A CHALLENGING CASE OF DYSPNEA IN A PATIENT WITH BREAST CARCINOMA. P.J. Bennett 1 , M. Panda 1 ; 1 University of Tennesee, Chattanooga, TN LEARNING OBJECTIVES: Use of appropriate diagnostic testing to differentiate the pulmonary tumor emboli syndrome from a thromboembolic event. Understand the diagnosis and management of pulmonary tumor emboli CASE INFORMATION: A 75 year old white female with a past history of poorly differentiated ductal adenocarcinoma of the right breast diagnosed in 7/95 presented with progressive shortness of breath for 4 ± 5 days. On exam, she was afebrile, tachypneic and tachycardic. She had decreased breath sounds bilaterally with crackles posteriorly in the right lower hemithorax. ABG revealed: pH 7.46, PCO2 26mmHg, PaO2 43mmHg, HC03 19meq, 82% saturation on room air. Chest films and CT were unchanged from previous of 8/98. There was no evidence of lymphangitic carcinomatosis. Echocardiogram revealed an EF of 72%, evidence of new moderate pulmonary hypertension and new tricuspid regurgitation, without tamponade. VQ scan revealed small unmatched peripheral deficits in the left upper lobe consistent with intermediate probability of pulmonary embolus. Subsequent pulmonary angiogram revealed no evidence of pulmonary embolism. Due to worsening hypoxia, bronchoscopy with transbronchial biopsy was performed. Biopsy revealed metastatic poorly differentiated carcinoma with prominent intravascular growth consistent with a breast primary. DISCUSSION: Pulmonary tumor embolism is more often a postmortem diagnosis in patients with known solid tumors such as breast, liver, prostate, and kidney. Potential mechanisms of tumor emboli to the lung include direct extension into the IVC, extension via the thoracic duct to pulmonary lymphatics or via the SVC & right side of the heart to the pulmonary arterioles. The tumor cells occlude the smaller arterioles without parenchymal involvement. Resulting intimal proliferation leads to increased pulmonary pressures and right ventricular strain. Progressive dyspnea is the most common symptom. Chest X-ray is often unremarkable. VQ scans may be normal, indeterminate, or reveal focal defects. Pulmonary angiography may only reveal slow blood flow. Occasionally, CT/MRI scans may reveal a tumor mass occluding the pulmonary artery. Diagnosis is proven by tissue biopsy. Treatment of patients with pulmonary tumor emboli is difficult. Tumor embolectomy may be an option in large proximal emboli. Chemotherapy and radiotherapy usually produce a poor response. Together with fat and amniotic fluid embolism, tumor embolism cause hypoxia with a normal pulmonary angiogram. As in our patient unrelenting hypoxia and new development of hypertension may be important diagnostic clues.`I A 40 year old white female with no significant medical history presented with a 5 month history of a slowly expanding rash on her lower trunk and proximal extremities associated with generalized fatigue. The rash was painless, nonpruritic and not associated with arthralgias, fever or chills. The patient admitted to taking several herbal medications which she had recently stopped. Her physical exam was unremarkable except for a pink, blanchable, nontender, confluent, macular rash involving the lower abdomen and proximal portions of the arms and legs. There were no bullae or pustules. Laboratory evaluation revealed a negative ANA, rheumatoid factor, SS-A and SS-B antibodies. The patient had normal levels of aldolase, CPK and sedimentation rate. Her CBC was unremarkable except for the presence of 26% eosinophils. A deep fascial biopsy of one of the left thigh lesions revealed an inflammatory infiltrate of the fascia consistent with eosinophilic fasciitis. Upon review of the patient's herbal medication list and available literature, the probable causative agents were glucosamine sulfate and the fever few leaf. The patient was started on steroids with slow improvement. DISCUSSION: Eosinophilia-myalgia syndrome was first described in 1989 when it was observed in 3 group of patients who developed scleroderma-like skin changes, myalgias, eosinophilia, and histologic findings similar to eosinophilic fasciitis after ingestion of Ltryptophan manufactured by a single company. However, as this case illustrates, other agents, including herbal medications can precipitate a similar syndrome. Other clinical manifestations include low grade fever, fatigue, dyspnea, cough, arthralgias/arthritis, erythematous rashes and myalgias. Myocarditis and pulmonary hypertension can occur. Usually significant peripheral eosinophilia is noted and striking tissue eosinophilia may be noted as well. Diagnosis is dependent on histologic findings from a deep biopsy including fascia and muscle. Response to treatment is variable but patients may respond to steroids, plaquenil, methotrexate, Dpenicillamine and cimetidine. The course of the disease is poorly defined but many patients spontaneously regress or remain unchanged for years. Use of herbal medications is becoming very common as these products are widely advertised and readily available. However clinical trails and adequate information on efficacy and adverse reactions are limited. This case stresses the importance of incorporating questions on use of herbal medications routinely on medication history and the need to have a hightened awareness of their possible implication in disease. A 74 year old previously healthy male presents complaining of a 2 month history of progressively worsening scrotal swelling. The patient denied urinary hesitancy, frequency, hematuria, dysuria, or incontinence, but admits to mild decrease in urine output with occasional urgency. Past medical history was negative, and the patient denied using any medications including NSAIDS. Physical exam was significant for marked scrotal, suprapubic, penile shaft, and foreskin edema with normal testicular size. No masses or hernias were detected. Routine labwork showed BUN 67, Creatinine 9.6. When seen for the same complaint 5 weeks earlier, the patient had normal electrolytes and creatinine 1.2. Foley catheter was successfully placed with approximately 50cc of residual volume obtained. Renal ultrasound showed mild to moderate right hydronephrosis, mild prominence of the left collecting system without hydronephrosis. Percutaneous nephrostomy of the right kidney failed to improve renal function, and hemodialysis was initiated. Left renal biopsy revealed normal glomerular structure. CT scan of pelvis showed calcification of the prostate, with thickened mucosa of the sigmoid colon and rectum and bilateral hydroceles. Prostate biopsy was negative for malignancy. Rectal biopsy revealed poorly differentiated carcinoma of probable uroepithelial etiology. After 7 days, urine output began to improve, and dialysis was discontinued. Hepatitis serologies, urine and serum protein electrophoresis, ANCA, and anti-GBM antibodies were negative. Cystoscopy showed bladder thickening with locally invasive disease and bilateral ureteral obstruction. Results of bladder biopsy showed high grade papillary transitional cell carcinoma with vascular invasion and extension to the pelvic wall and rectum. DISCUSSION: Approximately 4% of cases of renal failure due to obstructive uropathy present without dilation of the urinary tract. Of these cases, 60% are due to intrapelvic malignancy (prostate, bladder, colorectal). Proposed mechanisms for lack of dilation include ureteral encasement by tumor, ureteral edema, reabsorption, and interrupted peristalsis. Although renal ultrasound is often used to rule out urinary tract obstruction, the absence of hydronephrosis does not exclude obstructive uropathy as the cause of acute renal failure. In the presence of high clinical suspicion, additional studies such as cystoscopy, intravenous pyelogram, or retrograde pyelography must be pursued to evaluate patency of the upper and lower urinary tracts.