Severe SIRS Research Articles

293 Risk of Clostridium Difficile Enterocolitis in SJS/TENS Patients Treated with Antibiotics

Abstract Introduction Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis Syndrome (TENS) are both rare conditions derived from adverse drug reactions. SJS/TENS patients are often treated with antibiotics, both prophylactically and therapeutically, for secondary infections. However, the subsequent development of Clostridium Difficile (C. Difficile) enterocolitis is unknown. Due to the rarity of SJS/TENS, institution trials are limited in their data quantify the additional risk of sequelae such as enterocolitis development after antibiotic administration. Therefore, we used a large commercially available database derived from inpatient hospital coding data to assess the incidence of C. Difficile enterocolitis within 2 weeks of antibiotic administration after development of SJS/TENS. Methods : Our study utilized a large commercially available database. Inclusion criteria identified adult patients ( >18 years old) diagnosed with SJS/TENS between 2002 and 2022, who were treated with antibiotics within 2 weeks of diagnosis, and who subsequently went on to develop Clostridium Difficile enterocolitis within 6 months. We compared our cohort to a control group which did not receive antibiotics and propensity score matched them for age, sex, race, HIV status, cancer, transplant status, and severe sepsis and SIRS and analyzed the risk of developing C. Difficile enterocolitis. Results There were 4,792 SJS/TENS patients who did not receive antibiotics and 5,652 who did. Our matched cohorts contained 4,595 patients. The relative risk of mortality between our cohorts was 4.962 (RR: 2.562, CI 95% 2.125-3.088; p< 0.0001). SJS/TENS who received antibiotics developed C. Difficile 68/4595 vs 30/495 and had a relative risk of 0.827% (RR: 2.267, 1.478-3.476, CI 95%; p< 0.0001). Therefore, an SJS/TENS patient incurred a 2.267 times higher risk of developing C. difficile enterocolitis after receiving antibiotics. Conclusions While causality cannot be affirmed with retrospective data, our findings do suggest that patients with SJS/TENS due to the statistically significant risk of C. Difficile enterocolitis development. However, the overall absolute risk of C. difficile enterocolitis remains disproportionately low in this population that warrants further exploration. Applicability of Research to Practice SJS/TENS patients are difficult to develop evidence-based treatment plans for because of their rarity and the multitude of conflicting small cohort studies available in the literature. Our study utilizes a large database to more robustly suggest that clinicians should be cautious about administering antibiotics to patients diagnosed with SJS/TENS.

Autochthonous Babesia canis infections in 49 dogs in Germany.

Vector-borne diseases are of increasing importance in Germany. Since 2015, autochthonous cases have been increasingly documented in Berlin/Brandenburg. Describe autochthonous Babesia canis infection in the Berlin/Brandenburg region. Forty-nine dogs with autochthonous B. canis infection. Evaluation of history, clinical signs, laboratory abnormalities, treatment, and outcome. Dogs were presented between March and August (9) and September and January (40) in the years 2015-2021. Historical and clinical findings were lethargy (100%), pale mucous membranes (63%), fever (50%), and pigmenturia (52%). Common clinicopathological findings were thrombocytopenia (100%), anemia (85%), intravascular hemolysis (52%), pancytopenia (41%), and systemic inflammatory response syndrome (SIRS; 37%). Babesia detection was based on blood smear evaluation (n=40) and PCR targeting the 18S rRNA gene of piroplasms (n=49). Sequencing indicated 99.47% to 100% identity to B. canis sequences from GenBank. All dogs were treated with imidocarb (2.4-6.3mg/kg; median, 5mg/kg); 8 dogs received 1, 35 received 2, and 1 dog each received 3, 4, or 5 injections, respectively. Continued PCR-positive results were detected in 7 dogs after the 1st, in 5 after the 2nd, in 2 after the 3rd, and in 1 28 days after the 4th injection. Four dogs were euthanized and 3 dogs died. Autochthonous B. canis infections in Berlin/Brandenburg were associated with severe clinicopathological changes, SIRS, and multiorgan involvement. Testing by PCR during and after treatment is advisable to monitor treatment success. Screening of blood donors in high-risk areas and year-round tick protection is strongly recommended.

