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Background: Physical restraint is frequently used in intensive care units to prevent patients' life‐threatening removal of indwelling devices. In France, their use is poorly studied. Therefore, to evaluate the need for physical restraint, we have designed and implemented a decision support tool. Aims: Besides describing the prevalence of physical restraint use, this study aimed to assess whether the implementation of a nursing decision support tool had an impact on restraint use and to identify the factors associated with this use. Study Design: A large observational, multicentre study with a repeated one‐day point prevalence design was conducted. All adult patients hospitalized in intensive care units were eligible for this study. Two study periods were planned: before (control period) and after (intervention period) the deployment of the decision support tool and staff training. A multilevel model was performed to consider the centre effect. Results: During the control period, 786 patients were included, and 510 were in the intervention period. The prevalence of physical restraint was 28% (95% CI: 25.1%–31.4%) and 25% (95% CI: 21.5%–29.1%) respectively (χ2 = 1.35; p =.24). Restraint was applied by the nurse and/or nurse assistant in 96% of cases in both periods, mainly to wrists (89% vs. 83%, p =.14). The patient‐to‐nurse ratio was significantly lower in the intervention period (1:3.0 ± 1 vs. 1:2.7 ± 0.7, p <.001). In multivariable analysis, mechanical ventilation was associated with physical restraint (aOR [95% CI] = 6.0 [3.5–10.2]). Conclusion: The prevalence of physical restraint use in France was lower than expected. In our study, the decision support tool did not substantially impact physical restraint use. Hence, the decision support tool would deserve to be assessed in a randomized controlled trial. Relevance to Clinical Practice: The decision to physically restrain a patient could be protocolised and managed by critical care nurses. A regular evaluation of the level of sedation could allow the most deeply sedated patients to be exempted from physical restraint. [ABSTRACT FROM AUTHOR]

Objectives: In patients with spinal cord injury, spinal cord injury-immune depression syndrome induces pneumonia. We aimed to develop a new spinal cord injury-immune depression syndrome mouse model and to test antiprogrammed cell death 1 therapy.Design: Experimental study.Setting: Research laboratory.Subjects: RjOrl: SWISS and BALB/cJ mice.Interventions: Mouse model of spinal cord injury-immune depression syndrome followed by a methicillin-susceptible Staphylococcus aureus pneumonia. Lung injuries were assessed by histologic analysis. Membrane markers and intracytoplasmic cytokines were assessed by flow cytometry. Cytokine production was assessed by quantitative polymerase chain reaction (messenger RNA) and enzyme-linked immunosorbent assay (protein). Animals were treated with blocking antiprogrammed cell death 1 antibodies (intraperitoneal injection).Measurements and Main Results: Spinal cord injury mice were more susceptible to methicillin-susceptible S. aureus pneumonia (increased mortality rate). An early inflammatory response was observed in spinal cord injury mice characterized in lungs by a decreased percentage of aerated tissue, an increased production of proinflammatory cytokines (tumor necrosis factor-α). In spleen, an increased expression of major histocompatibility complex class II molecules on dendritic cells, and an increased production of proinflammatory cytokines (interleukin-12, interferon-γ) was observed. Following this pulmonary and systemic inflammation, spinal cord injury-immune depression syndrome was observed in spleens as acknowledged by a decrease of spleen's weight, a lymphopenia, a decrease of major histocompatibility complex class II expression on dendritic cells. An increase of interleukin-10 production and the increase of a cell exhaustion marker expression, programmed cell death 1 receptor on T-cell were also observed. Blockade of programmed cell death 1 molecules, improved survival of spinal cord injury infected mice and enhanced interferon-γ production by natural killer T cells as well as number of viable CD4 T cells.Conclusions: This model of spinal cord injury in mice mimics a clinical scenario rendering animals prone to a secondary pneumonia. We show for the first time an acute T-cell exhaustion-like phenomenon following an initial inflammatory response. Finally, inhibition of exhaustion pathway should be considered as a new therapeutic option to overcome spinal cord injury-immune depression syndrome and to decrease the rate of nosocomial pneumonia. [ABSTRACT FROM AUTHOR]

Background: Intravenous (IV) milrinone, in combination with induced hypertension, has been proposed as a treatment option for cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). However, data on its safety and efficacy are scarce. Methods: This was a controlled observational study conducted in an academic hospital with prospectively and retrospectively collected data. Consecutive patients with cerebral vasospasm following aSAH and treated with both IV milrinone (0.5 µg/kg/min−1, as part of a strict protocol) and induced hypertension were compared with a historical control group receiving hypertension alone. Multivariable analyses aimed at minimizing potential biases. We assessed (1) 6-month functional disability (defined as a score between 2 and 6 on the modified Rankin Scale) and vasospasm-related brain infarction, (2) the rate of first-line or rescue endovascular angioplasty for vasospasm, and (3) immediate tolerance to IV milrinone. Results: Ninety-four patients were included (41 and 53 in the IV milrinone and the control group, respectively). IV milrinone infusion was independently associated with a lower likelihood of 6-month functional disability (adjusted odds ratio [aOR] = 0.28, 95% confidence interval [CI] = 0.10–0.77]) and vasospasm-related brain infarction (aOR = 0.19, 95% CI 0.04–0.94). Endovascular angioplasty was less frequent in the IV milrinone group (6 [15%] vs. 28 [53%] patients, p = 0.0001, aOR = 0.12, 95% CI 0.04–0.38). IV milrinone (median duration of infusion, 5 [2–8] days) was prematurely discontinued owing to poor tolerance in 12 patients, mostly (n = 10) for "non/hardly-attained induced hypertension" (mean arterial blood pressure < 100 mmHg despite 1.5 µg/kg/min−1 of norepinephrine). However, this event was similarly observed in IV milrinone and control patients (n = 10 [24%] vs. n = 11 [21%], respectively, p = 0.68). IV milrinone was associated with a higher incidence of polyuria (IV milrinone patients had creatinine clearance of 191 [153–238] ml/min−1) and hyponatremia or hypokalemia, whereas arrhythmia, myocardial ischemia, and thrombocytopenia were infrequent. Conclusions: Despite its premature discontinuation in 29% of patients as a result of its poor tolerance, IV milrinone was associated with a lower rate of endovascular angioplasty and a positive impact on long-term neurological and radiological outcomes. These preliminary findings encourage the conduction of confirmatory randomized trials. [ABSTRACT FROM AUTHOR]

Pragmatically, because moderate-to-severe angiographic vasospasm, even if asymptomatic, was the trigger for the initiation of IV milrinone, ensuring that angiographic vasospasm resolved (at least partly) was key in the weaning process from IV milrinone in the Milrispasm study. Indeed, after 2 days of milrinone IV infusion, if vasospasm was stable or even worse compared with its aspect on the previous CT angiography, affirming that IV milrinone failed in vasospasm reversal is challenging because its natural course could have been a significantly more severe vasospasm at that time. [Extracted from the article]