Check out this month’s paper here
A golden oldie…..
Let me know what you think
Hope you enjoyed the paper!
So the VASST trial wanted to know whether adding in vasopressin to noradrenaline would improve outcomes in septic shock, which is a valid question. Patients with septic shock tend to be deficient in endogenous vasopressin (which is a potent directly acting vasopressor) and escalating doses of noradrenaline bring with them the problem of impaired splanchic perfusion which may in itself worsen outcomes, as the surgeons are always telling us…..
The problem is the study didn’t quite look at this. Essentially most of the patients in the study were “vasopressor responders” and by that I mean they weren’t in refractory shock (i.e receiving escalating levels of noradrenaline to try and maintain a MAP above 65). By the time the study drug was added the majority of patients had a MAP of above 70 on noradrenaline rates of approximately 0.2-0.3 mcg/kg/min. The study showed that in these situations adding in vasopressin doesn’t seem to affect outcomes (probably because they are already responding to treatment with relatively low doses of vasopressor)
However that isn’t really how we use vasopressin is it? We tend to reserved it for refractory shock where the patients are not fluid responsive and have noradrenaline requirements that have escalated above 0.5mcg/kg/min with a MAP below 65mmHg. In this group we are using it because we believe it will improve outcomes (along with steroids) through a noradrenaline sparing effect; however how confident are we that that is actually the case?
We use it because it is recommended by the surviving sepsis guidelines but until we have a study showing it’s benefit in catchocolamine refractory shock the evidence for using it will remain open to question…..
So should we always use it?
Let me know what you think.