Effect of CPB glucose levels on inflammatory response after pediatric cardiac surgery

BackgroundSystemic inflammatory response syndrome (SIRS) is a common complication after cardiac surgery. There are no definite optimal glycemic threshold for pediatric patients receiving open-heart surgery with CPB. The study aimed to investigate the optimal cardiopulmonary bypass (CPB) glucose in patients undergoing cardiac surgery.MethodsWe enrolled children with congenital heart disease who underwent surgical repair between June 2012 and December 2020. We included only patients who underwent cardiac surgery with CPB. The primary outcome was severe SIRS. A two-piece-wise regression model was applied to examine threshold effect of CPB glucose on severe SIRS.ResultsA total of 7350 patients were enrolled in the present study, of whom 3895 (52.99%) are female. After potential confounders were adjusted, non-linear relationship was detected between CPB glucose and severe SIRS, whose turning point was 8.1. With CPB glucose < 8.1 mmol/L, the estimated dose–response curve was consistent with a horizontal line. However, the prevalence of severe SIRS increased with increasing glucose up to the turning point (Glucose > 8.1 mmol/L); the odds ratio (OR) of the Glucose was 1.35 (95% CI 1.21, 1.50).ConclusionsThe present study indicates the association of CPB glucose with inflammatory response after pediatric cardiac surgery. The patients might have the best outcomes with the optimal CPB glucose no more than 8.1 mmol/L.

Supplemental immune globulins in sepsis: a critical appraisal

For 'the total population of patients with sepsis, sepsis syndrome or SIRS', the question of whether intravenous immune globulin (IVIG) reduces mortality is neither proved nor disproved. For the sepsis subgroups 'postoperative sepsis with a sepsis score more than 19' and 'endotoxaemic, early septic shock', a significant reduction in mortality by IVIG has been documented in a single, placebo-controlled, small trial of each subgroup; subsequent studies are needed for confirmation. The incidence of some severe infections in defined 'patients at risk' and 'operations at risk' is lowered by IVIG prophylaxis. Postoperative APACHE II-score identification of high-risk cardiac surgery patients prone to sepsis and severe SIRS may represent one approach to optimize individual, early therapy. Applying this concept to immune globulin treatment in a pilot study, the administration of IgG-IVIG and IgGMA-IVIG yielded similar results.

The severity of LPS induced inflammatory injury is negatively associated with the functional liver mass after LPS injection in rat model

BackgroundHigh levels of serum lipopolysaccharide (LPS) were observed in sepsis patients with liver injury and high mortality. However, the role of liver in modulation LPS induced inflammatory injury was ill investigated. In the present study, the severity of LPS induced inflammatory response was observed after liver resection or portal branch occlusion to decreasing functional liver mass. The local and systemic damage was observed to investigate the role of liver in modulation inflammatory injury.MethodsFirst, 30%, 70%, and 90% partial hepatectomy (PH) were performed, and serum TNF-α, survival rate, and hepatic LPS uptake was observed. Second, LPS-exposure of the functional liver mass was decreased by selectively blocking the RL prior to LPS-injection, which was given 30 min before a 70% PH, and the inflammatory response was compared in the occluded and the non-occluded liver. The control group was subjected to LPS injection 30 min prior to liver resection without blocking the RL transiently. The serum TNF-α, ALT, AST, creatinine levels, and urea levels, survival rate, hepatic LPS uptake, and hepatic inflammatory cytokines was observed.ResultsThe decreasing of functional liver mass after 90%, 70%, and 30% PH was associated with decreased serum TNF-α, survival rate, and increased hepatic LPS uptake after LPS injection. Occluding the right lobes (RL) prior to LPS administration reversed the liver injury caused by 70% PH, indicated by 100% survival rate and decreased liver and kidney injury, and systemic inflammatory response. The induction of inflammatory response in occluding liver lobes were lower than un-occluding liver lobes.ConclusionsThe severity of the LPS-induced systemic inflammatory injury is determined by functional liver volume. This observation suggests that the liver is the central organ for the initiation of the inflammatory response, and is involved in causing a severe SIRS with systemic damage and death.

