Post-thrombotic syndrome (PTS) is a long-term complication secondary to deep vein thrombosis (DVT), characterized by symptoms such as heaviness, pain, swelling, and ulcers in the affected limb. Due to the irreversible fibrosis of the venous wall in PTS, along with luminal occlusion leading to intractable ulcer formation, the treatment options are limited and their effectiveness is uncertain. Previous perspectives suggested that venous obstruction and dilation, as well as thrombus recanalization and valvular dysfunction, resulting from the progression of thrombosis, are the main pathogenic mechanisms leading to PTS. In recent years, it has been discovered that aseptic inflammatory thrombosis, primarily driven by neutrophils, is abnormally activated in a venous stasis environment. This activation can initiate a cascade of coagulation reactions, leading to intensified thrombus formation, known as the waterfall effect. During the phase of thrombus resolution, macrophages can promote neovascularization within the thrombus by secreting various inflammatory factors, thereby accelerating thrombus dissolution. However, they can also affect the venous wall, reducing compliance, inducing luminal fibrosis, and promoting unfavorable remodeling, ultimately contributing to the development of PTS. This article primarily focuses on the role of thromboinflammation in different stages of venous thrombosis formation, lysis, and venous wall fibrosis, and provides a comprehensive review regarding inflammatory markers and relevant anti-inflammatory target medications.