The treatment of septic conditions in critically ill patients is still one of medicine's major challenges. Cyclic nucleotides, adenosine and its receptors play a pivotal role in the regulation of inflammatory responses and in limiting inflammatory tissue destruction. The aim of this study was to verify the hypothesis that adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibition by erythro-9-[2-hydroxyl-3-nonyl]-adenine could be beneficial in experimental endotoxicosis/sepsis.

INTRODUCTION: Mast cells have been implicated in the aetiology of many diseases and are particularly important in evoking leukocyte-endothelial interactions during endotoxemia. Mast cell activity can be modified by histamine. There are only little data available whether serotonin (5-HT), another amine, is involved in alterations of mast cell activity, too. The aim of the study was to investigate the effects of the 5-HT-receptor antagonists methysergide (5-HT(1/2/7)-receptor antagonist), and ketanserin (5-HT(2A)-receptor antagonist) on mesenteric mast cell activation during endotoxemia. MATERIALS AND METHODS: In male Wistar rats, mast cell activity was determined in the mesentery using intravital microscopy. Rats were randomised in four groups of 12 animals each. Animals underwent laparotomy and the mesentery was exposed beneath an in-vivo videomicroscope. After baseline measurment endotoxemia was induced by continuous intravenous infusion of 2 mg/kg/h endotoxin (ETX group). Animals in the ETX/5-HT(1/2)-ANT group received methysergide (1 mg/kg body weight), animals in the ETX/5-HT(2A)-ANT group received ketanserin (1 mg/kg body weight) additionally prior to laparotomy and to the procedure described above. Animals in saline group served as controls and received equivalent volumes of NaCl 0.9%. Activated mast cells were stained by superfusion of the mesentery with ruthenium red. RESULTS: The relative mast cell activity to baseline value increased significantly in all groups. Values of the ETX-group versus the ETX/5-HT(1/2)-ANT group, the ETX/5-HT(2A)-ANT group, and the saline group were significantly higher at 120 min. CONCLUSIONS: Serotonin receptor antagonism using the 5-HT(1/2/7)-receptor antagonist methysergide or the 5-HT(2A)-receptor antagonist ketanserin reduces endotoxin-induced mast cell activation in-vivo, most probably via the 5-HT(2A)-receptor subtype.

A new adjunctive system to obtain higher PaO 2 with nasal cannula or catheter: double trunk mask

ObjectiveTo test the effects of dobutamine and dopexamine on hepatic portal and sinusoidal blood flow in a model of normodynamic endotoxemia. DesignRandomized, controlled trial. SettingExperimental laboratory. SubjectsMale Wistar rats (250–350 g). InterventionsA total of 40 male Wistar rats were randomized into four groups: a control group, which only received Ringer’s solution; an endotoxin group, which received a continuous infusion of 2 mg/kg body weight (bw)/hr of endotoxin; a dobutamine group, which received endotoxin and a continuous infusion of dobutamine (3 &mgr;g/kg bw/min); and a dopexamine group, which received endotoxin and dopexamine (2 &mgr;g/kg bw/min). The experimental period was 120 min. Measurements and Main Results Mean arterial blood pressure (MAP), heart rate (HR), and cardiac output (CO) were detected. Portal blood flow was measured using an ultrasonic flow probe positioned around the portal vein, and sinusoidal blood flow was detected in the left liver lobe using intravital microscopy. All detected variables remained stable in the control group. In the endotoxin group, HR increased significantly and MAP decreased significantly from 111 ± 10 mm Hg to 95 ± 8 mm Hg at 120 mins, whereas CO remained unchanged. Both in the dobutamine and the dopexamine group HR increased and MAP decreased more than in the endotoxin group. CO increased in both groups significantly. Portal blood flow (23 ± 4 mL/min to 16 ± 3 mL/min) and sinusoidal blood flow (38.6 ± 2.5 to 22.8 ± 1.2 103 &mgr;m3/sec) decreased significantly in the endotoxin group. In the dobutamine and the dopexamine group portal and sinusoidal blood flow remained at baseline values. ConclusionsIn our model of endotoxemia, dobutamine and dopexamine preserved systemic and hepatic blood flow. These preservations of hepatic blood flow during endotoxemia could portend beneficial effects but need to be studied further.

