Jean-Claude Chevrolet

Impact of a prevention strategy targeted at vascular-access care on incidence of infections acquired in intensive care.

BACKGROUND Intravascular devices are a leading cause of nosocomial infection. Specific prevention strategies and improved guidelines for the use of intravascular devices can decrease the rate of infection; however, the impact of a combination of these strategies on rates of vascular-access infection in intensive-care units (ICUs) is not known. We implemented a multiple-approach prevention programme to decrease the occurrence of vascular-access infection in an 18-bed medical ICU at a tertiary centre. METHODS 3154 critically ill patients, admitted between October, 1995, and November, 1997, were included in a cohort study with longitudinal assessment of an overall catheter-care policy targeted at the reduction of vascular-access infections and based on an educational campaign for vascular-access insertion and on device use and care. Incidence of ICU-acquired infections was measured by means of on-site surveillance. FINDINGS 613 infections occurred in 353 patients (19.4 infections per 100 admissions). The incidence density of exit-site catheter infection was 9.2 episodes per 1000 patient-days before the intervention, and 3.3 episodes per 1000 patient-days afterwards (relative risk 0.36 [95% CI 0.20-0.63]). Corresponding rates for bloodstream infection were 11.3 and 3.8 episodes per 1000 patient-days, respectively (0.33 [0.20-0.56]) due to decreased rates of both microbiologically documented infections and clinical sepsis. Rates of respiratory and urinary-tract infections remained unchanged, whereas those of skin or mucous-membrane infections decreased from 11.4 to 7.0 episodes per 1000 patient-days (0.62 [0.41-0.93]). Overall, the incidence of nosocomial infections decreased from 52.4 to 34.0 episodes per 1000 patient-days (0.65 [0.54-0.78]). INTERPRETATION A multiple-approach prevention strategy, targeted at the insertion and maintenance of vascular access, can decrease rates of vascular-access infections and can have a substantial impact on the overall incidence of ICU-acquired infections.

Activation of human macrophages by mechanical ventilation in vitro

Positive-pressure mechanical ventilation supports gas exchange in patients with respiratory failure but is also responsible for significant lung injury. In this study, we have developed an in vitro model in which isolated lung cells can be submitted to a prolonged cyclic pressure-stretching strain resembling that of conventional mechanical ventilation. In this model, cells cultured on a Silastic membrane were elongated up to 7% of their initial diameter, corresponding to a 12% increase in cell surface. The lung macrophage was identified as the main cellular source for critical inflammatory mediators such as tumor necrosis factor-α, the chemokines interleukin (IL)-8 and -6, and matrix metalloproteinase-9 in this model system of mechanical ventilation. These mediators were measured in supernatants from ventilated alveolar macrophages, monocyte-derived macrophages, and promonocytic THP-1 cells. Nuclear factor-κB was found to be activated in ventilated macrophages. Synergistic proinflammatory effects of mechanical stress and molecules such as bacterial endotoxin were observed, suggesting that mechanical ventilation might be particularly deleterious in preinjured or infected lungs. Dexamethasone prevented IL-8 and tumor necrosis factor-α secretion in ventilated macrophages. Mechanical ventilation induced low levels of IL-8 secretion by alveolar type II-like cells. Other lung cell types such as endothelial cells, bronchial cells, and fibroblasts failed to produce IL-8 in response to a prolonged cyclic pressure-stretching load. This model is of particular value for exploring physical stress-induced signaling pathways, as well as for testing the effects of novel ventilatory strategies or adjunctive substances aimed at modulating cell activation induced by mechanical ventilation.Positive-pressure mechanical ventilation supports gas exchange in patients with respiratory failure but is also responsible for significant lung injury. In this study, we have developed an in vitro model in which isolated lung cells can be submitted to a prolonged cyclic pressure-stretching strain resembling that of conventional mechanical ventilation. In this model, cells cultured on a Silastic membrane were elongated up to 7% of their initial diameter, corresponding to a 12% increase in cell surface. The lung macrophage was identified as the main cellular source for critical inflammatory mediators such as tumor necrosis factor-alpha, the chemokines interleukin (IL)-8 and -6, and matrix metalloproteinase-9 in this model system of mechanical ventilation. These mediators were measured in supernatants from ventilated alveolar macrophages, monocyte-derived macrophages, and promonocytic THP-1 cells. Nuclear factor-kappaB was found to be activated in ventilated macrophages. Synergistic proinflammatory effects of mechanical stress and molecules such as bacterial endotoxin were observed, suggesting that mechanical ventilation might be particularly deleterious in preinjured or infected lungs. Dexamethasone prevented IL-8 and tumor necrosis factor-alpha secretion in ventilated macrophages. Mechanical ventilation induced low levels of IL-8 secretion by alveolar type II-like cells. Other lung cell types such as endothelial cells, bronchial cells, and fibroblasts failed to produce IL-8 in response to a prolonged cyclic pressure-stretching load. This model is of particular value for exploring physical stress-induced signaling pathways, as well as for testing the effects of novel ventilatory strategies or adjunctive substances aimed at modulating cell activation induced by mechanical ventilation.

