Hemolytic

Hemolytic refers to hemolysis, the destruction of red blood cells leading to the release of hemoglobin into the blood plasma and, in some cases, into urine. Hemolysis can occur within blood vessels (intravascular) or outside vessels in organisms' organs such as the spleen or liver (extravascular). It is a feature of various disorders and can be acute or chronic.

Causes of hemolysis are diverse and are commonly categorized as immune-mediated or non-immune. Immune-mediated hemolysis results from antibodies or complement directed against red blood cells, as seen in autoimmune hemolytic anemia, alloimmune reactions (for example in newborns with maternal antibodies), and certain drug-induced immune hemolyses. Non-immune causes include mechanical destruction from artificial devices or severe turbulence (microangiopathic hemolytic anemia), oxidative damage in conditions like G6PD deficiency, infections, toxins, thermal injury, and various inherited red cell membrane disorders.

Pathophysiology typically involves premature red cell destruction, which reduces circulating red cell mass and triggers compensatory reticulocytosis. Intravascular hemolysis releases free hemoglobin into plasma and may lead to hemoglobinemia and hemoglobinuria. Extravascular hemolysis primarily increases bilirubin production, contributing to jaundice, and may cause splenomegaly. Laboratory findings often show anemia with elevated lactate dehydrogenase, low haptoglobin, increased indirect bilirubin, and reticulocytosis. Peripheral blood smear findings vary by cause and can include schistocytes (fragmented cells) in mechanical hemolysis, bite cells or Heinz bodies in G6PD deficiency, and spherocytes in autoimmune hemolytic anemia. A direct antiglobulin (Coombs) test helps distinguish immune from non-immune causes.

Management focuses on treating the underlying cause, stopping offending drugs when applicable, and providing supportive care such as transfusions for severe anemia. Specific therapies for immune-mediated hemolysis may include corticosteroids, rituximab, IVIG, or plasmapheresis, while mechanical or traumatic causes require removal or correction of the precipitating factor.