We compared psychomotor recovery after total intravenous anaesthesia (TIVA) with remifentanil/propofol and balanced anaesthesia (BAL) with etomidate/fentanyl/isoflurane in 40 patients, ASA I-III, aged > or =80 yr undergoing elective cataract surgery. Recovery times were recorded and psychomotor recovery was assessed according to simple reaction time, critical flicker fusion frequency (CFF) and short-term memory 30 min, 2 h and 1 day after surgery. Physical characteristics of patients in the two groups (19 in the TIVA group and 21 in the BAL group) were comparable. The TIVA group recovered significantly more quickly. Both groups showed a poorer psychomotor performance 30 min after surgery than at baseline assessment, but simple reaction time and short-term memory were close to baseline values 2 h after surgery. Only performance in the CFF test remained below baseline at this point. No deficits in psychomotor performance were noted on the first day after surgery. We conclude that there is only a minor deficit in psychomotor function in elderly patients 2 h after cataract surgery under general anaesthesia and that psychomotor function recovers completely by 24 h after surgery.

Background and aim We evaluated the costs and benefits of total intravenous anaesthesia compared with a balanced anaesthesia regimen. Methods One-hundred and twenty-four patients undergoing cataract surgery were randomized to either a propofol/remifentanil or an isoflurane/fentanyl group. In the propofol/remifentanil group, both drugs were used for induction and maintenance of anaesthesia; in the isoflurane/fentanyl group, anaesthesia was induced with etomidate and fentanyl and maintained with isoflurane and fentanyl. All patients received mivacurium for muscle relaxation and the lungs were ventilated mechanically. The use of propofol and remifentanil resulted in a faster emergence and an overall savings per case of € 12.25 due to a reduction in personnel costs which outweighs the higher drug acquisition costs. Results In the propofol and remifentanil group, more patients were satisfied and would accept the same anaesthetic again. Conclusion We conclude that propofol and remifentanil is more cost-effective than isoflurane/fentanyl due to its better recovery profile, reduced total direct costs and higher patient satisfaction.

PURPOSE:The purpose of this study was to investigate the role of histamine in mediating leukocyte-independent microvascular permeability and mast cell activation during endotoxemia. Microvascular permeability and mast cell activity were determined after inhibition of the L-selectin mediated leukocyte-adherence by fucoidin and after inhibition of histamine effects by the histamine H1-receptor antagonist diphenhydramine.MATERIALS AND METHODS:In male Wistar rats, leukocyte rolling, leukocyte adherence, microvascular permeability, and mast cell activity were determined in mesenteric postcapillary venules using intravital microscopy. After pretreatment with the histamine H1-receptor antagonist diphenhydramine, animals in the ETX/H1-ANT group received a continuous infusion of endotoxin. Animals in the ETX group underwent the same procedure, but received saline 0.9% instead of diphenhydramine. In both groups, leukocyte adherence was prevented by administration of fucoidin. Animals in the control group received volume-equivalent saline 0.9%.RESULTS:In the endotoxin-challenged groups, fucoidin prevented leukocyte rolling and reduced leukocyte adherence to values comparable to control group. In the ETX group and the ETX/H1-ANT group both microvascular permeability and mast cell activity increased significantly, starting at 60 minutes. Differences in mast cell activity between the ETX group and the ETX/H1-ANT group were significant at 60 minutes and at 120 minutes. Differences in microvascular permeability between the ETX/H1-ANT group and the ETX group were not significant.CONCLUSIONS:The leukocyte-independent microvascular damage during early endotoxemia cannot be inhibited efficiently by the H1-receptor antagonist diphenhydramine, indicating that histamine seems to play only a minor role in that pathophysiology. Furthermore, mast cells do not seem to be involved in the development of leukocyte-independent plasma extravasation during endotoxemia.

