Plasma levels of interleukin-8 and expression of interleukin-8 receptors on circulating neutrophils and monocytes after cardiopulmonary bypass in children.

OBJECTIVE: Cardiopulmonary bypass induces a systemic inflammatory response that causes substantial clinical morbidity. This study sought to determine cellular and humoral variables of inflammation. We hypothesized that chemokines are a major source of stimulation of neutrophils and monocytes in pediatric cardiac surgery. METHODS: We performed an observational prospective clinical study of 20 pediatric patients before and after cardiopulmonary bypass. Plasma levels of interleukin-6, interleukin-8, myeloperoxidase, and nitric oxide were measured by immunoassays. Expression of interleukin-8 receptors (CXCR1, CXCR2) and CD14 of circulating neutrophils and monocytes was assessed by flow cytometry. Clinical evaluations included length of inotropic support and mechanical ventilation as well as oxygenation. RESULTS: Two hours after cardiopulmonary bypass, plasma levels of interleukin-6 and interleukin-8 were strongly increased (P =.0001 and P =.0032, respectively). Interleukin-6 and interleukin-8 concentrations correlated with the length of inotropic support, as well as with the length of mechanical ventilation (r >.70, P .62, P

Inflammatory response of neutrophil granulocytes and monocytes after cardiopulmonary bypass in pediatric cardiac surgery.

OBJECTIVE: To determine whether the activation state of polymorphonuclear neutrophils (PMNs) and monocytes contributes to the inflammatory response after cardiopulmonary bypass (CPB) in pediatric cardiac surgery. DESIGN: Observational prospective clinical study. SETTING: Pediatric intensive care unit of a university hospital. PATIENTS: Twenty pediatric patients before and after open heart surgery with CPB. MEASUREMENTS: Cell counts of circulating PMNs and monocytes as well as phenotypic and functional analysis of these cells, and plasma levels of myeloperoxidase. RESULTS: Levels of myeloperoxidase (a marker of PMN degranulation) were significantly elevated after CPB (2.9+/-1.6 ng/ml before CPB versus 13.7+/-6.5 ng/ml after CPB, p=0.0001). However, PMN function, as measured by surface expression of CD11b/CD18 and phagocytic respiratory burst, was reduced. In contrast, the phagocytic respiratory burst of circulating monocytes was increased in some patients and there was a correlation with the increase of monocyte cell count after CPB (r=0.63, p=0.015). CONCLUSIONS: After the end of CPB, there was an ongoing inflammatory process. In particular, there was an activation of monocytes after the end of CPB.

Reproducibility of the blood flow index as noninvasive, bedside estimation of cerebral blood flow.

OBJECTIVE: To investigate the feasibility and reproducibility of the blood flow index (BFI) method for measuring cerebral blood flow. DESIGN AND SETTING: Prospective functional study in pediatric intensive care. PATIENTS AND PARTICIPANTS: 14 consecutive patients with median age of 2 months (range 1 days-11 years) requiring artificial ventilation, invasive arterial blood pressure monitoring, and central venous access. INTERVENTIONS: The first passage of an intravenous indocyanine green (ICG) bolus through the cerebral vasculature was monitored by noninvasive near-infrared spectroscopy. BFI was calculated by dividing maximal ICG absorption change by rise time. Reproducibility was evaluated by six ICG injections at 5-min intervals. RESULTS: Of all ICG injections 6% were canceled, and 4% were eliminated due to injection failures. Median BFI of 17 reproducibility determinations was 71 (range 12-213) and median coefficient of variation (CV) of BFI was 10% (4.9-18.5). The quantity of ICG bolus did not affect the CV (0.1 vs. 0.3 mg ICG/kg). Eight reproducibility tests in patients after cardiac surgery had smaller CV than the others, and the eight in newborns had higher CV than in older children. Patient parameters such as arterial blood pressure, endtidal CO(2), and percutaneous oxygen saturation were stable and showed CV below 2% during reproducibility determination. CONCLUSIONS: The BFI method allows rapid and repeated measurements of CBF with good feasibility and reproducibility. As a relative but not absolute measure of CBF, BFI seems to be suited for clinical evaluation of intraindividual CBF changes during determination of cerebrovascular reactivities or during therapeutic interventions.

Dynamic cerebral autoregulatory response to blood pressure rise measured by near-infrared spectroscopy and intracranial pressure.

OBJECTIVES: Noninvasive near-infrared spectroscopy (NIRS) continuously monitors changes in cerebral hemoglobin saturation (Hb(Diff) ) and content (Hb(Total)). It may allow visualization of the dynamic cerebral autoregulatory response to rapid blood pressure increases without relevant contamination of the NIRS signal from extracerebral hemoglobin. DESIGN: Prospective cohort study. SETTINGS: Multidisciplinary pediatric intensive care unit. PATIENTS: Six consecutive children in coma due to severe encephalopathy (head trauma, five patients; mumps encephalitis, one patient) requiring artificial ventilation, invasive arterial blood, and intracranial pressure monitoring. INTERVENTIONS: Frontotemporal recording of Hb(Diff) and Hb(Total) while rapidly elevating blood pressure by bolus injection of phenylephrine. MEASUREMENTS AND RESULTS: During an increase of blood pressure of 13 +/- 1 mm Hg with a "rise time" of 16 +/- 1 secs (mean of a total of 31 injections +/- sem), a significant linear correlation was found between Hb(Diff) and intracranial pressure signals (mean coefficient, 0.46 +/- 0.04) but not between Hb(Total) and intracranial pressure. Three response patterns were observed. First, Hb(Diff) and intracranial pressure reduction, corresponding with vasoconstriction and normal dynamic autoregulation (n = 3); second, Hb(Diff) and intracranial pressure increase, corresponding with persistent vasodilation and abolished autoregulation (n = 11); and third, transient Hb(Diff) and intracranial pressure increase followed by a decrease at peak blood pressure elevation, called impaired autoregulation (n = 15). In one patient with fatal brain swelling, phenylephrine testing showed no effect on NIRS signals (n = 2). Furthermore, there were significant correlations between 31 pooled interindividual pairs of Hb(Diff) changes with intracranial pressure changes (values at baseline averaged over 60 secs subtracted from values at peak blood pressure elevation averaged over 5 secs), with a correlation coefficient of .82 (p <.001). CONCLUSIONS: NIRS represents a new and promising technique for bedside determination of dynamic cerebral autoregulation during acutely induced blood pressure rise. The significant correlations found between NIRS signals and intracranial pressure excluded relevant extracerebral contamination of the NIRS signals. In our patients with severe encephalopathy, dynamic autoregulation was in most instances not fully preserved.