Mustapha Sebbane

Impact of systematic evaluation of pain and agitation in an intensive care unit.

Objective:To measure the impact of implementation of the systematic evaluation of pain and agitation by nurses using the Behavioral Pain Scale (BPS), the Numerical Rating Scale (NRS) for pain, and the Richmond Agitation Sedation Scale (RASS) associated with medical staff education in analgesia and sedation management in intensive care unit (ICU) patients. Design:Two-phase, prospective, controlled study. Setting:Twelve-bed medical-surgical ICU in a university hospital. Patients:Consecutive patients staying >24 hrs in ICU. Interventions:BPS, NRS, and RASS were measured twice daily, at rest, by independent observers during 21 wks (control group) and after 4 wks of training, by nurses during 29 wks (intervention group). In the intervention group, the treating physician was alerted in case of pain defined by BPS >5 or NRS >3 or in case of agitation defined by RASS >1. Measurements and Main Results:A total of 230 patients were included (control group, n = 100; intervention group, n = 130). Baseline characteristics were not significantly different. The incidence of pain and agitation decreased significantly in the intervention group: 63% vs. 42% (p = .002) and 29% vs. 12% (p = .002), respectively. Rate of severe pain and agitation events defined by NRS >6 and RASS >2, respectively, also decreased significantly. There were significantly more therapeutic changes in the intervention group in the way of an escalation but also in the way of a de-escalation for analgesic and psychoactive drugs. Compared with the control group, there was a marked decrease in the duration of mechanical ventilation (120 [interquartile range 48–312] vs. 65 (24–192) hrs, p = .01) and nosocomial infections rate (17% vs. 8%, p < .05) in the intervention group. There was no significant difference in median length of stay (9 [4, 15] vs. 7 [4, 13] days) and mortality in ICU (12 vs. 15%). Conclusions:Systematic evaluation of pain and agitation, and analgesics and sedatives need was associated with a decrease in incidence of pain and agitation, duration of mechanical ventilation and nosocomial infections.

Rapidly Progressive Diaphragmatic Weakness and Injury during Mechanical Ventilation in Humans

RATIONALE Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation (MV). Paradoxically, MV itself results in a rapid loss of diaphragmatic strength in animals. However, very little is known about the time course or mechanistic basis for such a phenomenon in humans. OBJECTIVES To determine in a prospective fashion the time course for development of diaphragmatic weakness during MV; and the relationship between MV duration and diaphragmatic injury or atrophy, and the status of candidate cellular pathways implicated in these phenomena. METHODS Airway occlusion pressure (TwPtr) generated by the diaphragm during phrenic nerve stimulation was measured in short-term (0.5 h; n = 6) and long-term (>5 d; n = 6) MV groups. Diaphragmatic biopsies obtained during thoracic surgery (MV for 2-3 h; n = 10) and from brain-dead organ donors (MV for 24-249 h; n = 15) were analyzed for ultrastructural injury, atrophy, and expression of proteolysis-related proteins (ubiquitin, nuclear factor-κB, and calpains). MEASUREMENTS AND MAIN RESULTS TwPtr decreased progressively during MV, with a mean reduction of 32 ± 6% after 6 days. Longer periods of MV were associated with significantly greater ultrastructural fiber injury (26.2 ± 4.8 vs. 4.7 ± 0.6% area), decreased cross-sectional area of muscle fibers (1,904 ± 220 vs. 3,100 ± 329 μm²), an increase of ubiquitinated proteins (+19%), higher expression of p65 nuclear factor-κB (+77%), and greater levels of the calcium-activated proteases calpain-1, -2, and -3 (+104%, +432%, and +266%, respectively) in the diaphragm. CONCLUSIONS Diaphragmatic weakness, injury, and atrophy occur rapidly in critically ill patients during MV, and are significantly correlated with the duration of ventilator support.

The Effectiveness of Noninvasive Positive Pressure Ventilation to Enhance Preoxygenation in Morbidly Obese Patients: A Randomized Controlled Study

