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Pierre-Edouard Bollaert

Publications and source records attributed to Pierre-Edouard Bollaert.

At least 19 recordsLinked to original sources

Modulation of the triggering receptor expressed on myeloid cells-1 pathway during pneumonia in rats.

BACKGROUND: Triggering receptor expressed on myeloid cells-1 (TREM-1) is a cell-surface molecule that has been identified on both human and murine polymorphonuclear neutrophils and mature monocytes. The activation of TREM-1 in the presence of microbial components amplifies the inflammatory response and may be responsible for the hyperresponsiveness observed during the initial stage of sepsis. The aim of the present study was to investigate the effect of the modulation of the TREM-1 pathway during experimental pneumonia in rats. METHODS: Adult male Wistar rats were intratracheally inoculated with Pseudomonas aeruginosa (PAO1 strain) and randomly treated or not treated with an analogue synthetic peptide derived from the extracellular moiety of TREM-1 (LP17). RESULTS: P. aeruginosa induced a severe pneumonia associated with signs of severe sepsis within the first 24 h. In septic rats, LP17 improved hemodynamic status, attenuated the development of lactic acidosis and hypoxemia, modulated lung and systemic inflammatory responses and coagulation activation, reduced lung histological damage, and improved survival. CONCLUSIONS: The modulation of the TREM-1 pathway by the use of such synthetic peptides as LP17 appears beneficial during P. aeruginosa pneumonia in rats in attenuating lung and systemic inflammatory responses.

Amino Acid Sequence↗

Effects of dexamethasone and L-canavanine on the intracellular calcium-contraction relation of the rat tail artery during septic shock.

The intracellular mechanism by which sepsis lowers vascular reactivity and the subsequent reversal by dexamethasone or nitric oxide synthase (NOS) inhibitors remain unclear. We measured the sensitivity of contraction of the rat tail artery to intracellular Ca2+ in a model of polymicrobial septic shock. At 22 h after cecal ligation and puncture (CLP), rats were treated with an anti-inflammatory glucocorticoid (dexamethasone, 1 mg/kg ip), an inducible NOS inhibitor (L-canavanine, 100 mg/kg ip), or saline. At 24 h after CLP, endothelium-denuded, perfused segments of tail artery were loaded with the intracellular Ca2+-sensitive dye fura 2 in vitro. Intracellular Ca2+ concentration and perfusion pressure were measured simultaneously. The rightward shift of the perfusion pressure-intracellular Ca2+ mobilization curve after norepinephrine stimulation subsequent to CLP indicates decreased intracellular Ca2+ sensitivity of contraction. The relation was restored by dexamethasone (which also restored in vivo blood pressure and flow), but not by L-canavanine (which restored perfusion pressure by further mobilization of intracellular Ca2+). We conclude that CLP lowers vasomotion by lowering intracellular Ca2+ sensitivity, which can be restored with glucocorticoid treatment. The involvement of inducible NOS does not solely account for the sepsis-induced reduction in Ca2+ sensitivity of contraction.

Animals↗

Surface triggering receptor expressed on myeloid cells 1 expression patterns in septic shock.

OBJECTIVE: To analyze the pattern of cell-surface expression of the triggering receptor expressed on myeloid cells (TREM) 1 during septic shock. DESIGN AND SETTING: Prospective clinical study in an adult 16-bed medical ICU. PATIENTS AND METHODS: 25 septic shock patients, 15 patients with shock of noninfectious origin and 7 healthy volunteers. Arterial blood was drawn within 12 h of admission and subjected to flow cytometry analysis after staining with anti-TREM-1 and anti-CD14 antibodies. Repeated sampling was performed on days 2, 3, 5, 7, and 14 in septic shock patients. RESULTS: Monocytic TREM-1 expression was significantly higher in septic shock patients (mean fluorescence intensity 2.3+/-0.2) than in nonseptic patients (1.0+/-0.1), and healthy volunteers (1.0+/-0.1). There was no difference in monocytic TREM-1 expression between nonseptic patients and healthy volunteers or between any of the three groups with respect to TREM-1 expression on neutrophils. The time course of TREM-1 expression on monocytes diverged significantly by day 3 between survivors and ns. CONCLUSIONS: The specificity of TREM-1 regulation by infection is highlighted. Moreover, surface TREM-1 expression on monocytes may prove useful in allowing the follow-up of septic patients during the course of the disease.

Aged↗

Risk factors of relative adrenocortical deficiency in intensive care patients needing mechanical ventilation.

