La Biblio du Mois: Juin 2015
Dans La Biblio du Mois: du choc hémorragique, des péridurales et des Pseudomonas aeruginosa toto-R. Et une revue de la littérature du NEJM sur les antagonistes de la vasopressine.
Bonne lecture !
Mesure du débit cardiaque par analyse de l’onde pouls en anesthésie neurochirurgicaleBackground Maintaining adequate organ perfusion during high-risk surgery requires continuous monitoring of cardiac output to optimise haemodynamics. Oesophageal Doppler Cardiac Output monitoring (DCO) is commonly used in this context, but has some limitations. Recently, the cardiac output estimated by pulse pressure analysis- (PPCO) was developed. This study evaluated the agreement of cardiac output variations estimated with 9 non-commercial algorithms of PPCO compared with those obtained with DCO.Methods High-risk patients undergoing neurosurgery were monitored with invasive blood pressure and DCO. For each patient, 9 PPCO algorithms and DCO were recorded before and at the peak effect for every haemodynamic challenge.Results Sixty-two subjects were enrolled; 284 events were recorded, including 134 volume expansions and 150 vasopressor boluses. Among the 9 algorithms tested, the Liljestrand-Zander model led to the smallest bias (0.03 litre min−1 [−1.31, +1.38] (0.21 litre min−1 [−1.13; 1.54] after volume expansion and −0.13 litre min−1 [−1.41, 1.15] after vasopressor use). The corresponding percentage of the concordance was 91% (86% after volume expansion and 94% after vasopressor use). The other algorithms, especially those using the Winkessel concept and the area under the pressure wave, were profoundly affected by the vasopressor.Conclusions Among the 9 PPCO algorithms examined, the Liljestrand-Zander model demonstrated the least bias and best limits of agreement, especially after vasopressor use. Using this particular algorithm in association with DCO calibration could represent a valuable option for continuous cardiac output monitoring of high risk patients.
50 coups pour acquérir une compétence acceptableBackground Cumulative sum (CUSUM) analysis has been used for assessing competence of trainees learning new technical skills. One of its disadvantages is the required definition of acceptable and unacceptable success rates. We therefore monitored the development of competence amongst trainees new to obstetric epidural anaesthesia in a large public hospital.Methods Obstetric epidural data were collected prospectively between January 1996 and December 2011. Success rates for inexperienced trainees were calculated retrospectively for (1) the whole database, (2) for each consecutive attempt and (3) each trainee’s individual overall success rate. Acceptable and unacceptable success rates were defined and CUSUM graphs generated for each trainee. Competence was assessed for each trainee and the number of attempts to reach competence recorded.Results Mean (SD) success rate for all inexperienced trainees was 76.8 (0.1%), range 63–90%. Consecutive attempt success rate produced a learning curve with a mean success rate commencing at 58% on attempt 1. After attempt 10 the attempt number had no effect on subsequent success rates. From these results, the acceptable and unacceptable success rates were set at 65 and 55% respectively. CUSUM graphs demonstrated 76 out of 81 trainees competent after a mean of 46 (22) attempts.Conclusions CUSUM is useful for assessing trainee epidural competence. Trainees require approximately 50 attempts, as defined by CUSUM, to reach competence.
