Please do not confuse recommendations with evidence. Induction of anesthesia does not cause DVTs, even theoretically. Risk of DVT is based on the procedure, not the anesthetic choice.
Okay so your recommendation is that there is no need for subq heparin or SCD before induction GA even in very high risk patients. (As long as they get it at some point?)
Also your words are technically incorrect as studies have show neuraxial anesthesia for ortho surgery has lower VTE rates than GA.
We give sub Q heparin or lovenox in preop holding for certain cases that are high risk for postop DVT, but it's a true minority of surgeries overall. The ones we don't give it to are not all of a sudden getting DVTs during the case. Similar with SCDs. Not every case gets SCDs, depends on the surgery. What heparin or SCDs or whatever don't depend on is the anesthetic drugs given.
Again you need to try to stop warping my words. I didn't say the anesthetic drugs cause clotting (second time I have to say this to you). I said it might cause hemodynamic changes which lead to nidus formation, and the nidus in certain high risk patient populations may grow and develop into VTE.
So now you do want to give subq heparin jn preop? I thought timing didn't matter? By your previous line of reasoning you don't need to do it jn preop specifically. You could just do it any time.
I talked about propensity for clot and risk. So while a tiny nidus may develop it may never actually form a VTE in a healthy patient going for lap appendectomy, but it might ultimately form a VTE later on in a frail, old, smoker who has GI cancer going for colorectal surgery.
Also, how in the heck would something like "valve cusp hypoxia" even be related to induction of anesthesia? We generally preoxygenate patients adequately and their PO2 is going to be way above normal which combined with a usual increase in cardiac output means tissue oxygen delivery is generally slightly higher immediately after induction than it was at baseline.
First of all, cardiac output doesn't always increase. The heart rate might increase. The blood pressure might increase or decrease. The blood flow and distribution of flow changes sometimes quite abruptly. Venous pooling can and does occur. (I think an interesting retrospective would be to examine the degree of hemodynamic swing with induction of GA and VTE outcomes in matched cohorts, although this would probably be very difficult to do)
Second of all, it is possible to have local hypoxia despite whole body hyperoxia.
I didn't make up the term valve cusp hypoxia. This has been around and was believed to be a mechanism for how some VTE might develop. Its probably the basis for our practice to give subq heparin PRIOR to induction of GA. The point of my thread is to question the actual evidence for this (decidedly not much, is it checkbox medicine?) but you haven't given much contrarian evidence either.
