A CURIOUS CASE OF CYANOSIS. C.T. Ko 1 , N. Spell 1 ; 1 Emory University, Atlanta, GA (Tracking ID #76425) LEARNING OBJECTIVES: 1. Recognize methemoglobinemia as a cause of cyanosis, even without G6PD deficiency. 2. Diagnose and treat methemoglobinemia by understanding its mechanism of action. 3. Recognize the drugs that can cause methemoglobinemia. CASE INFORMATION: A 26-year-old African-American female with HIV presented complaining of worsening shortness of breath, headaches, and generalized weakness. Her CD4 count was 11/mm3. She had been discharged from the hospital one week prior with treatment for presumptive Pneumocystis carinii pneumonia. Her discharge medications included clindamycin and primaquine. On physical exam, she was a thin, cachetic, pleasant female in mild respiratory distress. Vital signs included a temperature of 102.5F (39.2C), blood pressure 90/50 mm Hg, pulse 124 beats/minute, and respiratory rate 24 breaths/minute. Her pulse oximeter reading was 85% saturation on room air and 89% saturation with a 100% nonbreathing oxygen mask. She had conjunctival and mucosal pallor as well as cyanosis of her nail beds, diffuse shoddy lymphadenopathy, and tachycardia with no associated murmurs/rubs/ gallops. Lung fields were clear to auscultation with adequate airflow. Laboratory evaluation revealed white blood cells 3400/mm3 (47N, 46L, 6M), hemoglobin 7.0 g/dl, hematocrit 20.2%, platelets 130,000/mm3, and reticulocytes 1.4%. Her hematocrit one week prior was 35.5%. Chemistry profile showed total bilirubin 1.0 mg/dl, LDH 1374 U/L, and G6PD 10.6. All other chemistry values were within normal limits. Chest X-ray was unchanged from her previous films with minimal bilateral reticular prominence likely secondary to mild interstitial scarring. Arterial blood gas on room air showed pH 7.40, pCO2 28 mm Hg, pO2 73 mm Hg, oxyhemoglobin 73%, carboxyhemoglobin 0.2%, and methemoglobin 25%. Primaquine was discontinued, and methylene blue was administered. Methemoglobin level was 13.6% within one hour. One week later in outpatient follow-up, methemoglobin level was 2.6%. IMPLICATIONS/DISCUSSION: Methemoglobinemia causes cyanosis that is unresponsive to oxygen therapy. In addition, pulse oximeter readings are not accurate when there is methemoglobin in the blood. Etiologies of methemoglobinemia include medications, chemical agents, and hereditary causes. The goal of therapy in methemoglobinemia is to reduce heme iron in order to restore normal oxygen transport. year-old Asian-American woman presented with three weeks of progressive muscle weakness. She had difficulty combing her hair, lifting her arms or getting out of a chair. At presentation she could not walk. She had a dusky, almost dirty appearing rash on her chest and around her eyes. An erythematous rash was noted on the dorsal surface of the MCP and PIP joints of her hands. She could not lift either thigh off the bed. Laboratory values: CK 14,245, RF 273, ANA + >1:640 (speckled pattern), AST 605, ALT 207, ALK PHOS 95, LDH 150. Hepatitis B CAb +, Hep Sab +. Anti-RNP, Anti-Jo, Anti-SSA, Anti-SSB and anti-DS DNA were all negative. A presumptive diagnosis of dermatomyositis was made, a confirmatory muscle biopsy performed and prednisone begun. Malignancy workup was negative. She improved slightly and was discharged to a rehabilitation facility. IMPLICATIONS/DISCUSSION: Dermatomyositis (DM) is a rare idiopathic inflammatory myopathy that has a 2:1 female preponderance and presents most commonly in the fifth decade. The incidence of DM is 1:100,000. Pathogenetically, DM is associated with immune complex deposition in a perivascular and perifasicular distribution. The etiology is unknown although viruses have been implicated. The typical presentation of DM is proximal muscle weakness in association with classic dermatological findings. Gottren's papules, as seen in our patient, are the most commonly seen skin rash. The classic heliotrope rash is the most specific manifestation of DM but is only rarely seen. Other findings include acanthosis nigricans,`m echanics hands,'' diffuse flat erythema in a shawl like distribution, and periungual erythema. The elevated liver enzymes in this patient are problematic since DM alone can raise parenchymal liver enzymes. The hepatitis B profile is not suggestive of an acute infection and unlikely to be causing the elevated liver enzymes. Hepatitis B, however, has been implicated in the pathogenesis of some