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OBJECTIVE: Evaluation of selective decontamination of the digestive tract (SDD) on late mortality in ventilated trauma patients in an intensive care unit (ICU). METHODS: A multicenter, randomized controlled trial was undertaken in 401 trauma patients with Hospital Trauma Index-Injury Severity Score of 16 or higher. Patients were randomized to control (n=200) or SDD (n=201), using polymyxin E, tobramycin, and amphotericin B in throat and gut throughout ICU treatment combined with cefotaxime for 4 days. Primary endpoint was late mortality excluding early death from hemorrhage or craniocerebral injury. Secondary endpoints were infection and organ dysfunction. RESULTS: Mortality was 20.9% with SDD and 22.0% in controls. Overall late mortality was 15.3% (57/372) as 29 patients died from cerebral injury, 16 SDD and 13 control. The odds ratio (95% confidence intervals) of late mortality for SDD relative to control was 0.75 (0.40-1.37), corresponding to estimates of 13.4% SDD and 17.2% control. The overall infection rate was reduced in the test group (48.8% vs. 61.0%). SDD reduced lower airway infections (30.9% vs. 50.0%) and bloodstream infections due to aerobic Gram-negative bacilli (2.5% vs. 7.5%). No difference in organ dysfunction was found. CONCLUSION: This study demonstrates that SDD significantly reduces infection in multiple trauma, although this RCT in 401 patients was underpowered to detect a mortality benefit.

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OBJECTIVE: Critical illness-related colonic ileus (CIRCI) is characterized by the non-passage of stools in critically ill patients as a result of the absence of prokinetic movements of the colon, while the upper gastrointestinal tract functions properly and mechanical ileus is absent: We investigated whether neostigmine resulted in defecation in patients with CIRCI. DESIGN: Double-blinded, placebo-controlled prospective study. SETTING: Eighteen-bed intensive care unit. PATIENTS: Thirty ventilated patients with multiple organ failure with CIRCI for > 3 days. INTERVENTION: Continuous intravenous administration of neostigmine 0.4-0.8 mg/h over 24 h, or placebo. MEASUREMENTS AND RESULTS: Time to first defecation and adverse reactions were recorded. Thirty patients were randomized, 24 could be evaluated. The mean prestudy time was 5 days, mean APACHE II score on admission was 23.2, and mean MOF score on the day of the study was 6.4. Of the 13 patients receiving neostigmine, 11 passed stools, whereas none of the placebo-treated patients passed stools (P < 0.001). After 24 h, the non-responders received in a cross-over fashion neostigmine or placebo respectively. Eight out of the 11 neostigmine patients now passed stools (mean 11.4 h), and none of the placebo patients. Overall, in none of the patients did passage of stools occur during placebo infusion, whereas 19 of the 24 neostigmine-treated patients had defecation (79%). No acute serious adverse effects occurred, but three patients had ischemic colonic complications 7-10 days after treatment. CONCLUSION: Continuous infusion of 0.4-0.8 mg/h of neostigmine promotes defecation in ICU patients with a colonic ileus without important adverse reactions.

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OBJECTIVE: Whole-body hyperthermia (WBH) in combination with chemotherapy is a relatively new promising treatment modality for patients with cancer. The objective of this report is to present the development of an acute systemic inflammatory response syndrome (SIRS) with multiple organ dysfunction syndrome (MODS) following WBH in combination with chemotherapy. Although WBH can also induce cytokine production, MODS has not been described before in association with WBH. DESIGN: Case report. The patient was treated with WBH (core temperature 41.8 degrees C using a radiant heat device (Aquatherm) ) in combination with polychemotherapy (ifosfamide, carboplatin and etoposide (ICE) ) in the context of a clinical trial for metastatic sarcomas. SETTING: Department of medical oncology and intensive care unit of a university hospital. PATIENT: A 58-year-old Caucasian woman treated for disseminated leiomyosarcoma of the uterus, who developed SIRS with brain dysfunction, hypotension, respiratory failure and renal dysfunction following WBH/ICE. INTERVENTIONS: She was successfully treated in the intensive care unit by mechanical ventilation, inotropics and antibiotics. MEASUREMENTS AND RESULTS: There was a remarkable recovery within 2 days: she regained full conciousness, could be extubated, inotropic support was stopped and creatinine levels returned to pre-treatment levels. All cultures remained sterile. After almost complete recovery, 5 days later a second episode of fever during neutropenia occurred and, despite antibiotic treatment, she died of Bacteroides distasonis sepsis. CONCLUSION: WBH should be added as a new cause to the already known list of physical-chemical insults which can result in MODS.

