Superior vena cava syndrome (SVCS) is a clinical entity characterized by signs and symptoms arising from the obstruction or occlusion of the thin-walled superior vena cava (SVC) and can result in significant morbidity and mortality. Despite the rise of benign cases of SVCS, as a thrombotic complication of intravascular devices, it is most commonly seen secondary to malignancy as a consequence of thrombosis, direct invasion of tumor cells inside the vessel, or external compression. SVCS can be the initial presentation of a previously undiagnosed tumor in up to 60% of cases. Lung cancer and non-Hodgkin lymphoma (NHL) are responsible for up to 85%-90% of malignancy-related SVCS, while metastatic cancers account for approximately 10%. Herein, we review the pathophysiology, etiology, clinical presentation, diagnosis, and management of malignancy-related SVCS.

e13531 Background: It is known that malignancies exaggerate the risk of thrombosis up to 20%, while for Lung Cancer (LC) is articulated up to 14%. Likewise, thrombosis amplifies the LC progression, thrombosis-associated lung cancer (TALC). The pathophysiology promoting LCAT & TALC is multifactorial depending on the characteristics of LC, specific anti-cancer modalities, patient features, and biomarkers such as tissue factor, neutrophil extracellular traps released in response to cancer, cancer procoagulant, and cytokines. Low-molecular-weight heparins are used in prophylaxis and treatment for high-burden for thrombosis (HTB) patients, allowing specialists to focus on the cancer disease. Methods: iCaLT is a prospective observational study conducted in Thoracic Diseases General Hospital Sotiria (Athens, Greece) assessing the role of thromboprophylaxis with tinzaparin 10.000 Anti-Xa IU, OD with the systemic anti-cancer therapy (SACT). LC patients with active disease that are currently under treatment are enrolled after signing informed consent and monitored up to six months or until anticoagulation terminates. Results: Results from 106 patients reported, 29 (27%) are still ongoing: 79% were males. Histological results involve: adenocarcinomas 54%, squamous 25%, small cell 15%and others. LC patients received SACT: 55%, 23%, 10%, 6% in 1st, 2nd, 3rdand 4th line. HTB patients with active LC related to 4 factors: disease, treatment, biomarker and patient features are presented in table. On average patients accumulated 3.7±1.1risk factors, 91% of patients accumulated ≥3 risk factors. Median thromboprophylaxis duration was: 4.8 months (1st-3rd quartile: 2.8-6.0 months). One patient experienced thrombotic event in lower extremes and consequently pulmonary embolism (efficacy 99.1%, 95%CI: 94.6-99.8%), five patients experienced minor bleeding adverse events (haemoptysis) (4.7%, 95%CI: 2.0-10.6%), and two patients allergic reactions. Patients with haemoptysis had lower age (60 vs. 67, p=0.1357). Conclusions: Thromboprophylaxis with tinzaparin intermediate dose in high thrombotic burden patients with active lung cancer is effective and safe. Further research is needed.[Table: see text]

No abstract