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Results for “Systemic Inflammatory Response Syndrome”

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PubMed2002

Neutropenia and the development of the systemic inflammatory response syndrome.

OBJECTIVE: To determine outcome and natural course of systemic inflammatory response syndrome (SIRS) stages in adult febrile neutropenic patients. DESIGN AND SETTING: Retrospective cohort study in the medicine department and intensive care unit of a university hospital. PATIENT: Adults with cancer-related neutropenia and community-acquired fever. MEASUREMENTS AND RESULTS: Patients were classified on admission according to SIRS parameters, tumor type, and degree of neutropenia. Records of clinical and laboratory data during hospitalization were reviewed. Univariate and logistic regression analyses were performed. Seventy-nine events in 62 patients were analyzed. Overall mortality rate was 20.2% (16/79). Mortality increased as SIRS stage worsened on admission. No patients with stage 2 SIRS died (neutropenia and fever alone) but 11.1% of patients with SIRS 3, 43.4% with SIRS 4, 66.6% with sepsis induced hypotension, and 90% with septic shock. SIRS stage on admission was an independent predictor of death and was related directly to rate of progression to shock, i.e., none of the patients with SIRS 2, 2.7%(1/36) of those with SIRS 3, and 30.4% (7/23) of those admitted with SIRS 4. CONCLUSIONS: Mortality and progression to septic shock increased as more SIRS criteria were met on admission. SIRS stages could serve as a risk-assessing model in febrile neutropenic patients.

Analysis of Variance↗
PubMed2004

The clinical value of the systemic inflammatory response syndrome (SIRS) in abdominal aortic aneurysm repair.

OBJECTIVES: The systemic inflammatory response syndrome (SIRS) is common after major surgery. We examine the dynamics of SIRS in AAA patients, and assess the impact of the number of SIRS criteria on patient outcome. DESIGN: Prospective study of 151 consecutive patients with AAA, undergoing repair electively, urgently or with rupture. METHODS: SIRS scores and organ failure scores were recorded prospectively each day for all patients. Outcome measures included length of stay, evidence of organ failure and mortality. RESULTS: The majority of patients developed SIRS postoperatively. Elective patients with a cumulative SIRS score of > or =10 during postoperative days 1-4 were more likely to die, compared to patients with a SIRS score of <10 (p=0.02). The development of SIRS late in the postoperative period (day 5-10) was associated with adverse outcome (death) in elective patients (p=0.01). The actual number of SIRS criteria present did not significantly correlate with either outcome or the incidence of organ failure. CONCLUSIONS: SIRS is common in patients undergoing AAA repair. The SIRS score provides useful information regarding a patient's physiological state. High SIRS scores, and the development of SIRS late in the postoperative period are associated with adverse outcome in elective patients, and can therefore be used as an indicator of potential problems.

Aged↗
PubMed1996

Toward a theory regarding the pathogenesis of the systemic inflammatory response syndrome: what we do and do not know about cytokine regulation.

OBJECTIVES: The systemic inflammatory response syndrome (SIRS) is the massive inflammatory reaction resulting from systemic mediator release that may lead to multiple organ dysfunction. The objective of this review article is to analyze the roles of cytokines, cytokine production, and the relationship of cytokine production to the development of SIRS. DATA SOURCES: Previous research and clinical studies related to cytokines and their relationship to SIRS. STUDY SELECTION: From the studies reviewed, three critical questions are addressed. First, what is the definition of increased cytokine concentrations? Second, what other systemic illnesses besides sepsis can alter cytokine concentrations? Third, what are the right cytokines to measure? DATA SYNTHESIS: This article postulates a three-stage development of SIRS, in which stage 1 is a local production of cytokines in response to an injury or infection. Stage 2 is the protective release of a small amount of cytokines into the body's circulation. Stage 3 is the massive systemic reaction where cytokines turn destructive by compromising the integrity of the capillary walls and flooding end organs. CONCLUSIONS: While cytokines are generally viewed as a destructive development in the patient that generally leads to multiple organ dysfunction, cytokines also protect the body when localized. It will be necessary to study the positive effects of cytokines while also studying their role in causing SIRS. It will also be important to investigate the relationship between cytokines and their blockers in SIRS.

Animals↗
PubMedDate not supplied

Systemic inflammatory response syndrome treatment by powdered sorbent pheresis: the BioLogic-Detoxification Plasma Filtration System.

