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Not Enough Evidence to Use Plasma Exchange for Sepsis or Thrombocytopenia-Associated Multiple Organ Failure in Children.

To the Editor: We read with interest the article by Masse et al (1) published in the recent issue of Critical Care Medicine, in which the authors report that global cerebral blood flow (CBF) assessed by MRI arterial spin labeling is higher in sedated septic patients than in nonseptic sedated or unsedated controls. As noted by the authors, these findings differ from findings in older studies by Maekawa et al (2) and Bowton et al (3) that have showed reduced CBF in unsedated septic patients, which may indeed reflect differences between studies, including timing of measurements relative to shock onset as well as shock severity. A closer look at the data from the previous studies nevertheless unveils a distinct pathophysiologic pattern that is also present in the study by Masse et al (1). In the two previous studies, CBF and global cerebral metabolic rate of oxygen (CMRO 2 ) were measured by the Kety-Schmidt technique (using stable argon as the tracer) and the closely related Xe washout technique. In the two studies, individual CBF and CMRO 2 values are available from a total of nine patients (three from Bowton et al [3] and six from Maekawa et al [2]), and the pooled mean CBF in these patients is approximately 40% lower (29 [sd 8] mL 100 g min) while CMRO 2 is almost 70% lower CMRO 2 (0.5 [sd 0.1] μmol g min) than corresponding KetySchmidt-based values typically obtained in healthy humans (approximately 50 mL 100 g min and 1.5 μmol g min, respectively). Although CBF is reduced in these patients, they thus appear to exhibit a state of cerebral hyperperfusion “relative” to the cerebral metabolic requirements, which we informally refer to as “poor man’s luxury perfusion” with reference to the classical cerebrovascular luxury perfusion phenomenon originally described by Lassen (4). In contrast, the findings by Masse et al (1) indicate that septic patients may indeed exhibit manifest luxury perfusion with “absolute” cerebral hyperperfusion. Regrettably, the interpretation of the findings reported by Masse et al (1) is limited because the norepinephrine doses used to reach the target mean arterial pressure are not reported, as this may vary substantially between septic individuals. Furthermore, the vasopressor/inotropic properties of norepinephrine may vary distinctly at various doses, and one can thus only speculate how this may have affected findings. The substantial age-difference between the two study-populations should also be considered an important caveat. That being said, the presence of relative versus absolute cerebral hyperperfusion could be related to differences in timing of the cerebral hemodynamic assessments, as well as differences between patient populations (disease severity, sedation, blood gas values, etc.). Both phenomena nevertheless point toward increased cerebral capillary transit time heterogeneity, which has recently been suggested to limit cerebral oxygen extraction and predispose to cerebral ischemia in critically ill patients (5). In the efforts to identify mechanisms of sepsis-associated encephalopathy and/or long-term cognitive deficits in septic patients in future MRI studies, it may thus be worthwhile to include algorithms that assess this aspect of cerebrovascular function. The authors have disclosed that they do not have any potential conflicts of interest.