8.2: Macroangiopathic Hemolytic Anemias

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Traumatic Cardiac Hemolytic Anemia

In this condition, hemolysis is due to mechanical trauma caused by prosthetic cardiac valves. High blood flow around the prosthetic causes red blood cells to fragment leading to intravascular hemolysis. Any damaged cells that do not hemolyze in circulation are removed by the spleen via extravascular hemolysis.^1,2

Hemolytic anemia due to traumatic cardiac causes is uncommon and platelet count is not usually decreased drastically. Any hemolysis that occurs is often compensated by the bone marrow.^1,2

Laboratory Findings for Traumatic Cardiac Hemolytic Anemia:²

CBC:

PLT: Normal

Hb: Decreased

RETIC: Increased

PBS:

Schistocytes

Other Tests:

Unconjugated Bilirubin: Increased

LD: Increased

Haptoglobin: Decreased

Exercise-induced Hemoglobinuria

Transient hemolysis that occurs due to stress caused by exercise. Most often due to activities involving contact with hard surfaces such as running. Red blood cells become damaged as they pass through small vessels. Anemia usually does not develop unless hemolysis is severe.¹

Laboratory Findings for Exercise-induced Hemoglobinuria:²

CBC:

Hb: Increased

RETIC: Increased

MCV: Slight increase

PBS:

Schistocytes are NOT present

Other Tests:

Unconjugated Bilirubin: Increased

LDH: Increased

Haptoglobin: Decreased

Hemoglobinuria

Thermal Injury

Hemolytic anemia can develop after thermal burns to the body. Degree of hemolysis is dependent on the amount of surface area affected. Hemolysis is due to direct thermal damage to the red blood cells.¹

Laboratory Findings for Thermal Injury:¹

CBC:

Hb: Decreased

PBS:

Schistocytes

Micro-Spherocytes

Other Tests:

Hemoglobinuria

References:

1. Smith LA. Hemolytic anemia: nonimmune defects. In: Clinical laboratory hematology. 3rd ed. New Jersey: Pearson; 2015. p.372–87.

2. Keohane EM. Extrinsic defects leading to increased erythrocyte destruction – nonimmune causes. In: Rodak’s hematology clinical applications and principles. 5th ed. St. Louis, Missouri: Saunders; 2015. p. 394-410.