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.