Objectives Whole-body ischemia during out-of-hospital cardiac arrest triggers immediate activation of inflammatory systems leading to a sepsis-like syndrome. The aim was to investigate the association between level of systemic inflammation and mortality in survivors after out-of-hospital cardiac arrest treated with targeted temperature management.Design Post hoc analysis.Setting Single-center study of a prospective multicenter randomized study.Patients One hundred sixty-nine patients (99%) with available blood samples out of 171 patients included in the Target Temperature Management trial, randomly assigning patients to targeted temperature management at 33°C or 36°C.Intervention None.Measurements and Main Results At baseline and 24, 48, and 72 hours after out-of-hospital cardiac arrest, blood samples were obtained and screened for a battery of inflammatory markers. Level of interleukin-1β, interleukin-2, interleukin-4, interleukin-5, interleukin-6, interleukin-9, interleukin-10, interleukin-12, interleukin-13, tumor necrosis factor-α, interferon-γ, C-reactive protein, and procalcitonin were measured. Mortality at 30 days was evaluated by Cox analysis, and the predictive capability of inflammatory markers was evaluated by area under the curve. Level of all inflammatory markers changed significantly within 72 hours after out-of-hospital cardiac arrest (all p values < 0.001), but only procalcitonin levels showed overall differences between nonsurvivors and survivors (p = 0.0002). At baseline, interleukin-6 was independently associated with mortality, whereas both interleukin-6 levels (hazard ratio = 1.23 [1.01–1.49]; p = 0.04) and procalcitonin levels (hazard ratio = 1.20 [1.03–1.39]; p = 0.02) 24 hours after out-of-hospital cardiac arrest were associated with 30-day mortality with no interactions between targeted temperature management group and levels of interleukin-6 (p = 0.25) or procalcitonin (p = 0.85). None of the other inflammatory markers were independently associated with mortality. Area under the curve for procalcitonin and interleukin-6, 24 hours after out-of-hospital cardiac arrest, were 0.74 and 0.63, respectively.Conclusions Level of inflammation, assessed by interleukin-6 and procalcitonin, was independently associated with increased mortality with the highest discriminative value obtained 24 hours after out-of-hospital cardiac arrest. Interventions aiming at decreasing level of inflammation as a way to improve outcome may be investigated in future studies.
Rationale Several studies in mild chronic obstructive pulmonary disease (COPD) have shown a higher than normal ventilatory equivalent for carbon dioxide (V.e/V.co2) during exercise. Our objective was to examine pulmonary gas exchange abnormalities and the mechanisms of high V.e/V.co2 in mild COPD and its impact on dyspnea and exercise intolerance.
Methods: Twenty-two subjects (11 patients with GOLD [Global Initiative for Chronic Obstructive Lung Disease] grade 1B COPD, 11 age-matched healthy control subjects) undertook physiological testing and a symptom-limited incremental cycle exercise test with arterial blood gas collection.Measurements and Main Results Patients (post-bronchodilator FEV1: 94 ± 10% predicted; mean ± SD) had evidence of peripheral airway dysfunction and reduced peak oxygen uptake compared with control subjects (80 ± 18 vs. 113 ± 24% predicted; P < 0.05). Arterial blood gases were within the normal range and effective alveolar ventilation was not significantly different from control subjects throughout exercise. The alveolar–arterial O2 tension gradient was elevated at rest and throughout exercise in COPD (P < 0.05). V.e/V.co2, dead space to tidal volume ratio (Vd/Vt), and arterial to end-tidal CO2 difference were all higher (P < 0.05) in patients with COPD than in control subjects during exercise. In patients with COPD versus control subjects, there was significant dynamic hyperinflation and greater tidal volume constraints (P < 0.05). Standardized dyspnea intensity ratings were also higher (P < 0.05) in patients with COPD versus control subjects in association with higher ventilatory requirements. Within all subjects, Vd/Vt correlated with the V.e/V.co2 ratio during submaximal exercise (r = 0.780, P < 0.001).Conclusions High Vd/Vt was the most consistent gas exchange abnormality in smokers with only mild spirometric abnormalities. Compensatory increases in minute ventilation during exercise maintained alveolar ventilation and arterial blood gas homeostasis but at the expense of earlier dynamic mechanical constraints, greater dyspnea, and exercise intolerance in mild COPD.
BACKGROUND Whether noninvasive ventilation should be administered in patients with acute hypoxemic respiratory failure is debated. Therapy with high-flow oxygen through a nasal cannula may offer an alternative in patients with hypoxemia.
METHODS We performed a multicenter, open-label trial in which we randomly assigned patients without hypercapnia who had acute hypoxemic respiratory failure and a ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen of 300 mm Hg or less to high-flow oxygen therapy, standard oxygen therapy delivered through a face mask, or noninvasive positive-pressure ventilation. The primary outcome was the proportion of patients intubated at day 28; secondary outcomes included all-cause mortality in the intensive care unit and at 90 days and the number of ventilator-free days at day 28.