全身性炎症反応症候群（SIRS）におけるADVIA2120サイトグラムパターンおよびパラメータの有用性

全身性炎症反応症候群（SIRS）におけるADVIA2120サイトグラムパターンおよびパラメータの有用性

Sweet syndrome presents with severe SIRS

Sweet syndrome presents with severe SIRS

Antagonistic sepsis markers: Serum gelsolin and actin/gelsolin ratio

ObjectivesFor appropriate sepsis care, prognostic laboratory markers are mandatory. The aim of our study was to evaluate the predictive value of serum actin, gelsolin and the recently defined actin/gelsolin ratio during sepsis by comparison it to classical clinical and inflammatory laboratory parameters. Design & methodsWe analyzed sera of severe septic (n=32) and SIRS (n=12) patients for 5days. Ophthalmologic patients (n=27) served as controls. Besides serum actin, gelsolin and actin/gelsolin ratios classical laboratory parameters (WBC count, serum procalcitonin, hsCRP) and clinical scores (APACHE II, SAPS II, SOFA), were also assessed. ResultsSeptic patients showed significantly decreased first-day gelsolin levels and increased actin/gelsolin ratios compared to SIRS patients (p<0.05), furthermore, non-survivors had significantly lower gelsolin levels compared to survivors (p<0.05). Non-survivors had 11.4-fold higher 2nd day actin/gelsolin ratios than survivors. Besides procalcitonin (PCT) and hsCRP, gelsolin and actin/gelsolin ratios also proved to be useful in discriminating SIRS from sepsis in the ICU (p<0.05). Gelsolin had similar prognostic value to PCT when assessing 7-day mortality and the predictive capacity of the first-day actin/gelsolin ratios was similar to that of APACHE II score regarding ICU mortality in severe sepsis. ConclusionsSerum gelsolin and actin/gelsolin ratio might serve as efficient complementary prognostic markers in sepsis. However, for daily clinical usage, an automated laboratory assay of actin and gelsolin is still needed to be developed.

Early diagnosis of mild acute pancreatitis

to analyze the efficacy of early detection of patients with mild acute pancreatitis. 61 patients with acute pancreatitis who do not require intensive care were analyzed. Severity of condition was assessed using integral scales, i.e. modified index of severe pancreatitis severity (MITOP), BISAP, HAPS, SOFA, SIRS, CTSI and Atlanta classification (2012). Verification of mild course of disease according to MITOP scores ≤0.23 and BISAP scores ≤1 for the first 24 hours after admission and CTSI scores ≤3 within first 72 hours had high accuracy [AUC (CI 95%) 0.79 (0.66-0.91); 0.76 (0.66-0.87) and 0.99 (0.97-1.00) respectively], sensitivity and specificity (88.8 and 43.7%; 71.1 and 75.0%; 100 and 83.3% respectively). MITOP and BISAP scales are reliable to diagnose early mild acute pancreatitis. Their high positive diagnostic value (81.6 and 88.8%) allows to detect patients who do not require intensive care.

Cytokine Reduction in the Setting of an ARDS-Associated Inflammatory Response with Multiple Organ Failure.

A 45-year-old male was admitted to our hospital with a small bowel obstruction due to torsion and was immediately scheduled for surgical intervention. At anesthesia induction, the patient aspirated and subsequently developed a severe SIRS with ARDS and multiple organ failure requiring the use of ECMO, CRRT, antibiotics, and low dose steroids. Due to a rapid deterioration in clinical status and a concurrent surge in inflammatory biomarkers, an extracorporeal cytokine adsorber (CytoSorb) was added to the CRRT blood circuit. The combined treatment resulted in a rapid and significant reduction in the levels of circulating inflammatory mediators. This decrease was paralleled by marked clinical stabilization of the patient including a significant improvement in hemodynamic stability and a reduced need for norepinephrine and improved respiratory function as measured by PaO2/FIO2, ventilator parameters, lung mechanics, and indirect measures of capillary leak syndrome. The patient could be discharged to a respiratory weaning unit where successful respiratory weaning could be achieved later on. We attribute the clinical improvement to the rapid control of the hyperinflammatory response and the reduction of inflammatory mediators using a combination of CytoSorb and these other therapies. CytoSorb treatment was safe and well tolerated, with no device-related adverse effects observed.

