Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening hematologic condition characterized by widespread formation of small blood clots (thrombi) in arterioles and capillaries throughout the body. This leads to thrombocytopenia, microangiopathic hemolytic anemia, and multiorgan dysfunction, particularly affecting the brain, kidneys, and heart. Prompt diagnosis and treatment are essential to prevent irreversible organ damage and
Thrombotic disorders encompass a range of conditions where abnormal blood clot formation—thrombosis—occurs within blood vessels. These disorders pose significant health risks, as clots can obstruct blood flow and cause tissue ischemia or embolism. Thrombosis may occur in veins (venous thrombosis) or arteries (arterial thrombosis), each with distinct causes, risk factors, and consequences. Classification of Thrombotic
Thrombosis with thrombocytopenia syndrome (TTS) is a rare but life-threatening condition characterized by the combination of blood clots (thrombosis) and a low platelet count (thrombocytopenia). TTS has garnered global attention due to its association with certain adenoviral vector-based COVID-19 vaccines, though it can also occur independently or as part of autoimmune conditions. TTS shares pathological
Heparin-induced thrombocytopenia (HIT) is a severe prothrombotic immune complication of heparin exposure, particularly concerning in the setting of percutaneous coronary intervention (PCI). Despite its thrombocytopenic nature, HIT leads to paradoxical thrombosis that can compromise coronary perfusion, cause stent thrombosis, and lead to catastrophic outcomes during interventional procedures. A meticulous approach is required to safely manage
Heparin-induced thrombocytopenia (HIT) is a life-threatening, immune-mediated complication of heparin therapy, characterized by a significant drop in platelet count and an increased risk of thrombosis. Paradoxically, despite thrombocytopenia, patients with HIT are at an exceptionally high risk of both arterial and venous thrombotic events. Prompt diagnosis and intervention are critical to reducing morbidity and mortality.
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