BACKGROUND:The objective of this study was to determine the effects of a continuous infusion of the phosphodiesterase inhibitor enoximone on mucosal villus blood flow in a normotensive model of endotoxemia.METHODS:Twenty-four anesthetized and ventilated rats underwent laparotomy and a ileal portion was exteriorized and opened by an antimesenteric incision. The ileal segment was fixed on a plexiglass stage with the mucosal surface upward. Microcirculatory parameters were assessed by intravital videomicroscopy. The animals were randomly assigned to receive one of three treatments: infusion of Escherichia coli lipopolysaccharides (LPS, 2 mg/kg/h) without phosphodiesterase inhibitor pretreatment (LPS group); or infusion of LPS with enoximone pretreatment (10 microg x kg(-1) x min(-1), start 30 min before LPS infusion, enoximone group), or infusion of an eqivalent volume of NaCl 0.9% (control group). Macrohemodynamic parameters (MAP, HR) and microhemodynamic parameters of ileal mucosa (mean diameter of central arterioles = DA, and mean erythrocyte velocity within the arterioles = VE) were measured 30 min before and at 0, 60, and 120 min after induction of endotoxemia. Mucosal villus blood flow was calculated from DA and VE.RESULTS:In this normotensive endotoxemia model MAP remained stable in the control and the LPS group but significantly decreased in the enoximone group. The endotoxin-induced decrease of VE and DE of central arterioles of mucosal villi could be prevented. Thus, mucosal villus blood flow did not decrease compared to the LPS group.CONCLUSIONS:Our results indicate that enoximone during an early stage of sepsis contributes to systemic hypotension but prevents mucosal hypoperfusion.

The awareness of the diagnostic difficulty and the documented high mortality risk of perioperative myocardial infarction (PMI) has led to the wide use of work up to rule out PMI after major noncardiac operations.This has caused stable postoperative patients to be kept in monitored hospital beds for extended periods of time and to be subjected to additional tests.We hypothesized that the mortality of PMI is high and, therefore, the wide use of postoperative work up to identify these patients is justifiable.We performed the following study to prove our hypothesis.All patients in the recovery room after major noncardiac operations who underwent work up to rule out PMI were identified and followed.The PMI work up included care in an electronically monitored unit, physical assessment, continuous ECG monitoring, and three 12lead electrocardiograms and cardiac enzymes obtained at six to eight hour intervals.Data collection included patient demographics; preoperative cardiac risk factors; incidence of intraoperative hypotension, hemorrhage and ECG changes; type of anesthesia and operative procedures and their durations; postoperative ECG and cardiac enzyme results; the incidence of PMI and patient outcome.Two hundred patients were studied; 85 males and 115 females.Their mean age was 62.9 years.Preexisting conditions included hypertension in 162 patients, peripheral arterial disease in 102, diabetes mellitus in 97, angina in 30, previous myocardial infarction in 41, and smoking in 107.Of 200 patients, 164 had an abnormal preoperative ECG.Vascular operations were performed in 104 patients, nonvascular abdominal operations in 48, and other operations in the remaining 48.Intraoperatively, hypotension occurred in 29 patients, blood loss of >500 ml in 25 and ECG changes in 10.There were no deaths.PMI occurred in 5/200 (2.5%) patients.Four had undergone vascular operations and one had had an abdominal operation.The mean age of the patients with PMI was 64.2 years.The duration of operation and blood loss were similar to those of patients without PMI.None of these patients developed cardiac failure or cardiogenic shock and none of them died. Conclusion:The incidence of PMI among patients undergoing noncardiac surgery is low and its mortality is negligible.Physicians should become more selective in the use of monitored beds and in the ordering of a work up to rule out PMI. P2

Purpose: To determine whether the compromised intestinal villus blood flow in a rat model of endotoxemia could be improved by continuous infusion of the phosphodiesterase (PDE) inhibitor milrinone.

Cytokine production, neutrophil adhesion to endothelial cells, and release of reactive oxygen species are thought to be critical events in sepsis or ischemia/reperfusion. Modulation of leukocyte responses by anesthetics may have an important role in limiting tissue injury under these conditions. Therefore, we investigated the effect of ketamine on the expression of CD18, CD62L, and oxygen radical production of human neutrophils in vitro and on interleukin-6 production in endotoxin-stimulated human whole blood. Ketamine inhibited both the N- formyl-methionyl-leucyl-phenylalanine- and phorbol 12-myristate 13-acetate-induced up-regulation of CD18 and shedding of CD62L, determined by flow cytometry, in a concentration-dependent manner. Ketamine also caused a significant suppression of oxygen radical generation of isolated human neutrophils. In addition, there was a significant decrease in endotoxin-stimulated interleukin-6 production in human whole blood. The inhibitory effects were similar for racemic ketamine and its isomers S(+)-ketamine and R(-)-ketamine, suggesting that the inhibition of stimulated neutrophil function is most likely not mediated through specific receptor interactions. Implications Modulation of leukocyte responses by anesthetics may have an important role in limiting tissue injury in sepsis or ischemia/reperfusion. Therefore, we examined the effect of ketamine on stimulated neutrophil functions in vitro. These neutrophil functions were significantly inhibited by ketamine, independent of whether the racemic mixture or isomers were tested.