Percutaneous or surgical tracheostomy: a meta-analysis.

OBJECTIVE To compare percutaneous with surgical tracheostomy using a meta-analysis of studies published from 1960 to 1996. DATA SOURCES Publications obtained through a MEDLINE database search with a Boolean combination (tracheostomy or tracheotomy) and complications, with constraints for human studies and English language. STUDY SELECTION Publications addressing all peri- and postoperative complications. Studies limited to specific tracheostomy complications or containing insufficient details were excluded. Two authors independently selected the publications. DATA EXTRACTION A list of relevant surgical variables and complications was compiled. Complications were divided into peri- and postoperative groups and further subclassified into severe, intermediate, and minor groups. Because most studies of percutaneous tracheostomy were published after 1985, surgical tracheostomy studies were divided into two periods: 1960 to 1984 and 1985 to 1996. The articles were analyzed independently by three investigators, and rare discrepancies were resolved through discussion and data reexamination. DATA SYNTHESIS Earlier surgical tracheostomy studies (n = 17; patients, 4185) have the highest rates of both peri- (8.5%) and postoperative (33%) complications. Comparison of recent surgical (n = 21; patients, 3512) and percutaneous (n = 27; patients, 1817) tracheostomy trials shows that perioperative complications are more frequent with the percutaneous technique (10% vs. 3%), whereas postoperative complications occur more often with surgical tracheotomy (10% vs. 7%). The bulk of the differences is in minor complications, except perioperative death (0.44% vs. 0.03%) and serious cardiorespiratory events (0.33% vs. 0.06%), which were higher with the percutaneous technique. Heterogeneity analysis of complication rates shows higher heterogeneity in older and surgical trials. CONCLUSIONS Percutaneous tracheostomy is associated with a higher prevalence of perioperative complications and, especially, perioperative deaths and cardiorespiratory arrests. Postoperative complication rates are higher with surgical tracheostomy.

The effect of workload on infection risk in critically ill patients

Objective: There is growing evidence that low nurse staffing jeopardizes quality of patient care. The objective of the study was to determine whether low staffing level increases the infection risk in critical care. Design: Observational, single‐center, prospective cohort study. Setting: Medical intensive care unit of the University of Geneva Hospitals, Switzerland. Patients: All patients admitted over a 4‐yr period. Interventions: None. Measurements and Main Results: Study variables included all infections acquired in critical care, daily nurse‐to‐patient ratio, demographic characteristics, admission diagnosis and severity score, comorbidities, daily individual exposure to invasive devices, and selected drugs. Of a cohort of 1,883 patients totaling 10,637 patient‐days, 415 (22%) developed at least one healthcare‐associated infection while in critical care. Overall infection rate was 64.5 episodes per 1000 patient‐days. Infected patients experienced higher mortality with a longer duration of stay both in critical care and in the hospital than noninfected patients (all p < .001). Median 24‐hr nurse‐to‐patient ratio was 1.9. Controlling for exposure to central venous catheter, mechanical ventilation, urinary catheter, and antibiotics, we found that higher staffing level was associated with a >30% infection risk reduction (incidence rate ratio, 0.69; 95% confidence interval, 0.50–0.95). We estimated that 26.7% of all infections could be avoided if the nurse‐to‐patient ratio was maintained >2.2. Conclusions: Staffing is a key determinant of healthcare‐associated infection in critically ill patients. Assuming causality, a substantial proportion of all infections could be avoided if nurse staffing were to be maintained at a higher level.

