We used tunneled pleural catheters (TPC) to provide outpatient management of a patient with symptomatic, non-malignant pleural effusions secondary to thoracic venous thrombus.
A 49 year old female who had four prolonged hospital courses over a five month period developed symptomatic pleural effusions believed to be secondary to superior vena cava (SVC) syndrome. Initially she was found to have mitral valve fibroelastoma as the etiology for thromboembolic ischemic stroke. During the biopsy attempt she experienced laceration of the SVC. Post-operatively, elevated lupus anticoagulant and IgG anticardiolipin antibody was discovered along with the development of heparin induced thrombocytopenia with thrombosis. On presentation with dyspnea there were physical findings of facial, neck, bilateral upper extremity, and chest wall edema. Chest X-ray showed large bilateral pleural effusions. Progressive respiratory insufficiency required endotracheal intubation. Further imaging with CT scan and ultrasound revealed thrombus formation in the SVC, bilateral internal jugular, subclavian, and axillary veins. Uncomplicated, borderline, exudative pleural effusions were present. Pleural fluid analysis revealed a total protein and lactate dehydrogenase (LDH) ratio of 0.5 and 0.67, respectively. Absolute value of LDH= 184IU/L (upper limit of normal= 213IU/L), with a triglyceride level of 3mg/dL. Cultures were unremarkable for bacterial, fungal, and acid fast bacteria. Cytologic examination was negative for cancer on 3 separate occasions. Pleural effusions were managed with tube thoracostomy. Throughout her hospital course there was persistent high-ouput drainage. The multiple thrombi were determined to be non-intervenable by interventional radiology and surgical means. Chemical pleurodesis would have likely rendered a suboptimal outcome considering high-volume output. The risk of mechanical pleurodesis outweighed the benefit given the requirement for anticoagulation. In view of the refractory nature of the symptomatic pleural effusions, and prolonged hospitalization a novel approach was necessary. Bilateral TPCs (PleurX, Denver Biomedical) were placed at the bedside and the patient was discharged soon afterward. On follow up, pleural drainage had gradually trended down. Dyspnea was relieved without immediate or long-term complication at 150 days. Both catheters have been functional without intervention.
To our knowledge this is the first case describing both the presentation of large pleural effusions related to a benign cause of SVC syndrome, and the use of TPC in this situation. Pleural effusions concurrent with SVC syndrome has been reviewed.1 In cases of SVC syndrome due to a non-malignant cause 58% of patients had associated pleural effusions. Greater than half of the sampled pleural effusions in this population were exudative and 39% were bilateral. Pleural effusion occupied greater than half of the hemi-thorax only in patients with associated malignancy.Management of non-malignant pleural effusions with TPC has not been studied extensively. A retrospective analysis reported this intervention in 58 cases of pleural effusions related to malignant and non-malignant etiologies.2 Dyspnea was relieved in 86% without procedurally related mortalities. Complications in 7% of patients included pneumothorax, seroma, empyema, and pain syndrome. Pleural catheters remained in place for 5–330 days.
We have described an uncommon etiology of large pleural effusions uniquely managed with TPCs. Our patient had a non-malignant etiology for SVC syndrome leading to large, symptomatic pleural effusions. Limited use of conventional interventions necessitated an innovative strategy. We utilized TPCs to relieve dyspnea and as a bridge for anticipated formation of collateral venous flow. TPC placement was efficacious, safely performed at the bedside without complications on follow-up, and has been functional without the need for further intervention.
Shawn French, No Financial Disclosure Information; No Product/Research Disclosure Information