OBJECTIVE: To examine polymorphonuclear leukocyte respiratory burst function serially in patients with septic shock. DESIGN: Prospective, longitudinal, descriptive study. SETTING: Adult and pediatric (university hospital) intensive care units. PATIENTS: Eight critically ill patients, with septic shock and eight critically ill patients without evidence of infection or sepsis. MEASUREMENTS AND MAIN RESULTS: Severity of patient illness was estimated serially using the Acute Physiology and Chronic Health Evaluation (APACHE II) scoring system. For each patient, neutrophil superoxide anion synthesis was assayed spectrophotometrically in multiple blood samples over a period of 7 to 12 days after clinical identification of septic shock. The initial sample was obtained < 12 hrs after admission. Reaction velocities initially, at 2 to 3 mins, and at 4 to 5 mins (nmol superoxide anion/min/10(6) neutrophils), and extent of reaction at 5 mins (nmol superoxide anion/5 mins/10(6) neutrophils) were determined for each assay. On the day of admission, the mean APACHE II score and initial velocity for the septic shock group were 21.5 +/- 10 and 4.6 +/- 2 nmol superoxide anion/min/10(6) neutrophils, respectively. Over the next 7 to 12 days, as the patients recovered, there was a significant (paired t-test) decrease in APACHE II scores (p < .005) and increase in initial velocity (p < .0005). The increase in initial velocity correlated with the accompanying decrease in APACHE II scores (r2 = .46). Neutrophil superoxide anion generation in the critically ill group was not suppressed compared with the septic shock group and remained normal throughout the evaluation period. CONCLUSIONS: In vitro neutrophil respiratory burst function is significantly depressed during early septic shock. As patients improve clinically, as quantitated by decreasing APACHE II scores, neutrophil respiratory burst function recovers, approaching normal values.
OBJECTIVE: To examine polymorphonuclear leukocyte respiratory burst function serially in patients with septic shock. DESIGN: Prospective, longitudinal, descriptive study. SETTING: Adult and pediatric (university hospital) intensive care units. PATIENTS: Eight critically ill patients, with septic shock and eight critically ill patients without evidence of infection or sepsis. MEASUREMENTS AND MAIN RESULTS: Severity of patient illness was estimated serially using the Acute Physiology and Chronic Health Evaluation (APACHE II) scoring system. For each patient, neutrophil superoxide anion synthesis was assayed spectrophotometrically in multiple blood samples over a period of 7 to 12 days after clinical identification of septic shock. The initial sample was obtained < 12 hrs after admission. Reaction velocities initially, at 2 to 3 mins, and at 4 to 5 mins (nmol superoxide anion/min/10(6) neutrophils), and extent of reaction at 5 mins (nmol superoxide anion/5 mins/10(6) neutrophils) were determined for each assay. On the day of admission, the mean APACHE II score and initial velocity for the septic shock group were 21.5 +/- 10 and 4.6 +/- 2 nmol superoxide anion/min/10(6) neutrophils, respectively. Over the next 7 to 12 days, as the patients recovered, there was a significant (paired t-test) decrease in APACHE II scores (p < .005) and increase in initial velocity (p < .0005). The increase in initial velocity correlated with the accompanying decrease in APACHE II scores (r2 = .46). Neutrophil superoxide anion generation in the critically ill group was not suppressed compared with the septic shock group and remained normal throughout the evaluation period. CONCLUSIONS: In vitro neutrophil respiratory burst function is significantly depressed during early septic shock. As patients improve clinically, as quantitated by decreasing APACHE II scores, neutrophil respiratory burst function recovers, approaching normal values.
Authors: Angelike P Liappis; Kevin W Gibbs; Eric S Nylen; Bona Yoon; Richard H Snider; Baochong Gao; Kenneth L Becker Journal: Inflamm Res Date: 2010-10-17 Impact factor: 4.575
Authors: C Wenisch; B Parschalk; A Weiss; K Zedwitz-Liebenstein; B Hahsler; H Wenisch; A Georgopoulos; W Graninger Journal: Clin Diagn Lab Immunol Date: 1996-07