Purpose: The objective of this study was to determine the effects of a continuous infusion of the phosphodiesterase (PDE) inhibitor amrinone on mucosal villus blood flow in a normotensive model of endotoxemia. Materials and Methods: Twenty-four anesthetized and ventilated rats underwent laparotomy, and an ileal portion was exteriorized and opened by an antimesenteric incision. The ileal segment was fixed on a plexiglass stage with the mucosal surface upward. Microcirculatory parameters were assessed by intravital videomicroscopy. The animals were randomly assigned to receive one of three treatments: infusion of Escherichia coli lipopolysaccharides (LPS, 2 mg/kg/h) without phosphodiesterase inhibitor pretreatment (LPS group); or infusion of LPS with amrinone pretreatment (40 μg/kg/min, start 30 minutes before LPS infusion) (amrinone group), or infusion of eqivalent volumes of NaCl 0.9% (control group). Macrohemodynamic parameters (MAP, HR) and microhemodynamic parameters of ileal mucosa (mean diameter of central arterioles = DA and mean erythrocyte velocity within the arterioles = VE) were measured 30 minutes before and at 0, 60, and 120 minutes after induction of endotoxemia. Mucosal villus blood flow was calculated from DA and VE.Results: In this normotensive endotoxemia model, MAP remained stable in the control and the LPS group but significantly decreased in the amrinone group. The endotoxin-induced decrease of VE and DA of central arterioles of mucosal villi could be attenuated and prevented, respectively. Thus, the endotoxin-induced decrease of mucosal villus blood flow was diminished but not fully restored by amrinone infusion. Conclusion: Our results indicate that amrinone during an early stage of sepsis is of limited value. It attenuates mucosal hypoperfusion but contributes to systemic hypotension. Copyright © 2000 by W.B. Saunders Company

OBJECTIVES:To determine the effect of dopexamine, a synthetic catecholamine ligand for dopaminergic and beta2-adrenergic receptors, on intestinal release of adenosine 5'-triphosphate (ATP) degradation products and on intestinal tissue concentrations of high-energy phosphates during endotoxemia. DESIGN:Randomized, controlled trial. SETTING:Experimental laboratory. SUBJECTS:Twenty-one male Wistar rats. INTERVENTIONS:Rats given endotoxin (Escherichia coli lipopolysaccharide [LPS]; 1.5 mg/kg i.v. over 60 mins) were treated with a continuous infusion of dopexamine (DPX; 2.5 microg/kg/min, n = 7, group LPS + DPX) or 0.9% saline (n = 7, group LPS) during a study period of 120 mins. Animals in the control group (n = 7) received a volume-equivalent infusion of 0.9% saline without endotoxin. MEASUREMENTS AND MAIN RESULTS:In all groups, arterial and portal venous concentrations of adenosine, hypoxanthine, and uric acid were measured at baseline and at 60 and 120 mins after the endotoxin challenge, and we calculated the portal venous/arterial concentration differences as an indicator of the intestinal release of the purine compounds. Furthermore, at the end of the study, the intestinal tissue concentrations of the high-energy phosphates ATP, adenosine 5'-diphosphate (ADP), adenosine 5'-monophosphate (AMP), creatine phosphate, and adenosine were determined, and we calculated the adenine nucleotide pool, the ATP/ADP and AMP/adenosine ratios, and the adenylate energy charge of the intestinal tissue. Endotoxemia decreases intestinal tissue ATP, ADP, AMP, and creatine phosphate concentrations, increases tissue adenosine content, and increases the release of hypoxanthine and uric acid from the intestinal tract. Dopexamine attenuates the endotoxin-induced decrease of the intestinal tissue adenine nucleotide pool, the AMP/adenosine ratio, and the release of the ATP-degradation products hypoxanthine and uric acid from the intestinal tract. CONCLUSIONS:Normotensive endotoxemia is associated with a deterioration of the intestinal energy balance and an increased release of ATP degradation products, indicating intestinal tissue ischemia. Furthermore, these results suggest the beneficial effects of dopexamine on pathophysiologic alterations of the intestinal energy metabolism during endotoxemia.

