, constant, right-sided abdominal pain. Associated symptoms included anorexia, three days of constipation, with no bowel movement but some flaitus. She had no dysuria, normal menses, and no bloody bowel movements. She had one episode of``sweats'' and chills two days prior. On exam, she was afebrile and in moderate distress. Her vital signs were normal and abomen was soft with hypoactive bowel sounds and voluntary guarding in the right mid abdomen. Rectal exam was guiac negative. The remainder of the exam was normal. UA, CBC, LFTS, amylase, and lipase were normal. CT of the abdomen revealed a 5.3 cm mass( with a small air pocket) adjacent to the hepatic flexure with mesenteric stranding and sigmoid diverticulosis. Bowel rest and ampicillin -sulbactam were implemented. By the third day, her exam markedly improved. She was discharged on amoxicillin-clavulanate with follow up colectomy planned. IMPLICATIONS/DISCUSSION: The frequency of diverticulosis in younger patients is thought to be increasing. Most people will be asymptomatic. Overall, 15% will be right sided in western countries. Symptoms include bloating and abnormal bowel habits. About 20% develop clinical diverticulitis and of those, 10 to 20% will require surgery. Complications of diverticula include simple inflammation, abscess, bleeding, and fistula formation. Abscess may cause abdominal pain for several days duration, nausea, constipation and fever. WBC can be normal in up to 45% of patients. Treatment of complicated diverticulitis often requires combined medical and surgical approach. Evidence suggests more virulent disease in young people. Often these patients are treated with early colectomy. They have a higher incidence of right sided disease that can be mistaken for appendicitis. Longer lifespans lead to increased potential for morbidity. With CT guided drainage, the two part surgeries (with colostomy and then take down) decreased dramatically. Contained perforation is managed with antibiotics followed by partial colectomy. Offering colectomy after the second attack of uncomplicated diverticulitis has recently been challenged. Conservative treatment after the second attack is now considered a reasonable option in older patients. However, for younger individuals, with no medical comorbidities, early surgery may be the preferred option. The patient is a 33 year old female, gravida two para one, at eight weeks gestation who presents to the office. Her first pregnancy was complicated by a deep venous thrombosis at fifteen weeks gestation. At that time hypercoaguability work up was performed due to a positive family history. The patient had elevated protein C resistance and she was placed on full dose heparin through the duration of her pregnancy. Her third trimester she developed hypertension. She delivered at thirty-five weeks and remained on anticoagulation six weeks following delivery. Factor V leiden mutation was confirmed by gene testing following delivery. She had a seizure disorder as a child and took dilantin and multivitamin prior to pregnancy. Her father had a pulmonary embolus and has antithrombin III deficiency. She is a pharmacist and does not smoke or drink alcohol. Comprehensive physical exam is normal. The patient was placed on continuous subcutaneous infusion of heparin because she declined lovenox therapy. IMPLICATIONS/DISCUSSION: Factor V Leiden is the leading cause of thomboembolism in pregnancy (44%). Pulmonary embolus contributes greatly to maternal mortality rates. Venous thromboembolism occurs in one in 1500 pregnancies. The most prothrombotic time is immediately post partum. In addition factor V Leiden has been associated with HELLP, intrauterine growth retardation, miscarriage, and pregnancy induced hypertension. The activated protein C resistance test may be falsely positive because of changes that take place in the coagulation system during pregnancy. Diagnosis must be confirmed with gene testing. If factor V positive, patients have a three to five times greater risk of stillbirth. Factor V Leiden is present in 20±40% of abruptions. There have been no randomized control trials to demonstrate that full dose anticoagulation will reduce the risk of any of these complications. Treatment is based on extrapolation of data from nonpregnant patients. There is controversy over treatment of pregnant patients with factor V and a prior DVT. At present, patients are offered prophylactic dose heparin or full dose heparin or lovenox based on individual risk stratification (i.e homozygous vs. heterozygous). For individuals with factor V but no prior event, a variety of options exist: prophylactic subcutaneous heparin throughout the pregnancy with full dose anticoagulation postpartum for six weeks versus postpartum treatment only versus clinical surveillance alone. Lovenox will likely replace heparin because of its favorable side effect profile. Risks include a 2% major bleeding risk, heparin induced thrombocytopenia, and osteoporosis. (2) To review the presentation, treatment, and prognosis of CMV colitis among immunocompetent adults. CASE INFORMATION: A 17-year-old female was admitted to the hospital for a complaint of bloody diarrhea. She had been in good health until 4 months earlier when she noted intermittent passage of bright red blood and reddish tissue with her stool. Ten days before admission, she developed cramping periumbilical pain, soon followed by fever and watery diarrhea with hematochezia. Pertinent findings on examination included a temperature of 100.4 F, slightly pale conjunctivae, a soft abdomen with normoactive bowel sounds and minimal tenderness periumbilically, and bright red blood on digital rectal exam. Her white cell count was 8,200/mm3 with 37% neutrophils and 55% lymphocytes. Atypical lymphocytes were present. Stool samples were negative for ova, parasites, C. difficile toxin, and other bacterial enteropathogens. An abdominal CT scan showed thickening of the wall of the entire large bowel. On colonoscopy, there were diffuse inflammation in the colon, mucosal nodularities, and diminished haustral markings. Colonic biopsies demonstrated active colitis with CMV infection, but no architectural distortion to suggest an underlying chronic inflammatory bowel disease (IBD). A CMV antigenemia test came back positive, and anti-CMV IgM and IgG titers were both elevated. HIV serology, however, was negative and CD4 count was 354. Markers for IBD, including p-ANCA and ASCA, were likewise negative. The patient was treated with valganciclovir for 21 days.