OBJECTIVE: To study the factors associated with relative adrenocortical deficiency in mechanically ventilated, critically ill patients. DESIGN AND SETTING: Prospective observational study in a multidisciplinary ICU of a university-affiliated teaching hospital. PATIENTS: Sixty-two consecutive, acutely ill patients needing mechanical ventilation for more than 24 h. MEASUREMENTS AND RESULTS: A high-dose short corticotropin test 24 h after endotracheal intubation. Relative adrenocortical deficiency ("nonresponder" group of patients) was defined by a rise in cortisol less than 90 microg/l after stimulation. Twenty-seven patients were classified as nonresponders and 35 as responders. On univariate analysis nonresponders were more often men, had lower mean arterial pressure, required vasoactive agents more often, had lower creatinine clearance, higher SAPS II, higher organ dysfunction scores, and received etomidate as a single bolus for endotracheal intubation more often than responders. On multivariate analysis, only etomidate administration was related to relative adrenocortical deficiency (OR 12.21; 95% CI 2.99-49.74) while female gender was protective (OR 0.13; 95% CI 0.03-0.57). CONCLUSIONS: A single bolus infusion of etomidate could be a major risk factor for the development of relative adrenocortical deficiency in ICU patients for at least 24 h after administration. Female gender is an independent protective factor.

Addison Disease↗

Symptoms of anxiety and depression in family members of intensive care unit patients before discharge or death. A prospective multicenter study.

STUDY OBJECTIVES: More than two thirds of family members visiting intensive care unit (ICU) patients have symptoms of anxiety or depression during the first days of hospitalization. Identifying determinants of these symptoms would help caregivers support families at patient discharge or when death is imminent. DESIGN AND SETTING: Prospective multicenter study including 78 ICUs (1184 beds) in France. PARTICIPANTS: Family members completed the Hospital Anxiety and Depression Scale on the day of patient discharge or death to allow evaluation of the prevalence and potential factors associated with symptoms of anxiety and depression. RESULTS: Three hundred fifty-seven patients were included in the study, and 544 family members completed the Hospital Anxiety and Depression Scale. Symptoms of anxiety and depression were found in 73.4% and 35.3% of family members, respectively; 75.5% of family members and 82.7% of spouses had symptoms of anxiety or depression (P = .007). Symptoms of depression were more prevalent in family members of nonsurvivors (48.2%) than of survivors (32.7%) (P = .008). The multivariate model identified 3 groups of factors associated with symptoms: (1) patient-related: severity as assessed by the Simplified Acute Physiology Score II (odds ratio [OR] 1.017 per point) and patient age (OR 0.984 per year) predicted anxiety, and Simplified Acute Physiology Score II (OR, 1.015 per point), patient death (OR 2.092), and patient age (OR 0.981) predicted depression; (2) family-related: the spouse predicted anxiety (OR 2.085); and (3) ICU-related: a room with more than 1 bed (OR 1.539) predicted depression. CONCLUSION: The prevalence of symptoms of anxiety and depression remains high at the end of the ICU stay, whether the patient is well enough to be discharged or is near death.

Adult↗

Time-course of sTREM (soluble triggering receptor expressed on myeloid cells)-1, procalcitonin, and C-reactive protein plasma concentrations during sepsis.

OBJECTIVE: To describe the course of plasma sTREM (soluble triggering receptor expressed on myeloid cells)-1, procalcitonin (PCT), and C-reactive protein (CRP) concentrations during sepsis and their clinical informative value in predicting outcome. DESIGN: Prospective, noninterventional study. SETTING: Medical adult intensive care unit at a university hospital in France. PATIENTS: Sixty-three critically ill patients with sepsis, severe sepsis, or septic shock. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Soluble TREM-1 concentrations were significantly lower at admission in nonsurvivors (n = 21) than in survivors (n = 42) (94 [30-258] vs. 154 [52-435] pg/mL, p = .02), whereas PCT levels were higher among nonsurvivors (19.2 [0.3-179] vs. 2.4 (0-254) pg/mL, p = .001). CRP levels did not differ between the two groups of patients. Plasma PCT and CRP decreased during the 14-day period of study in both survivors and nonsurvivors. Conversely, sTREM-1 plasma concentrations remained stable or even increased in nonsurviving patients and decreased in survivors. An elevated baseline sTREM-1 level was found to be an independent protective factor with an odds of dying of 0.1 (95% confidence interval, 0.1-0.8). CONCLUSION: A progressive decline of plasma sTREM-1 concentration indicates a favorable clinical evolution during the recovery phase of sepsis. In addition, baseline sTREM-1 level may prove useful in predicting outcome of septic patients.

