Granulocyte colony-stimulating factor to prevent the progression of systemic nonresponsiveness in systemic inflammatory response syndrome and sepsis.
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Animals↗
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Results for “Systemic Inflammatory Response Syndrome”
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Shedding of L-selectin as a mechanism for reduced polymorphonuclear neutrophil exudation in patients with the systemic inflammatory response syndrome.
BACKGROUND: It has been recently shown that patients with the systemic inflammatory response syndrome (SIRS) have reduced neutrophil exudation. OBJECTIVE: To determine whether reduced neutrophil exudation, seen in patients with SIRS, is related to differential expression of cell adhesion molecules (CAMs), by studying endothelial and neutrophil CAM expression. SETTING: A tertiary care surgical intensive care unit in a university teaching hospital. DESIGN: Twenty-six patients with SIRS were compared with 18 healthy age-matched control subjects. Blister-type skin windows were created. Exudative neutrophils were harvested, and CAM expression was quantitated by using flow cytometry. Endothelial CAM expression was studied with immunohistochemical methods by using skin biopsy specimens that were taken following subdermal injections of saline solution or tumor necrosis factor alpha. RESULTS: Despite a significant reduction in neutrophil exudation in patients, we found no difference in the baseline expression of the endothelial intercellular adhesion molecule 1, P-selectin, or E-selectin in patients vs that in control subjects. There was a significant increase in E-selectin staining in response to recombinant human tumor necrosis factor alpha in patients with SIRS, but not in control subjects. However, up-regulation of P-selectin did not occur in patients in response to recombinant human tumor necrosis factor alpha, as was observed in control subjects. L-selectin expression on circulating neutrophils was lower in patients than in control subjects, while soluble serum L-selectin levels were higher. CONCLUSIONS: Alterations in neutrophil L-selectin, not endothelial CAMs, are important in decreased neutrophil exudation. Reduced levels of neutrophil L-selectin associated with increased levels of serum L-selectin in patients with SIRS suggest premature intravascular shedding of neutrophil L-selectin. This would compromise the initial interaction between neutrophils and the endothelium, and, consequently, impede exudation.
Case-Control Studies↗
[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↗
Energy metabolism of infants and children with systemic inflammatory response syndrome and sepsis.
OBJECTIVE: To evaluate whether critically ill children with systemic inflammatory response syndrome (SIRS) or sepsis have altered resting energy expenditure (REE) and substrate utilization. SUMMARY BACKGROUND DATA: Studies in adults with sepsis have shown increased energy expenditure and mobilization of endogenous fat. In infants and children, energy metabolism and substrate utilization during sepsis have not been characterized. METHODS: Metabolic studies were performed in 21 critically ill children with SIRS or sepsis. Twenty-one stable control children, matched for weight, were also studied. Seven patients required inotropic support and 17 received mechanical ventilation. Fifteen patients with SIRS had evidence of bacterial, fungal, or viral infection and were considered septic. Respiratory gas exchange was measured by computerized indirect calorimetry for 1 to 2 hours continuously. RESULTS: The REE of patients with SIRS or sepsis was not different from that of controls. Similarly, there were no differences in carbon dioxide production and oxygen consumption. Resting energy metabolism was not different between patients with SIRS and patients with sepsis. In addition, the presence of low platelet count or inotropic support did not affect resting energy metabolism. The median respiratory quotient of patients with SIRS or sepsis was 0.88 (range 0.75-1.12), indicating mixed utilization of fat and carbohydrate; this was not significantly different from that of controls. The Pediatric Risk of Mortality Score was not significantly correlated with REE or respiratory quotient. CONCLUSIONS: The energy requirements of children with SIRS or sepsis are not increased. Their resting metabolism is based on both carbohydrate and fat utilization. The authors speculate that these children divert the energy for growth into recovery processes.
Case-Control Studies↗
Systemic inflammatory response syndrome in the trauma intensive care unit: who is infected?
BACKGROUND: Systemic inflammatory response syndrome (SIRS) is common in trauma patients, and infection represents an important and treatable source of SIRS. C-Reactive protein (CRP), an acute phase protein, is elevated in infection and discriminates between infected and uninfected patients in other patient populations. Our goal was to examine the ability of CRP and other commonly used markers of infection (maximum temperature [Tmax], and white blood cell count [WBC]) to distinguish between infectious and noninfectious causes of SIRS. METHODS: This was a prospective study of a consecutive series of trauma patients who spent greater than 48 hours in the intensive care unit. Studied variables included CRP, Tmax, WBC, and culture-proven infection compared with standard definitions of infection and the presence of SIRS. The ability of these variables to correctly classify patients as infected (INF) or not infected was examined by using receiver operating characteristic curves. Values on the day of infection diagnosis in the INF group and on postadmission day 5 (the mean day of onset of infection in the INF group) in the not infected group were used. Multivariate discriminant analysis was used to examine the relative contributions of Tmax and CRP in predicting infection. Significance was defined as p < 0.05. RESULTS: Fifty-nine patients were admitted over a 4-month period. Of these, 35 patients (59%) had SIRS at the time of comparison (29 INF, 6 not infected). Thirty-three patients (56%) developed an infection. Both CRP and Tmax discriminated between patients with and without infection whereas WBC did not (areas under receiver operating characteristic curve: 0.86, 0.81, and 0.47, respectively). In patients with SIRS, cutoff values of 17 mg/dL for CRP (specificity 100%) and 102 degrees F for Tmax (specificity 83%) were identified. CRP added significant discriminatory power to Tmax in determining presence of infection in patients with SIRS (p = 0.003). CONCLUSION: Infection must be presumed to be the source of SIRS in patients with CRP more than 17 mg/dL and Tmax more than 102 degrees F after postinjury day 4. WBC is not useful in determining the presence of infection.
Adult↗
Systemic inflammatory response syndrome and surgical stress in thoracic surgery.
PURPOSE: To evaluate the clinical usefulness of postoperative systemic inflammatory response syndrome (SIRS) as an index of surgical stress in patients undergoing thoracic surgery. METHODS: Forty-five consecutive patients who underwent thoracic surgery with thoracotomy were enrolled. The SIRS criteria were examined daily during the first 7 postoperative days. The serum interleukin-6 (IL-6) level, operation time, intraoperative blood loss, amount of thoracic drainage, and C-reactive protein levels were also measured. RESULTS: Sixteen cases were categorized into the SIRS group, whereas 29 cases were categorized into the non-SIRS group. Among the patients who underwent thoracic surgery, the physiological responses of the patients to the surgery, such as serum IL-6 levels and C-reactive protein levels, were significantly higher in the SIRS group than in the non-SIRS group (P = .002 and .024, respectively). The serum IL-6 level on the first postoperative day was an independent factor associated with SIRS (95% CI 1.002-1.041; P = .030). Furthermore, there was a correlation between the number of SIRS days and the duration of the postoperative hospital stay (r = 0.379, P = .012). CONCLUSIONS: Our results demonstrated that SIRS reflected the degree of surgical stress, especially thoracotomic procedures, through the IL-6 levels, and affected the postoperative hospital stay. Systemic inflammatory response syndrome can be useful for the postoperative management of patients undergoing thoracic surgery.
Adult↗
[Systemic inflammatory response syndrome and disseminated intravascular coagulation: Sweet syndrome].
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Disseminated Intravascular Coagulation↗
Reduced ex vivo interleukin-8 production by neutrophils in septic and nonseptic systemic inflammatory response syndrome.
Ex vivo cytokine production by circulating lymphocytes and monocytes is reduced in patients with infectious or noninfectious systemic inflammatory response syndrome. Very few studies have addressed the reactivity of polymorphonuclear cells (PMN). To analyze further the relative contribution of systemic inflammatory response syndrome alone or in combination with infection we studied the interleukin-8 (IL-8) production by PMN isolated from patients who had undergone cardiac surgery with cardiopulmonary bypass (CPB) and patients with sepsis. Cells were activated with either lipopolysaccharide (LPS) or heat-killed streptococci. Compared with healthy controls, the release of IL-8 by PMN in both groups of patients was significantly reduced whether activated by LPS, independently of its concentration and origin, or by heat-killed streptococci. These observations suggest that stressful conditions related to inflammation, independently of infection, rapidly dampened the reactivity of circulating PMN. We investigated whether the observed diminished reactivity of PMN might reflect an endotoxin tolerance phenomenon. Our in vitro experiments with PMN from healthy controls indicated that PMN could not be rendered tolerant stricto sensu. However, our data suggested that LPS-induced mediators such as IL-10 may be responsible for the observed anergy in patients.
Adult↗
Improved outcome of APACHE II score-defined escalating systemic inflammatory response syndrome in patients post cardiac surgery in 1996 compared to 1988-1990: the ESSICS-study pilot project.
OBJECTIVE: Cardiac surgery using extracorporeal circulation leads to the release of cytokines and subsequently to a systemic inflammatory response syndrome, which is thought to be a negative prognostic factor for patients' outcome. A stratification for the risk of an escalating systemic inflammatory response syndrome had been achieved in a monocenter study carried out in 1988-1990, using APACHE II scoring on the morning of the 1st postoperative day. We now re-evaluated this concept prospectively in three independent centers. METHODS: The APACHE II based risk stratification was put to test in three independent heart surgery centers in the period from June to December 1996. Nine hundred and forty-five patients after elective cardiac surgery (excluding heart transplantation) with the assistance of the cardiopulmonary bypass were prospectively monitored. RESULTS: We found an increase in mortality with higher APACHE II score values determined on the 1st postoperative day. The mortality rose to nearly 50% with an APACHE II score of > or = 28. Patients at high risk for the development of a systemic inflammatory response syndrome (APACHE II score > or = 24) significantly differed from patients at lower risk (APACHE II score < 19) in the duration of mechanical ventilation and extracorporeal circulation, age and New York Heart Association (NYHA) classification (P < 0.05). CONCLUSION: The APACHE II score determined on the morning of the 1st postoperative day helps identifying the subgroup of patients with escalating systemic inflammatory response syndrome. Comparison with the data obtained in the years 1988-1990, suggests a better prognosis in the current trial for patients at high risk with a similar degree of escalating systemic inflammatory response syndrome.
APACHE↗
Systemic inflammatory response syndrome score at admission independently predicts infection in blunt trauma patients.
BACKGROUND: Systemic inflammatory response syndrome (SIRS) score has been demonstrated to be an accurate predictor of outcome in critical surgical illness. To our knowledge, there is a paucity of data using SIRS score as a tool to predict posttraumatic infection. Our goal was to determine whether the severity of SIRS score at admission is an accurate predictor of infection in trauma patients. METHODS: Prospective data were collected on 4,887 blunt trauma patients admitted to a primary adult resource center designated trauma center over an 18-month period. Patients were stratified by age and Injury Severity Score (ISS). SIRS score was calculated at admission. SIRS was defined as an SIRS score > or = 2. Each patient was screened for infection by an infectious disease specialist. Those at high risk for infection were then monitored daily throughout their hospitalization. Centers for Disease Control and Prevention guidelines were used to diagnose infection. RESULTS: Of the 4,887 patients, 1,850 (38%) were admitted > 24 hours and evaluated for subsequent infection (mean ISS, 16 +/- 9; mean age, 43 +/- 19, SD). Thirty-one percent (577) of the patients acquired an infection. The mean hospital length of stay (20.2 days vs. 6.5 days) and mortality (7.8% vs. 2.7%) were significantly greater in the infected group (p < 0.001). Of the four SIRS variables (temperature, heart rate, white blood cell count, and respiratory rate), hypothermia and leukocytosis were the most significant predictors of infection (p < 0.001) when adjusted for age and ISS. SIRS scores of > or = 2 were increasingly predictive of infection when analyzed by multiple logistic regression analysis. CONCLUSION: An admission SIRS score of > or = 2 is a significant independent predictor of infection and outcome in blunt trauma. Daily SIRS scores may be a meaningful method of assessing postinjury risk of infection, and may initiate earlier diagnostic intervention for determination of infection.
Adult↗
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↗
Fatal systemic inflammatory response syndrome following early bilateral femoral nailing.