3 months postpartum) presented with 5 days of cough, shortness of breath, palpitations, diaphoresis, fatigue, PND and orthopnea without chest discomfort, leg edema/pain, fevers/chills, urinary symptoms or recent illness. Meds: oral contraceptive. Family history: no cardiac disease

no pericardial effusion. The patient was given gentle diuresis, afterload reduction (initially ace inhibitors (ACE), then angiotensin receptor blockers (ARBs) after development of cough), digoxin, anticoagulation (lovenox and coumadin), beta-blockers (Toprol XL after symptoms of heart failure resolved), and sodium/water restriction; oral contraception was discontinued. She continues to do well as an outpatient (NYHA Class I heart failure) on this regimen. IMPLICATIONS/DISCUSSION: Postpartum cardiomyopathy (PPCM), a dilated CM, defined as LV dilatation and systolic dysfunction occurring between the 9th month of pregnancy and 5 months postpartum in the absence of other cardiac or metabolic conditions, affects 1000±1300 women/year in the US. Up to 50% recover sytolic function within 6 months of diagnosis (85% 5-yr mortality in those who do not recover systolic function.) Risk factors are poorly defined. The etiology may involve myocarditis, maladaptive immune or hemodynamic response to pregnancy, cytokines, prolonged tocolysis and/or a familial syndrome. Complications of dilated CM include arrhythmia, thromboembolism or sudden death. Diagnosis is based primarily on history, physical and echocardiography. Treatment consists of diuresis with lasix (and spironolactone in class IV CHF), afterload reduction (ACE, ARBs, hydralazine/nitrates), beta blockade (after decompensated heart failure symptoms are controlled), anticoagulation and digoxin. Given the hemodynamic stress of future pregnancy

Wiese 2 ; 1 Tulane University HSC (SL-12)

LEARNING OBJECTIVES: 1. Use Occam's razor as a cost-effective guide to investigate multiple complaints

His blood cultures grew Streptococcus viridans. An MRI of the lumbar spine showed edematous changes at T12-L1 with loss of disc space, consistent with discitis. An echocardiogram confirmed endocarditis. Further questioning revealed he had had a tooth extraction six months prior to presentation. IMPLICATIONS/DISCUSSION: DISCUSSION: Together the diagnoses of urinary tract infection and lower back strain adequately explained his symptoms, though each was unable to do so on its own. Integrating the two symptoms, per Occam's razor, pointed to endocarditis as a common diagnosis. The fever, bacteremia, and back pain generated sufficient pre-test probability for discitis to warrant an MRI for evaluation. Unlike the more common acute bacterial endocarditis from intravenous drug use, sub-acute endocarditis may exist with subclinical symptoms for months. Any bone or joint pain in the setting of suspected endocarditis should prompt evaluation for a metastatic infection

Wiese 2 ; 1 Society of General Internal Medicine

To illustrate the concept of Occam's Razor through a case that was initially misdiagnosed as two separate disease processes and later found to have a single cause. CASE INFORMATION: A 45 year-old Caucasian man presented with fever, chills, night sweats and back pain. Nine days prior, he had experienced fever and back pain. He had no history of trauma

RBC's; he was empirically treated for a urinary tract infection and lower back strain. He RIGHT VENTRICULAR INFARCTION PRECIPITATING A BIDIRECTIONAL SHUNT IN A PATIENT WITH INCIDENTAL ASD. N.I. Visweshwar 1 , R. Sudheendra 1 , A. Devarajan 1 , A. Ameen 1 , T. Vallur 1 ; 1 Jersey City Medical Center

He had a reportedly negative stress test, normal 2-D ECHO and EGD. 0/E, vitals were BP 120/80, HR 85/m, RR 14/m, T-998 F, SaO2-90%. Pt had raised JVD, normal carotids, PMI not felt, S1 normal intensity, S2 widely split and fixed, 2/6 ESM heard on Left sternal border. RS-normal. Extremities-no edema, 2+ pulses and equal on both sides. EKG-NSR,ST elevation in inferior leads and in V4R. CXR-Hilar prominence with pulmonary plethora

He had a cardiaccath, which showed 90% diffuse RCA stenosis with mild LV systolic dysfunction; A 3 cm ASD with bi-directional shunt. Oxymetry data: IVC 65%

Eisenmenger's is unlikely as the pt. has been asymptomatic with no cyanosis prior to this admission. The RV infarction caused an acute increase in the RA pressure with resultant bidirectional shunt, as is evidenced by the`step-up' between SVC (58%) & RA (75%) and a`step down'; between Left pulmonary vein (96%) & LA (84%). A difference of >5% in Oxymetry values is considered as significant. In summary, this pt. had an Infr. wall MI, RV infarction, diastolic equalization of pressures, 90% diffuse RCA stenosis, secundum ASD with a bi-directional shunt and moderate pulmonary. HTN. The patient underwent arterial by-pass graft of RCA and closure of a 3 cm ASD defect

