Introduction:
COVID-19 infection which was declared as a pandemic in March 2020 has now affected millions around the globe. The clinical features of COVID-19 vary widely from being purely asymptomatic to developing multi-organ dysfunction. The diffuse microvascular thrombi in multiple organs in autopsy cases of COVID-19 are similar to that of thrombotic microangiopathy (TMA).[1] TMA is a clinical entity encompassing thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and secondary TMAs. The classical pentad of TTP includes thrombocytopenia, MAHA, fever, altered mental status and acute kidney injury.[2]
TTP is primarily caused by a depletion of a disintegrin and metalloproteinase (ADAMTS13) which results in increase release of Von Willebrand Factor (VWF) leading to endothelial damage.[3] It is hypothesized that like other viral infections, SARS-CoV-2 virus itself stimulates the release of VWF and Factor VIII.[4] Initially TTP was almost universally fatal but improved treatment measures including exchange transfusions have reduced the mortality rate to 10-20%.[5]