#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

High- versus standard-volume haemofiltration in experimental peritonitis-induced sepsis


Authors: Sýkora Roman 1,2;  Chvojka Jiří 1,2;  Kroužecký Aleš 1,2;  Raděj Jaroslav 1,2;  Karvunidis Thomas 1,2;  Varnerová Veronika 2;  Novák Ivan 1,2;  Matějovič Martin 1,2
Authors place of work: Jednotka intenzivní péče, I. interní klinka, Fakultní nemocnice Plzeň 1;  Lékařská fakulta v Plzni, Univerzita Karlova v Praze 2
Published in the journal: Anest. intenziv. Med., 20, 2009, č. 5, s. 246-256
Category: Intensive Care Medicine - Original Paper

Summary

Objective:
The role of haemofiltration as an adjunctive treatment of sepsis remains a contentious issue. To address the role of the dose and to explore the biological effects of haemofiltration we compared the effects of standard and high-volume haemofiltration in a peritonitis-induced model of porcine septic shock.

Design and setting:
Randomized, controlled experimental study.

Materials and methods:
Hyperdynamic sepsis secondary to peritonitis was induced in 21 anaesthetized and mechanically ventilated pigs. After 12 hours of sepsis the animals were randomized to receive either supportive treatment (control group, CON, n = 7), standard haemofiltration (HF, 35 ml/kg/h, n = 7) or high-volume haemofiltration (HVHF, 100 ml/kg/h, n = 7).

Results:
Systemic and hepatosplanchnic haemodynamics, oxygen exchange, energy metabolism (lactate/pyruvate, ketone body ratios), ileal and renal cortex microcirculation and systemic inflammation (TNF-α, IL-6), nitrosative/oxidative stress (TBARS, nitrates, GSH/GSSG) and endothelial/coagulation dysfunction (von Willebrand factor, asymmetric dimethylarginine, platelet count) were assessed before and after 12, 18, and 22 hours of peritonitis. Although fewer haemofiltration-treated animals required noradrenalin support (86%, 43% and 29% animals in the control, HF and HVHF groups, respectively), neither of the haemofiltration doses reversed the hyperdynamic circulation and lung dysfunction, or ameliorated alterations in the gut and kidney microvascular perfusion. Both HF and HVHF failed to attenuate sepsis-induced alterations in surrogate markers of cellular energetics, nitrosative/oxidative stress, endothelial injury or systemic inflammation.

Conclusions:
In this porcine model of moderate septic shock, early HVHF proved superior in preventing the development of septic hypotension. However, neither of the haemofiltration doses was capable of reversing the progressive disturbances in microvascular, metabolic, endothelial and lung function at least within the timeframe of this study and this model severity.

Keywords:
sepsis – haemofiltration – high volume haemofiltration – microcirculation – energy metabolism – oxidative stress


Zdroje

1. Cariou, A. et al. Adjunctive therapies in sepsis: an evidence- based review. Crit. Care Med., 2004, 32, p. S562–570.

2. Honoré, P. M. et al. Blood and plasma treatments: the rationale of high-volume haemofiltration. Contrib. Nephrol., 2007, 156, p. 387–395.

3. Bellomo, R. et al. Extracorporeal blood treatment (EBT) methods in SIRS/Sepsis. Int. J. Artif. Organs., 2005, 28, p. 450–458.

4. Cole, L. et al. A phase II randomized, controlled trial of continuous haemofiltration in sepsis. Crit. Care Med., 2002, 30, p. 100–106.

5. Ronco, C. et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet, 2000, 356, p. 26–30.

6. Saudan, P. et al. Adding a dialysis dose to continuous haemofiltration increases survival in patients with acute renal failure. Kidney Int., 2006, 70, p. 1312–1317.

7. Schiffl, H. et al. Daily hemodialysis and the outcome of acute renal failure. N. Engl. J. Med., 2002, 31, p. 305–310.

8. Palevsky, P. M. et al. Intensity of renal support in critically ill patients with acute kidney injury. N. Engl. J. Med., 2008, 359, p. 7–20.

