Question

A patient underwent thrombectomy of femoro popliteal segment with poor outflow and was on heparin infusion. His platelet count dropped from 2 lakhs to 1 lakh/mm$^3$ on 6th day of infusion. Other blood parameters were normal and there was no feature of sepsis/infection.
What is the pathology behind the process?

Hint:

In HIT, antibodies against the heparin-PF4 complex activate platelets, leading to both thrombocytopenia and a pro-thrombotic state.

Answer 1

Step 1: Pathophysiology of HIT.
Heparin-induced thrombocytopenia (HIT) is an immune-mediated reaction caused by antibodies against the heparin-platelet factor 4 (PF4) complex. When heparin binds to PF4 on platelet surfaces, it forms a complex that triggers the production of antibodies in some individuals. These antibodies bind to the heparin-PF4 complex, leading to the activation of platelets. This activation promotes clot formation and platelet consumption, causing a drop in platelet count (thrombocytopeni.

Step 2: Mechanisms leading to thromboembolic complications.
In addition to thrombocytopenia, the activated platelets can form aggregates, which may lead to thromboembolic events, including deep vein thrombosis (DVT), pulmonary embolism (PE), or arterial thrombosis. This paradoxical pro-thrombotic state despite low platelet counts is a hallmark of HIT.

Step 3: Conclusion.
The pathophysiology of HIT involves the formation of antibodies against the heparin-PF4 complex, leading to platelet activation, consumption, and increased thromboembolic risk.