By which mechanism of Virchows triad leads to a hyper-coaguable state in ice hockey players?
Hi Michael,
The notorious cases of blood clots in ice hockey players concerned individuals with inherited mild coagulation disorders, e.g. protein C deficiency. Additional factors, inherent in ice hockey career, e.g. repeated traumas, surgeries, stick-handling, frequent team flights on season etc. only added to their risk of thrombotic events and elicited the symptoms which had not been seen in their family members.
Answering your broader question regarding the Virchow's triad, in those most covered cases you could say that both flow and blood were abnormal.
I hope this helps.
Hi Michael
Repetitive and vigorous activity or trauma may cause a blood clot to form in the veins of the upper extremities(also called "Paget-Schroetter syndrome"). The clot is caused by damage to the vein from repetitive efforts of the upper extremity or compression of the vein by other internal structures (tendons, the first rib, or the clavicle). In ice hockey players the clot may be caused as a result of obstruction of veins by their equipment/sportwear. For example, elbow pads putting on the arm very tightly may impact the blood flow. Regarding Virchow's triad, as mentioned by Radoslaw, it causes stasis or blood flow obstruction. Risk factor like dehydration causes hyperviscosity of the blood during prolonged activity which also contributes to blood be more thick (hypercoagulability).
Best regards
Gleb
Both of these answers have shed some valuable light on the subject. Yes, professional ice hockey players do fly quite often, so in one aspect you have stasis of blood due to flying, as well as frequent injuries, either to the macro or micro vasculature, therefore injury to the endothelial tissue. Plus the final piece of the triangle, a hypercoagubility state in the form of for example Protein C deficiency or dehydration. I just wondered how could high performance athletes be prone to a disorder (deep vein thrombosis) primarily thought of as a condition of the sick and bed-ridden. Once a clot is discovered, I would assume a form of anti-coagulation regime would be started, either via new generation selective factor II or X inhibitors, which would increase the risk of bleeding, and thereby limiting the playing time of the hockey player. A very vicious circle indeed. Due to high performance sports, I imagine the viscosity of the blood would increase due to increased hematocrit. Would hockey players be prone to an increased erythrocyte count due to constant traning/events?
Thanks for the feedback on the question.
I think that violent activity are not fully recovery is the main reason as well as to the causes of disease in the player
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