Removal of mediators by continuous hemofiltration in septic patients.
Continuous hemofiltration currently represents standard renal replacement therapy in critically ill patients. Because higher ultrafiltration rates are related to better survival rates in experimental and clinical studies and hemofiltration results in fewer cardiovascular side effects than does conventional hemodialysis, the use of inflammatory mediator removal by this extracorporeal procedure has emerged. This article reviews clinically relevant principles of compound transport and the experimental and clinical effects of hemofiltration during sepsis. Hemofiltration did not have a major impact on plasma concentrations of prominent inflammatory cytokines (tumor necrosis factor-a and interleukins 1b, 6, and 8) and seems therefore not to be able to counterbalance endogenous cytokine production despite considerable cytokine removal in the filtrate. Contradictory results in the literature are discussed under the viewpoint of membrane-related sieving coefficients and plasma cytokine measurement. A significant reduction in plasma anaphylatoxin concentrations by hemofiltration is associated with impressive immunomodulatory and cardiodepressive ultrafiltrate effects. Thus far, however, the use of hemofiltration for nonrenal indications remains experimental and is not supported by controlled clinical trials. Modern strategies of blood purification that may be associated with a high degree of effectiveness for mediator removal (high-volume hemofiltration and heparin-induced extracorporeal lipoprotein-fibrinogen precipitation) are discussed.
Hoffmann
J N
JN
Department of Surgery, Klinikum Grosshadern, Ludwig-Maximilians University, Marchioninistrasse 15, D-81377 Munich, Germany.
Faist
E
E
D000706:Anaphylatoxins / Q000032:analysis; D000818:Animals; D001781:Blood Component Removal; D019446:Endotoxemia / Q000503:physiopathology / Q000628:therapy; D006440:Hemofiltration; D006801:Humans; D018836:Inflammation Mediators; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D009102:Multiple Organ Failure / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D018805:Sepsis / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000706:Anaphylatoxins; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha