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.