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Information about the patient's health status and about medical problems in general, play an important role in stratifying a patient population for quality assurance of intensive care. A terminological system which supports both the description of health problems for daily care practice and the aggregation of diagnostic information for evaluative research, is desirable for description of the patient population. This study describes the engineering of an ontology that facilitates a terminological system for intensive care diagnoses. We analyzed the criteria for such an ontology and evaluated existing terminological systems according to these criteria. The analysis shows that none of the existing terminological systems completely satisfies all our criteria. We describe choices regarding design, content and representation of a new ontology on which an adequate terminological system is based. The proposed ontology is characterized by the explicit and formal representation of the domain model, the metaspecification of its concepts, the vocabulary to define concepts and the nomenclature to support the composition of new concepts.

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BACKGROUND: Food in the intestine drives the enterohepatic circulation of bile components. OBJECTIVE: We investigated whether parenteral or enteral delivery of nutrients alters serum and biliary lipids in critically ill patients. DESIGN: Eight intensive care unit (ICU) patients who had received >/= 5 d of total parenteral nutrition (TPN) were compared with 8 ICU patients who had fasted for >/=5 d. Both groups were studied before and after 5 d of enteral nutrition (EN). Each patient served as his or her own control. Duodenal bile was analyzed for biliary lipid content and serum lipids were determined simultaneously. Duodenal bile samples from 18 healthy persons served as controls. RESULTS: Bile salt concentrations in all ICU patients were 17% of control values before EN (P < 0.005) and 34% of control values after 5 d of EN (P < 0.005). Phospholipid concentrations were 12% of control before EN (P < 0. 0005) but increased almost 4-fold after EN (P < 0.0005). Biliary cholesterol concentrations were 20% of control values before EN (P < 0.001) and did not improve afterward. No difference in bile composition was observed between fasted ICU patients and those who received TPN. The inverse correlation between the severity of illness and biliary lipid concentrations observed before EN disappeared with enteric stimulation. The low serum concentrations of HDL cholesterol and apolipoprotein A-I increased significantly with EN in all ICU patients. CONCLUSION: Lack of EN during critical illness was associated with profound decrements in biliary lipid concentrations that normalized partially after 5 d of EN. We hypothesize that loss of enteric stimulation in ICU patients impairs hepatic lipid metabolism.

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BACKGROUND: To compare continuous cardiac output obtained by simulation of an aortic input impedance model to bolus injection thermodilution (TDCO) in critically ill patients with septic shock. METHODS: In an open study, mechanically ventilated patients with septic shock were monitored for 1 (32 patients), 2 (15 patients), or 3 (5 patients) days. The hemodynamic state was altered by varying the dosages of dopamine, norepinephrine, or dobutamine. TDCO was estimated 189 times as the series average of four automated phase-controlled injections of iced 5% glucose, spread equally over the ventilatory cycle. Continuous model-simulated cardiac output (MCO) was computed from radial or femoral artery pressure. On each day, the first TDCO value was used to calibrate the model. RESULTS: TDCO ranged from 4.1 to 18.2 l/min. The bias (mean difference between MCO and TDCO) on the first day before calibration was -1.92 +/- 2.3 l/min (mean +/- SD; n = 32; 95% limits of agreement, -6.5 to 2.6 l/min). The bias increased at higher levels of cardiac output (P < 0.05). In 15 patients studied on two consecutive days, the precalibration ratio TDCO:MCO on day 1 was 1.39 +/- 0.28 (mean +/- SD) and did not change on day 2 (1.39 +/- 0.34). After calibration, the bias was -0.1 +/- 0.8 l/min with 82% of the comparisons (n = 112) < 1 l/min and 58% (n = 79) < 0.5 l/min, and independent of the level of cardiac output. CONCLUSIONS: In mechanically ventilated patients with septic shock, changes in bolus TDCO are reflected by calibrated MCO over a range of cardiac output values. A single calibration of the model appears sufficient to monitor continuous cardiac output over a 2-day period with a bias of -0.1 +/- 0.8 l/min.