RESULTS A total of 310 patients were included in the analyses. The intubation rate (primary outcome) was 38% (40 of 106 patients) in the high-flow–oxygen group, 47% (44 of 94) in the standard group, and 50% (55 of 110) in the noninvasive-ventilation group (P=0.18 for all comparisons). The number of ventilator-free days at day 28 was significantly higher in the high-flow–oxygen group (24±8 days, vs. 22±10 in the standard-oxygen group and 19±12 in the noninvasive-ventilation group; P=0.02 for all comparisons). The hazard ratio for death at 90 days was 2.01 (95% confidence interval [CI], 1.01 to 3.99) with standard oxygen versus high-flow oxygen (P=0.046) and 2.50 (95% CI, 1.31 to 4.78) with noninvasive ventilation versus high-flow oxygen (P=0.006).
CONCLUSIONS In patients with nonhypercapnic acute hypoxemic respiratory failure, treatment with high-flow oxygen, standard oxygen, or noninvasive ventilation did not result in significantly different intubation rates. There was a significant difference in favor of high-flow oxygen in 90-day mortality.
Solutions hypertoniques et chocs hémorragiques traumatiques: attention à l’hypocoagulation et hyperfibrinolyse !
Impaired hemostasis frequently occurs after traumatic shock and resuscitation. The prehospital fluid administered can exacerbate subsequent bleeding and coagulopathy. Hypertonic solutions are recommended as first-line treatment of traumatic shock; however, their effects oncoagulation are unclear. This study explores the impact of resuscitation with various hypertonic solutions on early coagulopathy after trauma. We conducted a prospective observational subgroup analysis of large clinical trial on out-of-hospital single-bolus (250 mL) hypertonic fluid resuscitation of hemorrhagic shock trauma patients (systolic blood pressure, ≤70 mmHg). Patients received 7.5% NaCl (HS), 7.5% NaCl/6% Dextran 70 (HSD), or 0.9% NaCl (normal saline [NS]) in the prehospital setting. Thirty-four patients were included: 9 HS, 8 HSD, 17 NS. Treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. The HSD-resuscitated patients had higher admission international normalized ratio values and more hypocoagulable patients, 62% (vs. 55% HS, 47% NS; P < 0.05). Prothrombotic tissue factor was elevated in shock treated with NS but depressed in both HS and HSD groups. Fibrinolytic tissue plasminogen activator and anti–fibrinolytic plasminogen activator inhibitor type 1 were increased by shock but not thrombin-activatable fibrinolysis inhibitor. The HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in more hypocoagulability and hyperfibrinolysis. We concluded that resuscitation with hypertonic solutions, particularly HSD, worsens hypocoagulability and hyperfibrinolysis after hemorrhagic shock in trauma through imbalances in both procoagulants and anticoagulants and both profibrinolytic and antifibrinolytic activities.
Objectives Resistance to all β-lactams is emerging among Pseudomonas aeruginosa (PA) clinical isolates. Aztreonam and cefepime act synergistically in vitro against AmpC overproducing PA isolates. The objective of this study was to evaluate the clinical efficacy of this treatment in ICU patients infected with multidrug-resistant PA.
Material and methods Retrospective study (2 years, 2 ICUs) in a tertiary university hospital. Inclusion criteria were proven infection with evidence of a bacterial strain of PA resistant to all β-lactams and treated with the association of at least aztreonam plus cefepime. Treatment was considered effective for pneumonia using CPIS scores at the end of treatment and for other infections, using the SOFA score and signs of infection improvement at the end of treatment. Infectious episodes were classified as cure or failure.
Results Thirteen patients were included (10 nosocomial pneumonia, 3 nosocomial intra-abdominal infections). The median [25th–75th percentiles] admission SAPS2 score was 54 [51–69] and the median SOFA score at the beginning of infection was 7 [4–8]. The median CPIS scores for pneumonia at the beginning and end of treatment were 9 [7–10.5] and 2 [0.75–5.5]. The duration of treatment with the combination of aztreonam plus cefepime was 14 days [9.5–16]. Nine episodes were classified as cures and 4 as failures, indicating a clinical efficacy of 69.2%. Overall mortality was 38.5%.
Discussion These data suggest that the association of cefepime plus aztreonam could be an attractive alternative in the treatment of infections with multidrug-resistant PA to all β-lactams with a clinical efficacy rate of 69%.