Direct Coombs test was positive. Repeat antibody screening showed anti-Kell antibody. Coagulation screen showed PT 12.5 secs, PTT 85 secs and fibrinogen 220 mg/dl. Factor VIII level was 3%. Mixing studies of the patients' plasma and normal plasma showed (50:50) immediate correction of PTT to 30 secs, but PTT done after incubation of one hour was 66 secs confirming a delayed inhibitor. At this time he had a positive hemoccult and bloody gastric aspirate. The tests for ANA and dsDNA were negative. He was prescribed oral Prednisone 60 mg /day and Prevacid 30 mg/day and inj. Procrit 40,000 units SC/ week. Over the next few days he improved with no fresh bleeding and was discharged

This was replaced about 2 months later as it had migrated from its original location. IMPLICATIONS/DISCUSSION: The differential for a mediastinal mass is usually compartmentalized into abnormalities in the anterior, middle and posterior mediastinal segments. This differential includes: 1) anteriorly: thymoma, thymic carcinoma, thymolipoma, thymic cysts, teratomas, seminoma, germ cell tumor, thyroid goiter, lymphangioma, and parathyroid adenoma; 2) middle and posterior: lymphoma foregut cysts, pericardial cysts, neurofibomatoma, schwannoma, ganglioma, ganglioneuroblastomas, neuroblastoma, and lateral thoracic meningocele. Fibrosing mediastinitis, often considered``benign,'' causes a variety of clinical syndromes secondary to compression and/or erosion into the surrounding mediastinal structures. It often presents with superior vena cava syndrome, pulmonary vein or artery compression, extrinsic compression of the tracheo-bronchial tree, and rarely with constrictive pericarditis. It is a rare disease and has a reported association with Histoplasma and Mycobacterium tuberculosis. The mass is comprised of dense fibrotic tissue in the mediastinal area which often causes symptoms secondary to compression of adjacent structures. The disease is histologically and pathologically similar to sclerosing cervicitis and retroperitoneal fibrosis, and thus, is often viewed as a``variable manifestation of a single disease

Wu 1 , M. Maher 1 , L. Mermel 1 , L. Glasser 1 ; 1 Rhode Island Hospital

To recognize the tenuous course of HLH and manage it accordingly. CASE INFORMATION: An 88-year-old male with a PMH of Sjogren's syndrome and rheumatoid arthritis presented to an outside hospital with 2 weeks of fevers, weight loss, night sweats, and fatigue. He had splenomegaly, elevated LFTs, and pancytopenia. Bone marrow biopsy, pan-cultures, and a hepatitis panel were unrevealing. He received empiric antibiotics and was discharged. Recurrence of fever prompted admission to our hospital. Physical examination revealed a temperature of 38.58C and splenomegaly

2 g/dl, and total bili 4.3 mg/dl. ESR was 56 mm/hr. Abdominal CT revealed mild splenomegaly, a 2-cm low density splenic mass, bilateral pleural effusions, para-aortic lymphadenopathy, and ascites. Bacterial, viral, fungal, and parasitic cultures were negative. Epstein-Barr virus (EBV) IgG Ab titer to viral capsid antigen was 1:10240

IMPLICATIONS/DISCUSSION: Hemophagocytic lymphohistiocytosis (HLH) is an unusual syndrome characterized by fever, splenomegaly, jaundice, and the pathologic finding of hemophagocytosis on bone marrow examination. It is associated with familial and infectious etiologies. Familial cases have been observed in children. EBV-associated HLH is the most common form and can occur at any age. Our patient's serology suggested recent EBV infection or more likely, reactivation. Overall prognosis in HLH remains poor. Familial HLH is an important variant to diagnose, as patients have done well with bone marrow transplantation. Patients with other forms of HLH may respond to etoposide with or without cyclosporine A. Treatment of underlying bacterial, fungal, or parasitic infection is imperative; however, antiviral treatment of patients with EBV-associated disease has not been found to be helpful. HOT HANDS, COLD HANDS: APPROACHING VASCULAR DYSFUNCTION OF THE EXTREMITIES

To develop an evidence-based approach to the evaluation and treatment of these disorders. CASE INFORMATION: A 40 year-old woman with long-standing RP reported a six month history of intermittent``hot hands and feet'' associated with redness and pain. Symptoms were exacerbated by heat, exercise and alcohol, and relieved by immersion in ice water. Past medical history revealed only mitral valve prolapse. The patient denied tobacco, alcohol or drug use. Her mother had also complained for many years of``hot, painful hands''. Physical examination revealed a blood pressure of 116/89 and heart rate of 97. The patient was a well-appearing white female. No abnormality was noted except marked erythema and warmth of both hands. Normal capillary beds were visualized at the periungual folds. Pulses were symmetric and strong. Labs revealed normal CBC, lytes, renal function, and TSH. ANA was 1:40 in a speckled pattern, and ESR was 4. Given the otherwise unremarkable history and physical exam, the patient's symptoms were consistent with primary EM. She was instructed to avoid extreme heat, and avoid ice water immersion given the risk of skin necrosis

Although most cases represent a relatively benign primary disease, up to one fifth of cases seen by internists accompany serious underlying disorders. Treatment consists of environmental measures, and evidence favors calcium-channel blockers as first-line drug therapy. In contrast, EM is a rare condition resulting in episodes of red, warm, and painful extremities. The primary form of disease constitutes 60% of cases. Among patients with underlying disorders, myeloproliferative diseases are most common. Approaches to diagnosis and treatment remain poorly studied