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Accidents, Traffic↗
Polymorphonuclear leukocyte dysregulation during the systemic inflammatory response syndrome.
Altered polymorphonuclear leukocyte (PMN) function is thought to contribute to organ dysfunction during the systemic inflammatory response syndrome (SIRS). To test this hypothesis, we evaluated whole blood PMN function adherent to fibronectin or laminin in patients with mild or severe acute pancreatitis as a paradigm for sirs. Whole-blood PMN intracellular H2O2 production, expression of CD32w (Fc gamma R II), CD16 (Fc gamma R III), and phagocytosis were performed using dichlorofluorescein diacetate, fluorescein isothiocyanate-labeled anti-CD32w, CD16, and serum-opsonized fluorescent microspheres. Group I (n x 7) represents normal control individuals; group II (n x 11) represents patients with mild acute pancreatitis. Group III (n x 15) represents critically ill patients with severe acute pancreatitis. Adherence of PMN from groups I and II to matrix proteins resulted in a 5% to 20% increase in each PMN function assayed whereas adherence of PMN from group III to matrix proteins resulted in 50% to 75% increases in each PMN function assayed. Pertussis toxin, pentoxifylline, and dibutyryl cyclic adenosine monophosphate (cAMP) each reduced group I-II H2O2 production and phagocytosis. Pentoxifylline and dibutyryl cAMP but not pertussis toxin reduced group III H2O2 production. Both intracellular H2O2 and phagocytosis assays from group III but not groups I-II showed exaggerated upregulation when exposed to NaF (4 mmol/L). Anti-interleukin-6 reduced the increase in intracellular H2O2 production in group III patients and significantly altered the exaggerated oxidative response to NaF. Longitudinal studies of group III whole-blood PMN showed persistent upregulation of intracellular H2O2 production in those patients whose hospital courses were complicated by multiple system organ failure. These results demonstrate abnormal whole blood PMN function during the systemic inflammatory response syndrome in the presence of fibronectin, or laminin and that this is mediated in part via a pertussis toxin insensitive altered guanosine triphosphate-binding protein.
Cell Adhesion↗
Disseminated intravascular coagulation is a frequent complication of systemic inflammatory response syndrome.
To evaluate the role of disseminated intravascular coagulation (DIC) and to determine the influence of antithrombin, protein C, and plasminogen activator inhibitor 1 on multiple organ dysfunction syndrome (MODS) and outcome in patients with systemic inflammatory response syndrome (SIRS), we made a prospective cohort study. The study subjects consisted of thirty-five patients who exhibited two or more of the conditions of SIRS for more than three consecutive days. They were classified into subgroups of survivors (n = 13) and nonsurvivors (n = 22). The global coagulation and fibrinolytic markers, antithrombin, protein C, and plasminogen activator inhibitor 1 were measured on the day of the diagnosis of SIRS, and also on the 1st, 3rd, and 5th days. The results of these measurements, demographic data, criteria of severity, incidence of MODS were compared between the subgroups. For prediction of patient's death, a receiver operating characteristic (ROC) curve analysis was made. DIC was frequently associated with SIRS patients (29/35, 82.9%). A significant decrease in the DIC score was found in the survivors (p = 0.0001). None of them suffered from DIC on the 5th day. In the nonsurvivors, low levels of protein C and antithrombin and markedly high values of plasminogen activator inhibitor 1 continued up to the 5th day, no improvement of the DIC was observed during the study period and the number of the dysfunctioning organs were significantly higher than in the survivors. Plasminogen activator inhibitor 1 on the 5th day had prognostic value for the prediction of death on the SIRS patients. In conclusion, DIC occurs commonly in patients with SIRS and may be the main determinant for the outcome of these patients. Changes in antithrombin, protein C, and plasminogen activator inhibitor 1 are one of the aggravating factors of MODS. Furthermore, plasminogen activator inhibitor 1 is a good predictor of death in these patients.
APACHE↗
[SIRS (systemic inflammatory response syndrome): clinical entity, definitions, and the significance].
