16 Sept 2026
Patient history
A 38-year-old woman has three days of easy bruising, gum bleeding and worsening fatigue. Today her husband found her briefly confused about where she was, resolving within minutes. There has been no diarrhea, recent illness or new medication.
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Thrombotic thrombocytopenic purpura (TTP)
Urgent plasma exchange (plus corticosteroids)
Schistocytes with a high LDH, low haptoglobin and a negative Coombs test establish that red cells are being destroyed mechanically rather than by antibody: they are being physically sheared, not marked for removal. Pair that with severe thrombocytopenia and the differential is short, and the discriminators are all present here. Normal PT, aPTT and fibrinogen argue against disseminated intravascular coagulation, where the clotting cascade is consumed wholesale. Renal impairment that is only mild, with neurological signs that fluctuate, argues for thrombotic thrombocytopenic purpura over haemolytic uraemic syndrome, in which renal failure dominates and a diarrhoeal illness usually precedes it. The mechanism explains every finding at once. ADAMTS13 normally cleaves ultra-large von Willebrand factor multimers as they are released; without it those multimers persist, platelets adhere to them spontaneously throughout the microcirculation, and the resulting thrombi both consume platelets and shred the red cells passing through. That is why treatment cannot wait for the confirmatory ADAMTS13 assay. Plasma exchange is started within hours of suspicion because it does two things at once, removing the autoantibody and replacing the missing enzyme, and because untreated mortality approaches 90 per cent against roughly 10 to 20 per cent with prompt exchange. High-dose corticosteroids are added, with caplacizumab and rituximab where available. Platelets are withheld unless bleeding is life-threatening, since transfusing them feeds the same microvascular thrombosis.