The Fontan procedure is a palliative surgical intervention performed in patients with single-ventricle congenital heart defects. This operation reroutes systemic venous return directly to the pulmonary arteries, bypassing the heart. While it improves oxygenation and survival, it creates a non-pulsatile, low-flow venous circulation that predisposes patients to thrombosis. Hemodynamic Features Increasing Thrombotic Risk These conditions
Heparin-induced thrombocytopenia (HIT) is a prothrombotic, immune-mediated adverse reaction to heparin exposure. Paradoxically, HIT causes thrombosis rather than bleeding, despite the hallmark of thrombocytopenia. It typically occurs 4–14 days after initiation of heparin and can lead to arterial or venous thromboembolism, making it a hematologic emergency requiring immediate intervention. Pathophysiology of HIT-Associated Thrombosis Thrombosis in
Thromboembolism due to prosthetic heart valves represents a significant clinical concern, particularly in patients with mechanical valve replacements. These complications arise when thrombi form on or near the valve surface, dislodge, and embolize to systemic or pulmonary circulation. Valve-related thromboembolic events can result in ischemic stroke, organ infarction, or prosthetic valve dysfunction—necessitating prompt diagnosis, effective
Thromboembolic disorders are conditions characterized by the abnormal formation and migration of blood clots within the circulatory system. These clots, or thrombi, may form in veins or arteries and can travel through the bloodstream, causing embolic events that obstruct blood flow to vital organs. This disruption can lead to severe clinical outcomes, including pulmonary embolism,
Thrombocytosis is defined as a sustained elevation in platelet count exceeding 450,000/μL. When occurring in the context of myeloproliferative neoplasms (MPNs), this hematologic abnormality is typically a result of clonal proliferation of megakaryocytes in the bone marrow. Unlike reactive thrombocytosis, which is a response to inflammation or tissue damage, MPN-related thrombocytosis reflects an intrinsic defect
Thrombocytopenia is a common hematologic manifestation in patients with chronic hepatitis C virus (HCV) infection. It is characterized by a platelet count below 150,000/µL and is often multifactorial in origin. As the disease progresses, thrombocytopenia becomes more prominent, particularly in the context of cirrhosis and portal hypertension. Its presence may serve as both a marker
Thrombocytopenia, defined as a platelet count below 150,000/µL, is a frequent hematological abnormality in patients with chronic hepatitis. It is most commonly observed in those with chronic hepatitis B (CHB), chronic hepatitis C (CHC), and advanced liver disease such as cirrhosis. The condition results from a multifactorial pathogenesis involving hypersplenism, impaired thrombopoietin (TPO) production, bone