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OBJECTIVE: To determine whether translocation of bacteria or endotoxin occurred into the thoracic duct in patients with multiple organ failure (MOF). SUMMARY BACKGROUND DATA: Translocation of bacteria or endotoxin has been proposed as a causative factor for MOF in patients without an infectious focus, although it has rarely been demonstrated in patients at risk for MOF. Most studies have investigated the hematogenic route of translocation, but it has been argued that lymphatic translocation of bacteria or endotoxin by the thoracic duct is the major route of translocation. METHODS: The thoracic duct was drained for 5 days in patients with MOF caused either by generalized fecal peritonitis (n = 4) or by an event without clinical and microbiologic evidence of infection (n = 4). Patients without MOF who were undergoing a transthoracic esophageal resection served as controls. In lymph and blood, concentrations of endotoxin, proinflammatory cytokines, and antiinflammatory cytokines were measured. RESULTS: Endotoxin concentrations in lymph and blood of patients with MOF ranged from 39 to 63 units per liter and were not significantly different from concentrations in patients without MOF. The quantity of endotoxin transported by the thoracic duct in the study group was small. In patients with MOF, low levels of proinflammatory cytokines and high levels of antagonists of these cytokines were found. CONCLUSION: This study provides evidence that translocation (especially of endotoxin) occurs into the thoracic duct. However, these data do not support the concept that the thoracic duct is a major route of bacterial translocation in patients with MOF.

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BACKGROUND: Studies to assess the prognostic value of early neurological and neurophysiological findings in patients with anoxic-ischaemic coma have not led to precise, generally accepted, prognostic rules. We did a systematic review of the relevant literature to assess whether such rules could be derived from the combined results of these studies. METHODS: From Medline and Embase databases we selected studies concerning patients older than 10 years with anoxic-ischaemic coma in which findings from early neurological examination, electroencephalogram (EEG), or somatosensory evoked potentials (SSEP) were related to poor outcome--defined as death or survival in a vegetative state. We selected variables with a specificity of 100% for poor outcome in all studies, and expressed the overall prognostic accuracy of these variables as pooled positive-likelihood ratios and as 95% CIs of the pooled false-positive test rates. FINDINGS: In 33 studies, 14 prognostic variables were studied, three of which had a specificity of 100%: absence of pupillary light reflexes on day 3 (pooled positive-likelihood ratio 10.5 [95% CI 2.1-52.4]; 95% CI pooled false-positive test rate 0-11.9%); absent motor response to pain on day 3 (16.8 [3.4-84.1]; 0-6.7%); and bilateral absence of early cortical SSEP within the first week (12.0 [5.3-27.6]; 0-2.0%). EEG recordings with an isoelectric or burst-suppression pattern had a specificity of 100% in five of six relevant studies (pooled positive-likelihood ratio 9.0 [2.5-33.1]; 95%CI pooled false-positive test rate 0.2-5.9%). These characteristics were present in 19%, 31%, 33%, and 33% of pooled patient populations, respectively. For the 11 SSEP studies, results did not significantly differ between studies in which the treating physicians were or were not masked from the test result, prospective and retrospective studies, studies with short and long follow-up periods, and studies with high or low overall poor outcome. INTERPRETATION: SSEP has the smallest CI of its pooled positive-likelihood ratio and its pooled false-positive test rate. Because evoked potentials are also the least susceptible to metabolic changes and drugs, recording of SSEP is the most useful method to predict poor outcome.