BACKGROUND: Noninvasive positive-pressure ventilation (NPPV) with pressure support-ventilation and positive end-expiratory pressure are effective in providing oxygenation during intubation in hypoxemic patients. We hypothesized administration of oxygen (O2) using NPPV would more rapidly increase the end-tidal O2 concentration (ETo2) than preoxygenation using spontaneous ventilation (SV) in morbidly obese patients. METHODS: Twenty-eight morbidly obese patients were enrolled in this prospective randomized study. Administration of O2 for 5 min was performed either with SV group or with NPPV (pressure support = 8 cm H2O, positive end-expiratory pressure = 6 cm H2O) (NPPV group). ETo2 was measured using the anesthesia breathing circuit, and is expressed as a fraction of atmospheric concentration. The primary end-point was the number of patients with an ETo2 >95% at the end of O2 administration. Secondary end-points included the time to reach the maximal ETo2 and the ETo2 at the conclusion of O2 administration. RESULTS: A larger proportion of patients achieved a 95% ETo2 at 5 min with NPPV than SV (13/14 vs 7/14, P = 0.01). The time to reach the maximal ETo2 was significantly less in the NPPV than in the SV group (185 ± 46 vs 222 ± 42 s, P = 0.02). The mean ETo2 at the conclusion of O2 administration was larger in the NPPV group than the SV group (96.9 ± 1.3 vs 94.1 ± 2.0%, P < 0.001). A modest, although significant, increase in gastric distension was observed in the NPPV group. No adverse effects were observed in either group. CONCLUSION: Administration of O2 via a facemask with NPPV in the operating room is safe, feasible, and efficient in morbidly obese patients. In this population NPPV provides a more rapid O2 administration, achieving a higher ETo2.

Adaptive support ventilation prevents ventilator-induced diaphragmatic dysfunction in piglet: an in vivo and in vitro study.

Background:Contrary to adaptive support ventilation (ASV), prolonged totally controlled mechanical ventilation (CMV) results in the absence of diaphragm activity and causes ventilator-induced diaphragmatic dysfunction. Because main-taining respiratory muscles at rest is likely a major cause of ventilator-induced diaphragmatic dysfunction, ASV may prevent its occurrence in comparison with CMV. The aim of our study was to compare the effects of ASV with those of CMV on both in vivo and in vitro diaphragmatic properties. Methods:Two groups of six anesthetized piglets were ventilated during a 72-h period. Piglets in the CMV group (n = 6) were ventilated without spontaneous ventilation, and piglets in the ASV group (n = 6) were ventilated with spontaneous breaths. Transdiaphragmatic pressure was measured after bilateral, supramaximal transjugular stimulation of the two phrenic nerves. A pressure–frequency curve was drawn after stimulation from 20 to 120 Hz of the phrenic nerves. Diaphragm fiber proportions and mean sectional area were evaluated. Results:After 72 h of ventilation, transdiaphragmatic pressure decreased by 30% of its baseline value in the CMV group, whereas it did not decrease in the ASV group. Although CMV was associated with an atrophy of the diaphragm (evaluated by mean cross-sectional area of both the slow and fast myosin chains), atrophy was not detected in the ASV group. Conclusion:Maintaining diaphragmatic contractile activity by using the ASV mode may protect the diaphragm against the deleterious effect of prolonged CMV, as demonstrated both in vitro and in vivo, in healthy piglets.

Lung morphology predicts response to recruitment maneuver in patients with acute respiratory distress syndrome.

Objectives:The impact of recruitment maneuvers on gas exchange, hemodynamics, alveolar recruitment, and hyperinflation is highly variable among patients with acute respiratory distress syndrome. The objective was to determine whether differences in lung morphology, defined as differences in the pulmonary distribution of aeration loss, predict the response to recruitment maneuvers. Design:Prospective study. Setting:A 16-bed medical–surgical intensive care unit in a university hospital. Measurements and Main Results:Nineteen consecutive patients with early acute lung injury/acute respiratory distress syndrome were studied. Computed tomography scans, respiratory mechanics, hemodynamics, and gas exchange were obtained at zero end-expiratory pressure during an open-lung ventilation (controlled mode, tidal volume 6 mL/kg of ideal body weight, positive end-expiratory pressure set 2 cm H2O above the lower inflection point of the inspiratory pressure volume curve at zero end-expiratory pressure) during a recruitment maneuver (continuous positive airway pressure of 40 cm H2O for 40 secs), and, finally, 5 mins after the recruitment maneuver during open-lung ventilation. Nine patients presented focal and 10 presented nonfocal lung morphology at zero end-expiratory pressure. Recruitment maneuver-induced recruited volume after 5 mins of open-lung ventilation was 48 ± 66 mL and 417 ± 293 mL in patients with focal and nonfocal lung morphology, respectively (p = .0009). Recruitment maneuver-induced alveolar hyperinflation represented 23% ± 14% and 8% ± 9% of total lung volume in patients with focal and nonfocal morphology, respectively (p = .007). In patients with focal lung morphology, hyperinflated lung volume was significantly greater during and 5 mins after (316 ± 155 mL) than immediately before recruitment maneuvers (150 ± 175 mL; p = .0407. Conclusion:Lung morphology at zero end-expiratory pressure predicts the response to recruitment maneuvers. Patients with focal lung morphology are at risk for significant hyperinflation during the recruitment maneuvers, and lung recruitment is rather limited.