Michelini 1 , E.F. Yee 2 , M. Davis 1 ; 1 GLAVAHCS/ UCLA±San Fernando Valley Program

Urine eosinophils 7%. HIV, and urine fungus, AFB, chlamydia, and gonorrhea were all negative. Prostate exam unremarkable. Post void residual 43 cc. Repeat CT revealed diverticuli, and thickened bladder wall with air suggestive of colovesicular fistula. He was given po levofloxacin and flagyl and a surgical appointment scheduled. Four months after initial presentation, colovesicular fistula repair, and sigmoid resection with primary anastomosis were performed. IMPLICATIONS/DISCUSSION: It is important to recognize clinical clues such as fecaluria, dysuria, pneumaturia, irritative symptoms, abdominal pain, diarrhea, hematuria, and rectal urine passage in order not to miss the diagnosis of colovesicular fistula and delay treatment or incur unneccessary work up of other diagnoses. Aseptic pyuria from fungus, TB, or chlamydia, aseptic prostatitis, bladder mass/malignancy, eosinophilic cystitis, interstitial nephritis, nephrolithiasis, and fistula were all considered in this patient's differential. He was treated for multiple UTI's (common) due to a colovesicular fistula (rare) from diverticulitis, the most common cause of this type of fistula. CT, BE, colonscopy, cystoscopy, and intravenous urogram are all diagnostic modalities

LEARNING OBJECTIVES: 1) To recognize the clinical manifestations of meningovascular syphilis

To recognize that meningovascular syphilis should be considered in the differential diagnosis of HIV patients who present with focal neurological findings

After treatment with ten days of high dose intravenous penicillin, his symptoms resolved, his CSF VDRL was negative, and his MRI/ MRA normalized. IMPLICATIONS/DISCUSSION: Meningovascular syphilis is a clinical entity marked by stroke symptoms secondary to a vasculitis. Clinical manifestations are characterized by an acute onset of hemiparesis. Other possible symptoms include aphasia, seizures, and a prodrome of headaches, dizziness, mood changes, or impaired memory. Population based studies in the literature have demonstrated higher rates of neurosyphilis among HIV co-infected individuals. This vignette demonstrates that HIV patients who present with focal neurological findings deserve a work-up that includes testing for meningovascular syphilis

After excluding cases of individuals above 70 years of age, on immunosuppressive therapy, and with associated diseases such as AIDS, cancer, chronic renal failure, inflammatory bowel disease, or co-infection with another enteropathogen, a literature search from the mid-1960's to 2002 identified less than 15 cases of CMV colitis in truly immunocompetent adults. The youngest of these patients was 22 years old, and the most common presenting manifestations were diarrhea (100%), fever (82%), hematochezia (64%), and abdominal pain (27%). The outcomes ranged from death to development of a chronic illness indistinguishable from IBD

Exercise echocardiogram was also normal with no ischemia. EP study was performed with IV epinephrine and procainamide challenge, no QT prolongation nor Brugadar syndrome were identified. Finally, MRI of the heart shown fatty infiltrate of the right ventrical free wall. Arrythmogenic right ventricular dysplasia (ARVD) was diagnosed and patient was discharged home with an AICD placement. IMPLICATIONS/DISCUSSION: Discussion: Sudden cardiac death (SCD) in young healthy men or women is a catastrophic event. In this country, majority of the cases are due to hypertrophic cardiac myopathy (HCM). Coronary artery disease (CAD) is by far the most common cause of SCD in people who are above the age of 35. It is crucial to rule out HCM and CAD by using echocardiogram. The next common cause of SCD is acquired or congenital QT prolongation induced VF/VT. Therefore, a detailed family history and medication are very important in identify this disease

