Volume kinetics in a translational porcine model of stabilized sepsis with fluid accumulation

Volume kinetics in a translational porcine model of stabilized sepsis with fluid accumulation

Hong, S.L., Dumargne, H., Hahn, R.G. et al. Volume kinetics in a translational porcine model of stabilized sepsis with fluid accumulation. Crit Care 29, 92 (2025). https://doi.org/10.1186/s13054-025-05308-8


Summary of "Volume Kinetics in a Translational Porcine Model of Stabilized Sepsis with Fluid Accumulation"


Abstract

Fluid dynamics in sepsis remains complex, influencing both resuscitation strategies and fluid removal protocols. This study investigated volume kinetics before and after sepsis in a porcine model to better understand fluid distribution and accumulation during the late phase of sepsis. Findings suggest that sepsis alters fluid compartment behavior, shifting fluid distribution towards fast-exchange interstitial spaces while promoting interstitial albumin recruitment and lymphatic flow acceleration.

Key Points

  1. Sepsis-Induced Fluid Accumulation: Sepsis results in fluid accumulation, particularly in the slow-exchange interstitial compartment, contributing to persistent fluid overload.
  2. Hemodynamic Changes in Late Sepsis: Sepsis leads to hypoalbuminemia and mild hypovolemia, altering the balance between vascular and interstitial fluid compartments.
  3. Fluid Kinetics and Distribution: Before sepsis, infused fluids distributed transiently into plasma and interstitial compartments. After sepsis, fluids preferentially accumulated in the fast-exchange compartment rather than the slow-exchange space.
  4. Increased Lymphatic Flow: In the late sepsis phase, lymphatic return was significantly enhanced, suggesting that fluid shifts were influenced by lymphatic function recovery.
  5. Albumin Recruitment and Plasma Expansion: Infused fluid promoted interstitial albumin movement into the plasma, facilitating improved volume expansion compared to the baseline pre-sepsis phase.
  6. Cardiac Index and Fluid Distribution: A higher cardiac index correlated with greater expansion of the fast-exchange compartment, demonstrating that hemodynamic factors influence fluid kinetics.
  7. Reduced Urine Output in Late Sepsis: Despite fluid infusion, urine output remained lower in the late sepsis phase, supporting the hypothesis that fluid retention persists despite systemic hemodynamic recovery.
  8. Persistent Fluid Overload and Body Weight Gain: Sepsis-induced fluid accumulation resulted in an 8.3% increase in body weight, reinforcing the importance of fluid management in septic patients.
  9. Implications for Fluid Resuscitation and Removal: Findings support the need for individualized fluid strategies, emphasizing lymphatic recovery and interstitial albumin mobilization as key factors in fluid removal.
  10. Future Research Directions: Further studies should explore real-time fluid monitoring techniques and targeted de-resuscitation strategies to optimize fluid balance in sepsis management.


Study Design. VK: volume kinetic

Conclusion

Sepsis alters volume kinetics, leading to fluid accumulation in slow-exchange compartments, but late-phase sepsis is characterized by increased lymphatic flow and improved plasma expansion. These findings highlight the importance of understanding fluid distribution dynamics in critically ill patients to optimize resuscitation and de-resuscitation strategies. Future research should focus on refining individualized fluid management approaches, leveraging biomarkers and advanced monitoring techniques to guide therapy.


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Volume kinetics in a translational porcine model of stabilized sepsis with fluid accumulation
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Discussion Questions

  1. How can volume kinetics models improve fluid management in sepsis patients undergoing resuscitation and de-resuscitation?
  2. What role does lymphatic function play in fluid removal during late-phase sepsis, and how can it be optimized clinically?
  3. Should individualized fluid removal strategies be integrated into sepsis treatment guidelines based on patient-specific hemodynamic and fluid distribution characteristics?


Javier Amador-Casta?eda, BHS, RRT, FCCM

Interprofessional Critical Care Network (ICCN)


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