Performance characteristics of five new anesthesia ventilators and four intensive care ventilators in pressure-support mode: a comparative bench study.

Background:During the past few years, many manufacturers have introduced new modes of ventilation in anesthesia ventilators, especially partial-pressure modalities. The current bench test study was designed to compare triggering and pressurization of five new anesthesia ventilators with four intensive care unit ventilators. Methods:Ventilators were connected to a two-compartment lung model. One compartment was driven by an intensive care unit ventilator to mimic “patient” inspiratory effort, whereas the other was connected to the tested ventilator. The settings of ventilators were positive end-expiratory pressures of 0 and 5 cm H2O, and pressure-support ventilation levels of 10, 15, and 20 cm H2O with normal and high “patient” inspiratory effort. For the anesthesia ventilators, all the measurements were obtained for a low (1 l/min) and a high (10 l/min) fresh gas flow. Triggering delay, triggering workload, and pressurization at 300 and 500 ms were analyzed. Results:For the five tested anesthesia ventilators, the pressure-support ventilation modality functioned correctly. For inspiratory triggering, the three most recent anesthesia machines (Fabius, Drägerwerk AG, Lübeck, Germany; Primus, Drägerwerk AG; and Avance, GE-Datex-Ohemda, Munchen, Germany) had a triggering delay of less than 100 ms, which is considered clinically satisfactory and is comparable to intensive care unit machines. The use of positive end-expiratory pressure modified the quality of delivered pressure support for two anesthesia ventilators (Kion, Siemens AG, Munich, Germany; and Felix, Taema, Antony, France). Three of the five anesthesia ventilators exhibited pressure-support ventilation performance characteristics comparable to those of the intensive care unit machines. Increasing fresh gas flow (1 to 10 l/min) in the internal circuit did not influence the pressure-support ventilation performance of the anesthesia ventilators. Conclusion:Regarding trigger sensitivity and the system’s ability to meet inspiratory flow during pressure-supported breaths, the most recent anesthesia ventilators have comparable performances of recent-generation intensive care unit ventilators.

Predicting peripheral venous access difficulty in the emergency department using body mass index and a clinical evaluation of venous accessibility.

BACKGROUND Peripheral venous (PV) cannulation, one of the most common technical procedures in Emergency Medicine, may prove challenging, even to experienced Emergency Department (ED) staff. Morbid obesity (body mass index [BMI] ≥ 40) has been reported as a risk factor for PV access failure in the operating room. OBJECTIVES We investigated PV access difficulty in the ED, across BMI categories, focusing on patient-related predicting factors. METHODS Prospective, observational study including adult patients requiring PV lines. Operators were skilled nurses and physicians. PV accessibility was clinically evaluated before all cannulation attempts, using vein visibility and palpability. Patient and PV placement characteristics were recorded. Primary outcome was failure at first attempt. Outcome frequency and comparisons between groups were examined. Predictors of difficult cannulation were explored using logistic regression. A p-value <0.05 was considered significant. RESULTS PV lines were placed in 563 consecutive patients (53 ± 23 years, BMI: 26 ± 7 kg/m(2)), with a success rate of 98.6%, and a mean attempt of 1.3 ± 0.7 (range 1-7). Failure at the first attempt was recorded in 21% of patients (95% confidence interval [CI] 17.6-24.4). Independent risk factors were: a BMI ≥ 30 (odds ratio [OR] 1.98, 95% CI 1.09-3.60), a BMI < 18.5 (OR 2.24; 95% CI 1.07-4.66), an unfavorable (OR 1.66, 95% CI 1.02-2.69), and very unfavorable clinical assessment of PV accessibility (OR 2.38, 95% CI 1.15-4.93). CONCLUSION Obesity, underweight, an unfavorable, and a very unfavorable clinical evaluation of PV accessibility are independent risk factors for difficult PV access. Early recognition of patients at risk could help in planning alternative approaches for achieving rapid PV access.

Comparison of conventional and high-sensitivity troponin in patients with chest pain: A collaborative meta-analysis