prolonged course of immunosuppression as the antibody has been noted to be present for a long time. Although the acquisition of Factor VIII inhibitor in Hep C infection is known, this case is being presented for the excellent response to steroids, in spite of continued Hep C infection, is less well known.ACUTE MYOPERICARDITIS PRESENTING AS MI. N. Visweshwar 1 , R. Sudheendra 1 , A. Devarajan 1 , T. Vallur 1 ; 1 Jersey City Medical Center, Jersey City, NJ (Tracking ID #74205) LEARNING OBJECTIVES: 1. A bedside Echo would delineate acute pericarditis from an acute MI in case of suspision which also averts the disastorous complications of thrombolytic therapy 2. Failure of St segment to revert back to isoelectric line following thrombolytic therapy should alert the physician to consider a bedside echocardiography to differentiate acute myocarditis from acute myocardial infarction. CASE INFORMATION: A 40-year-old caucasian male presented with history of crushing central chest pain 9/10 in intensity at the retrosternal region radiating to the neck. This was associated with profuse sweating for about three hours prior to his arrival in ER. Patient had taken aspirin at home. In ER, patient was given two tablets of nitroglycerin with no response. A 12 lead EKG showed ST segment elevation in the anterior wall leads and PR segment depression. The cardiac injury profile showed CPK 1635, CKMB 171 and troponin 192. As the history and investigations were consistent with acute myocardial infarction, patient was started on thrombolytic therapy with TNK 40 mg IV and heparin infusion. Repeat EKG done at 10 minute and 20 minute interval showed no change and patient continued to have the same intensity of chest pain. Patient needed two doses of morphine sulphate 4 mg IV to relieve his pain. As the patient did not respond to thrombolytic therapy, he had an echocardiogram that showed no evidence of segmental hypokinesia. The left ventricular ejection fraction was 45%. A diagnosis of acute myopericarditis was made, anticoagulant therapy was discontinued and patient was treated conservatively in intensive care unit. Cardiac catheterization was done on the second day of admission. During catheterization the coronary vasculature was found to be normal. Patient recovered with ST segment elevation reverting back to isoelectric line within the next three days. IMPLICATIONS/DISCUSSION: Acute myocarditis usually presents with preceding viral prodrome followed by pleuropericardial pain and anginal type of Chest pain is uncommon. Patients may have tachycardia, gallop rhythm and other evidence of heart failure or conduction defect. EKG may show nonspecific ST-T changes and conduction disturbances. Chest x-ray is nonspecific but cardiomegaly may be seen. The confirmation is by endomyocardial biopsy that may reveal round cell infiltration with patchy areas of necrosis. Treatment with immunosuppressive therapy with corticosteroids, NSAIDs and cyclophosphamide has been advised but none has been shown to be of beneficial value. Most of these cases resolve spontaneously and some may progress to dilated cardiomyopathy; but the exact proportion of patients with viral myocarditis progressing to dilated cardiomyopathy is not known. In a series of 9 patients from a single center with myocarditis presenting as MI, there has been no recorded case of death from inadvertent treatment with thrombolytic therapy, In case of suspicion, especially when there is no change in EKG following thrombolytic therapy bedside echocardiography has been advised as a way of differentiating myocarditis from acute myocardial infarction.HOMOCYSTEINEMIA AND CLASSICAL HOMOCYSTINURIA. D. Waggoner 1 , D. Babovic-Vuksanovic 2 ; 1 Mayo Clinic Jacksonville, Jacksonville, FL; 2 Mayo Clinic Rochester, Rochester, MN (Tracking ID #74963) LEARNING OBJECTIVES: Diagnose classical homocystinuria by history, physical exam and laboratory analysis. Treatment modalities for individuals affected by classical homocystinuria. CASE INFORMATION: A 22-year-old male, previously diagnosed with duodenitis, presented with complaints of a cold left foot. An abdominal CT revealed a massive thrombus involving the abdominal vessels and the major arteries of the lower extremity. The patient was taken to surgery and underwent an aorto-iliac thromboembolectomy, a segmental jejunal resection, and a left tibial thromboembolectomy. Coagulation studies were unrevealing. Genetic studies demonstrated heterozygosity for the MTHR common variant. The homocysteine level was 277 umol/L. The patient was started on pyridoxine 1 mg/day and cyanocobalamin 1,000 mcg/day. On physical exam, the patient was noted to be minimally dysmorphic with mild mid-facial hypoplasia, a narrow palate with crowded teeth, myopia, and skin with areas of striae atrophicae about the upper extremities. Further diagnostic studies included quantitative plasma amino acids and a formal eye exam. Folic acid was increased to 5 mg/day and pyridoxine was increased to 100 mg/twice a day. Homocysteine levels normalized, and no further thrombotic events have occurred. IMPLICATIONS/DISCUSSION: Homocysteinemia is seen in a variety of conditions including homocystinuria, an inherited disorder involving the metabolism of the amino acid methionine. It is an autosomal recessive disorder commonly due to beta-synthetase deficiency that affects approximately 1:200,000 people. Affected individuals may present with myopia, dislocation of the lens of the eye, and a tendency to develop venous and arterial clots. Newborns appear normal. Symptoms, if present, tend to be mild. Mental retardation is usually present, but some affected people have normal IQs. Untreated, the mental retardation is progressive and irreversible. Homocystinuria has several features in common with Marfan's syndrome: dislocation of the lens, a tall and thin build with long limbs, arachnodactyly, and a pectus deformity. High arches of the feet, genu valgum, and scoliosis may be present. The most worrisome manifestation of homocystinuria is thromboembolic events. Diagnosis is aided by physical exam, blood and urine homocysteine levels, fiboblast culture, and enzyme assay for beta-cystathionine synthase. In addition to high dose pyridoxine, larger doses of folic acid than used for other forms of homocysteinemia are required. Unfortunately, only about 50% of patients will respond to treatment. Those that fail treatment generally require a low methionine diet.WAS IT REALLY HYPOTENSION? G. Wali 1 , M. Panda 1 , N. Desbiens 1 ; 1 University of Tennessee±Chattanooga Unit, Chattanooga, TN (Tracking ID #77000) LEARNING OBJECTIVES: 1. Recognize the limitations of accurate blood pressure (BP) measurement and that arm blood pressure readings may not reflect central perfusion pressure. 