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In 2 patients with severe haemorrhage (a 63-year-old man with haemophilia A (the factor VIII level was 29%) and a 44-year-old woman), of an inhibitory antibody against factor VIII was diagnosed. The development of recombinant factor VIIa (eptacog alpha) has made available a new therapeutic option for patients with an inhibitory antibody against a coagulation factor. Both patients were treated successfully with the new factor after other forms of treatment had failed. The new concept of the coagulation cascade on which the treatment with eptacog alpha is based assumes that the lack of an amplifying loop in the coagulation which takes place via factor IX (in combination with factor VIII) can be compensated by extra stimulation of the principal route (tissue factor-factor VIIa --> factor X) by pharmacological amounts of factor VIIa.

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Disseminated intravascular coagulation (DIC) can be caused by a variety of diseases. Experimental models of DIC have provided substantial insight into the pathogenesis of this disorder, which may ultimately result in improved treatment. Disseminated coagulation is the result of a complex imbalance of coagulation and fibrinolysis. Simultaneously occurring tissue factor-dependent activation of coagulation, depression of natural anticoagulant pathways and shutdown of endogenous fibrinolysis all contribute to the clinical picture of widespread thrombotic deposition in the microvasculature and subsequent multiple organ failure. Cornerstone for the treatment of DIC is the optimal management of the underlying disorder. At present, specific treatment of the coagulation disorders themselves is not based on firm evidence from controlled clinical trials. Plasma and platelet transfusion are used in patients with bleeding or at risk for bleeding and low levels of coagulation factors or thrombocytopenia. The role of heparin and low molecular weight heparin is controversial, but their use may be justified in patients with active DIC and clinical signs of extensive fibrin deposition such as those with meningococcal sepsis. There is some evidence to indicate that low molecular weight heparin is as effective as unfractionated heparin but may be associated with a decreased bleeding risk. Antithrombin III (AT III) replacement appears to be effective in decreasing the signs of DIC if high doses are administered, but effects on survival or other clinically significant parameters are at best uncertain. If AT III supplementation is used, the dosage should be selected to achieve normal or supranormal plasma levels of 100% or higher. Results of studies on protein C concentrate, thrombomodulin or inhibitors of tissue factor are promising, but the efficacy and safety of these novel strategies remains to be established in appropriate clinical trials.

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OBJECTIVE: To assess the agreement between the functions of seven configurations of Patient Data Management Systems (PDMS) and the Dutch specifications prepared by the users prior to use. DESIGN: An observational descriptive study with hospital visits of seven configurations of five different PDMS systems including three commercial systems and two locally developed systems. SETTING: Seven Dutch level I intensive care units in university and teaching hospitals. MEASUREMENTS AND RESULTS: A substantial disagreement was found between the Dutch specifications and the actual functions of the PDMS configurations tested. Between the PDMS configurations, major differences in key features, including "automated charting", "information and care planning", and "management information", were observed. Automated charting is adequately supported by the three commercial systems. All configurations tested had limited functions supporting care planning. In none of the configurations tested was the required function present to support unit management with reports on resource utilisation and outcome performance. The automatic calculation of prognostic scores was either absent or incorrect. The implementation, the (continuous) configuration and the training required a substantial investment in costs and human resources. CONCLUSION: Today, none of the PDMSs tested satisfy the Dutch specifications. This can be explained by technical impossibilities of the systems and shortcomings in the actual configuration or in the unit organisation. The PDMS might become a valuable tool in improving the quality of ICU practice, but full implementation of these systems according to the specifications still has a long way to go.