Effects of the prone position on gas exchange and hemodynamics in severe acute respiratory distress syndrome.

OBJECTIVES To address the following issues regarding the use of prone position ventilation in patients with severe acute respiratory distress syndrome (ARDS): a) response rate; b) magnitude and duration of improved oxygenation in responders during a 12-hr trial and the consequences of returning to the supine position; c) effects of the prone position on gas exchange and hemodynamics; d) consequences of oxygenation in nonresponders; and e) effects of repeated prone position trials. DESIGN Prospective, nonrandomized interventional study. SETTING Medical intensive care unit, university tertiary care center. PATIENTS Nineteen consecutive, mechanically ventilated patients (age 45+/-20 yrs, mean+/-SD) with ARDS and severe hypoxemia, defined as PaO2/FiO2 of < or = 150 with FiO2 of > or = 0.6 persisting for < or =24 hrs, and a pulmonary artery occlusion pressure of <18 mm Hg. INTERVENTIONS Patients were turned prone for 2 hrs. Nonresponders were returned supine, but responders were maintained prone for 12 hrs before being returned to the supine position. The procedure was repeated on a daily basis in all patients, until inclusion criteria were no longer met or the patients died. MEASUREMENTS AND MAIN RESULTS Hemodynamic, blood gas, and gas exchange measurements were performed at the following time points: a) baseline supine; b) after 30 mins prone; and c) after 120 mins prone. Additional measurements for nonresponders were taken after 30 mins supine. For responders, additional measurements were taken after 12 hrs prone and 30 mins supine. Patients were considered responders if an increase in PaO2 of > or = 10 torr (> or =1.3 kPa), or increase in the PaO2/FiO2 ratio of >20 occurred within 120 mins. Eleven (57%) patients responded to the prone position. There was no difference in initial baseline parameters between responders and nonresponders. After 30 mins, the prone position in responders increased PaO2 and decreased calculated venous admixture (Qva/Qt). This improvement was the maximal obtained, and was maintained throughout the 12-hr prone period. After 12 hrs prone, mean FiO2 had been lowered from 0.85+/-0.16 to 0.66+/-0.18 (p < .05). Thirty minutes after the patients were returned supine, PaO2, PaO2/FiO2, and Qva/Qt were not different from 12-hr prone values, and were improved in comparison with baseline supine values. There was no worsening of gas exchange or hemodynamics in nonresponders. After the initial trial, a total of 28 additional episodes of prone position ventilation were performed in nine of the 19 patients. Of the 24 additional episodes in the responders, there was a response in 17 (71%) of 24 episodes. In the four additional episodes in nonresponders, there was a response in only one (25%) of four episodes. Response was accompanied by the same beneficial effects on gas exchange and Qva/Qt and absence of effect on hemodynamics as in the initial trial. There was no worsening in gas exchange or hemodynamics in nonresponder trials. CONCLUSIONS Based on the data from this study, the prone position can improve oxygenation in severely hypoxemic ARDS patients without deleterious effects on hemodynamics. This beneficial effect does not immediately disappear on return to the supine position. In our patients, an absence of response to this technique was not accompanied by worsening hypoxemia or hemodynamic instability. Repeated daily trials in the prone position should be considered in the management of ARDS patients with severe hypoxemia.

