Hemolytic Anemia

Confirm the hemolysis picture - CBC with reticulocyte count, LDH, unconjugated bilirubin, and haptoglobin, plus a peripheral smear looking for schistocytes, spherocytes, or bite cells. Reticulocytosis with high LDH, high indirect bilirubin, and low haptoglobin is the signature.

Sort immune from non-immune - A direct antiglobulin (Coombs) test with warm and cold agglutinin testing tells you whether this is antibody-driven. It changes everything downstream, including how hard the blood bank has to work for compatible units.

Avoid oxidant exposure - In G6PD deficiency and other oxidant-sensitive anemias, oxidant drugs drive Heinz body formation and hemolysis. Known offenders include acetaminophen, vitamin K1, phenothiazines, and dapsone. Once the diagnosis is known the patient must avoid the drugs and foods that worsen oxidative stress.

Watch for methemoglobinemia - Oxidative stress converts ferrous to ferric iron and cuts oxygen-carrying capacity further. Co-oximetry gives you the methemoglobin level; pulse oximetry alone will not.

Keep the patient warm - Cold agglutinin disease and cold hemoglobinuria are among the immune causes. Forced-air warming, warmed fluids, and a warm room cost nothing and remove one trigger.

Protect the kidneys - Intravascular hemolysis produces hemoglobinemia and hemoglobinuria. Keep volume up and urine flowing; diuresis is one of the immediate interventions in severe hemolysis alongside transfusion and plasmapheresis.

Transfuse for severe anemia - Transfusion is the mainstay when anemia is severe, particularly with active bleeding. Get the type and crossmatch started early — an antibody workup takes time you will not have once the case is bleeding.

Expect a tachycardic, high-output circulation - Anemic patients compensate with increased heart rate and respiratory rate; long-standing anemia brings high-output heart failure, angina, and arrhythmias. A baseline 12-lead ECG is worth having before you start.

Ask about splenectomy - Splenectomy, steroids, monoclonal antibodies, and immunosuppressants are used for autoimmune hemolytic anemia, hereditary spherocytosis, and sickle cell disease. Asplenic patients are at risk of overwhelming sepsis from encapsulated organisms, and chronic steroids raise the question of perioperative supplementation.

Hemolytic anemia is a normocytic anemia (MCV 80 to 100 fL) in which red cells are destroyed faster than the marrow can replace them. Causes split into intracorpuscular defects — hemoglobinopathies (sickle cell disease, thalassemia), membranopathies (hereditary spherocytosis, hereditary elliptocytosis), and enzymopathies (G6PD deficiency, pyruvate kinase deficiency) — and extracorpuscular causes: immune-mediated destruction (warm and cold agglutinins, transfusion reactions), mechanical shear from prosthetic valves or microangiopathy (TTP, DIC, HELLP), and infections such as malaria and babesiosis. Destruction happens intravascularly or extravascularly in the spleen.

What matters at the board is that oxygen-carrying capacity is already reduced and the marrow is already running flat out to compensate. Any added insult — an oxidant drug, hypoxia, surgical blood loss, a mismatched unit — drops hemoglobin faster than in a normal patient.