BACKGROUND:The intestinal mucosa is the portion of the gut most susceptible to impaired perfusion and oxygen delivery. The phosphodiesterase (PDE) inhibitor amrinone has been proposed to improve oxygen delivery and tissue perfusion during sepsis. The objective of this study was to investigate the effects of amrinone on arterial oxygenation (Pao(2)) and tissue oxygenation (Ptio(2)) of jejunal mucosa during endotoxemia.MATERIALS AND METHODS:Forty anesthetized and ventilated rats were laparotomized and a jejunal portion was exteriorized and fixed on a plexiglass stage. The jejunum was punctured and a Clark-type microcatheter Po(2) probe and a microthermocouple were placed on the mucosa to measure Ptio(2). The animals were randomly assigned to receive one of the four treatments: infusion of Escherichia coli lipopolysaccharides (LPS, 2 mg/kg/h) without amrinone pretreatment (LPS group); infusion of LPS with amrinone pretreatment (40 microg/kg/min, start 30 min before LPS infusion, amrinone + LPS group); no treatment with either amrinone or LPS (control group); treatment with amrinone without LPS infusion (amrinone group). Mean arterial pressure (MAP), heart rate (HR), Pao(2), and Ptio(2) were measured 30 min before and 0, 60, and 120 min after induction of endotoxemia.RESULTS:MAP remained stable in the control and LPS groups. In the amrinone + LPS group MAP decreased within the first 30 min of amrinone infusion and decreased further during endotoxemia. Pao(2) remained stable in the control group and decreased in the LPS group. This endotoxin-induced decrease in Pao(2) was attenuated in the amrinone + LPS group. The mucosal Ptio(2) decreased in the LPS group but remained stable in both the control and amrinone + LPS groups.CONCLUSIONS:Pretreatment with amrinone was able to diminish a decrease in Pao(2) during endotoxemia, indicating that pulmonary dysfunction was attenuated. Endotoxin-induced tissue hypoxia of the intestinal mucosa, however, could be fully prevented, indicating that an additional improvement in compromised tissue perfusion had occurred.

To the Editor:—The mortality rate of septic patients increases progressively with increasing severity of encephalopathy caused by sepsis. Several mechanisms have been suggested as the cause of septic encephalopathy, including direct central nervous system infection, endotoxin and cytokine effects on the brain, inadequate cerebral perfusion, metabolic derangements, or complications of medical therapy. Neuropathologic examinations of 12 septic patients who died during protracted, severe septic encephalopathy showed microabscesses in eight cases and vascular lesions in approximately half. We assessed the ability of the neuron-specific enolase (NSE), the neuronal isomer of the glycolytic enzyme 2-phospho-D-glycerate hydrolase, and the central nervous system–specific isoforms of S100 to predict mortality in patients with severe sepsis or septic shock. Both NSE and S100 have been shown to be specific parameters for the assessment of Table 2. Comparison of Tidal Volume and Peak Inspiratory Pressure When Sealing between Laryngeal Mask Airway and Endotracheal Tube and/or Laryngeal Mask Airway Cuff Inflation was Performed