Biomarkers↗

Surface and soluble triggering receptor expressed on myeloid cells-1: expression patterns in murine sepsis.

OBJECTIVE: To examine the expression patterns of the triggering receptor expressed on myeloid cells (TREM)-1 during experimental septic shock. DESIGN: Animal study. SETTING: Animal research laboratory. SUBJECTS: Male BALB/c mice, 7-9 wks of age. INTERVENTIONS: Septic shock was induced by cecal ligation and puncture in eight mice. Eight additional animals were sham-operated and served as a control group. All animals were resuscitated by fluid infusion and administered antibiotics. Kill was performed under anesthesia 12, 24, or 48 hrs later. MEASUREMENTS AND MAIN RESULTS: Surface expression of TREM-1 was analyzed using flow cytometry on peripheral blood cells, peritoneal macrophages and neutrophils, splenic macrophages, and Kupffer cells. Gene expression was also studied in these same cells using reverse transcription-polymerase chain reaction. Tumor necrosis factor-alpha, interleukin-1beta, and soluble TREM-1 concentrations were determined in plasma and peritoneal lavage fluid. Sepsis strongly induced TREM-1 gene expression, which translated into an up-regulation of TREM-1 surface expression on neutrophils and monocytes/macrophages both at the focus on infection as well as distally. Moreover, sepsis induced the release of significant levels of soluble TREM-1. Plasma soluble TREM-1 concentrations negatively correlated with tumor necrosis factor-alpha and interleukin-1beta levels at 12 hrs. CONCLUSIONS: These results provide new information as to the regulation of TREM-1 during sepsis. Considering that both cell-surface and soluble TREM-1 were strongly up-regulated during infection, this study may add support to the putative usefulness of TREM-1 as a diagnostic tool.

Animals↗

Cardiovascular response to dopamine and early prediction of outcome in septic shock: a prospective multiple-center study.

OBJECTIVES: To compare mortality rates between dopamine-sensitive (Dopa-S) and dopamine-resistant (Dopa-R) septic shock patients, the latter group defined by a mean arterial pressure <70 mm Hg despite the use of 20 mug/kg/min dopamine. DESIGN: A human, prospective observational, multiple-center, clinical trial. SETTING: Ten intensive care units from ten hospitals. PATIENTS: 110 patients with septic shocks. INTERVENTIONS: Following volume resuscitation, patients were treated by a rapid increase in dopamine infusion from 10 to 20 mug/kg/min. If mean arterial pressure remained <70 mm Hg, dopamine treatment was promptly switched to norepinephrine or epinephrine. MEASUREMENTS AND MAIN RESULTS: Dopamine sensitivity, arterial gas, lactate, and organ system failure scores were measured at admission and after 6, 12, 24, 48, 72, 96, and 120 hrs. The overall 28-day mortality rate was 54% for the entire population under study. In multivariate analysis, independent predictors of death were dopamine resistance (odds ratio, 9.5; 95% confidence interval, 3-25), arterial lactate >3.5 mmol/L (odds ratio, 1.75; 95% confidence interval, 1.06-2.55), and Sepsis-related Organ Failure Assessment score >10 (odds ratio, 1.40; 95% confidence interval, 1.07-2.12). Of the 110 patients studied, 66 were observed to be resistant to dopamine (60%). In the Dopa-S group, the 28-day mortality rate was 16% (seven of 44 patients) compared with 78% (52 of 66 patients) in the Dopa-R group (p = .0006). The capacity of dopamine resistance to predict death was associated with a sensitivity of 84% and a specificity of 74%. At 24 hrs, the association of dopamine resistance to a lactate level >3.5 mmol/L improved the prognostic value (sensitivity, 90%, specificity, 92%). CONCLUSIONS: Dopamine sensitivity is associated with decreased mortality rate. Early recognition of dopamine resistant septic shock could allow for better screening of patients with an ominous prognosis.

Adult↗

A soluble form of the triggering receptor expressed on myeloid cells-1 modulates the inflammatory response in murine sepsis.

