Severe Severe Systemic Inflammatory Response Syndrome Research Articles

Effect of perfusate oxygenation on inflammatory response in congenital heart disease children from low versus high altitude

ObjectiveTo examine the altitude differences in the optimal perfusate oxygenation (PpO2) in patients who underwent cardiac surgery. MethodsWe included children (aged 1 month to 18 years) with congenital heart diseases surgically repaired between 2012 and 2018. We included only patients who underwent cardiac surgery with arrested heart cardiopulmonary bypass. Primary outcome was severe systemic inflammatory response syndrome (SIRS). Logistic regression was used to evaluate the association between arterial PpO2 on continuous and categorical scales and severe SIRS by altitude. We established PpO2 thresholds that equated to a risk probability of roughly 0.185 or greater for developing severe SIRS in each group of altitude. ResultsAmong 3918 patients from low altitudes and 2384 from high altitudes, high-altitude patients were older (median, 42.3 [interquartile range 22.8-75.8] vs 37.1 [17.7-69.1] months, P < .001) and had lower arterial PpO2 (289 [237-342] vs 301 [246-362] mm Hg, P < .001). Greater PpO2 was associated with increased risk of severe SIRS overall (adjusted odds ratio, 1.221 [95% confidence interval, 1.167-1.278] per standard deviation increase), with a stronger monotonic associations for low-altitude patients than for high-altitude patients (adjusted odds ratio, 1.302 [95% confidence interval, 1.229-1.379] vs adjusted odds ratio, 1.083 [95% confidence interval, 1.003-1.170] per standard deviation increase) (Pinteraction = .0003). A PpO2 level of 310 mm Hg identified low-altitude patients with a risk probability of roughly 0.185 or greater of severe SIRS, whereas the cutoffs ranged from 200 mm Hg to 325 mm Hg for high-altitude patients. ConclusionsThis study suggests altitude differences in the association of arterial PpO2 with inflammatory response following pediatric cardiac surgery.

Severe Systemic Inflammatory Response Syndrome with Multi-Organ Failure Following Zoledronic ACID Infusion

ABSTRACT Objective: We report a new, life-threatening adverse effect of zoledronic acid. One of the adverse effects of zoledronic acid is acute phase reaction (APR). Mild APR is characterized by arthralgia, myalgia, headache, and fever, which are usually self-limiting. Here, we present a case of severe systemic inflammatory response syndrome (SIRS) following zoledronic acid infusion, leading to multi-organ failure. Methods: A 63-year-old female presented to the emergency department with fever, headache, and myalgia within hours after zoledronic acid infusion. Approximately 24 hours later, she developed progressive weakness and confusion. She was febrile, tachycardic, and tachypneic on presentation. Subsequently, she developed acute respiratory distress syndrome, stress or Takotsubo cardiomyopathy, shock with hypotension, and acute tubular necrosis with acute kidney failure. Results: All infectious work-up was unrevealing. She was diagnosed with severe SIRS leading to multi-organ failure. She needed aggres...

Treatment of Post-Cardiopulmonary Bypass SIRS by Hemoadsorption: A Case Series

The use of cardiopulmonary bypass (CPB) in cardiothoracic surgery results in a well-known activation of the immunologic response. In some cases, however, this triggered immunologic response may be excessive, leading to a severe systemic inflammatory response syndrome (SIRS) and induced organ dysfunction. For example, patients frequently develop hemodynamic instability with hypotension and low systemic vascular resistance. To date, different therapeutic approaches, such as steroids, have been tried to control this maladaptive postoperative SIRS response, yet definitive proof of clinical efficacy is missing. A new cytokine adsorber device (CytoSorb; CytoSorbents) may be a useful approach to control hyperinflammatory systemic reactions by reducing a broad range of proinflammatory cytokines and other inflammatory mediators. This may, in turn, help to reestablish a physiologic immune response and help to restore deranged clinical parameters in these patients. In this retrospective case series study, we describe 16 cardiac surgery patients following prolonged CPB with post-CPB SIRS and subsequent acute kidney injury, who were then treated with hemoadsorption using CytoSorb in combination with continuous renal replacement therapy (CRRT). Treatment of patients with CytoSorb who presented with severe post-CPB SIRS resulted in a reduction of elevated cytokine levels, which was associated with a clear stabilization of deranged hemodynamic, metabolic, and organ function parameters. Treatment was well tolerated and safe, with no device-related adverse events occurring. CytoSorb therapy combined with CRRT is a potentially promising new treatment approach to achieve hemodynamic stability, cytokine reduction, and improved organ function in cardiac surgery patients who develop post-CPB SIRS.

