![]() ![]() Unconjugated bilirubin levels rise as its production exceeds elimination capability. Haptoglobin binds to free hemoglobin, and levels decrease in hemolysis. Lactate dehydrogenase is intracellular, and levels increase when RBCs rupture. When anemia is identified, testing should include measurement of lactate dehydrogenase, haptoglobin, reticulocyte, and unconjugated bilirubin levels, as well as urinalysis ( Table 3). The initial workup of hemolytic anemia begins with a complete blood count illustrating normocytic (mean corpuscular volume of 80 to 100 μm 3 ) or macrocytic (mean corpuscular volume greater than 100 μm 3) anemia ( Figure 1). Malignant hypertension, systemic lupus erythematosus, scleroderma, liver disease, vasculitides, hypersplenismĮndovascular devices, aortic stenosis, extracorporeal membrane oxygenation, arteriovenous malformation, march hemoglobinuria, burns Plasma exchange, steroids, delivery, drug withdrawal ![]() Peripheral blood smear (showing schistocytes), assessment of ADAMTS13 activity, liver enzyme tests, coagulation study, culture Thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, disseminated intravascular coagulation, HELLP syndrome, drug-induced thrombotic microangiopathy Microangiopathic hemolytic anemia/thrombotic microangiopathy Splenectomy, eculizumab (Soliris paroxysmal nocturnal hemoglobinuria) ![]() Osmotic fragility test, eosin-5-maleimide binding Hereditary spherocytosis, hereditary elliptocytosis, paroxysmal nocturnal hemoglobinuria Malaria, Babesia, Bartonella, Clostridia, Rickettsia, Haemophilus influenzae, human immunodeficiency virus Sickle cell disease, thalassemias, hemoglobin defects Steroids, avoidance, treatment of other diseaseĭrug-induced thrombotic microangiopathy, drug-induced immune hemolytic anemia, oxidative hemolysisĭirect, toxin, phagocytosis, fragmentation Transfusion reactions, hemolytic disease of the fetus and newborn A rapid onset of anemia or significant hyperbilirubinemia in the neonatal period should prompt consideration of a hemolytic anemia. Medications can cause hemolytic anemia through several mechanisms. Extrinsic nonimmune causes include the thrombotic microangiopathies, direct trauma, infections, systemic diseases, and oxidative insults. ![]() Hemolytic diseases are classified into hemoglobinopathies, membranopathies, enzymopathies, immune-mediated anemias, and extrinsic nonimmune causes. A peripheral blood smear should be performed when hemolysis is present to identify abnormal red blood cell morphologies. The direct antiglobulin test further differentiates immune causes from nonimmune causes. Laboratory test results that confirm hemolysis include reticulocytosis, as well as increased lactate dehydrogenase, increased unconjugated bilirubin, and decreased haptoglobin levels. Patients with hemolysis may present with acute anemia, jaundice, hematuria, dyspnea, fatigue, tachycardia, and possibly hypotension. Mechanisms include poor deformability leading to trapping and phagocytosis, antibody-mediated destruction through phagocytosis or direct complement activation, fragmentation due to microthrombi or direct mechanical trauma, oxidation, or direct cellular destruction. Hemolysis may occur intravascularly, extravascularly in the reticuloendothelial system, or both. It should be part of the differential diagnosis for any normocytic or macrocytic anemia. Hemolytic anemia is defined by the premature destruction of red blood cells, and can be chronic or life-threatening. ![]()
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