The triggering receptor expressed on myeloid cells (TREM)-1 is a recently discovered receptor expressed on the surface of neutrophils and a subset of monocytes. Engagement of TREM-1 has been reported to trigger the synthesis of proinflammatory cytokines in the presence of microbial products. Previously, we have identified a soluble form of TREM-1 (sTREM-1) and observed significant levels in serum samples from septic shock patients but not controls. Here, we investigated its putative role in the modulation of inflammation during sepsis. We observed that sTREM-1 was secreted by monocytes activated in vitro by LPS and in the serum of animals involved in an experimental model of septic shock. Both in vitro and in vivo, a synthetic peptide mimicking a short highly conserved domain of sTREM-1 appeared to attenuate cytokine production by human monocytes and protect septic animals from hyper-responsiveness and death. This peptide seemed to be efficient not only in preventing but also in down-modulating the deleterious effects of proinflammatory cytokines. These data suggest that in vivo modulation of TREM-1 by sTREM peptide might be a suitable therapeutic tool for the treatment of sepsis.

Amino Acid Sequence↗

Plasma level of a triggering receptor expressed on myeloid cells-1: its diagnostic accuracy in patients with suspected sepsis.

BACKGROUND: Previous experimental studies have suggested that the triggering receptor expressed on myeloid cells-1 (TREM-1) is specifically upregulated in the presence of microbial products. OBJECTIVE: To evaluate the diagnostic value of plasma levels of the soluble form of TREM-1 in patients admitted with clinical suspicion of infection. DESIGN: Prospective, noninterventional study conducted between July and September 2003. SETTING: Medical adult intensive care unit at a university hospital in France. PARTICIPANTS: 76 consecutive newly admitted patients who presented with clinically suspected infection and fulfilled at least 2 criteria of the systemic inflammatory response syndrome. MEASUREMENTS: Sensitivity and specificity of plasma soluble TREM-1 levels at admission for the diagnosis of infection. Two independent intensivists blinded to the results of soluble TREM-1 assays retrospectively classified patients as having the systemic inflammatory response syndrome, sepsis, severe sepsis, or septic shock. RESULTS: The systemic inflammatory response syndrome was diagnosed in 29 patients (38%), and sepsis, severe sepsis, or septic shock was diagnosed in the remaining 47 (62%). A plasma soluble TREM-1 level higher than 60 ng/mL was more accurate than any other clinical or laboratory finding for indicating infection (sensitivity, 96% [95% CI, 92% to 100%]; specificity, 89% [CI, 82% to 95%]; positive likelihood ratio, 8.6 [CI, 3.8 to 21.5]; negative likelihood ratio, 0.04 [CI, 0.01 to 0.2]). LIMITATIONS: The study did not enroll patients with mild infections not requiring intensive care unit hospitalization, patients older than 80 years of age, or patients who were immunocompromised. CONCLUSION: In newly admitted critically ill patients, measurement of plasma levels of soluble TREM-1 could help to rapidly identify those with infection.

Blotting, Western↗

Soluble triggering receptor expressed on myeloid cells and the diagnosis of pneumonia.

BACKGROUND: The diagnosis and treatment of bacterial pneumonia in patients who are receiving mechanical ventilation remain a difficult challenge. The triggering receptor expressed on myeloid cells (TREM-1) is a member of the immunoglobulin superfamily, and its expression on phagocytes is specifically up-regulated by microbial products. The presence of soluble TREM-1 (sTREM-1) in bronchoalveolar-lavage fluid from patients receiving mechanical ventilation may be an indicator of pneumonia. METHODS: We conducted a prospective study of 148 patients receiving mechanical ventilation in whom infectious pneumonia was suspected. A rapid immunoblot technique was used to measure sTREM-1 in bronchoalveolar-lavage fluid. Two independent intensivists who were unaware of the results of the sTREM-1 assay determined whether community-acquired pneumonia and ventilator-associated pneumonia were present or absent. RESULTS: The final diagnosis was community-acquired pneumonia in 38 patients, ventilator-associated pneumonia in 46 patients, and no pneumonia in 64 patients. The presence of sTREM-1 by itself was more accurate than any clinical findings or laboratory values in identifying the presence of bacterial or fungal pneumonia (likelihood ratio, 10.38; sensitivity, 98 percent; specificity, 90 percent). In multiple logistic-regression analysis, the presence of sTREM-1 was the strongest independent predictor of pneumonia (odds ratio, 41.5). CONCLUSIONS: In patients receiving mechanical ventilation, rapid detection of sTREM-1 in bronchoalveolar-lavage fluid may be useful in establishing or excluding the diagnosis of bacterial or fungal pneumonia.