Rapid and Sustained Long‐Term Decrease of Fecal Short‐Chain Fatty Acids in Critically Ill Patients With Systemic Inflammatory Response Syndrome

The gut is an important target organ for injury after severe insult. Short-chain fatty acids (SCFAs) are end-products of fermentation of dietary fibers by anaerobic microbiota. They are related to intestinal energy, motility, and transport and to protective effects against infection and inflammation. However, there are few clinical data on SCFAs in critically ill patients. We evaluated serial change in fecal SCFAs in patients with severe systemic inflammatory response syndrome (SIRS). This study included 140 intensive care unit (ICU) patients who fulfilled the criteria of SIRS and had a serum C-reactive protein level of >10 mg/dL. A fecal sample was used for quantitative measurement of fecal SCFA (butyrate, propionate, and acetate) concentrations by high-performance liquid chromatography. Fecal SCFAs were evaluated weekly for 6 weeks after admission. Data obtained from patients were compared with corresponding data from healthy volunteers. SIRS resulted from infection in 78 patients, trauma in 30, burns in 12, and other causes in 20. Fecal concentrations of butyrate, propionate, and acetate in these patients decreased significantly compared with those in healthy volunteers and remained low throughout the 6 weeks of the patients' ICU stay. Fecal concentrations of SCFAs in the patients with gastrointestinal complications, including enteritis and dysmotility, were lower than those in the patients without gastrointestinal complications. Concentrations of fecal SCFAs in patients with severe SIRS were significantly lower than those in healthy volunteers over a 6-week period. Maintenance of SCFAs may have therapeutic potential to prevent gastrointestinal complications in critically ill patients.

Prognostic Value of Central Venous Oxygen Saturation and Blood Lactate Levels Measured Simultaneously in the Same Patients with Severe Systemic Inflammatory Response Syndrome and Severe Sepsis

Blood lactate levels and central venous oxygen saturation (ScvO(2)) are known to be useful indicators of global tissue hypoxia. However, it is unclear whether ScvO(2) correlates with lactate levels when measured simultaneously and whether changes in ScvO(2) or lactate levels in serial measurements have prognostic value. We investigated the correlation between ScvO(2) and lactate levels measured simultaneously and their association with clinical outcomes. We performed a prospective observational study of patients with severe systemic inflammatory response syndrome (SIRS) and severe sepsis who were admitted to the medical intensive care unit. ScvO(2) and lactate levels were measured simultaneously at the time of study enrollment, every 6 h for 24 h, and then every 24 h until the goal was reached. Twenty-five patients were enrolled in the study; 13 have died and 12 have survived. There was no correlation between lactate levels and ScvO(2). Neither lactate levels nor ScvO(2) at the time of admission differed between nonsurvivors and survivors. Normalization of lactate levels within 48 h was significantly associated with survival. In patients with severe SIRS and severe sepsis, simultaneously measured ScvO(2) and lactate levels showed no correlation, and normalization of lactate levels within 48 h was a predictive factor for survival.