The clinical entity, definitions, and the significance of SIRS (systemic inflammatory response syndrome) were reviewed. The term, SIRS was proposed to define sepsis and its sequelae clearly in 1991, in order to make early detection of the disease possible, and to improve the ability to compare innovative potential diagnostic and therapeutic modalities by standardizing terms. Although the criteria of SIRS is not strict and too sensitive, SIRS has been shown to be useful as a warning sign of severe condition in clinical setting. We also discussed about a new concept, CARS (compensatory anti-inflammatory response syndrome), which was characterized as anti-inflammatory mediators-dominant condition, in this issue.
Cytokines↗
Recombinant bactericidal/permeability-increasing protein attenuates the systemic inflammatory response syndrome in lower limb ischemia-reperfusion injury.
OBJECTIVES: Hind limb ischemia-reperfusion (I/R) injury increases gut permeability, and resultant endotoxemia is associated with an amplified systemic inflammatory response syndrome leading to multiple organ dysfunction syndrome. We studied the potential role of recombinant bactericidal/permeability-increasing protein (rBPI(21) ), a novel antiendotoxin therapy, in modulating endotoxin-enhanced systemic inflammatory response syndrome in hind limb I/R injury. METHODS: In this prospective, randomized, controlled, experimental animal study, 48 male Wistar rats, weighing 300 to 350 g, were randomized to a control group (sham) and five groups undergoing 3 hours bilateral hind limb ischemia with 2 hours reperfusion (I/R) (n = 8 per group). The control and untreated I/R groups received thaumatin, a control-protein preparation, at 2 mg/kg. Treatment groups were administered rBPI(21) intravenously at 1, 2, or 4 mg/kg body weight at the beginning of reperfusion; an additional group was administered rBPI(21) intravenously at 2 mg/kg after 1 hour of reperfusion. Plasma interleukin-6 concentration was estimated by bioassay as a measure of systemic inflammation. Plasma endotoxin concentration was determined by use of an amebocyte lysate chromogenic assay. Crossreactive immunoglobulin G and M antibodies to the highly conserved inner core region of endotoxin were measured by use of an enzyme-linked immunosorbent assay. The lung tissue wet-to-dry weight ratio and myeloperoxidase concentration were used as markers of edema and neutrophil sequestration, respectively. RESULTS: I/R provoked highly significant elevation in plasma interleukin-6 concentrations (1351.20 pg/mL [860.16 - 1886.40 pg/mL]) compared with controls (125.32 pg/mL [87.76-157.52 pg/mL; P <.0001]), but treatment with rBPI(21) 2 mg/kg at onset of reperfusion (715.89 pg/mL [573.36-847.76 pg/mL]) significantly decreased interleukin-6 response compared with the nontreatment group ( P <.016). I/R increased plasma endotoxin concentrations significantly (21.52 pg/mL [6.20-48.23 pg/mL]), compared with control animals (0.90 pg/mL [0.00-2.30 pg/mL; P <.0001]), and treatment with rBPI(21) 4 mg/kg at reperfusion significantly decreased endotoxemia (1.30 pg/mL [1.20-2.20 pg/mL]), compared with the untreated group ( P <.001). The lung tissue myeloperoxidase level was significantly increased in the untreated I/R group (208.18% [128.79%-221.81%]), compared with in controls (62.00% [40.45%-80.92%; P <.0001]), and attenuated in those treated with rBPI(21) 2 mg/kg (129.54% [90.49%-145.78%; P <.05]). Data represent median and interquartile range, comparisons made with the nonparametric Mann-Whitney U test. CONCLUSIONS: These findings show that hind limb ischemia-reperfusion injury is associated with endotoxemia, elevations in plasma interleukin-6, and pulmonary leukosequestration. Treatment with rBPI(21) after ischemia reduces endotoxemia, the interleukin-6 response, and attenuates pulmonary leukosequestration in response to hind limb reperfusion injury.
Animals↗
Diffusive vs. convective therapy: effects on mediators of inflammation in patient with severe systemic inflammatory response syndrome.