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The aim of this study was to investigate the effects of a gelatin-based plasma expander on blood coagulation and haemostasis in human subjects. Six healthy men were studied in a randomised, controlled cross-over study to investigate the effects of a 60 min intravenous infusion of either 1 l gelatin-based plasma substitute (Gelofusine) or 0.9% NaCl (control). The infusion of gelatin resulted in a 1.7 fold increase in bleeding time at 60 min and a 1.4 fold increase at 120 min, while saline had no effect (p <0.05). Aggregation studies revealed a significant impairment of ristocetin-induced platelet aggregation (p <0.05), associated with a substantial decrease of vWF:ag (-32% vs. -5%, p <0.05) and ristocetin co-factor (-29% vs. +1%, p <0.05) and without in vitro impairment of the platelet glycoprotein 1b receptor. Gelatin caused a decrease in thrombin-antithrombin complexes (-45% vs. -4%, p <0.05) and F1+2 (-40% vs. +1%, p <0.05). The decrease in circulating levels of vWF:ag, vWF R:Co, thrombin-antithrombin complexes and F1+2 was more than could be expected by the calculated plasma-dilution generated by Gelofusine. Our results demonstrated that the administration of a gelatin-based plasma substitute results in a significant impairment of primary haemostasis and thrombin generation. The defect in primary haemostasis appears to be related to a gelatin-induced reduction in von Willebrand factor, whereas the decreased thrombin generation may be due to the dilution of coagulation factors induced by Gelofusine.

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In the present in vitro study we investigated filtration and adsorption of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) during predilution and postdilution hemofiltration with polysulfone, polyacrylonitrile, polyamide and cellulose triacetate membranes. The median sieving coefficient (SC) for all membranes was 0.0 for TNF-alpha, below 0.15 for IL-6 and below 0.15 for IL-8 during postdilution hemofiltration. Differences in SC between filtration modes were less than 0.05. Maximal differences in SC between membranes were 0.11 for IL-6, 0.0 for TNF-alpha, and 0.11 for IL-8. The progressive decrease in cytokine concentrations was identical between the two filtration modes and most pronounced with the polyacrylonitrile membrane (reduction 77% for IL-6, 39% for TNF-alpha and 95% for IL-8 after 4 h of hemofiltration). The relative contribution of adsorption to the reduction in cytokines was 100% for TNF-alpha for all membranes, between 53 (cellulose triacetate) and 83% (polyacrylonitrile) for IL-6, and for IL-8 between 0 (polysulfone) and 100% (polyacrylonitrile). In conclusion, the reduction in TNF-alpha, IL-6 and IL-8 was most impressive with the polyacrylonitrile membrane after 4 h of hemofiltration and was largely due to adsorption. Adsorption of TNF-alpha, IL-6 and IL-8 was also seen with the other membranes. None of the membranes filtered TNF-alpha. Sieving of IL-6 and IL-8 was low for all membranes with only marginal differences between membranes or between filtration modes.

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BACKGROUND: A body of evidence exists for the occurrence of bacterial translocation and its relationship to multiple organ failure (MOF). METHODS: Relevant articles on bacterial translocation (the phenomenon defined as the passage of microbes and endotoxin across the intestinal barrier) in patients prone to develop MOF and in representative animal studies were selected. To interpret and evaluate the evidence for bacterial translocation in current literature, the endpoints generally used are discussed. RESULTS: Fractional data from individual manuscripts were tabulated and assessed for statistical significance with chi 2 analysis. Various clinically relevant stimuli, postulated as important causative factors for the development of MOF, appeared to be interrelated and related to bacterial translocation itself. CONCLUSIONS: Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.

