Some interesting questions were asked. For example, is lactate an indicator of tissue oxygenation in sepsis? Evidence suggests it may be due to a metabolic effect instead, unrelated to tissue hypoxia, that is, type b lactic acidosis. Nevertheless it appears to be a useful marker to follow. Certainly its elevation portends a worse outcome but maybe not by the mechanism we think. See here. All this is not to say that type a lactic acidosis does not exist (that is, is not due to tissue ischemia in other forms of shock, in low cardiac output states or in high demand states).
How strong is the evidence in favor of fluid resuscitation in sepsis? Pretty weak. The author talks around the idea, but comes short, of saying we should stop doing it. He also talks around the idea, but comes just short, of saying there is equipoise for a controlled trial of fluid resuscitation versus no fluid resuscitation.