cases of DM and raises the question of a delayed slowly progressive humorally mediated immune reaction. The relationship between the two conditions is unknown although a few select reported cases suggest it may be more than coincidental. There was no history of smoking, travel, or prolonged immobilization. His ROS was otherwise negative. His medications were aspirin, metaprolol, lisinopril, and sulfasalazine. After initial treatment for pulmonary edema at an outside hospital, he was transferred to our institution. He was intubated due to worsening hypoxia. A bronchoscopy was performed: bronchoalveolar lavage (BAL) was bloody. VS: Temp -378C, BP -124/60 mmHg, HR -110/min, SaO2 -98% on assist control ventilation. Exam was notable for bilateral rales and absence of S3 or JVD. Initial labs revealed Na-127, creatinine -1.0, CK-MB -15, Troponin I -10.2. EKG was normal; CXR showed interstitial pulmonary edema. Echocardiogram showed EF of 35%. A highresolution chest CT showed ground glass appearance consistent with ARDS. He was treated with ceftriaxone and azithromycin. His hospital course was complicated by right middle and anterior cerebral artery ischemic stroke, ARF (BUN/Cr 118/3.3), anemia and ultimately shock. He expired on the ninth hospital day. Autopsy reports confirmed thrombotic microangiopathy consistent with HUS. BAL culture subsequently grew influenza A. IMPLICATIONS/DISCUSSION: Influenza, occurring as outbreaks in winter seasons, is usually self-limited; but causes increased morbidity and mortality in high-risk populations. Such high-risk group includes patients with underlying cardiac, pulmonary, and immunosuppressive diseases, nursing home residents and older than 65. Primary viral pneumonia is the most severe pulmonary complication that tends to occur in individuals with elevated left atrial filling pressures, and pulmonary diseases. Systemic complications include rhabdomyolysis, Reye syndrome, transverse myelitis, and myocarditis. Other rare complications, such as hemolytic uremic syndrome and toxic shock syndrome worsen the clinical outcome. Apart from the tissue culture, the virus can be detected in throat swabs and by serologic methods. This high-risk patient presented with acute severe respiratory failure from primary influenza A pneumonia complicated by HUS leading to renal failure and anemia. Increasing the pretest probability by clinical evaluation will be helpful in initiating treatment earlier in the course rather than be fooled by the flu. LEARNING OBJECTIVES: 1. To recognize the clinical and pathologic presentation of talcosis, also known as foreign body granulomatosis. To recognize the sequelae of talcosis, specifically panlobular emphysema, acute pulmonary hypertension, ARDS, and spontaneous pneumothorax. 2. To recognize signs and symptoms of factitious disorders (Munchausen's). 3. To discuss differences between factitious disorders, somatoform disorders and malingering. CASE INFORMATION: A 50 year-old Oregon man with an extensive past medical history including chronic pain syndrome involving his hip, knee, and groin, total hip replacement surgery with multiple revisions and post-surgical complications presented with a recent history of hypertensive episodes and syncope. He was referred to VMMC for evaluation of a possible pheochromocytoma. In addition to syncope, the history and physical revealed an antecubital abscess and fevers. The patient was admitted and an Infectious Disease consult ordered. He reported that In March, 2002, he developed increasing frequency of attacks characterized by chill, abrupt fever, hypertensive episodes, and syncope. In mid-March, he noted swelling, redness and warmth in his right antecubital fossa and continued to have fever every few days. The patient's hospital course was complicated by multiple episodes of fever >39 oC, witnessed and unwitnessed syncopal episodes, frequently infliltrated intravenous lines, polymicrobial blood cultures, increasing oxygen needs, infected PICC, and atrial fibrillation. His medical work-up was extensive. He ultimately underwent a chest CT which showed multiple 2-3mm, bilateral pulmonary nodules. The patient had thoracoscopic lung biopsy of several nodules. The pathology revealed near complete occlusion of small and medium vessels by extracellular refracticle material. The patient was confronted with these findings and confessed to having crushed and injected oxycontin on several hundred occasions.