Innate Immune Functions of Immature Neutrophils in Patients With Sepsis and Severe Systemic Inflammatory Response Syndrome*

A hallmark of sepsis and severe systemic inflammatory response syndrome (SIRS) is the massive recruitment of immature neutrophils from the bone marrow into the circulation (left shift, band forms). Their capacity to participate in innate defense against bacteria is ill defined. We aimed at comparing various innate immune functions of mature vs. immature neutrophils circulating during sepsis and SIRS. Prospective, observational cohort study. Tertiary level ICU and associated research laboratory. : Thirty-three ICU patients with sepsis; 12 ICUs with SIRS; 32 healthy volunteers. Twenty milliliters of whole heparinized blood was used for in vitro studies including neutrophil viability and apoptosis, surface expression of CD16, Toll-like receptors () 4 and TLR2, CD14, MD-2, HLA-DP,-DQ and -DR, and CXCR2, chemotaxis, phagocytosis, bacterial killing, and tumor necrosis factor-α/interleukin-10 baseline intracellular cytokine levels. Immature neutrophils were capable of mediating important innate immune functions such as bacterial phagocytosis and killing via the production of reactive oxygen species, although less efficiently than mature neutrophils. Immature neutrophils had a longer life span and resistance to spontaneous apoptosis, and could mature ex vivo. They expressed lower levels of receptors for bacterial molecules such as CD14 and MD-2 and migrated less efficiently than mature granulocytes. Immature neutrophils had higher basal intracellular tumor necrosis factor-α/interleukin-10 ratio than that of mature neutrophils, suggesting a proinflammatory phenotype. No significant differences were observed between immature neutrophils isolated from patients with sepsis and those from patients with severe SIRS. Despite their "immaturity", band forms are capable of mediating crucial innate immune functions during severe infections and sepsis. Their fate and capacity to mature in vivo remain to be determined.

Gastrointestinal dysmotility is associated with altered gut flora and septic mortality in patients with severe systemic inflammatory response syndrome: a preliminary study

The gut is an important target organ for injury after severe insult, and resolution of feeding intolerance is crucial for critically ill patients. We investigated gut flora and motility to evaluate the impact of gastrointestinal dysmotility on septic complications in patients with severe systemic inflammatory response syndrome (SIRS). Sixty-three ICU patients with severe SIRS were divided into two groups depending on their intestinal condition. Patients with feeding intolerance comprised patients who had feeding intolerance, defined as ≥ 300 mL reflux from nasal gastric feeding tube in 24 h, and patients without feeding intolerance comprised patients with no feeding intolerance. We compared fecal microflora, incidences of bacteremia, and mortality between these groups. Analysis of feces showed that patients with feeding intolerance had significantly lower numbers of total obligate anaerobes including Bacteroidaceae and Bifidobacterium, higher numbers of Staphylococcus, lower concentrations of acetic acid and propionic acid, and higher concentrations of succinic acid and lactic acid than those in patients without feeding intolerance (P ≤ 0.05). Patients with feeding intolerance had higher incidences of bacteremia (86%vs 18%) and mortality (64%vs 20%) than did patients without feeding intolerance (P ≤ 0.05). Gut flora and organic acids were significantly altered in patients with severe SIRS complicated by gastrointestinal dysmotility, which was associated with higher septic mortality in SIRS patients.

Patterns of Gram-Stained Fecal Flora as a Quick Diagnostic Marker in Patients with Severe SIRS

BackgroundThe gut is an important target organ of injury during critically ill conditions. Although Gram staining is a common and quick method for identifying bacteria, its clinical application has not been fully evaluated in critically ill conditions.AimsThis study’s aims were to identify patterns of Gram-stained fecal flora and compare them to cultured bacterial counts and to investigate the association between the patterns and septic complications in patients with severe systemic inflammatory response syndrome (SIRS).MethodsFifty-two patients with SIRS were included whose Gram-stained fecal flora was classified into three patterns. In a diverse pattern, large numbers of multiple kinds of bacteria completely covered the field. In a single pattern, one specific kind of bacteria or fungi predominantly covered the field. In a depleted pattern, most bacteria were diminished in the field.ResultsIn the analysis of fecal flora, the numbers of total obligate anaerobes in the depleted pattern was significantly lower than those in the diverse pattern and single pattern (p < 0.05). The concentrations of total organic acids, acetic acid, and propionic acid in the depleted pattern were significantly lower than those in diverse pattern and single pattern (p < 0.05). Mortality due to multiple organ dysfunction syndrome for the single pattern (52%) and the depleted pattern (64%) was significantly higher than that for the diverse pattern (6%) (p < 0.05).ConclusionsGram-stained fecal flora can be classified into three patterns and are associated with both cultured bacterial counts and clinical information. Gram-stained fecal bacteria can be used as a quick bedside diagnostic marker for severe SIRS patients.