ABSTRACT 603

Background and aims: The inducible 90-kDa-heat-shock-protein (HSP90α) is involved in the heat-shock (HS) and lipopolysaccharide (LPS)-stress response. Aims: We investigated the LPS or HS HSP90α induction in cultured peripheral blood mononuclear cells (PBMCs) of Severe Sepsis (SS) or SIRS patients compared to healthy-controls (H) and any possible modulating Glutamine (Gln)-effects. Methods: PBMCs from 11/H, 5/SS, 4/SIRS patients were incubated either without stimulation or with 1μg/ml LPS or 43oHS. In each group 3 experiments involved L-Ala-Gln10mM incubation 1h before (Gln-b) or after (Gln-a) induction, or none (640 measurements). Intracellular Mean Fluorescence Intensity (MFI) levels of monocytes (mHSP90α) or lymphocytes (lHSP90α) determined using Flow Cytometry. (IRB approved). Results: Baseline septic PBMCs express higher mHSP90α (147 ± 34 vs. 111 ± 21MFI p<0.04) and lHSP90α (75 ± 15 vs. 44 ± 7MFI, p<0.05) compared to H. In SS the LPS-induced lHSP90α (87 ± 41 vs. 75 ± 15MFI, p<0.02) and the HS-induced lHSP90α (86 ± 12 vs. 75 ± 15MFI, p<0.05) showed declining trends by Gln-a or Gln-b (78 ± 11MFI, p<0.05). In healthy, HS mainly induced lHSP90 (HS 59 ± 11 vs. LPS 48 ± 10MFI, p<0.04) but LPS mainly induced mHSP90α (LPS 142 ± 22 vs. HS 122 ± 19MFI, p<0.03). Gln did not influence these effects, the induction differences remaining unaltered in healthy controls. Conclusions: Septic PBMCs express higher baseline mHSP90α and lHSP90α, expression further induced by LPS or HS. Gln pre-treatment may attenuate the induced HSP90α only in septic PBMCs. Grant Acknowledgment: This research has been co-financed by the European Union (European Social Fund (ESF)) and Greek national funds through the Operational Program ‘‘Education and Lifelong Learning’’ of the National Strategic Reference Framework (NSRF)-Research Funding Program: THALES.

Presence of Hypogammaglobulinemia – A Risk Factor of Mortality in Patients with Severe Sepsis, Septic Shock, and SIRS

In this retrospective study we assessed the frequency of hypogammaglobulinemia in 708 patients with SIRS, severe sepsis and septic shock. We evaluated the relationship between hypogammaglobulinemia IgG, IgM and 28 day mortality. Total of 708 patients and 1,513 samples were analyzed. In the three subgroups we investigated, patients met the criteria of SIRS, severe sepsis and septic shock. IgG hypogammaglobulinemia was demonstrated in 114 patients with severe sepsis (25.2%), 11 septic shock patients (24.4%), and in 29 SIRS patients (13.9%). IgM hypogammaglobulinemia was documented in 55 patients with severe sepsis (12.2%), 6 septic shock patients (13.3%), and in 17 SIRS patients (8.1%). Mortality of patients with severe sepsis and normal IgG levels was significantly lower (111 patients; 32.8%) compared with those with IgG hypogammaglobulinemia (49 patients; 43.0%; p=0.001). Mortality of patients with septic shock and IgG hypogammaglobulinemia (n=5) was significantly higher compared with those with normal IgG levels (45.5% vs. 38.2%; p=0.001). Mortality of patients with severe sepsis and IgM hypogammaglobulinemia did not differ from that of patients with normal IgM levels (37.0 vs. 41.8%). Mortality of patients with septic shock and IgM hypogammaglobulinemia was significantly higher compared with those with normal IgM levels (50% vs. 38.5%; p=0.0001). This study documented relatively high incidence of hypogammaglobulinemia IgG and IgM in patients with severe sepsis, septic shock and SIRS respectively. The presence of IgG hypogammaglobulinemia in patients with severe sepsis is independent factor of mortality.

Predictive ability of the ISS, NISS, and APACHE II score for SIRS and sepsis in polytrauma patients