2. Recognize the cardinal clinical signs of shock. CASE INFORMATION: A 68-year old white female with a history of hypertension, CVA and bilateral carotid endarterectomy was brought to the ED because of falling, right-sided weakness and decreased responsiveness. Vital signs revealed BP: 76/35 mmHg, pulse: 94/min, resp: 24/min, temp: 98.8F. She was minimally responsive and did not follow commands. There were no signs of trauma or active bleeding. Pupils were 3 mm and reactive. She had a regular rate and rhythm with no jugular venous distension. Lung exam revealed decreased breath sounds bilaterally with no wheezing or rales. Upper and lower extremities were cold without edema. Femoral pulses are 1+ and the dorsalis pedis pulses were not felt. She had a right sided facial droop and hypotonia. She remained hypotensive despite aggressive IV fluids and large doses of dopamine (40 ug/kg/min). EKG, CXR, CT of head & abdomen, echocardiogram, urine drug screen, ABG and complete lab evaluation failed to identify a cause of hypotension. Urgent cardiac catheterization was performed which showed 70% stenosis of the proximal RCA, significant atherosclerotic disease in both subclavian arteries, central aortic systolic pressure of 149/52 mmHg, compared to simultaneous cuff pressure in either arm (98/51 mmHg). Only the left thigh pressure correlated well with central pressure measurements and was used to monitor BP throughout remainder of the hospitalization. Repeat CT revealed a new left tempo-parietal infarct. The patient's alertness improved but had a receptive and expressive aphasia. She was transferred to a nursing home with instructions to measure BP on the left thigh with an appropriately sized cuff. IMPLICATIONS/DISCUSSION: The presentation of shock is challenging and requires prompt assessment and management. The cardinal clinical signs of shock include hypotension, altered mental status, cool extremities and later decreased urine output. Our patient presented with 3 of these 4 signs. However in our patient the arm BP readings did not reflect the perfusion pressure to her major organs. Her urine output remained normal and her poor responsiveness was most likely related to her CVA. Her upper and lower extremities remained cool secondary to her severe PVD. Accurate BP measurement both in the acute and the ambulatory setting is an essential part of optimal patient care. Severe peripheral vascular disease can interfere with accurate blood pressure measurement and thus its management. Measurement of lower extremity BP would be helpful and possibly prevent invasive diagnostic studies in patients with hypotension that does not respond to fluid and pressors, though even this approach might not work in patients who have severe atherosclerosis in all extremities. year-old man with a long history of type 2 diabetes mellitus, severe peripheral vascular disease, and medical noncompliance was admitted for further management of progressive bilateral lower extremity infections. He recently underwent bilateral BKA and developed soft tissue infections at the amputation sites. He consented to initial surgery, and was found to have extensive necrosis in his legs, hip and pelvis. He underwent a left AKA and aggressive debridement, with a plan to return to the operating room for more radical surgery including a possible hemicorpectomy. This plan became thwarted by the patient's indecision about further surgery. Multiple medical and surgical consultation teams held discussions with the patient. He was informed of the nature of the operation, its consequent disabilities, and of the high likelihood of death without surgery. Yet the patient persisted in postponing a decision. He expressed clear comprehension of the treatment alternatives and expected outcomes, but remained unable to choose between life with severe disability or death. In the meantime, his clinical status slowly deteriorated. After two weeks, the involved physicians decided to present a firm recommendation against surgery. They informed the patient that they interpreted his indecision as a decision to forego surgery, and that his condition had declined to the point where surgery was of high risk. His care was redirected towards palliation and he was discharged to home. The patient accepted this recommendation. IMPLICATIONS/DISCUSSION: The modern model of medical decision-making is grounded in the ethical principles of informed consent and respect for patient autonomy. In this model, the physician's role is to provide sufficient information and support to allow the patient to make an autonomous decision±one that is free from coercive influence and made with the capacity to understand and intend a certain outcome. Sometimes, however, the physician's role in decision-making may need to be expanded; simply providing information and support may not be enough. In our case, the patient was capable but unwilling to make a decision, so his physicians were compelled to decide on his behalf. They interpreted the patient's indecision as a refusal of surgery, based upon his past ambivalence regarding medical attention, his aversion to future disabilities, and his passive allowance of his further decline. The patient then fully assented to the physicians' decision. This case illustrates how respecting the autonomy of an indecisive patient might require physicians to assume an active role in decision-making, undertaking a cautious assessment of their patients' values, experiences and decisional capacity, and fully informing and allowing the patient to disagree with the decision. LEARNING OBJECTIVES: 1. To recognize that captopril can cause severe cholestatic jaundice 2. To discuss the management of captopril induced cholestasis CASE INFORMATION: 48 yo Filipino female presented