Synbiotics Decrease the Incidence of Septic Complications in Patients with Severe SIRS: A Preliminary Report

The purpose of this study was to evaluate if synbiotic therapy can correct the deteriorated gut flora and environment in patients with severe systemic inflammatory response syndrome (SIRS). Twenty-nine SIRS patients, who fulfilled a serum C-reactive protein (CRP) level >10 mg/dl, received synbiotics (Bifidobacterium breve, Lactobacillus casei, and galactooligosaccharides) (S group) and were compared with previous observations in 26 patients without synbiotics (NS group). Analysis of fecal flora confirmed that patients in the S group had significantly greater levels of beneficial Bifidobacterium, Lactobacillus, and total organic acids (particularly short-chain fatty acids) than those in the NS group. The incidence of infectious complications such as enteritis, pneumonia, and bacteremia was significantly lower in the S group than in the NS group. Synbiotics maintain the gut flora and environment and decrease the incidence of septic complications in patients with severe SIRS. Further randomized controlled study is necessary to determine the effects of synbiotics.

Immunoglobulin G treatment of postcardiac surgery patients with score-identified severe systemic inflammatory response syndrome—The ESSICS study*

A minority of patients develop severe systemic inflammatory response syndrome (SIRS) with high mortality following cardiopulmonary bypass-assisted cardiac surgery. We assessed whether intravenous immunoglobulin G (ivIgG) improves postoperative short-term (5-day) morbidity and reduces 28-day mortality in these patients. Randomized, double-blind, placebo-controlled, multicenter trial. Intensive care units of 11 cardiothoracic centers. Of 6,984 patients screened, we identified 244 with severe SIRS (Acute Physiology and Chronic Health Evaluation II score > or = 28 on the first postoperative day). The 244 patients with severe SIRS were randomly assigned to receive an intravenous infusion of either albumin 0.1% (placebo group, 6 mL [6 mg]/kg of body weight on day 1 and 3 mL [3 mg]/kg of body weight on day 2) or immunoglobulin G 10% (ivIgG group, 6 mL [600 mg]/kg of body weight on day 1 and 3 mL [300 mg]/kg of body weight on day 2). The prospectively defined primary end points were improvement in morbidity on day 5 and death from any cause assessed on day 28. A total of 218 patients received both doses of the study drug (placebo n = 108, ivIgG n = 110). Acute Physiology and Chronic Health Evaluation II scores in the placebo group decreased from 31.8 +/- 4.0 (day 1) to 25.8 +/- 9.3 (day 5) and in the ivIgG group from 31.8 +/- 3.4 (day 1) to 25.9 +/- 10.3 (day 5), with no significant difference between the groups (p = .56). The 28-day mortality rate was not significantly different between the groups (per protocol population, placebo group 31.5%, ivIgG group 39.1%; intent-to-treat population, placebo group 37.2%, ivIgG group: 44.7%). No effect of ivIgG on plasma levels of interleukin-6, tumor necrosis factor, and tumor necrosis factor receptor I/II was observed. Drug-related adverse events were rare in both groups. Patients undergoing cardiac surgery (involving cardiopulmonary bypass) who develop severe SIRS derive no improvement in short-term morbidity or 28-day mortality from ivIgG.

