Q. How come the PT and PTT are not increased in TTP and HUS? You have clots all over, so why don’t the coag tests go up like they do in DIC?

A. Great question! Bear with me…lots of acronyms coming up.

In disseminated intravascular coagulation (DIC), the coagulation system is activated (for many different possible reasons). The patient makes clots (consisting of platelets sealed up with fibrin) all over the place – and the prothrombin time (PT) and partial thromboplastin time (PTT) go up because the patient is using up all his/her coagulation factors! The platelet count goes down too, due to consumption.

In thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS), you’re right – there are clots all over. However, these clots aren’t really the same kind of clots that you see in DIC. In TTP and HUS, the problem is that platelets get caught in long von Willebrand factor multimers, and you get platelet clumping. The “clots” are really platelet clumps – not traditional clots (coated with fibrin). So the PT and PTT don’t go up much if at all. ย A fine point, perhaps, but a potentially important one when you have a patient that has a microangiopathic hemolytic anemia (MAHA) and you’re trying to figure out what to do. Most patients with TTP should get plasma exchange – and fast! So if you have a patient with MAHA, thrombocytopenia, and normal (or barely elevated) PT/PTT ย – start thinking TTP/HUS.