Both passive leg raising and intravascular volume expansion improve sublingual microcirculatory perfusion in severe sepsis and septic shock patients.

Intensive Care Med

Unité EA 3509, Département d'Anesthésie-Réanimation, Centre Hospitalier Universitaire de Bicêtre, Assistance Publique Hôpitaux de Paris, Université Paris 11, 78 rue du Général Leclerc, 94275, Le Kremlin-Bicêtre Cedex, France.

Published: November 2010

Purpose: To assess sublingual microcirculatory changes following passive leg raising (PLR) and volume expansion (VE) in septic patients.

Methods: This prospective study was conducted in two university hospital intensive care units and included 25 mechanically ventilated patients with severe sepsis or septic shock who were eligible for VE in the first 24 h of their admission. Pulse pressure variation (ΔPP), cardiac output (CO) and sublingual microcirculation indices were assessed at five consecutive steps: (1) semi-recumbent position (Baseline 1), (2) during PLR manoeuvre (PLR), (3) after returning to semi-recumbent position (Baseline 2), (4) at the time when VE induced the same degree of preload responsiveness as PLR (VE(∆PP = PLR)) and (5) at the end of VE (VE(END)). At each step, five sublingual microcirculation sequences were acquired using sidestream darkfield imaging to assess functional capillary density (FCD), microcirculatory flow index (MFI), proportion of perfused vessels (PPV) and flow heterogeneity index (FHI).

Results: The PLR, VE(∆PP = PLR) and VE(END) induced a significant increase in CO and a significant decrease in ΔPP compared to Baseline 1 and Baseline 2 values. Both PLR and VE induced significant increases in FCD, MFI and PPV and a significant decrease in FHI compared to Baseline 1 and Baseline 2 values.

Conclusions: In preload responsive severe septic patients examined within the first 24 h of their admission, both PLR and VE improved sublingual microcirculatory perfusion. At the level of volume infusion used in this study, these changes in sublingual microcirculation were not explained by changes in rheologic factors or changes in arterial pressure.

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Source
http://dx.doi.org/10.1007/s00134-010-1966-6DOI Listing

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