Enhanced Expression of Intracellular Heme Oxygenase-1 in Deactivated Monocytes From Patients With Severe Systemic Inflammatory Response Syndrome

Monocyte deactivation is an important contributor to infectious susceptibility in critically ill patients. However, the mechanism of monocyte deactivation has not been fully elucidated. Recently, intracellular heme oxygenese-1 (HO-1), an anti-inflammatory heat-shock protein, was reported to be activated by Toll-like receptors (TLRs), and to inhibit inflammatory cytokine production such as that of TNF-alpha. In the present study, we evaluated the expression of intracellular HO-1 and TLRs in monocytes from patients with severe systemic inflammatory response syndrome (SIRS) and examined the role of HO-1 in monocyte deactivation. Twenty-seven patients who fulfilled the criteria for severe SIRS and had a serum C-reactive protein (CRP) level >10 mg/dL were included in this study. The cause of SIRS was sepsis in 16 patients, trauma in 7, and other in 4. Expression of intracellular HO-1, surface TLR2 and TLR4, and intracellular cytokines (TNF-alpha, Interleukin-6) stimulated via TLR activation were measured in circulating monocytes by flow cytometry. Intracellular HO-1 expression was evaluated in normal monocytes stimulated with patient serum. Serum cytokine levels were also measured. Patient data were compared with data from healthy volunteers (n = 16). Cytoplasmic HO-1 was clearly detected by fluorescence microscopy. Expression of HO-1, TLR2, and TLR4 in monocytes was significantly enhanced in patients with severe SIRS compared with that in healthy volunteers, whereas intracellular TNF-alpha expression with peptidoglycan was significantly decreased (p < 0.05) in patients compared with that in healthy volunteers. HO-1 expression was significantly enhanced in normal monocytes stimulated with patient serum. Intracellular HO-1 levels were positively related to serum TNF-alpha levels in patients (r = 0.46). Expression of intracellular HO-1 and of TLRs was enhanced in deactivated monocytes from patients with SIRS. Increased production of intracellular HO-1 in response to serum factors may play a role in monocyte deactivation after systemic inflammation.

Altered Gut Flora and Environment in Patients with Severe SIRS

The gut is considered an important target organ of injury after severe insult such as sepsis, trauma, and shock. The impact of bacterial translocation or mesenteric lymph on systemic inflammatory response and multiple organ damage has been investigated in animals, but dynamic changes in the gut flora and environment have not been fully clarified in critically ill patients. In the present study, we quantitatively evaluated changes in the gut microflora and environment in patients with severe systemic inflammatory response syndrome (SIRS). Twenty-five patients with severe SIRS, who fulfilled the criteria for SIRS, had a serum CRP level >10 mg/dL, and were treated in the intensive care unit for more than 2 days, were included in our study. SIRS was a result of sepsis in 18 patients, trauma in 6, and burn in 1. A fecal sample was used for quantitative evaluation of microflora (bacterial counts of 10 key groups including Bifidobacterium and Lactobacillus) by plate or tube technique and of the gut environment (pH and 9 organic acids by high speed liquid chromatography). Data obtained from patients were compared with corresponding data from healthy volunteers. Analysis of fecal flora confirmed that patients with severe SIRS had significantly lower total anaerobic bacterial counts (especially 2-4 log fewer "beneficial" Bifidobacterium and Lactobacillus) and 2 log higher "pathogenic" Staphylococcus and Pseudomonas group counts than those of healthy volunteers. Concentrations of total organic acids (especially "beneficial" short-chain fatty acids such as acetic acid, propionic acid, and butyric acid) in the feces were significantly decreased in the patients, whereas pH was markedly increased. The gut flora and environment are significantly altered in patients with severe SIRS. Abnormal gut flora and environment may affect systemic inflammatory response after severe insult.

