A well-performed study by Bouattour et al1  concluded that preload dependence was associated with reduced sublingual microcirculation during major abdominal surgery. Fluid administration successfully restored microvascular perfusion. This finding suggests immediate correction of preload dependence to avoid reduced microcirculation. In the future, microvascular sublingual parameters could serve as additional indicators when deciding to administer fluids.

By this conclusion, the authors suggest that the presence of preload responsiveness might be associated with impaired sublingual microcirculatory perfusion and thus an abnormal microcirculatory perfusion might be an indicator of vascular volume. In this conclusion, however, we miss two important aspects. First, in general, fluid responsiveness is a normal physiological state2  accompanied by a normal sublingual microcirculation.3  When from this state cardiac output is decreased by decreasing venous return either by tamponade, sepsis, or lower body negative pressure, the sublingual microcirculatory perfusion will deteriorate,3–5  and restoration of venous return, in these contexts, will improve sublingual microcirculatory perfusion.3–5  In the context of sepsis there is no real hypovolemia, but rather a decrease in venous return due to increased vascular capacitance of the venous circulation (unstressed volume). This is frequently referred to, clinically, as relative hypovolemia. In absolute hypovolemia (e.g., hemorrhage) the decrease in venous return results from an absolute loss of intravascular volume. In both these cases, sublingual microcirculatory perfusion will improve after fluid resuscitation. From this, it’s clear that an improvement in sublingual microcirculatory perfusion is not indicative of hypovolemia, but rather decreased venous return resulting from decreased stressed volume (mean systemic filling pressure). To further complicate the picture, after initial resuscitation in sepsis, patients’ fluid responsiveness can be associated with normal sublingual microcirculatory perfusion.6  In the study by Bouattour et al.1  the context of the patient is not clear, as the patients most likely started the procedure in a state of fluid responsiveness and normal microcirculation. The response of the microcirculation to fluid resuscitation in this context doesn’t necessarily clarify this, as both increased vasodilation during the surgery and bleeding will decrease venous return where fluid resuscitation is likely to improve microcirculatory perfusion.

The authors declare no competing interests.

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