Systemic inflammatory response syndrome (SIRS) is one of the most common causes of death in intensive care unit patients. The detoxification plasma filtration (DTPF) system (HemoCleanse, Inc., West Lafayette, IN) combines the DT hemodiabsorption system in series with a push-pull pheresis PF system (a suspension of powdered sorbents surrounding 0.5 microm plasma filter membranes). Bidirectional plasma flow (at 80-100 ml/min) across the PF membranes provides direct contact between plasma proteins and powdered sorbents, as well as clearance of cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) at a rate of 15-25 ml/min, without evidence of saturation for 90 minutes. In a U.S. Food and Drug Administration approved study we treated eight patients with SIRS and organ failure with a single DTPF treatment, using powdered charcoal as sorbent in four patients and powdered charcoal and silica in four patients. Treatments proceeded for 6 hours with proper heparin anticoagulation (activated clotting time 250-300 sec) and appeared safe. All patients improved during the treatments and each had increased blood pressure and decreased need for pressor agents. Plasma cytokine levels stabilized or decreased during treatment and were significantly lower the morning after treatment. Multiple organ dysfunction (MOD) and Acute Physiology Chronic Health Evaluation II scores and organ function gradually improved in most patients, and two patients survived for more than 28 days and two for more than 14 days. The DTPF System may prove beneficial in treatment of patients with sepsis.

Adult↗
PubMed2004

Cutting edge: an endogenous pathway to systemic inflammatory response syndrome (SIRS)-like reactions through Toll-like receptor 4.

Systemic inflammatory response syndrome (SIRS) is typically associated with trauma, surgery, or acute pancreatitis. SIRS resembles sepsis, triggered by exogenous macromolecules such as LPS acting on Toll-like receptors. What triggers SIRS in the absence of infection, however, is unknown. In this study, we report that a SIRS-like response can be induced in mice by administration of soluble heparan sulfate, a glycosaminoglycan associated with nucleated cells and extracellular matrices, and by elastase, which cleaves and releases heparan sulfate proteoglycans. The ability of heparan sulfate and elastase to induce SIRS depends on functional Toll-like receptor 4, because mutant mice lacking that receptor or its function do not respond. These results provide a molecular explanation for the initiation of SIRS.

Animals↗
PubMed1997

Systemic inflammatory response syndrome and organ dysfunction following gastrointestinal surgery.

OBJECTIVES: Progression from systemic inflammatory response syndrome (SIRS) to sepsis, severe sepsis, and septic shock has been demonstrated in a variety of patients. However, the presence of SIRS alone was not helpful in predicting the development of multiple organ dysfunction syndrome (MODS) since SIRS includes many nonprogressive conditions. This study was conducted to investigate the clinical significance of SIRS in postoperative patients. DESIGN: Retrospective study. SETTING: The surgical department of a university hospital. PATIENTS: Two hundred ninety-two consecutive patients who received elective common gastrointestinal surgery (esophagectomy, pancreatoduodenectomy, hepatectomy, gastrectomy, colorectal resection, and laparoscopic cholecystectomy) between 1992 and 1995. INTERVENTIONS: Patients were analyzed for preoperative physiologic status, surgical stress parameters, and postoperative status of SIRS, complications, and end-organ dysfunction. MEASUREMENTS AND MAIN RESULTS: Duration of SIRS or positive criteria's number of SIRS after surgery significantly correlated with surgical stress parameters (blood loss/body weight and operation time) and peak serum C-reactive protein concentrations. SIRS that continued or reappeared after postoperative day 3 was an early sign of postoperative complications. SIRS continuing consecutively for 2 days after postoperative day 3 had a 70.6% positive predictive value and a 92.5% negative predictive value for postoperative complications. Septic complications and prolongation of SIRS were associated with MODS. Five of six patients who met the SIRS criteria for >30 days developed severe MODS, and three of them died. CONCLUSIONS: SIRS is a useful criterion for the recognition of postoperative complications and end-organ dysfunctions. Early recovery from SIRS may arrest the progression of organ dysfunction.

Aged↗
PubMed2005

[Clinical study on effects of ulinastatin on patients with systemic inflammatory response syndrome].

