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.