Percutaneous Versus Surgical Tracheostomy: A Double-Blind Randomized Trial

OBJECTIVE To compare surgical (SgT) and percutaneous (PcT) tracheostomies. BACKGROUND Percutaneous tracheostomy has been said to provide numerous advantages over classical SgT. METHODS A prospective randomized trial with a double-blind evaluation was used to compare SgT and PcT. SgT and PcT were performed according to established techniques (n = 70). The procedure was performed at the bedside in the intensive care unit in 21 cases (30%). The outcome measures were divided into procedure-related variables, perioperative complications, and postoperative complications. The procedure-related variables (location, duration, and difficulty) were evaluated by the surgeon. The perioperative and postoperative complications were divided into serious, intermediate, and minor. Perioperative and early postoperative (14 days) complications were evaluated daily by an intensive care unit nurse blinded to the technique used. Long-term postoperative complications were evaluated 3 months after decannulation by a surgeon blinded to the surgical technique. RESULTS There were no major complications in either group. Most variables studied were not statistically different between the PcT and SgT groups. The only variables to reach statistical significance were the size of the incision (smaller with PcT, p < 0.0001), minor perioperative complications (greater with PcT, p = 0.02), and difficult cannula changes (greater with PcT; p < 0.05). Among nonsignificant differences, difficult procedures and false passages were more frequent with PcT, whereas long-term unesthetic scars were more frequent with SgT. CONCLUSIONS Both techniques are associated with a low rate of serious or intermediate complications when performed by experienced surgeons. There were more minor perioperative complications with PcT and more minor long term complications with SgT.

Impact of a public campaign on pre-hospital delay in patients reporting chest pain.

OBJECTIVE: To decrease pre-hospital delay in patients with chest pain. DESIGN: Population based, prospective observational study. SETTING: A province of Switzerland with 380000 inhabitants. SUBJECTS: All 1337 patients who presented with chest pain to the emergency department of the Hôpital Cantonal Universitaire of Geneva during the 12 months of a multimedia public campaign, and the 1140 patients who came with similar symptoms during the 12 months before the campaign started. MAIN OUTCOME MEASURES: Pre-hospital time delay and number of patients admitted to the hospital for acute myocardial infarction (AMI) and unstable angina. RESULTS: Mean pre-hospital delay decreased from 7h 50 min before the campaign to 4 h 54 min during it, and median delay from 180 min to 155 min (P < 0.001). For patients with a final diagnosis of AMI, mean delay decreased from 9 h 10 min to 5 h 10 min and median delay from 195 min to 155 min (P < 0.002). Emergency department visits per week for AMI and unstable angina increased from 11.2 before the campaign to 13.2 during it (P < 0.02), with an increase to 27 (P < 0.01) during the first week of the campaign; visits per week for non-cardiac chest pain increased from 7.6 to 8.1 (P = NS) during the campaign, with an increase to 17 (P < 0.05) during its first week. CONCLUSIONS: Public campaigns may significantly reduce pre-hospital delay in patients with chest pain. Despite transient increases in emergency department visits for non-cardiac chest pain, such campaigns may significantly increase hospital visits for AMI and unstable angina and thus be cost effective.

Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.

ObjectiveTo measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS).DesignProspective study.Setting: 18-bed, medical intensive care unit, university hospital.Patients11 mechanically ventilated ARDS patients.InterventionPatients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30–60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h.ResultsMinute ventilation was reduced from 13.5±6.1 to 8.2±4.1l/min (mean±SD), PaCO2 increased (40.3±6.6 to 59.3±7.2 mmHg), pH decreased (7.40±0.05 to 7.26±0.05), and P50 increased (26.3±2.02 to 31.1±2.2 mmHg) (p<0.05). Systemic vascular resistance decreased (865±454 to 648±265 dyne·s·cm−5, and cardiac index (CI) increased (4±2.4 to 4.7±2.4 l/min/m2) (p<0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29±5 to 32±6 mmHg,p<0.05). PaO2 remained unchanged, while saturation decreased (93±3 to 90±3%,p<0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2>90%. PvO2 increased (36.5±5.7 to 43.2±6.1 mmHg,p<0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545±240 to 621±274 ml/min/m2,p<0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3±12.3 to 32.8±13.2,p<0.05).ConclusionsThese data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.

