Abstract
Background: Thrombotic microangiopathy (TMA) is a potentially life-threatening condition caused by small-vessel platelet microthrombi. The estimated incidence of clopidrogel-associated TMA is 1 per 1600 to 5000. The principal treatment is to withdraw clopidrogel. However, the diagnosis of clopidrogel induced TMA may be challenging because of the subtle presentation and co-morbidities confounding the diagnosis of TMA. Case: A 57 y.o. female presented with h/o hypertension, dyslipidemia with suspected cryptogenic strokes since 2018 (left thalamic stroke in 6/2020, left parietal stroke in 4/2020, chronic infarcts in frontal lobes from MRI brain on 9/17/2020 with normal CT angiogram of neck and brain and echocardiography ). She was on clopidrogel since April 2020. Patient was admitted on 6/14/2020 with racing thoughts for four weeks. The psychiatrist confirmed delirium. The EEG showed no focal lesion. Hematological workup revealed thrombocytopenia, elevated LDH and red cell fragments. The ADAMTS13 (a disintegrin and metalloproteinase, with a thrombospondin type 1 motif, member 13) level was <3%. Thrombotic microangiopathy was diagnosed. Steroids and plasma exchange were initiated and clopidrogel discontinued. Patient was discharged on prednisone. However, ADAMTS13 on 7/17/2020 was still <3%. As initial ANA and anti-ds-DNA were reported positive, patient was started on rituximab 375mg/m 2 weekly infusions with which ADAMTS13 increased to 75%. The repeat ANA and anti-ds-DNA were negative. When patient was reviewed on 5/20/2021 she was off steroids and independant of her ADLs. Discussion: Thrombotic microangiopathy is a medical emergency, with a mortality of 90% if untreated. Treatment with plasma exchange and corticosteroids significantly reduces the mortality to ∼10% to 15%. Early diagnosis of TMA is prudent, as recovery from TMA may appear to be complete, but patients may have persistent cognitive abnormalities if the diagnosis is not made early.
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