9. Cole, L. et al. High-volume haemofiltration in human septic shock. Intensive Care Med., 2001, 27, p. 978–986.

10. Honore, P.M. et al. Prospective evaluation of short-term, high-volume isovolemic haemofiltration on the hemodynamic course and outcome in patients with intractable circulatory failure resulting from septic shock. Crit. Care Med., 2000, 28, p. 3581–3587.

11. Ratanarat, R. et al. Pulse high-volume haemofiltration for treatment of severe sepsis: effects on haemodynamics and survival. Crit. Care, 2005, 9, p. 294–302.

12. Oudemans-van Straaten, H. M. et al. Outcome of critically ill patients treated with intermittent high-volume haemofiltration: a prospective cohort analysis. Intensive Care Med., 1999, 25, p. 814–821.

13. Joannes-Boyau, O. et al. Impact of high volume haemofiltration on hemodynamic disturbance and outcome during septic shock. ASAIO J., 2005, 50, p. 102–109.

14. Piccinni, P. et al. Early isovolaemic haemofiltration in oliguric patients with septic shock. Intensive Care Med., 2006, 32, p. 80–86.

15. Cornejo, R. et al. High-volume haemofiltration as salvage therapy in severe hyperdynamic septic shock. Intensive Care Med., 2006, 32, p. 713–722.

16. Grootendorst, A.F. et al. High volume haemofiltration improves right ventricular function in endotoxin-induced shock in the pig. Intensive Care Med., 1992, 18, p. 235–240.

17. Ullrich, R. et al. Continuous venovenous haemofiltration improves arterial oxygenation in endotoxin-induced lung injury in pigs. Anesthesiology, 2001, 95, p. 428–436.

18. Yekebas, E. F. et al. Attenuation of sepsis-related immunoparalysis by continuous veno-venous haemofiltration in experimental porcine pancreatitis. Crit. Care Med., 2001, 29, p. 1423–1430.

19. Bellomo, R. et al. The effect of intensive plasma water exchange by haemofiltration on haemodynamics and soluble mediators in canine endotoxemia. Am. J. Respir. Crit. Care Med., 2000, 161, p. 1429–1436.

20. Rogiers, P. et al. Continuous venovenous haemofiltration improves cardiac performance by mechanisms other than tumor necrosis factor-alpha attenuation during endotoxic shock. Crit. Care Med., 1999, 27, p. 1848–1855.

21. Bouman, C. S. et al. Haemofiltration in sepsis and systemic inflammatory response syndrome: the role of dosing and timing. J. Crit. Care, 2007, 22, p. 1–12.

22. Matejovic, M. et al. Selective inducible nitric oxide synthase inhibition during long-term hyperdynamic porcine bacteremia. Shock, 2004, 21, p. 458–465.

23. Matejovic, M. et al. Effects of tempol, a free radical scavenger, on long-term hyperdynamic porcine bacteremia. Crit. Care Med., 2005, 33, p. 1057–1063.

24. Matejovic, M. et al. Effects of combining inducible nitric oxide synthase inhibitor and radical scavenger during porcine bacteremia. Shock, 2007, 27, p. 61–68.

25. Tugtekin, I. F. et al. Increased ileal-mucosal-arterial PCO2 gap is associated with impaired villus microcirculation in endotoxic pigs. Intensive Care Med., 2001, 27, p. 757–766.

26. De Backer, D. et al. How to evaluate the microcirculation: report of a round table conference. Crit. Care, 2007, 10, 11, p. R101.

27. Yekebas, E. F. et al. Impact of different modalities of continuous venovenous haemofiltration on sepsis-induced alterations in experimental pancreatitis. Kidney Int., 2002, 62, p. 1806–1818.

28. Asfar, P. et al. Catecholamines and vasopressin during critical illness. Crit Care Clin., 2006, 22, p. 131–149.

29. Landry, D. W. et al. The pathogenesis of vasodilatory shock. N. Engl. J. Med., 2001, 345, p. 588–595.

30. Takakura, K. et al. Modification of alfa-1 adrenoreceptors by peroxynitrite as a possible mechanism of systemic hypotension in sepsis. Crit. Care Med., 2002, 30, p. 894–899.

31. Takakura, K. et al. Deactivation of noradrenaline by peroxynitrite as a new pathogenesis in the hypotension of septic shock. Anestesiology, 2003, 98, p. 928–934.