OBJECTIVE: To evaluate the value of ulinastatin in hindering systemic inflammatory response syndrome (SIRS) to proceed to multiple organ dysfunction syndrome (MODS). METHODS: Sixty patients were randomly divided into routine treatment group (n=30) and ulinastatin treatment group (n=30). Both groups were given routine treatment, while the patients of the ulinastatin treatment group were given ulinastatin (100 kU intravenously drip, once every 8 hours, and continued for 5 days) in addition. Additionally, 15 healthy persons were enrolled as normal control group. Temperature (T), heart rate (HR), respiration rate (RR) and white blood cell (WBC) count were observed everyday. The duration of SIRS, the number of organ dysfunction, and mortality were also compared. Serum C reactive protein(CRP), tumor necrosis factor-alpha (TNF-alpha), interleukin-6(IL-6) and IL-10 levels were measured before treatment and 5 days after in ulinastatin treatment group, routine treatment group, and in normal control group at the time of health examination. RESULTS: All of the SIRS markers were not different both in ulinastatin group and routine treatment group before treatment. T, RR, HR and WBC were reduced significantly after 3 days in ulinastatin groups(P<0.05 or P<0.01), but HR was not lowered significantly after 5 days and WBC after 7 days of treatment in regular treatment group (P<0.05 or P<0.01). All of the cytokines in ulinastatin treatment group and routine treatment group were higher than normal control group before treatment. Serum CRP, TNF-alpha and IL-6 levels were reduced significantly after 5 days of treatment in both ulinastatin treatment group and routine treatment group(P<0.01), but in ulinastatin treatment group the reduction was faster than routine treatment group(both P<0.01). IL-10 level was elevated significantly after treatment in ulinastatin treatment group(P<0.01), but it showed no significant change in routine treatment groups(P>0.05). The number of patients with duration of SIRS longer than 3 days were fewer and the incidence of MODS was lower in ulinastatin treatment group than those in routine treatment group(10.00% vs. 36.67%, P<0.05), and the fatality rate was reduced significantly with ulinastatin(3.33% vs. 20.00%, P<0.05). CONCLUSION: Ulinastatin significantly improves the inflammatory symptom and signs of SIRS, such as T, HR, RR, and WBC, inhibits the production of inflammatory cytokines, and enhance the anti-inflammatory cytokines in the treatment of SIRS. It can effectively prevent SIRS to proceed to MODS.

Adult↗
PubMed2004

[Coagulation dysfunctions in patients with systemic inflammatory response syndrome].

OBJECTIVE: To study the effects of coagulation dysfunctions on patients with the development of systemic inflammatory response syndrome (SIRS). METHODS: All the patients studied were divided into 2 groups: SIRS and non-SIRS according to the criteria for selection of SIRS. The SIRS group included 100 patients and the non-SIRS group 50 patients. A control group included 50 healthy adults. SIRS group was further divided into two subgroups: survivor and non-survivor. Levels of platelet (PLT), D-dimer, protein C (PC), protein S (PS), antithrombin III (ATIII), thrombomodulin (TM), tissue plasminogen activator (TPA), plasminogen-activator inhibitor (PAI-1), prothrombin test (PT), thrombin time (TT), activated partial thromboplastin time (APTT) and fibrinogen (FBG) were measured in all the patients and healthy persons. RESULTS: (1) Levels of TT, APTT, PT, D-dimer, TM, PAI-1 were significantly higher in SIRS than those in non-SIRS and the control group (P < 0.05). Levels of PC, PS, TPA, PLT, FBG were significantly lower in SIRS group than those in non-SIRS and the control group (P < 0.05). (2) Levels of ATIII were not different among SIRS, non-SIRS and the control group (P > 0.05). (3) Survivors levels of D-dimer, APTT and PAI-1 in SIRS group were significantly higher than there in non-survivors (P < 0.05); they were both negatively correlated with the prognosis of SIRS (P < 0.01). CONCLUSIONS: (1) There are dysfunctions of coagulation in patients with systemic inflammatory response syndrome. (2) Fibrinolytic system plays an important role in the development of SIRS. (3) Levels of PAI-1 and D-dimer are both negatively correlated with the prognosis of SIRS.

Adult↗
PubMed1998

Lymph of patients with a systemic inflammatory response syndrome inhibits lipopolysaccharide-induced cytokine production.

In patients with systemic inflammatory response syndrome (SIRS), tolerance of peripheral blood mononuclear cells to a second challenge with lipopolysaccharide (LPS) has been described. Thoracic duct lymph transports LPS and represents the extravascular, interstitial fluid compartment of the body. The aim of this study was to determine the capacity of lymph to influence LPS-induced cytokine production in vitro. Thoracic duct lymph was obtained from patients with SIRS and without SIRS (controls). The effect of lymph and simultaneously collected plasma on LPS-induced cytokine production by normal peripheral blood mononuclear cells was assessed. Both lymph and plasma of patients with SIRS reduced LPS-induced tumor necrosis factor-alpha and interleukin-6 production (P < .01); lymph of controls also inhibited cytokine production (P < .01), although to a lesser extent. This study suggests that LPS tolerance may occur both in the intra- and extravascular compartments.

