Explain HIT

In many cases, the mechanism is related to an autoimmune reaction. Do a quick Google search and you should find several sites that explain the disorder in detail.

Can anyone explain how HIT comes about? I understand it is caused by use of heparin and causes a reduction in platelets. I can't wrap my head around how this happens in the body and then it leads to irreversible platelet clumping? Please explain.

In short, heparin + certain antibodies = an immune complex that causes platelets to activate (prone to sticking to each other and vessel walls). This results in the formation of "platelet clumps" (microparticles) or clots on vessel walls. It doesn't destroy platelets so much as causes them to form abnormal clots.

When we say "thrombocytopenia" in reference to HIT, what we really mean is that there are fewer circulating platelets because they have all formed clots and clumps. That's why you are "thrombocytopenic" on lab analysis, but hypercoagulable clinically.

BTW, if you don't have an emedicine user name and password, get one. It is free (unlike that UpToDate crap, which is grossly overpriced and I hate with a passion).

I just read about this in Nursing 2007 Critical Care (Nov 2007, "Managing the patient with HIT"). Its an excellent article and if possible you should read it.

According to the article, vascular injury (surgery, cariopulmonary bypass, trauma) induces platelet activation. Part of the cascade of factors released is platelet factor 4. Heparin occasionally binds PF4 and some pt develop antibodies to the PF4-heparin complex. The antibody-PF4-heparin complex induces even greater platelet aggregation, which activates the blood coagulation system and thrombin induced clot formation.

The antibody coated platelets reduce the overall platelets available in the blood (thrombocytopenia). DVT, PE and other thromboses are common due to clot formation. Can present in 1-3 days but more commonly in 5-14 days.

Unfractionated heparin seems to produce this rxn more than low molecular wt heparin.

Recommended therapy includes removal of heparin from all coated lines, no hep flushes, and use of direct thrombin inhibitors.