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Improvement of haemodynamic and respiratory parameters during coupled plasma filtration and adsorption correlates with the clearance of inflammatory mediators

Introduction

Sepsis is the leading cause of mortality in intensive care, but data on new therapies are inconclusive. Coupled plasma filtration adsorption (CPFA) is a new extracorporeal technology for septic shock and may improve haemodynamic respiratory function and mortality. The aim of this study is to evaluate during CPFA the haemodynamic response and respiratory function and the reduction of inflammatory markers.

Methods

Eighteen septic patients have been enrolled in this study within 8 hours from sepsis diagnosis. Every patient had three CPFA treatments for 8 hours with Q blood = 200 ml/hour, Q ultrafiltration = 30 ml/kg/hour and Q plasma = 20% of Q blood. At T0 (basal), T1 (after first cycle), T2 (after second cycle), T3 (after third cycle) and T4 (after 72 hours) we evaluated haemodynamic parameters, norepinephrine dosage, PaO2/FiO2 ratio and plasma IL-6, and procalcitonin. All data are expressed as the mean ± SD. ANOVA was used to compare changes during the times of study. P < 0.05 was statistically significant.

Results

Table 1 presents the main results of the study.

Table 1 (abstract P284)

Conclusion

In contrast with a recent experimental study in septic pigs [1], data from this study confirm that CPFA improves haemodynamics during septic shock. This improvement may be related to the reduction of IL-6 and first of all of procalcitonin. Procalcitonin clearance during CPFA may have a role in the improvement of shock-related vasoparalysis, as calcitonin receptor family complexes have been implicated recently in the pathogenesis of sepsis.

References

  1. Sykora R, et al.: Coupled plasma filtration adsorption in peritonitis induced septic shock. Shock 2008, in press.

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Turani, F., Lanini, G., Alessandrini, C. et al. Improvement of haemodynamic and respiratory parameters during coupled plasma filtration and adsorption correlates with the clearance of inflammatory mediators. Crit Care 13 (Suppl 1), P284 (2009). https://doi.org/10.1186/cc7448

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  • DOI: https://doi.org/10.1186/cc7448

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