INTRODUCTION: Tumor emboli to the pulmonary vasculature has been described in hepatocellular, renal cell, gastric, breast and prostate carcinoma. We report a case of a distantly treated urothelial carcinoma with a metastatic presentation of tumor emboli causing progressive pulmonary hypertension.
CASE PRESENTATION: A 69 year old man presented with a complaint of dyspnea, pleuritic chest pain and blood-streaked sputum for 3 days. His past medical history was significant for urothelial carcinoma of the left renal pelvis (high-grade, pT3NxM0) successfully treated 1 year ago with nephrectomy and partial ureterectomy followed by adjuvant chemotherapy with carboplatin and gemcitabine. He had been in good health up until this admission. Oxyhemoglobin saturation (Sa02) was 91% in room air. Physical examination was significant for right-sided crackles. Chest X-ray showed bibasilar interstitial markings. Chest CT revealed pulmonary emboli (PE) in the bilateral lower lobe segments, nodular and confluent ground glass opacities in the bibasilar and right upper lobes. Echocardiogram demonstrated normal left ventricular function with a dilated and poorly functioning right ventricle (RV) and a calculated pulmonary artery systolic pressure (PASP) of 67 mmHg. The patient was anticoagulated for PE and given a 14 day course of moxifloxacin for presumed pneumonia and discharged. The patient returned 10 days later complaining of worsening hemoptysis. Repeat chest CT showed no interval change. His hemoptysis was presumed to be due to pulmonary infarction. His hemoptysis improved without intervention and he was discharged on anticoagulation. Three weeks later, the patient returned to the emergency department, complaining of increasing dyspnea and persistent hemoptysis. He was found to be tachypneic with a respiratory rate of 24 breaths per minute and SaO2 of 91%. Physical exam again showed crackles over the right lung. Laboratory values demonstrated a white blood cell count 10,600/mm3 and an INR of 2.1. Repeat chest CT again revealed the previously noted multiple PEs and further progression of ground glass opacities to the left upper lobe. Abdominal CT did not show any evidence of local or metastatic recurrence of urothelial carcinoma. Repeat echocardiogram showed worsening PASP of 87 mmHg with persistent RV dysfunction. Treatment for presumed hospital acquired pneumonia was begun with a combination of ticarcillin/clavulanate and vancomycin. Anticoagulation therapy for PE was continued. His dyspnea continued to worsen requiring increasing FiO2. Open lung biopsy was performed on the 14th day of admission. During the biopsies, the patient developed a refractory shock state and subsequently died the following day. Pathologic examination of the lung biopsies revealed metastatic urothelial carcinoma predominantly present in the form of widespread intra-arterial emboli.
DISCUSSIONS: Tumor emboli from urothelial carcinoma is an uncommon occurrence. Only two prior cases have been reported in the literature. This underreporting may be due to the fact that RV failure in such cases is often thought to be due to venous thromboemboli. Pathologic confirmation is generally not performed. One possible clue of tumor pulmonary emboli is that patients will continue to have refractory dyspnea and worsening pulmonary hypertension despite adequate anticoagulation. This case was unique for that fact that the patient had no evidence of tumor recurrence. Tumor emboli was considered as a possible diagnosis due to his lack of improvement. Unfortunately, the definitive diagnosis was made late in the clinical course.
CONCLUSION: When patients with a history of cancer present with dyspnea and pulmonary hypertension, tumor emboli to pulmonary vasculature should be considered in the differential diagnosis. If clinical improvement is not observed after an appropriate period of anticoagulation, lung biopsy should be promptly considered. Only early diagnosis of tumor emboli may prevent fatal disease as there is a reluctance to retreat with chemo therapy without proof of progression.
DISCLOSURE: Taro Minami, None.