Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria). Lead poisoning or poisoning by arsine or stibine causes non-immune hemolytic anemia. Runners can develop hemolytic anemia due to "footstrike hemolysis", the destruction of red blood cells in feet at foot impact. Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. Intravascular hemolysis
Intravascular hemolysis describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red blood cell are released into the general circulation, leading to hemoglobinemia and increasing the risk of ensuing hyperbilirubinemia.Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by damage by parasites such as Babesia. Additionally, thrombotic microangiopathy (TMA) can result in hemolysis of red blood cells. TMA is frequently observed in aHUS patients where clots form in the small vessels of the kidney resulting in damaged red blood cells as they attempt to pass through the restricted vessels. Extravascular hemolysis
Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes. In this case little hemoglobin escapes into blood plasma. The macrophages of the reticuloendothelial system in these organs engulf and destroy structurally-defective red blood cells, or those with antibodies attached, and release unconjugated bilirubin into the blood plasma circulation.
Red blood cells (erythrocytes) have a short lifespan (approximately 120 days), and old (senescent) cells are constantly removed and replaced with new ones via erythropoiesis. This breakdown/replacement process is called erythrocyte turnover. In this sense, erythrolysis or hemolysis is a normal process that happens continually. However, these terms are usually used to indicate that the lysis is pathological. Complications
Pulmonary hypertension has been gaining recognition as a complication of chronic hereditary and acquired hemolysis. Free hemoglobin released during hemolysis inactivates the vasodilator nitric oxide (NO). Hemolysis also releases arginase that depletes L-arginine, the substrate needed for NO synthesis. This reduces NO-dependent vasodilation and induces platelet activation, thrombin generation, procoagulant factors and tissue factor activation, contributing to the formation of thrombosis. This can lead to esophageal spasm and dysphagia, abdominal pain, erectile dysfunction, systemic hypertension, decreased organ perfusion, promotion of inflammation and coagulation, and thrombosis.Chronic hemolysis may also lead to endothelial dysfunction, heightened endothelin-1-mediated responses and vasculopathy. The release of heme leads to the production of bilirubin and depletion of plasma proteins, such as albumin, haptoglobin, and hemopexin, which may lead to jaundice. It may also lead to increased levels of the heme breakdown product stercobilin in the stool.Splenectomy of those with hemolytic disorders appears to increase risk of developing pulmonary thrombosis.Complications may also arise from the increased workload for the kidney as it secretes erythropoietin to stimulate the bone marrow to produce more reticulocytes (red blood cell precursors) to compensate for the loss of red blood cells due to hemolysis.