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.