In diseases such as hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and malignant hypertension, the endothelial layer of small vessels is damaged with resulting fibrin deposition and platelet aggregation.
As red blood cells travel through these damaged vessels, they are fragmented resulting in intravascular hemolysis.
The resulting schistocytes (red cell fragments) are also increasingly targeted for destruction by the reticuloendothelial system in the spleen, due to their narrow passage through obstructed vessel lumina.
[1] Microangiopathic hemolytic anemia may be suspected based on routine medical laboratory tests such as a CBC (complete blood cell count).
[2] In all causes, the mechanism of MAHA is the formation of a fibrin mesh due to increased activation of the system of coagulation.