complaining of 2 weeks of worsening yellow skin, nausea, vomiting, weight loss and total body pruritus. Her PMH was significant for HTN diagnosed three week prior to admission for which she was started on captopril. The patient denied abdominal pain, diarrhea, constipation, clay colored stool, bright red blood per rectum, melena, fever, cough, or the use of other medications, alcohol or drugs. Vital signs were stable and physical exam was significant for severe jaundice and dry mucous membranes. Laboratory results were notable for: AST 230, ALT 455, Alk phos 252, Tbili 7.1, Dbili 6.3. Lipase, Amylase, electrolytes, CBC, albumin, PT/PTT, panel for hepatitis a, b, and c, ANA, anti-mitochondrial antibody, ferritin, and blood cultures were all normal. The patient underwent abdominal U/S, CT scan, and two ERCPs, which were notable for the presence of cholelithiasis without biliary duct dilation. Her captopril was stopped and it was concluded that her cholestasis was an adverse effect of this medication. A liver biopsy was contemplated but not performed because the Gastroenterology team felt that it would not change management. They would consider liver biopsy if liver tests remained elevated for greater than one year. After her intitial discharge the patient required several admissions for IV hydration because of severe nausea and vomiting. Two weeks after her initial discharge, her total bilirubin had increased to 27 mg/dl with a direct bilirubin of 24 mg/dl. These values normalized after six months. Seven months after her initial presentation, she had recovered fully except that her alk phos and ALT remained mildly elevated IMPLICATIONS/DISCUSSION: This case demonstrates a rare adverse effect of captopril. To date there have been several dozen reported cases of captopril induced cholestatic jaundice. Case reports demonstrate an equal incidence in gender and a latent period to development of symptoms of 1 to 20 months. Management is largely supportive following cessation of captopril with improvement of jaundice within 1 week to 6 months. Total bilirubin, alk phos and AST are almost always elevated. The exact mechanism for this drug-induced cholestatic jaundice is unknown but appears to be a hypersensitivity reaction. As such, features of a drug hypersensitivity reaction (i.e. fever, chills, and eosinophilia) often accompany the jaundice and associated pruritus. The diagnosis is one typically of exclusion. Liver biopsy can be helpful in distinguishing cholestatic jaundice from other forms of parenchymal liver damage induced jaundice. Based on the common use of captopril, it is important that practitioners are aware that cholestasis is a potential and serious complication of this medication. LEARNING OBJECTIVES: Consider tick-borne illness early when managing a patient with meningitis. CASE INFORMATION: A 68 year old white male presented with fever, altered mental status, and respiratory distress. He is an avid outdoorsman and lives alone. He was found unresponsive at home after coworkers reported him missing for two days. He was febrile, orthostatic, with diffuse rhonchi and a fine macular truncal rash. Laboratory studies revealed mild anemia, hepatitis (AST = 306), renal failure (creatinine = 7.2) and thrombocytopenia (platelets = 28,000). White cell count was 5600 with 33% bands. Lumbar puncture chemistries suggested bacterial meningitis. Cerebrospinal fluid gram stain revealed intracellular clusters of gram negative bacteria in cytoplasmic vacuoles of mononuclear cells. Doxycycline, begun early for coverage of tick-borne illnesses, was continued upon receipt of the gram stain. Four days after admission, ehrlichia indirect fluorescent IgG antibody test returned at 1:64. Twelve days later, IgG antibody was 1:4096. IMPLICATIONS/DISCUSSION: Two forms of human ehrlichiosis are found in North American, human monocytic ehrlichiosis (HME) and human granulocytic ehrlichiosis (HGE). HME is predominant in the south, is caused by Ehrlichia chaffeensis, and is transmitted by the lone star tick, Amblyomma americanum. Symptoms of ehrlichiosis are generally nondescript. Common signs are hepatitis (85±90%), thrombocytopenia (50±75%), and rash (36%). Although neurologic symptoms are not common, abnormal CSF chemistries are common (55%) when lumbar puncture is performed. When CSF is abnormal, mortality is high (19%). CDC case definition includes antigen, antibody, PCR, and/or culture data. Our patient met case definition by his Y fourfold rise in IgG antibody.LEGIONNAIRES' DISEASE, RASH AND RENAL FAILURE. C. Wells 1 , D. Balkovetz 1 ; 1 University of Alabama at Birmingham, Birmingham, AL (Tracking ID #76633) LEARNING OBJECTIVES: Review a case of Legionnaires' Disease (LD) associated with acute renal failue (ARF) and rash. CASE INFORMATION: A 50 year-old male presented with a 5-day history of fever to 1048F, abdominal pain, non-bloody diarrhea, malaise, and an erythematous, non-pruritic rash. Physical examination was significant for fever, tachycardia, hypotension, cardiac murmur, crackles in the left lung field, and a diffuse erythematous maculopapular rash. Hospital evaluation revealed pneumonia and ARF with creatinine of 7.1. The patient was treated for community-acquired pneumonia (CAP) with vancomycin and ceftriaxone. Renal function deteriorated further with peak creatinine of 13.6, a renal biopsy was consistent with acute interstitial nephritis (AIN), and the patient required hemodialysis. Legionella urine antigen sent on hospital day #3 was positive, and the patient's renal and pulmonary function began to improve with the initiation of doxycycline. IMPLICATIONS/DISCUSSION: Legionella pneumophila, the causative organism in LD, is responsible for 2±9% of cases of CAP. Classic associations include abdominal pain and diarrhea. ARF and rash are less common. ARF was described in 14 of the original 123 patients from the outbreak in 1976, three of which required hemodialysis. At least 45 more patients with LD and ARF have been described with various pathology including ATN, AIN, and RPGN. Only three cases of rash associated with LD are documented in English journals. In each case the rash developed after antibiotics. In this patient the rash was observed on presentation and resolved with doxycycline.