Acute-Phase Proteins↗
PubMed2000

Procalcitonin (PCT) in cardiac surgery: diagnostic value in systemic inflammatory response syndrome (SIRS), sepsis and after heart transplantation (HTX).

PURPOSE: Since it is of great importance to distinguish between a systemic inflammatory response syndrome (SIRS) and an infection caused by microbes especially after heart transplantation (HTX), we examined patients following heart surgery by determining procalcitonin (PCT), because PCT is said to be secreted only in patients with microbial infections. METHODS: Sixty patients undergoing coronary artery bypass grafting (CABG) and 14 patients after heart transplantation were included in this prospective study. In the CABG group we had 30 patients without any postoperative complications (group A). Furthermore we took samples of 30 patients who suffered postoperatively from a sepsis (group B, n=15) or a systemic inflammatory response syndrome (C, n=15). In addition we measured the PCT-levels in 65 blood samples of 14 patients after heart transplantation (Group I: rejection > IIa, II: viral infection (CMV), III: bacterial/fungal infection, IV: controls). RESULTS: In all patients of group A the pre- and intraoperative PCT-values and the measurement at arrival on intensive care unit (ICU) were less than 0.2 ng/ml. On the second postoperative day the PCT-value was 0.33+/-0.15 ng/ml in the control group. At the same time it was 19.6+/-6.2 ng/ml in sepsis and 0.7+/-0.4 ng/ml in systemic inflammatory response syndrome patients (P<0.05). In transplanted patients we could find the following PCT-values: Gr.I: 0.18+/-0.06 II: 0.30+/-0.09 III: 1.63+/-1.16 IV: 0.21+/-0.09 ng/ml (P<0.05 comparing group III with I, II and IV). CONCLUSIONS: These results show that extracorporeal circulation (ECC) and systemic inflammatory response syndrome do not initiate a PCT-secretion. Septic conditions cause a significant increase of PCT. In addition, PCT is a reliable indicator concerning the essential differentiation of bacterial or fungal--not viral--infection and rejection after heart transplantation.

Aged↗
PubMedDate not supplied

Suppression of postoperative systemic inflammatory response syndrome with clarithromycin following lung cancer surgery.

We examined whether clarithromycin (CAM), a 14-membered macrolide, can control the postoperative systemic inflammatory response syndrome that occurs following lung cancer surgery. In the control group (n = 16), prophylactic antibiotics (flomoxef) were administered for 4-7 days following surgery. In the CAM group (n = 10), 400 mg/day of CAM were administered orally for 14 days prior to surgery and for 7 days following surgery, in addition to the postoperative administration of flomoxef. The incidence and duration of the systemic inflammatory response syndrome in the CAM group (30%, 0.3 days) were significantly lower than those in the control group (81%, 1.6 days). There were no significant differences between the control and CAM groups in both the amount and frequency of nonsteroidal anti-inflammatory drugs following surgery. In conclusion, our study suggests that CAM may suppress the postoperative systemic inflammatory response syndrome in lung cancer patients.

Adult↗
PubMed2003

Therapeutic potential for transient inhibition of adenosine deaminase in systemic inflammatory response syndrome.

OBJECTIVE: We sought to determine the potential usefulness of 2'-deoxycoformycin (pentostatin), an inhibitor of adenosine deaminase, as a postinsult, or prophylactic treatment for systemic inflammatory response syndrome resulting from fecal peritonitis. DESIGN: Prospective, randomized, controlled experiment. SETTING: Small animal basic science laboratory. SUBJECTS: Male Spague-Dawley rats, weighing 300 to 350 g. INTERVENTIONS: Rats with fecal peritonitis (intraperitoneal cecal slurry) were treated with 1 mg/kg pentostatin intraperitoneally 24 hrs before, or intravenously when signs of illness presented (2 hrs after induction of peritonitis). Signs of illness included tachycardia, tachypnea, and leukopenia. All rats received 50 mL/kg 0.9% saline resuscitative fluid at 2 hrs. MEASUREMENTS AND MAIN RESULTS: Survival to day 6 was 100% in nonseptic sham rats, but 33% in untreated septic rats. In rats given pentostatin either 2 hrs after the insult, or 24 hrs before the insult, 6-day survival improved to 81% and 78%, respectively. Histology revealed diffuse peritonitis, and evidence of systemic inflammatory response syndrome, including local and distant site vascular damage and leukocyte activation. These responses to the septic challenge were abrogated by pentostatin treatment. Return of significant amount of tissue adenosine deaminase activity by 24 hrs and later recovery of white blood cell counts argue against any potential for inappropriate immunosuppression by pentostatin. CONCLUSIONS: These data indicate that the novel use of pentostatin to prevent systemic inflammatory response syndrome secondary to fecal peritonitis shows uncommon promise as a therapeutic tool. All indices of systemic inflammatory response syndrome were abrogated and survival improved when pentostatin was not given until after signs of the illness became manifest. Because protection was afforded with treatment 24 hrs in advance of the inciting insult, pentostatin also has the unique potential for use as a true prophylactic agent.

