Thoracic duct outflow obstruction increases thoracic duct pressure above central venous pressure supporting thoracic duct decompression.

Objective: Thoracic duct outflow obstruction is a recognized cause of refractory lymphatic leakage; however, the physiological consequences of such obstruction on thoracic duct pressure and its relationship to central venous pressure have not been fully characterized in vivo. This study aimed to evaluate changes in thoracic duct pressure and the pressure gradient between the thoracic duct and the central venous system in an experimental model of thoracic duct outflow obstruction. Methods: In a swine model, thoracic duct pressure and central venous pressure were directly measured using intravascular catheters positioned at matched vertebral levels. Thoracic duct embolization was performed at the upper thoracic level using coils and cyanoacrylate and was used as an experimental model of thoracic duct outflow obstruction. Pressure measurements were obtained before embolization and after confirmation of complete thoracic duct occlusion. Changes in thoracic duct pressure, central venous pressure, and the pressure relationship between the two systems were analyzed using paired statistical comparisons. Results: Thoracic duct outflow obstruction resulted in a significant increase in upstream thoracic duct pressure, with a median increase of approximately 6 to 8 mmHg compared with preobstruction values. Following obstruction, thoracic duct pressure consistently exceeded central venous pressure, creating a pressure gradient indicative of lymphatic hypertension. In contrast, central venous pressure did not change significantly after thoracic duct obstruction. No consistent cranio-caudal longitudinal pressure gradient along the thoracic duct was identified. Conclusions: Thoracic duct outflow obstruction induces lymphatic hypertension, as demonstrated by an increase in thoracic duct pressure relative to central venous pressure. This experimentally demonstrated pressure gradient provides physiological support for decompressive interventions by demonstrating a pressure gradient favorable for lymphatic drainage into the venous system. By directly quantifying intralymphatic and venous pressures in vivo, this study offers mechanistic insight into the pathophysiology of lymphatic leakage associated with thoracic duct obstruction and may help inform treatment selection between occlusive and decompressive strategies in lymphatic interventions. Clinical Relevance: Thoracic duct outflow obstruction is a cause of lymphatic leakage, yet the consequences of obstruction on thoracic duct pressure and its relationship to central venous pressure have remained unclear. In this experimental study, in vivo measurements demonstrated that thoracic duct outflow obstruction results in an increase in thoracic duct pressure, creating a pressure gradient relative to central venous pressure. This pressure relationship reflects lymphatic hypertension caused by outflow obstruction and supports decompressive interventions aimed at restoring lymphatic outflow.