H. Whelan 1 , G. Applebaum 1 ; 1 Olive View±UCLA Medical Center, Sylmar, CA (Tracking  ID #75573) LEARNING OBJECTIVES: 1. Hyperkalemic periodic paralysis(HYPP) as a rare cause of weakness 2. Review clinico-pathologic presentation of HYPP 3. Highlight iatrogenic precipitants of HYPP CASE INFORMATION: A 64 year old Hispanic man with a history of CHF, atrial fibrillation, pacemaker and chronic renal insufficiency presented complaining of 2 weeks of progressive weakness of his extremities. He reported that his lower extremity weakness gave him the inability to walk and upper extremity weakness made it difficult to lift a glass to drink. The patient denied headache, diplopia, dysphagia, dysarthria, paresthesia, or ataxia. Furthermore, he reported no history of a febrile illness or upper respiratory symptoms. The patient did, however, report having loose stools over 2 weeks and that he had increased his potassium supplementation during this time period. Physical exam was remarkable for 4/5 strength in bilateral upper and lower extremities and 3/5 in left hip flexion. The patient was unable to rise from a chair. His deep tendon reflexes were present and symmetric. Lab data was remarkable for potassium 7.6 and creatinine 1.9. The initial EKG showed a paced rhythm with widening of the QRS and peaking of the T waves. Initial management consisted of calcium gluconate, glucose and insulin. The patient was further treated with kayexalate and furosemide and his serum potassium decreased to 4.9. In 24 hours, the patient demonstrated resolution of his weakness. IMPLICATIONS/DISCUSSION: While hypokalemia is more commonly recognized to cause periodic paralysis, hyperkalemic periodic paralysis (HYPP) is a rare cause of weakness. HYPP is caused by a defect in the muscle sodium channel which is linked to an autosomal dominant gene mutation. Clinically, HYPP is characterized by episodic bouts of weakness lasting hours to days, during which time the serum potassium is elevated although it can occasionally be normal. Attacks can be precipitated by exercise, cold, and during pregnancy. Common iatrogenic causes include potassium supplementation, glucocorticoids and potassium sparing diuretics. Treatment of HYPP includes acute management of hyperkalemia with EKG changes, and then lowering of serum potassium by usual means. The diagnosis is suggested when muscular weakness resolves with potassium normalization.HYDROCHLOROTHIAZIDE-INDUCED HEMOLYTIC ANEMIA? K.C. Wilson 1 ; 1 University of Illinois at Peoria, Peoria, IL (Tracking ID #76998) LEARNING OBJECTIVES: 1. Recognize the clinical and laboratory features of druginduced autoimmune hemolytic anemia (DIAHA). 2. Recognize treatment and need for referral in DIAHA. CASE INFORMATION: A 55-year-old Caucasion female presented with nausea, myalgias, and jaundice 2 weeks status post rectal surgery. At that time she had received cefotetan perioperatively, as well as hydrochlorothizide (HCTZ) prior to discharge. Review of systems revealed pronounced fatigue, myalgias, dark colored urine, nausea, and jaundice. Medical history was significant for hypertension, tobacco use, and remote history of blood transfusion. She was allergic to sulfa, which caused a rash. She denied alcohol or intravenous drug use. She denied any abdominal pain, hematochezia, melena, or recent viral illness but reported some dyspnea on exertion. Medications included atenolol,estrogen, sertraline, and the newly prescribed thiazide. Her vitals were stable except for a pulse of 120. On physical exam, the skin was jaundiced with rare ecchymosis but without rashes. The conjunctivae and mucous membranes were pale and scleral icterus was evident. The remainder of the exam was normal including abdominal exam. Hemoglobin was 3.5 g/dl, WBC 34,000, total bilirubin 4.1, LDH 1070, haptoglobin was low,and direct Coombs was positive. HIV and viral hepatitis studies were negative. CT of the chest was negative for lymphoma. Methylprednisolone and gamma globulin were begun for presumed DIAHA, and patient was tranfused blood products. A hematologist suspected HCTZ as the culprit, given her sulfa allergy. Other possibilities included cefotetan. Patient markedly improved and was discharged 5 days later on oral predisone. IMPLICATIONS/DISCUSSION: With advancements in pharmacologic medicine have come an increasing incidence of drug-related reactions, including DIAHA. Common drugs implicated in DIAHA include high-dose penicillin, sulfa-based drugs, cephalosporins (e.g. cefotetan and ceftriaxone), methyldopa, procainamide, quinidine, isoniazide, and primaquine. HCTZ has the potential to cause allergic reactions and hemolytic anemia due to its sulfacomponent. Other causes of hemolytic anemia to be ruled out include viral infections (HIV, etc.), autoimmune diseases,lymphoma, hypersplenism, and microangiopathy (DIC, HUS, TTP). DIAHA typically presents with jaundice, anemia, low haptoglobin, elevated LDH, positive direct Coombs test, and elevated indirect bilirubin. Treatment requires removal of the offending drug, corticosteroids, and hematology referral for gamma globulin therapy.FIBROSIS, NOT SO BENIGN. M. Woodske 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA (Tracking ID #74956) LEARNING OBJECTIVES: 1. To recognize the differential diagnosis of extrinsic lung masses. 2. To recognize the causes, associated syndromes, and treatment of fibrosing mediastinitis. CASE INFORMATION: A 49 year old male, a smoker with 75 pack-years, with additional medical history of occupational exposures to petrochemicals from auto body repair and multiple recurrent pneumonias over the last 3 years, presented to an outside hospital approximately 2 months prior to admission with hemoptysis and progressive dyspnea. The ROS was unremarkable and the patient denied weight loss. The patient's hemoptysis and dyspnea initially resolved with a course of antibiotics. However, a chest x-ray and subsequent CT scans revealed a soft tissue density between the left mainstem bronchus and esophagus, compressing the left mainstem bronchus. Split function ventilation perfusion scans showed minimal function in the left lung. A malignancy work up including EGD, colonoscopy, CT of the abdomen and pelvis, and multiple labs test was unrevealing. Several attempts at bronchoscopy only revealed dense fibrosis. The patient then had an open thoracotomy to