Aged↗

Comparative effects of dexamethasone and L-canavanine in experimental septic shock.

Glucocorticoids can reverse hemodynamic disturbances and dependence on catecholamines in septic shock. The relevant beneficial mechanisms of steroids in septic shock are unknown, although inducible nitric oxide synthase could account for them. The aim of this study was to compare the effects of dexamethasone, a glucocorticoid and L-canavanine, a selective inhibitor of inducible nitric oxide synthase, in a rodent model of sepsis. Mean arterial pressure was restored by dexamethasone and L-canavanine administration at 24 h, no longer at 30 h. Dexamethasone but not L-canavanine improved aortic blood flow at 24 and 30 h. Although both dexamethasone and L-canavanine administration significantly reduced nitrite/nitrate production, and improved survival, steroids did better for survival. In conclusion, dexamethasone and L-canavanine displayed similar vasopressor effects. In addition, steroids improved blood flow suggesting that steroid-induced hemodynamic improvement in sepsis is not solely due to inhibition of inducible nitric oxide synthase.

Animals↗

Effects of epinephrine and norepinephrine on hemodynamics, oxidative metabolism, and organ energetics in endotoxemic rats.

OBJECTIVE: To determine whether epinephrine increases lactate concentration in sepsis through hypoxia or through a particular thermogenic or metabolic pathway. DESIGN: Prospective, controlled experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTIONS: Three groups of anesthetized, mechanically ventilated male Wistar rats received an intravenous infusion of 15 mg/kg Escherichia coli O127:B8 endotoxin. Rats were treated after 90 min by epinephrine ( n=14), norepinephrine ( n=14), or hydroxyethyl starch ( n=14). Three groups of six rats served as time-matched control groups and received saline, epinephrine, or norepinephrine from 90 to 180 degrees min. Mean arterial pressure, aortic, renal, mesenteric and femoral blood flow, arterial blood gases, lactate, pyruvate, and nitrate were measured at baseline and 90 and 180 min after endotoxin challenge. At the end of experiments biopsy samples were taken from the liver, heart, muscle, kidney, and small intestine for tissue adenine nucleotide and lactate/pyruvate measurements. MEASUREMENTS AND RESULTS: Endotoxin induced a decrease in mean arterial pressure and in aortic, mesenteric, and renal blood flow. Plasmatic and tissue lactate increased with a high lactate/pyruvate (L/P) ratio. ATP decreased in liver, kidney, and heart. The ATP/ADP ratio did not change, and phosphocreatinine decreased in all organs. Epinephrine and norepinephrine increased mean arterial pressure to baseline values. Epinephrine increased aortic blood flow while renal blood low decreased with both drugs. Plasmatic lactate increased with a stable L/P ratio with epinephrine and did not change with norepinephrine compared to endotoxin values. Nevertheless epinephrine and norepinephrine when compared to endotoxin values did not change tissue L/P ratios or ATP concentration in muscle, heart, gut, or liver. In kidney both drugs decreased ATP concentration. CONCLUSIONS: Our data demonstrate in a rat model of endotoxemia that epinephrine-induced hyperlactatemia is not related to cellular hypoxia.

Acidosis, Lactic↗

Spectrum of acute allergic diseases in an emergency department: an evaluation of one years' experience.

OBJECTIVE: There is limited available literature on the incidence of allergic diseases in ED. The objective of this study was to investigate the clinical records of patients admitted to the ED with a suspected allergic reaction. METHODS: A 1 year retrospective study was carried out and data were collected from the patients' computerized medical reports. RESULTS: A total of 324 patients were admitted for an allergic event. Of those, 165 patients (50.9%) were female and their mean age was 55 +/- 18.5 years. Diagnoses included: asthma in 100 patients (30.9%); hymenoptera allergy in 78 patients (24.1%); food allergy in 31 patients (9.5%); drug allergy in 25 patients (7.7%); and allergic conjunctivitis in 12 patients (3.7%). No diagnosis was found in the medical records of 78 patients (24.1%). Anaphylactic shock was observed in 12 patients (3.7%) with a diagnosis of food allergy (six cases), drug allergy (three cases) and hymenoptera allergy (three cases). Ninety patients (27.7%) were hospitalized in the following units: 38 in allergy unit (42.2%); 20 in intensive care unit (22.2%); 10 in pulmonary unit (11.1%); eight in the dermatology unit (8.9%); six in the internal medicine unit (6.7%); and eight in other units (8.9%). Overall, 42 patients (12.9%) were evaluated by an allergologist after ED discharge with positive allergy results in 28 cases (66.6%). CONCLUSIONS: Acute allergic diseases are not rare in ED, representing 1% of the annual visits in our series. A low rate of allergologist referral was observed. Emergency physicians must work closely with allergologists to ensure a better evaluation, long-term care and preventive management of patients with allergic diseases admitted to the ED.