OBJECTIVE: To compare two forms of continuous renal replacement therapy, continuous venovenous hemofiltration (CVVH) vs. continuous venovenous hemodialysis (CVVHD), in terms of the removal of inflammatory mediators from the blood of patients with systemic inflammatory response syndrome and acute renal failure. DESIGN: Randomized crossover, clinical study. SETTING: University teaching hospital. PATIENTS: Thirteen patients with systemic inflammatory response syndrome and acute renal failure receiving continuous renal replacement therapy. INTERVENTION: Patients were randomized to receive either convective clearance using CVVH or diffusive clearance using CVVHD for the first 24 hrs, followed by the other modality for 24 hrs. All treatments utilized AN69 hemofilters. CVVH was performed with an ultrafiltration rate of 2 L/hr and CVVHD with a dialysis outflow rate of 2 L/hr. MEASUREMENTS AND MAIN RESULTS: Plasma and ultrafiltrate concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, and sL-selectin were measured at 0, 1, 3, 6, 12, and 24 hrs by radioimmunoassay. Plasma endotoxin concentrations were also measured at 0, 12, and 24 hrs by chromogenic assay. CVVH was associated with a 13% decrease in plasma TNF-alpha concentrations compared with a 23% increase while on CVVHD (p < .05). Mean plasma concentrations of IL-6, IL-10, and sL-selectin were unchanged over time and between therapies. Only minimal amounts of mediators were recovered in the effluents with either therapy except for IL-6. The clearances for IL-6 were different between therapies, 1.9+/-0.8 (SD) mL/min for CVVHD and 3.3+/-1.5 mL/min for CVVH, (p< .01). Plasma endotoxin concentrations were not different between therapies. CONCLUSION: CVVH resulted in a decrease in plasma TNF-alpha concentrations as compared with CVVHD, while the type of transport mechanism used did not influence plasma concentrations of IL-6, IL-10, soluble L-selectin, or endotoxin. Differences in clearance for IL-6 between CVVH and CVVHD did not translate into significant changes in circulating IL-6 concentrations.
Acute Kidney Injury↗
Blockade of transdiaphragmatic lymphatic absorption reduced systemic inflammatory response syndrome during experimental peritonitis: evaluation with body oxygen kinetics in rats.
OBJECTIVE: To assess the effect of blockade of transdiaphragmatic lymphatic absorption of infected peritoneal fluid on systemic inflammatory response syndrome during experimental peritonitis by evaluating body oxygen kinetics in rats. DESIGN: Randomised controlled experimental study. SETTING: Teaching hospital, Turkey. MATERIAL: 30 Wistar-albino rats, 10 in each group. INTERVENTIONS: Control group, sham laparotomy; peritonitis alone group, faecal peritonitis induced by caecal puncture; and lymphatic blockade and peritonitis group, transdiaphragmatic lymphatic absorption was blocked by fibrosis created by a sheet of braided polyester (Mersilene) mesh, and peritonitis induced with caecal puncture. MAIN OUTCOME MEASURES: Aerobic culture of peritoneal contents and blood. Arterial and mixed venous blood gas analysis, plasma lactate concentrations. Indicators of body oxygen kinetics were calculated from these variables. RESULTS: Bacterial peritonitis was detectable in all 20 animals in the experimental groups. Blood cultures grew pathogens in 9/10 animals in the peritonitis alone group and 4/10 in the lymphatic blockade group (p = 0.057). Among the measured blood gas variables there were significant differences in PvO2 (p = 0.006) and in PaCO2 (p = 0.02), and as indicators of tissue perfusion and acidosis there were significant differences in all calculated blood gas variables and in plasma lactate concentration (p = 0.0001) between the two experimental groups. Hypoxia as judged by the oxygen utilisation coefficient of over 0.5 and oxygen saturation of mixed venous blood of less than 50%, eight animals were hypoxic in the peritonitis alone group compared with one in the lymphatic blockade group (p = 0.006). CONCLUSION: Animals in which transdiaphragmatic drainage was obstructed had fewer positive blood cultures and better body oxygen balance during peritonitis, indicating that blockade of transdiaphragmatic lymphatic absorption of peritoneal contents reduced systemic inflammatory response syndrome.
Absorption↗