Adenosine Deaminase↗
PubMed1995

Prognostic value of assessing contact system activation and factor V in systemic inflammatory response syndrome.

OBJECTIVE: To test if serially sampled determinations of the contact system proteins and factor V have prognostic value for death in patients who develop the systemic inflammatory response syndrome. DESIGN: Prospective, observational study with sequential measurements in an inception cohort. SETTING: Medical intensive care unit (ICU) in a community hospital. PATIENTS: Over a 1-yr period, a population base sample of 23 patients was selected from all ICU admissions who met established criteria for the systemic inflammatory response syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Components of the contact system, factor XII, prekallikrein, high-molecular-weight kininogen, factor XI, alpha 2-macroglobulin-kallikrein complexes and factor V values were measured in plasma samples collected serially (day of admission, and at 2, 12, 24, 48 and/or 72 hrs or at discharge). Data were analyzed to determine if admission values or serially obtained values within 48 hrs were useful in predicting outcome. Fourteen patients survived and nine died. At admission, in all patients, assay values indicated that prekallikrein, high-molecular-weight kininogen, and factor V were significantly lower than normal (as observed in a range of 20 to 23 healthy adults), alpha 2-macroglobulin-kallikrein complexes were higher than normal, while concentrations of factor XII and factor XI were in the normal range. No differences were detected in the admission values between survivors and nonsurvivors, nor between patients with positive or negative blood cultures. However, subsequent values demonstrated a difference in values between survivors and nonsurvivors. Survivors showed improvement in high molecular weight kininogen values and higher than normal factor V values, as compared with nonsurvivors. CONCLUSIONS: Low or persistently low serial factor XII, high-molecular-weight kininogen and factor V values are associated with a poor prognosis, whereas high or increasing values of factor XII, high-molecular-weight kininogen, prekallikrein, and factor V all correlate with a favorable outcome.

Aged↗
PubMed1997

[Clinical study of systemic inflammatory response syndrome and multiple organ dysfunction syndrome in critically patients].

We defined the epidemiology of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in critically ill patients, and evaluated the procession from SIRS to MODS and the therapeutic strategies. 230 patients were studied prospectively until discharge or death. On admission, the morbidity rate of SIRS was 71.3%. The mortality rate of the patients with SIRS was 18.9%. MODS was developed in 65 patients (28.3%), and 33 patients dided (50.8%). In SIRS patients with non-infectious SIRS, sepsis and septic shock, the morbidity rates of MODS were 22.8%, 61.1% and 85.7%, and the mortality rates were 11.4%, 30.6% and 50.0% respectively. The outcome of critically ill patients may be improved if SIRS is early diagnosed and the body inflammatory response is reglulated properly.

China↗
PubMed1996

Immunologic dissonance: a continuing evolution in our understanding of the systemic inflammatory response syndrome (SIRS) and the multiple organ dysfunction syndrome (MODS)

Our current understanding of sepsis and multiple organ dysfunction needs to be revised, as the uniformly negative results of new therapies for these disorders suggest. Previous theories for the pathogenesis of these conditions are incomplete; reasons for this include the following. First, the surrogate models that have been used to study these disorders are not analogous to the clinical situation. Second, patients who have less severe manifestations of these diseases are often overlooked. And third, patients' preexisting conditions have not been taken into account. Considerable new evidence indicates that, in addition to a massive proinflammatory reaction, a compensatory anti-inflammatory response contributes to the onset of these disorders. At a local site of injury or infection and during the initial appearance of pro- and anti-inflammatory mediators in the circulation, the beneficial effects of these mediators outweigh their harmful effects. Only when the balance between these two forces is lost do these mediators become harmful. Sequelae of an unbalanced systemic proinflammatory reaction include shock, transudation into organs, and defects in coagulation. An unbalanced systemic compensatory anti-inflammatory response can result in anergy and immunosuppression. The proinflammatory and anti-inflammatory forces may ultimately reinforce each other, creating a state of increasingly destructive immunologic dissonance.

Humans↗