Purpose: The objective of this study was to determine the effects of epinephrine and norepinephrine on mucosal villous blood flow in a normotensive model of endotoxemia.Materials and Methods: Thirty-two anesthetized rats were laparotomized, and a jejunal portion was exteriorized and opened by an antimesenteric incision. The jejunal segment was fixed on a plexiglass stage with the mucosal surface upward. Microcirculatory parameters were assessed by intravital videomicroscopy. The animals were randomly assigned to receive one of four treatments: infusion of Escherichia coli lipopolysaccharides (LPS, 2 mg/kg/h) without catecholamine pretreatment (LPS group); or infusion of LPS with epinephrine pretreatment (0.2 mu g/kg/min, start 30 minutes before LPS infusion) (E group), or infusion of LPS with norepinephrine pretreatment (0.2 mu g/kg/min, start 30 minutes before LPS infusion) (IUE group). The control group did not receive either catecholamines or LPS, Mean diameter of central arterioles (D-A) and mean erythrocyte velocity within the arterioles (V-E) were measured 30 minutes before and at 0, 60, and 120 minutes after induction of endotoxemia, Mucosal villous blood flow was calculated from D-A and V-E Results: LPS infusion alone and norepinephrine plus LPS infusion led to a significant vasoconstriction of central arterioles, which was associated with a similar decrease in mucosal villous blood flow. Epinephrine infusion alone led to a vasodilation and an increase in villous blood flow within the first 30 minutes. After induction of endotoxemia, D-A returned to baseline values and villous blood flow was as low as in the LPS and the norepinephrine group after 120 minutes.Conclusion: In this experimental rat model, the catecholamines epinephrine and norepinephrine in a dosage of 0.2 mu g.kg(-1).min(-1) neither diminish nor improve mucosal villous blood flow during the early phase of endotoxemia. Copyright (C) 1999 by W.B, Saunders Company.

Background: C1-esterase inhibitor (C1-INH) has been shown to have beneficial effects in patients with sepsis. However, the microcirculatory effects of C1-INH during sepsis are unknown. This study investigated the influence of C1-INH on leukocyte-endothelial cell adhesion, vascular leakage, and venular microhemodynamics in postcapillary venules of rat mesentery during endotoxemia. Methods: Thirty-two anesthetized Wistar rats randomly received 1 of 4 treatments: pretreatment with infusion of C1-INH in a concentration of 7.5 U · kg -1 body weight (C1-INH-7.5 group, n = 8) or in a concentration of 15 U · kg -1 body weight (C1-INH-15 group, n = 8) followed by continuous infusion of Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 8) was pretreated with saline solution 30 minutes before LPS infusion. The control group (n = 8) received equivalent amounts of saline infusion. Leukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules of rat mesentery were determined every 60 minutes during a period of 120 minutes using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from mean red blood cell velocity and vessel diameter. Results: LPS infusion induced a decrease in venular wall shear rate and an increase in leukocyte adherence and vascular permeability in postcapillary venules of rat mesentery. All microcirculatory disturbances were attenuated by pretreatment with C1-INH, showing no significant difference between the 2 concentrations. Conclusions: Pretreatment with C1-INH attenuates endotoxin-induced leukocyte adherence and macromolecular leakage in postcapillary venules of rat mesentery, indicating that complement inhibition might be a therapeutic tool in the treatment of sepsis. (Surgery 1999;125:280-7.)

OBJECTIVE:To investigate whether endotoxin, interleukin-6, and circulating adhesion molecules, measured sequentially in blood, can predict mortality and organ dysfunction in sepsis. DESIGN:Inception cohort study with follow-up for 28 days. SETTING:Surgical intensive care unit at a university hospital. PATIENTS:A total of 14 consecutive patients were enrolled in the study within the first 24 hrs after onset of septic shock. Seven healthy subjects were studied as controls. INTERVENTIONS:Patients were analyzed for mortality and development of organ dysfunction. MEASUREMENTS AND MAIN RESULTS:At the end of the 28-day follow-up period, seven of the patients were still alive (survivors) but the other seven (nonsurvivors) had died. At the time of enrollment in the study (day 0), the Acute Physiology and Chronic Health Evaluation II score was 28.4 in survivors (n = 7) and 28.7 in nonsurvivors (n = 7). In contrast, circulating intercellular adhesion molecule-1 (ICAM-1) was significantly higher in nonsurvivors than in survivors. Circulating ICAM-1 predicted mortality in patients with septic shock with a sensitivity and a specificity of 71.4% each. Endotoxin, interleukin-6, circulating L-selectin, P-selectin, E-selectin, and platelet endothelial cell adhesion molecule-1, however, did not distinguish between survivors and nonsurvivors. In addition, circulating ICAM-1 at day 0 showed a significant correlation with the highest serum bilirubin observed during the entire study period (r2 = 0.963). CONCLUSIONS:Because only circulating ICAM-1 was higher in nonsurvivors than in survivors at day 0, circulating ICAM-1 may serve as an early prognostic marker for outcome in septic shock. In addition, measurement of circulating ICAM-1 facilitates identification of those patients with the highest risk of developing liver dysfunction.