Systemic inflammatory response syndrome (SIRS) and sepsis as causes of multiple organ dysfunction syndrome (MODS) remain challenging to treat in polytrauma patients. In this study, the focus was set on widely used scoring systems to assess their diagnostic quality. A total of 512 patients (mean age: 39.2±16.2, range: 16-88years) who had an Injury Severity Score (ISS) ≥17 were included in this retrospective study. The patients were subdivided into four groups: no SIRS, slight SIRS, severe SIRS, and sepsis. The ISS, New Injury Severity Score (NISS), Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, and prothrombin time were collected at admission. The Kruskal-Wallis test and χ(2)-test, multinomial regression analysis, and kernel density estimates were performed. Receiver operating characteristic (ROC) analysis is reported as the area under the curve (AUC). Data were considered as significant if p<0.05. All variables were significantly different in all groups (p<0.001). The odds ratio increased with increasing SIRS severity for NISS (slight vs. no SIRS, 1.06, p=0.07; severe vs. no SIRS, 1.07, p=0.04; and sepsis vs. no SIRS, 1.11, p=0.0028) and APACHE II score (slight vs. no SIRS, 0.97, p=0.44; severe vs. no SIRS, 1.08, p=0.02; and sepsis vs. no SIRS, 1.12, p=0.0028). ROC analysis revealed that the NISS (slight vs. no SIRS, AUC 0.61; severe vs. no SIRS, AUC 0.67; and sepsis vs. no SIRS, AUC 0.77) and APACHE II score (slight vs. no SIRS, AUC 0.60; severe vs. no SIRS, AUC 0.74; and sepsis vs. no SIRS, AUC 0.82) had the best predictive ability for SIRS and sepsis. Quick assessment with the NISS or APACHE II score could preselect possible candidates for sepsis following polytrauma and provide guidance in trauma surgeons' decision-making.

How tissue injury alarms the immune system and causes a systemic inflammatory response syndrome

Systemic inflammation is very prevalent among critically ill patients, particularly those with extensive tissue injury. Although downstream mediators (cytokines) and effector cells (phagocytes) have been identified, proximal mediators originating from injured tissues remained elusive. Alarmins (“danger signals”) released by necrotic/injured cells have been identified recently and certainly play a role in triggering local and systemic inflammation in critically ill patients. The most promising alarmin candidates are of mitochondrial origin, i.e. mitochondrial DNA and the chemotactic factor fMet-Leu-Phe (fMLP). ATP also is released from necrotic tissues and stimulates the assembly of the inflammasome, leading to the production of proinflammatory cytokines, such as interleukin (IL)-1ß. The identification of novel alarmins opens new therapeutic avenues for the treatment of severe SIRS, and SIRS-dependent organ dysfunction.

Generating Evidence Based Interpretation of Hematology Screens via Anomaly Characterization

Introduction: We propose a simple, workable algorithm that provides assistance for interpreting any set of data from the screen of a blood analysis with high accuracy, reliability, and inter-operability with an electronic medical record. This has been made possible at least recently as a result of advances in mathematics, low computational costs, and rapid transmission of the necessary data for computation. Materials and Methods: The database used for this study is a file of 22,000 laboratory hemograms generated by two Beckman-Coulter Gen-S analyzers over a two month period in a 630 bed acute care facility in Brooklyn. All control samples, patient identifiers, and patients under 23 years old were stripped from the dataset. An experienced medical practitioner reviewed all of the data used in generating the algorithm described. The differential diagnoses were outlined prior to beginning the study, and preliminary studies were done to determine the reference ranges for each predictor. An algorithm for anomaly detection and classification via anomaly characterization is proposed. For each patient, the algorithm characterizes its anomalous profile and builds a differential metric to identify similar patients who are mapped into a classification. Results: The algorithm successfully classified patients into the diagnosis that were sufficient in sample size, and others are still under observation. The algorithm correctly classified the patients as follows: Microcytic Anemia - 99.63%, Normocytic Anemia - 98.03%, Mild SIRS - 73.42%, Thrombocytopenia - 99.52%, Leukocytopenia - 84.83%, Moderate / Severe SIRS - 96.69% and Normal - 93.18%. Discussion: This limited analysis of automated hematological results can be extended to the case of more complicated conditions than presented, and can be extended to a combination of chemistry, hematology, immunology, and other data.