32. Macarthur, H. et al. Modulation of serum cytokine levels by a novel superoxide dismutase mimetic, M40401, in an Escherichia coli model of septic shock: correlation with preserved circulating catecholamines. Crit. Care Med., 2003, 31, p. 237–245.

33. Rokyta Jr., R. et al. Effects of continuous venovenous haemofiltration-induced cooling on global haemodynamics, splanchnic oxygen and energy balance in critically ill patients. Nephrol. Dial. Transplant., 2004, 19, p. 623–630.

34. Marsh, J. D. et al. Mechanism of diminished contractile response to catecholamines during acidosis. Am. J. Physiol., 1988, 254, p. H20–27.

35. Kellum, J. A.et al. Effects of hyperchloremic acidosis on arterial pressure and circulating inflammatory molecules in experimental sepsis. Chest, 2004, 125, p. 243–248.

36. Rogiers, P. et al. Blood warming during haemofiltration can improve haemodynamics and outcome in ovine septic shock. Anesthesiology, 2006, 104, p. 1216–1222.

37. Ronco, C. et al. Interpreting the mechanisms of continuous renal replacement therapy in sepsis: the peak concentration hypothesis. Artif. Organs, 2003, 27, p. 792–801.

38. Hoffmann, J. N. et al. Effect of haemofiltration on haemodynamics and systemic concentrations of anaphylatoxins and cytokines in human sepsis. Intensive Care Med., 1996, 22, p. 1360–1367.

39. Silvester, W. Mediator removal with CRRT: complement and cytokines. Am. J. Kidney Dis., 1997, 30, p. S38–43.

40. Wang, Y. et al. Polymyxin B binds to anandamide and inhibits its cytotoxic effect. FEBS Lett., 2000, 24, 470, p. 151–155.

41. Trzeciak, S. et al. Early microcirculatory perfusion derangements in patients with severe sepsis and septic shock: relationship to haemodynamics, oxygen transport, and survival. Ann. Emerg. Med., 2007, 49, p. 88–98.

42. Leverve, X. M. From tissue perfusion to metabolic marker: assessing organ competition and co-operation in critically ill patients? Intensive Care Med., 1999, 25, p. 890–892.

43. Li, C. M. et al. Continuous veno-venous haemofiltration attenuates myocardial mitochondrial respiratory chain complexes activity in porcine septic shock. Anaesth. Intensive Care, 2007, 35, p. 911–919.

44. Joannes-Boyau, O. et al. Haemofiltration: The case for removal of sepsis mediators from where they do harm. Crit. Care Med., 2006, 34, p. 2244–2246.

45. Honoré, P.M. et al. Extracorporeal removal for sepsis: Acting at the tissue level – the beginning of a new era for this treatment modality in septic shock. Crit. Care Med., 2004, 32, p. 896–897.

46. Ronco, C. The immunomodulatory effect of extracorporeal therapies in sepsis: A reconciliation of three theories. Int. J. Artif. Organs, 2007, 30, p. 855–857.

47. Hack, C. E. et al. The endothelium in sepsis: source of and target for inflammation. Crit. Care Med., 2001, 29, p. S21–27.

48. Schouten, M. et al. Inflammation, endothelium, and coagulation in sepsis. J. Leukoc. Biol., 2008, 83, p. 536–545.

49. Reinhart, K. et al. Markers of endothelial damage in organ dysfunction and sepsis. Crit. Care Med., 2002, 30, p. S302–312.

50. Polanska, K. et al. Effect of regional citrate anticoagulation on thrombogenicity and biocompatibility during CVVHDF. Ren. Fail., 2006, 28, p. 107–118.

51. Honoré, P.M. et al. The big bang of haemofiltration: the beginning of a new era in the third millennium for extra-corporeal blood purification! Int. J. Artif. Organs, 2006, 29, p. 649–659.

52. Mink, S. N. et al. Early but not delayed continuous arteriovenous haemofiltration improves cardiovascular function in sepsis in dogs. Intensive Care Med., 1999, 25, p. 733–743.

Štítky
Anaesthesiology, Resuscitation and Inten Intensive Care Medicine
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#