smartcane wrote:KingDavid wrote:smartcane wrote:
Most of what you said is incorrect. You don't have to taper off coumadin. It can be stopped and easily reversed with him eating leafy vegetables that contain V-K or he can be given Vit - k. There is no concern for swelling. In term of flight it isn't flights per say it immobility that increases the risk of clots forming but if he moves around normally he will be ok. The treatment for an elite athlete may be less because they have high lung capacity and their body uses O2 more efficiently. That is why he was able to keep playing even though he was losing lung capacity. He only went to the doctor because of the pain. You or I would have died from not sufficient O2. The best example of the above facts is UD. He had the same thing and recovered in about 3 months.
Oh ok thanks for the correction. But I thought ud only had one clot vs the multiple ones Bosh had?
It's incredible that he was able to play this game like that. I really wish I could see his o2 sat %.
It really doesn't matter the amount of clot but rather the amount of lung capacity that is affected. It is actually worse to have one large clot rather than multiple small ones. It is easier for the body to break down and less likely to completely obstruct blood flow to the lungs like a saddle emboli ( a large clot that affects both lungs due to it' size) typically does.
Ohhh...thanks a lot for the info. So why isn't there an infarct of lung tissue from the occlusion(s) even though he was suffering from what seemed to be hemodynamic instability (sob, cp, weakness, pale, etc)? Is it because the clots weren't complete blocks and he was still getting some form perfusion? I was really worried about that for Bosh long term.
I think I'm confusing p.e. with ACS and mixing up treatment. School is killing me lols. Seriously, thank you for calling me out on being wrong; it means I have to read up a bit harder before midterms next week.