Additive beneficial effects of the prone position, nitric oxide, and almitrine bismesylate on gas exchange and oxygen transport in acute respiratory distress syndrome

OBJECTIVE To test the hypothesis that prone position ventilation, nitric oxide, and almitrine bismesylate, each acting by a different mechanism to improve arterial oxygenation, could exert additive beneficial effects when used in combination in patients with severe acute respiratory distress syndrome (ARDS). DESIGN Prospective, nonrandomized, interventional study. SETTING Medical and surgical intensive care units at a university tertiary care center. PATIENTS Twelve patients with ARDS and severe hypoxemia, defined as PaO2/FIO2 of < or = 150 and FIO2 of > or = 0.6, with pulmonary artery occlusion pressure of < 18 mm Hg. INTERVENTIONS Inhaled nitric oxide (20 parts per million for 15 mins) in the supine and prone position, and intravenous almitrine bismesylate while prone (1 mg/kg/hr for 60 mins), alone or combined with nitric oxide. MEASUREMENTS AND MAIN RESULTS Hemodynamic, blood gas, and gas exchange measurements were performed at sequential time points as follows: a) baseline supine; b) nitric oxide in the supine position; c) after return to baseline supine; d) after 30 mins prone; e) after 120 mins prone; f) nitric oxide while prone; g) after return to baseline prone; h) almitrine bismesylate prone; and i) nitric oxide and almitrine bismesylate combined, for 15 mins prone. Patients were considered responders to the prone position if a gain in PaO2 of > or = 10 torr (> or = 1.3 kPa) or a gain in the PaO2/FIO2 ratio of > or = 20 was observed. Seven patients (58%) responded to being turned prone. Compared with supine baseline conditions, nitric oxide and supine position increased arterial oxygen saturation from 89 +/- 1 (SD)% to 92 +/- 3% (p < .05) and nitric oxide plus prone position increased arterial oxygen saturation (94 +/- 3% vs. 89 +/- 4%, p < .05) and decreased the alveolar-arterial oxygen difference from 406 +/- 124 torr (54 +/- 15 kPa) to 387 +/- 108 torr (51 +/- 14 kPa) (p < .05). Almitrine bismesylate increased PaO2/FIO2 vs. baseline (122 +/- 58 vs. 84 +/- 21, p < .05). Almitrine bismesylate decreased the alveolar-arterial oxygen difference vs. baseline from 406 +/- 124 torr (53.9 +/- 16.5 kPa) to 386 +/- 112 torr (51.3 +/- 14.8 kPa) and vs. nitric oxide and supine position from 406 +/- 111 torr (53.9 +/- 14.7 kPa) to 386 +/- 112 torr (51.3 +/- 14.8 kPa) (p < .05). Prone position alone did not improve oxygenation. However, the combination of nitric oxide and almitrine bismesylate increased PaO2/FIO2 vs. nitric oxide supine and nitric oxide prone conditions (147 +/- 69 vs. 84 +/- 25 and 91 +/- 18, respectively; p < .05). In patients responding to the prone position (n = 7), combining nitric oxide and almitrine bismesylate led to further improvement in PaO2 compared with the prone position alone, with PaO2 increasing from 78 +/- 12 torr (10.3 +/- 1.6 kPa) to 111 +/- 55 torr (14.7 +/- 7.3 kPa) (p < .05), which was not the case when either nitric oxide or almitrine bismesylate was added separately. Heart rate and cardiac output were increased by almitrine bismesylate compared with all other measurements. Mean pulmonary arterial pressure was decreased by nitric oxide (27 +/- 7 vs. 30 +/- 7 mm Hg nitric oxide supine vs. baseline supine and 29 +/- 7 vs. 33 +/- 8 mm Hg nitric oxide prone vs. baseline prone, p < .05) and increased by almitrine bismesylate (36 +/- 9 vs. 30 +/- 7 mm Hg baseline supine, 27 +/- 7 mm Hg nitric oxide supine, 33 +/- 8 mm Hg baseline prone, and 29 +/- 7 mm Hg nitric oxide prone; p < .05). The increase in mean pulmonary arterial pressure was totally abolished by nitric oxide (31 +/- 5 vs. 36 +/- 9 mm Hg, p < .05). Minute ventilation, respiratory system compliance, physiologic deadspace, and PaCO2 remained unchanged. CONCLUSION In ARDS patients with severe hypoxemia, arterial oxygenation can be improved by combining the prone position, nitric oxide, and almitrine bismesylate, without deleterious effects.