Gut flora and Synbiotic therapy in patients with severe SIRS

Gut flora and Synbiotic therapy in patients with severe SIRS

Oral Presentation

Introduction: Serum lactate is considered to be a marker of tissue hypoxia (1) Cut-off values >4 mM predict poor outcome, yet many patients after resuscitation according Surviving Sepsis Campaign guidelines (SSCG) (2) have high mortality despite decreases in blood lactate. Our hypothesis was that dynamic, rather than absolute blood lactate concentrations predict survival. Further we tested the ability of microdialysis lactate (MD-lac) to follow dynamic changes in blood levels, and whether this was also predictive of survival. Methods: Prospective, observational, single-centre cohort study in a mixed-bed university hospital ICU. About 53 consecutive patients with SIRS and circulatory failure despite adequate fluid resuscitation according to the SSCG were included. Arterial blood lactate (B-lac) was measured 6- hourly and MD-lac in subcutaneous tissue measured 4- hourly. Changes in B- and MD-lac from baseline were also calculated. Results: There were no differences in absolute values of B- lac or MD-lac between survivors and non-survivors during the first 24 h, nor were there differences in the change in MD-lac. In contrast changes in B-lac were greater in survivors. Among patients who reached P-lac > 4 mM during the study period of 7 days, the mortality rate was 37% as compared to 21% in the others, although this did not reach statistical significance. Conclusions: Survivors of severe SIRS were characterized by greater changes in B-lac compared to baseline. This supports the concept of lactate clearance, rather than absolute values, as a useful end point for fluid resuscitation, as opposed to the traditional endpoints used in the SSCG. In contrast MD- lac was not a useful predictor of mortality in this population. (Less)

Adenosine A2A Receptor Hyperexpression in Patients With Severe SIRS After Cardiopulmonary Bypass

ObjectiveAdenosine (ADO) is an endogenous nucleoside, which has been involved in blood pressure failure during severe systemic inflammatory response syndrome (severe SIRS) after cardiac surgery with cardiopulmonary bypass (CPB). Adenosine...

Does severe non-infectious SIRS differ from severe sepsis?

To compare the time course of organ dysfunction/failure, mortality and cause of death in patients with severe sepsis (SS) and patients with severe non-infectious systemic inflammatory response syndrome (SNISIRS). Secondary analysis of a multi-centre inception cohort study. Twenty-three multidisciplinary intensive care units (ICUs) in Australia and New Zealand. 3,543 ICU admissions > or = 48 h or <48 h if SIRS and organ dysfunction present. None. ICU prevalence of SS and SNISIRS was 20% (707/3,543) and 28% (980/3,543), respectively. ICU mortality was similar in patients with SNISIRS and with SS (25 vs. 27%, P = 0.40). Central nervous system (CNS) failure occurred more frequently in patients with SNISIRS (33 vs. 22%, P < 0.001) and resulted in death more commonly than in SS (relative risk = 1.6, 95% confidence interval 1.4-1.7, P < 0.001). The time to peak organ dysfunction (0.67 vs. 0.91 days, P = 0.004), overall episode length (3.6 vs. 5.6 days, P < 0.001) and ICU stay (geometric mean: 4.1 vs. 5.8 days, P < 0.001) were significantly shorter in patients with SNISIRS. Whilst SNISIRS and SS have similarities, including their crude mortality rate, important differences exist. SNISIRS is more common on admission to the ICU, and is more commonly coupled with CNS dysfunction and death from neurological failure. SIRS/sepsis: clinical studies.

Systemic inflammatory complications after cardiopulmonary bypass (CPB): Influence of cytokines and complement system in correlation to endothelial activation

Objective: To investigate the role of cytokines and complement system in the inflammatory response after CPB we looked for correlations between cytokine-/complement-levels and clinical parameters. Methods: 40 consecutive CABG-patients were included in a prospective study. Blood samples were analyzed for CRP, PCT and for C3a and C5a. We also determined TNF-a, interleukin-1,-6,-8 and -10, as well as ET1, ICAM-1, ICAM-3, VCAM-1 and ELAM-1. Results: IL-1b was not elevated in the plasma at any sample time point. TNF-a was significantly increased in 4 patients after onset of CPB. 3 patients showed a significant TNF-elevation already preoperatively (268.5 pg/ml vs. <10 pg/ml in the other patients). In these 3 patients, which were the only to develop a severe SIRS, we also found significantly higher preoperative levels of ET1 (2.5±0.3 vs. 1.2±0.4 pg/ml), ICAM-1, ICAM-3 and ELAM-1. IL-6 and IL-10 rose significantly and peaked 88 respectively 50 minutes after end of CPB. C3a and C5a were significantly elevated during CPB with maximum levels 30 minutes after CPB. Peak values of IL-6 and -10 could be correlated to the duration of aortic crossclamping. Conclusions: CPB does not induce systemic release of TNF-a and IL-1b. A preoperative TNF-elevation in combination with an activation of the endothelium seems to be an indicator of an increased risk for systemic inflammation. Furthermore our results confirm the presence of complement activation preceding the production of IL-6 and IL-10. IL-6 may contribute to adverse systemic reactions after CPB, since its release could be correlated to the duration of myocardial ischemia.