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 Â 2cm Â 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 Â 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.