This most often occurs when the mother has previously been exposed to blood antigens present on the fetus but foreign to her, through either a blood transfusion or a previous pregnancy. Hemolytic anemia
Because in vivo hemolysis destroys red blood cells, in uncontrolled, chronic or severe cases it can lead to hemolytic anemia. Hemolytic crisis
A hemolytic crisis, or hyperhemolytic crisis, is characterized by an accelerated rate of red blood cell destruction leading to anemia, jaundice, and reticulocytosis. Hemolytic crises are a major concern with sickle-cell disease and G6PD deficiency. Toxic agent ingestion or poisoning
Paxillus involutus ingestion can cause hemolysis. Space hemolysis
Spaceflight can cause hemolysis. Intrinsic causes
Hemolysis may result from intrinsic defects in the red blood cell itself:
Defects of red blood cell membrane production (as in hereditary spherocytosis and hereditary elliptocytosis)
Defects in hemoglobin production (as in thalassemia, sickle-cell disease and congenital dyserythropoietic anemia)
Defective red cell metabolism (as in glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency)
Paroxysmal nocturnal hemoglobinuria (PNH), sometimes referred to as Marchiafava-Micheli syndrome, is a rare, acquired, potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia. Extrinsic causes
Extrinsic hemolysis is caused by the red blood cells environment:
Immune-mediated causes could include transient factors as in Mycoplasma pneumoniae infection (cold agglutinin disease) or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as systemic lupus erythematosus, rheumatoid arthritis, Hodgkins lymphoma, and chronic lymphocytic leukemia). Spur cell hemolytic anemia
Any of the causes of hypersplenism (increased activity of the spleen), such as portal hypertension.
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.