Article Text

  1. A W Schadenberg1,
  2. P R deJong2,
  3. B J Prakken2,
  4. N J Jansen1
  1. 1Paediatric Intensive Care Unit, Wilhelmina Children’s Hospital, UMC Utrecht, Utrecht, The Netherlands
  2. 2Paediatric Immunology Department, Wilhelmina Children’s Hospital, UMC Utrecht, Utrecht, The Netherlands


Objectives Immune deactivation has been well described in patients following acute inflammatory events such as sepsis, trauma and major surgery. During the recovery phase of a systemic inflammatory response patients are at risk of developing serious infectious complications. We studied the immune response of children recovering from cardiac surgery to gain an understanding of the mechanisms involved in the hypoinflammatory phase.

Methods 20 children, who underwent cardiac surgery for a septum defect, were included in the study. Samples were taken before surgery and at several time points, up to 48 h postoperatively. Monocytes were characterised by flow cytometry. Plasma cytokines were determined by multiplex immunoassay. In-vitro plasma studies included stimulation assays with plasma and lipopolysaccharide, followed by intracellular cytokine staining.

Results Cardiac surgery ignited a systemic inflammatory response, illustrated by rapid cytokine changes in plasma. Most notably IL-10 levels soared immediately after surgery, followed closely by typical pro-inflammatory cytokines such as IL-8 and IL-6. Monocytes showed phenotypic characteristics of immune deactivation by reduced HLA-DR expression, with the nadir at 24 h post-surgery. Culture with plasma 4 h after surgery gave a significant decrease of intracellular cytokine staining (IL-6 and TNFα) in monocytes compared with culture with plasma before surgery.

Conclusion Children undergoing cardiac surgery show a rapid systemic inflammatory response. Together with increased pro-inflammatory cytokines, monocytes have characteristics of immune deactivation. Alongside the general immune activation after cardiac surgery, there are soluble factors reducing this response and protecting against unbridled inflammatory damage.

Vesikari et al

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