Polymorphonuclear leukocyte activation. An early marker of the postsurgical sepsis response
C. H. Wakefield, P. D. Carey, S. Foulds, J. R. Monson and P. J. Guillou
Academic Surgical Unit, St Mary's Hospital Medical School, London, England.
It has been suggested that major surgery induces polymorphonuclear
leukocyte (PMNL) dysfunction, which exposes patients to the development of
sepsis. Conversely, the sepsis response and multisystem organ failure in
patients after surgery is thought to be mediated by activated PMNLs. In a
preliminary attempt to investigate this paradox, we studied functional
(hydrogen peroxide production) and phenotypic (the adhesion/complement
receptor CD11b) markers of PMNL activation in 28 patients undergoing
elective major resectional surgery; 11 (39%) of these patients developed
postoperative sepsis (the septic group). The mean (SEM) preoperative level
of neutrophil CD11b expression (97.8 [6.2] mean channel fluorescence [MCF]
and 101.42 [7.9] MCF; P = .74) and hydrogen peroxide production (109.51
[4.91] MCF and 104.53 [6.3] MCF; P = .5) were similar for the uncomplicated
and septic groups, respectively. However, on the first postoperative day,
both mean CD11b expression and hydrogen peroxide production were greater in
those patients who subsequently developed postoperative sepsis (192.5 [38]
MCF vs 128.6 [8.1] MCF for the septic group vs the uncomplicated group,
respectively [P < .05], and 120.43 [2.56] MCF vs 109.61 [3.05] MCF for
the septic group vs the uncomplicated group, respectively [P < .0001]).
We suggest that an exaggerated PMNL activation response to surgery is an
early event in those patients destined to develop postsurgical sepsis.