Acute Disease↗

Baseline cortisol levels, cortisol response to corticotropin, and prognosis in late septic shock.

The prognostic value of basal and corticotropin-stimulated cortisol concentration in patients with sepsis remains a controversial issue. In a retrospective cohort study, 82 consecutive patients with septic shock underwent a short corticotropin test performed more than 24 h after the onset of vasopressor therapy. Forty-one (50%) patients died within 28 days after the onset of septic shock. The mean (SD) basal cortisol level was 22.7 (10.6) microg/dL. With threshold values of 7 and 9 microg/dL maximal increases in cortisol level, 28 (34%) and 31 (38%) patients were, respectively, classified as nonresponders to the short corticotropin test. On multivariate analysis, a cortisol level >20 microg/dL (P = 0.0002), a maximal response to corticotropin <9 microg/dL (P = 0.044), abnormal lactate values (P = 0.0098), and positive blood cultures (P = 0.004) were independent predictors of 28-day mortality. In conclusion, high basal cortisol and low increase on corticotropin stimulation are predictors of a poor outcome in late septic shock. The underlying mechanisms of these prognostic patterns remain to be elucidated.

Adrenocorticotropic Hormone↗

Gastric capnometry with air-automated tonometry predicts outcome in critically ill patients.

CONTEXT: Contrary to tonometer gastric intramucosal pH, there is currently no validated threshold prognostic value for Pco2 gap (tonometer gastric mucosal Pco2 minus arterial Pco2) in the critically ill patient. OBJECTIVE: To demonstrate a relationship between Pco2 gap and mortality in mechanically ventilated patients. DESIGN AND SETTING: Inception cohort study from a 9-month prospective survey of 95 consecutively ventilated critically ill patients in a teaching hospital. PATIENTS: All the ventilated patients of the intensive care unit were included at their admission. MEASUREMENTS AND MAIN RESULTS: Gastric Pco2 using regional capnometry with air-automated tonometry, arterial gas, lactate, and organ system failure score were measured at admission and after 6, 12, 24, 48, 72, 96, and 120 hrs. For the entire population, the 28-day mortality was 44%. In multivariate analysis, independent predictors of death were organ system failure score (odds ratio, 2.12; 95% confidence interval, 1.02-3.14), 24-hr Pco2 gap (odds ratio, 1.57; 95% confidence interval, 1.10-2.24), and 24-hr lactate (odds ratio, 1.48; 95% confidence interval, 1.06-2.05). We found a threshold value of 20 mm Hg for Pco2 gap and 2.5 mmol/L for lactate, which was associated with a sensitivity of 0.70 and 0.72, respectively, and a specificity of 0.72 and 0.73, respectively. CONCLUSION: The Pco2 gap is a marker of mortality in ventilated patients in the intensive care unit.

Adult↗

Opinions about surrogate designation: a population survey in France.

OBJECTIVE: Many patients go through periods when they are too ill to give consent or to participate in decisions. When this occurs, patient autonomy is best maintained when a surrogate designated by the patient and familiar with his or her values can speak for the patient. The objective of this study was to determine whether people who are not yet ill are ready to accept surrogate designation. Attitudes toward family participation in care were explored also. DESIGN: Population survey by telephone. Because refusal of life-sustaining treatment is a dramatic example of patient autonomy, the survey used questions about ICU admission. SETTING: General population in France. SUBJECTS: Representative random sample of 8000 residents of France aged 18 yrs or more. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The survey investigated attitudes. RESULTS: Most respondents said they would like to designate a surrogate (7205 [90%]) and to have their family share in their care (6691 [84%] for bathing, 5629 [70%] for feeding, and 4139 [52%] for tracheal suctioning) and in decisions about their management (6120 [76%]). Among respondents with a spouse, 79% said they would designate the spouse to speak for them. The attitudes were not influenced by ethnicity, religion or education level. CONCLUSIONS: Most people living in France would want a surrogate to represent them should they be incompetent and admitted to an ICU. Primary care physicians should inform their patients about the benefits of discussing illness-related issues among friends and family.

Adult↗