High concentrations of N-BNP are related to non-infectious severe SIRS associated with cardiovascular dysfunction occurring after off-pump coronary artery surgery

Procalcitonin (PCT) blood concentrations are known to be an appropriate marker of severe systemic inflammatory response syndrome (SIRS) induced by coronary artery surgery with and without cardiopulmonary bypass. Pro-brain natriuretic peptide (N-BNP) is a newly described cardiac hormone considered to be an effective marker of severity and prognosis of acute coronary syndromes and congestive heart failure. We evaluated the perioperative time courses of PCT and N-BNP and investigated their role as early markers of severe SIRS (SIRS with cardiovascular dysfunction) induced by off-pump coronary artery bypass (OPCAB). Sixty-three patients were prospectively included. The American College of Chest Physicians Classification was used to diagnose SIRS and organ system failure to define severe SIRS. Serum concentrations of PCT and N-BNP were determined before, during and after surgery. Receiver operating characteristic curves and cut-off values were used to assess the ability of these markers to predict postoperative severe SIRS. SIRS occurred in 25 (39%) patients. Nine of them (14%) showed severe SIRS. Significantly higher serum concentrations of N-BNP and PCT were found in patients with severe SIRS with peak concentrations respectively at 8887 pg ml(-1) (range 2940-29372 pg ml(-1)) for N-BNP and 9.50 ng ml(-1) (range 1-65 ng ml(-1)) for PCT. The area under the curve using N-BNP to detect postoperative severe SIRS was 0.799 before surgery (0.408 for PCT; P<0.01) and 0.824 at the end of surgery (0.762 for PCT; P<0.05). N-BNP may be an appropriate marker indicating the early development of non-infectious postoperative severe SIRS after OPCAB.

Early activation of gammadelta T lymphocytes in patients with severe systemic inflammatory response syndrome.

Innate immunity plays an important role in host defense after severe insult. gammadelta T lymphocytes are recognized as the first line of defense against microbial invasion. In this study, we evaluated gammadelta T lymphocytes in the peripheral blood of patients with severe systemic inflammatory response syndrome (SIRS), and examined on role of these cells. Thirty-seven patients with severe SIRS (SIRS criteria and serum C-reactive protein > or = 10 mg/dL) and 27 healthy volunteers were studied. Severe SIRS was caused by trauma in 14 patients (Injury Severity Score of 30.1 +/- 10.8) and by sepsis in 23 patients. The counts of gammadelta and alphabeta T lymphocytes were determined by flow cytometry of cells stained with monoclonal antibodies to gammadelta and alphabeta T lymphocyte receptors. The activation of these cells was evaluated by flow cytometry of cells stained with monoclonal antibodies to CD69 and HLA-DR. Serial counts and activation of gammadelta and alphabeta T lymphocytes were also determined in eight trauma patients (Injury Severity Score of 31.0 +/- 13.5) during a 2-week observation period. The count of gammadelta T lymphocytes in the peripheral blood of SIRS patients (30.1 +/- 6.0/microL) was significantly lower (P < 0.05) than that of the healthy volunteers (104.3 +/- 10.9/microL). The expression of CD69, an index of early activation of T lymphocytes, was significantly greater on gammadelta T lymphocytes from SIRS patients (patients 23.9% +/- 3.4%, healthy controls 4.8% +/- 0.6%, P < 0.05). In trauma patients, the expression of CD69 on gammadelta T lymphocytes increased rapidly within 48 h after injuries. In conclusion, gammadelta T lymphocytes are activated and decreased in the peripheral blood of severe SIRS patients. In trauma patients, the activation of gammadelta T lymphocytes occurs in the fairly acute phase after injuries. These results suggest a significant role for gammadelta T lymphocytes as early responders after severe insult.