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Aspiration of oropharyngeal and/or gastrointestinal (GI) contents is the main cause of ventilator-associated pneumonia. A number of nonantibiotic measures have been proposed to prevent aspiration eg, drainage of subglottic secretions or the semirecumbent position or to prevent gastric microbial overgrowth by stress-ulcer prophylaxis with sucralfate or early enteral feeding. Critical review of the studies shows that subglottic drainage does not prevent colonization or infection of the respiratory tract with intensive care unit-acquired Enterobacteriaceae or Pseudomonas aeruginosa. The effect of subglottic drainage on primary endogenous infections caused by Staphalococcus aureus and Streptococcus spp in patients not receiving antibiotics is only found in a post-hoc subgroup analysis and might reflect differences in carriage of community-acquired potentially pathogenic microorganisms (PPM) caused by previous antibiotic treatment, rather than a true treatment effect. The semirecumbent position may reduce the incidence of aspiration, particularly in patients without a nasogastric tube, but the aspiration rate remains high even in the short observation periods of the studies. There is no evidence that it reduces the ventilator-associated pneumonia rate. Sucralfate may reduce the increased pneumonia rate caused by H2-antagonists and/or antacids, but it remains to be proven whether it is superior to placebo. Sucralfate has no effect on the oropulmonary route of infection and has therefore no effect on early-onset (primary endogenous) pneumonia, which is characteristically caused by PPM carried in the oropharynx. Early enteral feeding is preferable to total parenteral feeding. However, there is limited evidence that it prevents ventilator-associated pneumonia. The studies showing a benefit of early enteral feeding were relatively small studies, partly in nonventilated patients, and used poorly defined criteria for pneumonia. The oropulmonary route is the most important route in the pathogenesis of pneumonia. Preventive strategies (both antibiotic and nonantibiotic strategies) have to block both the oropulmonary route and the gastropulmonary route to be fully effective. Because microaspiration cannot be fully prevented in critically ill patients, preventive strategies should attempt to eliminate PPM from the oropharynx and GI-tract.

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Recently in an observational study the use of a pulmonary artery catheter in critically ill patients was associated with an increase in both mortality and utilization of resources when compared with case-matched control patients. The authors corrected for selection bias by using a propensity score. The publication of this article elicited a flood of commentary in both medical journals and the lay press. Critical assessment of this study and other studies about pulmonary artery catheterization in our opinion supports the view that it is probably not the use of the catheter itself, but physicians' insufficient knowledge of right heart catheterization and the specific treatment resulting from its use that is at fault.

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In a randomized, double-blind clinical study in 29 patients undergoing elective coronary artery surgery, we assessed the role of ketanserin, an inhibitor of serotonin-induced vasoconstriction and weak alpha 1 sympathetic blocker, in reducing endotoxaemia and postoperative hypermetabolism. Male patients without major organ dysfunction were allocated randomly to receive either ketanserin or placebo. Hypermetabolism was defined as an increase in oxygen consumption in the early postoperative hours (delta Vo2). Circulating endotoxin (P = 0.04) and postoperative delta Vo2 (P = 0.03) were lower in the ketanserin patients. Endotoxaemia was associated also with low vascular filling. From these preliminary results we conclude that treatment with ketanserin during cardiac surgery may reduce but not abolish endotoxaemia and postoperative hypermetabolism.

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OBJECTIVE: To determine whether standard P50 after cardiac surgery decreases and whether decreased P50 is related to the transfusion of red blood cells (RBCs), acid-base changes, body temperature, oxygen parameters and/or duration of cardiopulmonary bypass (CPB). DESIGN: Pilot study in cardiac surgery patients. SETTING: University hospital. PATIENTS: 12 Consecutive elective cardiac surgery patients. INTERVENTIONS: Blood was taken before surgery, after CPB and in the intensive care unit until 18 h post-operatively. Cardiac output and oxygen consumption were measured. Buffy coat-poor RBCs were transfused, anticoagulated with citrate-phosphate-dextrose buffer and stored in saline-adenine-glucose-mannitol at 4 degrees C, when haemoglobin was < 5.6 mmol.l-1. MEASUREMENTS AND RESULTS: Standard P50 was calculated from measured partial pressure of oxygen and of carbon dioxide, pH and oxygen saturation in mixed venous blood (SvO2) using the Severinghaus formula. Median length of RBC storage was 25 days. Standard P50 after surgery was significantly lower than baseline value (p = 0.0001). The number of RBC units transfused and duration of CPB were conjointly associated with P50 (R2 = 0.72). Patients who received more RBCs consumed more oxygen. CONCLUSION: Cardiac surgery patients receiving more RBC units have lower standard P50 and consume more oxygen. P50 decreased more when the CPB took longer. Because a decrease in P50 implies a low ratio of mixed venous oxygen tension (PvO2) to SvO2, a shift in P50 should be taken into account when using SvO2 as a measure of global oxygen availability. When a direct measurement of SvO2 is not available, PvO2 should be used instead of calculated SvO2.

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