Beneficial effects of helium:oxygen versus air:oxygen noninvasive pressure support in patients with decompensated chronic obstructive pulmonary disease

OBJECTIVE To test the hypothesis that, in decompensated chronic obstructive pulmonary disease (COPD), noninvasive pressure support ventilation using 70:30 helium:oxygen instead of 70:30 air:oxygen could reduce dyspnea and improve ventilatory variables, gas exchange, and hemodynamic tolerance. DESIGN Prospective, randomized, crossover study. SETTING Medical intensive care unit, university tertiary care center. PATIENTS Nineteen patients with severe COPD (forced 1-sec expiratory volume of 0.83+/-0.3 l) hospitalized in the intensive care unit for noninvasive pressure support ventilation after initial stabilization with noninvasive pressure support for no more than 24 hrs after intensive care unit admission. INTERVENTIONS Noninvasive pressure support ventilation was administered in the following randomized crossover design: a) 45 min with air:oxygen or helium:oxygen; b) no ventilation for 45 min; and c) 45 min with air:oxygen or helium:oxygen. MEASUREMENTS AND MAIN RESULTS Air:oxygen and helium:oxygen decreased respiratory rate and increased tidal volume and minute ventilation. Helium:oxygen decreased inspiratory time. Both gases increased total respiratory cycle time and decreased the inspiratory/total time ratio, the reduction in the latter being significantly greater with helium:oxygen. Peak inspiratory flow rate increased more with helium:oxygen. PaO2 increased with both gases, whereas PaCO2 decreased more with helium:oxygen (values shown are mean+/-SD) (52+/-6 torr [6.9+/-0.8 kPa] vs. 55+/-8 torr [7.3+/-1.1 kPa] and 48+/-6 torr [6.4+/-0.8 kPa] vs. 54+/-7 torr [7.2+/-0.9 kPa] for air:oxygen and helium:oxygen, respectively; p<.05). When hypercapnia was severe (PaCO2 >56 torr [7.5 kPa]), PaCO2 decreased by > or =7.5 torr (1 kPa) in six of seven patients with helium:oxygen and in four of seven patients with air:oxygen (p<.01). Dyspnea score (Borg scale) decreased more with helium:oxygen than with air:oxygen (3.7+/-1.6 vs. 4.5+/-1.4 and 2.8+/-1.6 vs. 4.6+/-1.5 for air:oxygen and helium:oxygen, respectively; p<.05). Mean arterial blood pressure decreased with air:oxygen (76+/-12 vs. 82+/-14 mm Hg; p<.05) but remained unchanged with helium:oxygen. CONCLUSION In decompensated COPD patients, noninvasive pressure support ventilation with helium:oxygen reduced dyspnea and PaCO2 more than air:oxygen, modified respiratory cycle times, and did not modify systemic blood pressure. These effects could prove beneficial in COPD patients with severe acute respiratory failure and might reduce the need for endotracheal intubation.