Enhanced Production of Endothelial Microparticles With Increased Binding to Leukocytes in Patients With Severe Systemic Inflammatory Response Syndrome

The vascular endothelium sustains substantial damage after severe insult. Recently, activated endothelial cells have been reported to produce microparticles in vitro. The objective of this study was to evaluate endothelial microparticle formation and microparticle-leukocyte interaction among patients with severe systemic inflammatory response syndrome (SIRS). The participants in this study were 28 patients with severe SIRS (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 18 healthy volunteers. Endothelial microparticles in the blood, microparticle-polymorphonuclear leukocyte (PMNL) binding, and PMNL oxidative activity were measured by flow cytometry. Soluble E-selectin, thrombomodulin, and plasminogen activator inhibitor-1 levels in the blood, variables representing systemic vascular endothelial cell activation and damage, and coagulative activity in the blood also were measured. Endothelial microparticle levels in the blood, microparticle binding to PMNLs, and oxidative activity in PMNLs increased significantly in patients with severe SIRS, as compared with the values in healthy volunteers. Soluble E-selectin, thrombomodulin, plasminogen activator inhibitor-1, and procoagulant activity in the blood also increased in these patients. Activated vascular endothelial cells with increased procoagulant activity enhance production of microparticles with increased binding to leukocytes in patients with severe SIRS. Endothelial microparticles may be involved in the pathogenesis of endothelial injury after severe insult.

Postoperative extracorporeal membrane oxygenation for severe intraoperative SIRS 10 h after multiple trauma

A 34-yr-old male suffered multiple trauma in a road traffic accident. He required right thoracotomy and laparotomy to control exanguinating haemorrhage, and received 93 u blood and blood products. Intraoperatively, he developed severe systemic inflammatory response syndrome (SIRS) with coagulopathy and respiratory failure. At the end of the procedure, the mean arterial pressure (MAP) was 40 mm Hg, arterial blood gas analysis showed a pH of 6.9, PaCO2 12 kPa, and PaO2 4.5 kPa, and his core temperature was 29°C. There was established disseminated intravascular coagulation. The decision was made to stabilize the patient on veno-venous extracorporeal membrane oxygenation (ECMO) only 10 h after the accident, in spite of the high risk of haemorrhage. The patient was stabilized within 60 min and transferred to the intensive care unit. He was weaned off ECMO after 51 h. He had no haemorrhagic complications, spent 3 weeks in the intensive care unit, and has made a good recovery.

Hyperprocalcitonemia is related to noninfectious postoperative severe systemic inflammatory response syndrome associated with cardiovascular dysfunction after coronary artery bypass graft surgery

Objective: To investigate the role of 3 inflammatory parameters as early markers of severe systemic inflammatory response syndrome (SIRS) induced by coronary artery bypass graft surgery. Design: Prospective study. Setting: University hospital. Participants: Patients (n = 63) undergoing elective coronary artery bypass graft surgery with cardiopulmonary bypass. Measurements and Main Results: The American College of Chest Physicians/Society of Critical Care Medicine classification was used to diagnose SIRS. Organ system failures were used to define severe SIRS. Serum concentrations of the inflammatory parameters (procalcitonin [PCT], C-reactive protein, leukocyte count) were determined before, during, and after surgery. SIRS occurred in 30 (47%) patients after surgery. Seven patients (11%) showed SIRS with ≥1 organ dysfunction (severe SIRS), whereas patients without SIRS had no organ dysfunction. Significantly higher serum levels of PCT were found in patients with severe SIRS from the 6th postoperative hour until the 3rd postoperative day with a peak level of 10.7 ± 13.2 ng/mL. No significant difference was detected between serum PCT of patients with SIRS but without any organ dysfunction and patients without SIRS. PCT levels of these patients remained lower than 1.7 ng/mL. Compared with PCT, plasma concentrations of C-reactive protein peaked later on the 2nd postoperative day and were not able to confirm the severity of SIRS. Leukocyte counts were not significantly modified. Conclusions: PCT seems to be an appropriate marker to identify the early development of noninfectious postoperative severe SIRS after coronary artery bypass graft surgery with cardiopulmonary bypass. Copyright 2002, Elsevier Science (USA). All rights reserved.