Platelet clumping

Heparin-induced thrombocytopenia A clinical syndrome of IgG antibody production against the heparin-platelet factor 4 complex occurring in approximately 1% to 5% of patients exposed to either heparin or low-molecular-weight heparin. Heparin-induced thrombocytopenia results in excess production of thrombin, platelet aggregation, and thrombocytopenia (due to platelet clumping), often leading to venous and arterial thrombosis, amputation of extremities, and death. 

Aggregation of blood platelets is the requisite first event for the maintenance of intact circulation in the face of any break in a blood vessel. It is the platelet clump that starts the long and complicated process leading to closure of the broken vessel by an organized blood clot. Though this property of platelets is vital to maintenance of the circulatory system, an excessive tendency to aggregation can also lead to problems. Thus platelet clumps formed in blood vessels in the absence of injury can lead to blockade of blood circulation and subsequent injury. Strokes and some types of myocardial infarcts have thus been associated with platelet clumps. The nonsteroid antiinflammatory... 

Artefactual pseudothrombocytopenia is typically an error of automated cell counters. When platelet clumps are mistaken for leukocytes this can result in pseudoleukocytosis (30,36). Edetic acid can also cause agglutination of granulocytes, and confusing findings such as combined pseudothrombocytopenia, pseudoneutropenia, and pseudolymphocytosis can occur (28). 

Hemolytic uremic syndrome—A condition characterized by the breakup of red blood cells (hemolysis) and kidney failure. Platelets clump together within the kidney s small blood vessels resulting in ischemia leading to kidney failure. 

Figure 20. Higher magnification of a section of Figure 19 showing primarily platelets with extended pseudopodia. No platelet clumps are present.

Figure 22. Fibrinogen-coated PVC after 15 min of blood contact (representing time of maximum deposition). Extensive fibrin network basal to attached platelets and platelet clumps is shown. Fibrin is the predominant species present.

Defects or imperfections as small as 10 microns [in an artificial heart] were sufficient to form platelet clumps leading to thromboembolic complications. 

The exposed collagen fiber of the subendothelial layers may form the trap for the circulating platelets. Indeed, when collagen fibers are added to platelet-rich plasma, platelet clumps form at the surface of the fiber. The adhesion requires ADP and is inhibited by EDTA and collagenase. Thus, in vascular injury, the release of an ADP-like substance and the denudation of collagen fiber appear to play a determinant role in platelet adhesion. 

Decreased blood flow results from narrowing of the arteries from coronary artery disease (CAD), which may be complicated by platelet clumping, thrombus formation, and vasospasm. 

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