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]