Internal jugular vein (IJV) thrombosis is a rare finding and is usually associated with central venous catheterization, neck infections, or local trauma. Neuroendocrine tumors (NETs) rarely predispose to central vein thrombosis. The usual presentation of pulmonary NET depends on tumor location and is usually non-specific. It ranges from asymptomatic to cough, hemoptysis, dyspnea, etc. Here we present the case of a 52-year-old male with right-sided neck swelling. Ultrasound imaging of the neck revealed right IJV and right subclavian vein thrombosis. Further imaging with computed tomography (CT) scan of the chest showed mediastinal mass. Histopathology findings were consistent with NET of pulmonary origin. Patient was started immediately on anti-coagulation and radiology oncology was consulted for tumor-specific treatment. This case highlights an association of central vein thrombosis with underlying mediastinal and lung malignancies.

Central vein thrombosis is defined as thrombosis of the major vessels draining either the upper or lower extremities. It presents most commonly in the upper limb, where it affects the subclavian veins and the superior vena cava; in the lower limb, it affects the common iliac veins and the inferior vena cava. These different anatomical segments pose unique challenges in both acute and chronic settings, and this article will summarize the current best practice treatment options.

Vanishing bone disease with multisystemic involvement may mimic systemic autoimmune or autoinflammatory diseases. We present a 19-year-old man who was hospitalized due to chest pain following a progressive osteolysis of the bony thorax. The disease later expanded into the pleura, peritoneum and pericardium in a form of massive chylous polyserositis. The patient also developed thrombosis of multiple central veins, which in turn worsened the chylothorax by increasing the pressure in the thoracic duct. This is the first case of vanishing bone disease complicated by triple chylous effusions and central vein thrombosis.

Central vein thrombosis as a cause of chylothorax is uncommon, and in a few cases in the literature was related to thrombotic complications of central venous access devices (CVAD). Superior vena cava (SVC) occlusion-induced chylothorax has been described in adult sickle cell disease (SCD) in a setting of chronic indwelling CVAD. There are limited reports on chylothorax induced by central venous thrombosis secondary to chronic CVAD in children with SCD. We describe an 8-year-old male patient, with a history of SCD, maintained on long term erythrocytapheresis for primary prevention of stroke, and whose clinical course was complicated by chylothorax which was successfully treated with a pleuroperitoneal shunt.