BACKGROUND Multiple studies have evaluated the diagnostic and prognostic performance of conventional troponin (cTn) and high-sensitivity troponin (hs-cTn). We performed a collaborative meta-analysis comparing cTn and hs-cTn for diagnosis of acute myocardial infarction (AMI) and assessment of prognosis in patients with chest pain. METHODS MEDLINE/PubMed, Cochrane CENTRAL, and EMBASE were searched for studies assessing both cTn and hs-cTn in patients with chest pain. Study authors were contacted and many provided previously unpublished data. RESULTS From 17 included studies, there were 8,644 patients. Compared with baseline cTn, baseline hs-cTn had significantly greater sensitivity (0.884 vs 0.749, P < .001) and negative predictive value (NPV; 0.964 vs 0.935, P < .001), whereas specificity (0.816 vs 0.938, P < .001) and positive predictive value (0.558 vs 0.759, P < .001) were significantly reduced. Based on summary receiver operating characteristic curves, test performance for the diagnosis of AMI was not significantly different between baseline cTn and hs-cTn (0.90 [95% CI 0.85-0.95] vs 0.92 [95% CI 0.90-0.94]). In a subanalysis of 6 studies that alternatively defined AMI based on hs-cTn, cTn had lower sensitivity (0.666, P < .001) and NPV (0.906, P < .001). Elevation of baseline hs-cTn, but negative baseline cTn, was associated with increased risk of death or nonfatal myocardial infarction during follow-up (P < .001) compared with both negative. CONCLUSION High-sensitivity troponin has significantly greater early sensitivity and NPV for the diagnosis of AMI at the cost of specificity and positive predictive value, which may enable early rule in/out of AMI in patients with chest pain. Baseline hs-cTn elevation in the setting of negative cTn is also associated with increased nonfatal myocardial infarction or death during follow-up.

Adaptive support and pressure support ventilation behavior in response to increased ventilatory demand.

Background:Dual-control modes of ventilation adapt the pressure delivery to keep a volume target in response to changes in respiratory mechanics, but they may respond poorly to changes in ventilatory demand. Adaptive support ventilation (ASV), a complex minute volume-targeted pressure-regulated ventilation, was compared to adaptive pressure ventilation (APV), a dual-mode in which the pressure level is adjusted to deliver a preset tidal volume, and to pressure support ventilation (PSV) when facing an increase in ventilatory demand. Methods:A total of 14 intensive care unit patients being weaned off mechanical ventilation were included in this randomized crossover study. The effect of adding a heat-and-moisture exchanger to augment circuit dead space was assessed with a same fixed level of ASV, PSV, and APV. Results:Arterial blood gases, ventilator response, and patient respiratory effort parameters were evaluated at the end of the six periods. Adding dead space significantly increased minute ventilation and Paco 2 values with the three modes. Indexes of respiratory effort (pressure-time index of respiratory muscles and work of breathing) increased with all ventilatory modes after dead-space augmentation. This increase was significantly greater with APV than with PSV or ASV (P < 0.05). The assistance delivered during APV decreased significantly with dead-space from 12.7 ± 2.6 to 6.7 ± 1.4 cm H2O, whereas no change occurred with ASV and PSV. Conclusions:ASV and PSV behaved differently but ended up with similar pressure level facing acute changes in ventilatory demand, by contrast to APV (a simple volume-guaranteed pressure-control mode), in which an increase in ventilatory demand results in a decrease in the pressure support provided by the ventilator.

Early rule out of acute myocardial infarction in ED patients: value of combined high-sensitivity cardiac troponin T and ultrasensitive copeptin assays at admission☆ , ☆☆

OBJECTIVE We sought to evaluate the added value of ultrasensitive copeptin (us-copeptin) for early rule out of acute myocardial infarction in a prospective cohort of emergency department (ED) patients with acute chest pain. METHODS This was a prospective study including consecutive patients with acute chest pain presenting to the ED within 12 hours of symptom onset. High-sensitivity cardiac troponin T (hs-cTnT, Roche Diagnostics, Meylan, France) and us-copeptin (ThermoFisher Scientific, Clichy, France) were blindly assayed from venous blood samples obtained at admission. Diagnosis was made by 2 ED physicians using all available data and serial cardiac troponin I as the biochemical standard. Diagnostic performances of us-copeptin combined with hs-cTnT were assessed using logistic regression. Analysis was conducted in all patients and in patients without ST-elevation myocardial infarction. RESULTS A total of 194 patients were included (age, 61 [48-75] years; male sex, 63%). Acute myocardial infarction occurred in 52 (27%) patients, including non-ST-elevation myocardial infarction (NSTEMI) in 25 (13%). Patients with acute myocardial infarction had higher levels of hs-cTnT (50 [95% confidence interval, 19-173] ng/L) and us-copeptin (30 [13-113] pmol/L) at admission compared with those without (P < .05). Combination of markers significantly improved receiver operating characteristic area under the curve (from 0.89 [0.85-0.92] for hs-cTnT alone to 0.93 [0.89-0.97], P = .018). Sensitivity and negative predictive value were increased, particularly for NSTEMI diagnosis (sensitivity, 76% [54.9-90.6] to 96% [79.6-99.9]; negative predictive value, 95% [90.4-98.3] to 98.9% [94.2 to 100]). CONCLUSION Assessment of us-copeptin combined with hs-cTnT on ED admission could allow safe and early rule out of NSTEMI for patients with negative results on both markers and help identify patients who may be suitable for discharge.