Doubling Intensive Care Unit Capacity by Surging Onto Medical-Surgical Units During the COVID-19 Pandemic.

INTRODUCTION: The ability of an organization to accommodate a large influx of patients during a prolonged period is dependent on surge capacity. The aim of this article is to describe the surge experience with space, supplies, and staff training in response to COVID-19 and provide guidance to other organizations. BACKGROUND: A hospital's response to a large-scale event is greatly impacted by the ability to surge and, depending on the type of threat, to maintain a sustained response. To identify surge capacity, an organization must first consider the type of event to appropriately plan resources. PREPARATION PROCESS: An epidemic surge drill, conducted in 2012, served as a guide in planning for the COVID-19 pandemic. The principles of crisis standards of care and a hospital incident command structure were used to clearly define roles, open lines of communication, and inform our surge plan. Preparation began by collaborating with multidisciplinary groups to acquire the most appropriate space, as well as adequate supplies, and identify and train staff. IMPLEMENTATION: Teams were formed to identify the necessary resources to expand the intensive care unit (ICU) environment quickly and efficiently. Educational training was developed for redeployed staff. OUTCOMES: Beth Israel Deaconess Medical Center experienced the largest surge of ICU patients within a hospital system in the state of Massachusetts. The ICU capacity was expanded by 93% from 77 to 149 beds, and the surge was maintained for approximately 9 weeks. Shadowing experiences before the actual surge were extremely valuable. CONCLUSIONS: Planning for the surge of critically ill patients required a thoughtful, collaborative approach. Ongoing staff support and communication from nursing leadership were necessary to ensure safe, effective care for critically ill patients in a new and dynamic environment.

Automated surveillance for ventilator-associated events.

BACKGROUND: The US Centers for Disease Control and Prevention has implemented a new, multitiered definition for ventilator-associated events (VAEs) to replace their former definition of ventilator-associated pneumonia (VAP). We hypothesized that the new definition could be implemented in an automated, efficient, and reliable manner using the electronic health record and that the new definition would identify different patients than those identified under the previous definition. METHODS: We conducted a retrospective cohort analysis using an automated algorithm to analyze all patients admitted to the ICU at a single urban, tertiary-care hospital from 2008 to 2013. RESULTS: We identified 26,466 consecutive admissions to the ICU, 10,998 (42%) of whom were mechanically ventilated and 675 (3%) of whom were identified as having any VAE. Any VAE was associated with an adjusted increased risk of death (OR, 1.91; 95% CI, 1.53-2.37; P < .0001). The automated algorithm was reliable (sensitivity of 93.5%, 95% CI, 77.2%-98.8%; specificity of 100%, 95% CI, 98.8%-100% vs a human abstractor). Comparison of patients with a VAE and with the former VAP definition yielded little agreement (κ = 0.06). CONCLUSIONS: A fully automated method of identifying VAEs is efficient and reliable within a single institution. Although VAEs are strongly associated with worse patient outcomes, additional research is required to evaluate whether and which interventions can successfully prevent VAEs.

When policy gets it right: variability in u.s. Hospitals' diagnosis of ventilator-associated pneumonia*.

OBJECTIVE: The Centers for Disease Control has recently proposed a major change in how ventilator-associated pneumonia is defined. This has profound implications for public reporting, reimbursement, and accountability measures for ICUs. We sought to provide evidence for or against this change by quantifying limitations of the national definition of ventilator-associated pneumonia that was in place until January 2013, particularly with regard to comparisons between, and ranking of, hospitals and ICUs. DESIGN: A prospective survey of a nationally representative group of 43 hospitals, randomly selected from the American Hospital Association Guide (2009). Subjects classified six standardized vignettes of possible cases of ventilator-associated pneumonia as pneumonia or no pneumonia. SUBJECTS: Individuals responsible for ventilator-associated pneumonia surveillance at 43 U.S. hospitals. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We measured the proportion of standardized cases classified as ventilator-associated pneumonia. Of 138 hospitals consented, 61 partially completed the survey and 43 fully completed the survey (response rate 44% and 31%, respectively). Agreement among hospitals about classification of cases as ventilator-associated pneumonia/not ventilator-associated pneumonia was nearly random (Fleiss κ 0.13). Some hospitals rated 0% of cases as having pneumonia; others classified 100% as having pneumonia (median, 50%; interquartile range, 33-66%). Although region of the country did not predict case assignment, respondents who described their region as "rural" were more likely to judge a case to be pneumonia than respondents elsewhere (relative risk, 1.25, Kruskal-Wallis chi-square, p = 0.03). CONCLUSIONS: In this nationally representative study of hospitals, assignment of ventilator-associated pneumonia is extremely variable, enough to render comparisons between hospitals worthless, even when standardized cases eliminate variability in clinical data abstraction. The magnitude of this variability highlights the limitations of using poorly performing surveillance definitions as methods of hospital evaluation and comparison, and our study provides very strong support for moving to a more objective definition of ventilator-associated complications.

Estimated nursing workload for the implementation of ventilator bundles.

BACKGROUND: Ventilator-associated pneumonia is a common healthcare-associated infection with high attributable morbidity and mortality. Prevention strategies, including prevention bundles, have been widely adopted across the USA. However, the nursing resources required to implement these bundles, and their effect on other aspects of intensive care unit patient care, are unknown. METHODS: We conducted a survey of all critical care nurses at our institution to determine the time required, and impact of, a prevention bundle at our hospital. RESULTS: Nurses estimated that the standard ventilator bundle requires a median of 115 min (IQR: 74-182) per patient per day. Although the majority of nurses did not perceive that other patient care tasks were delayed by these prevention activities, this was not universal; 29% (95% CI 21% to 39%) of respondents reported that other patient care tasks were sometimes delayed because time was allocated to ventilator bundle activities. CONCLUSIONS: Our estimates may serve as potentially important inputs for cost-effectiveness and decision analyses related to intensive care unit prevention activities. Further research should include direct observations about nursing time allocation related to prevention activities.

[Utrophin, a way to cure Duchenne muscle dystrophy]. / Guérir la myopathie de Duchenne par l'utrophine ?

Duchenne muscle dystrophy results from the absence of dystrophin, a cytoskeletal protein of the muscle fibre. Dystrophin plays an essential role in the integrity of the membrane-associated protein complexes connected to the extracellular matrix. On chromosome 6 is located the gene of a protein presenting 80 % homology with dystrophin : utrophin, which is expressed at the neuromuscular junction. The review examines if utrophin can replace dystrophin and correct the structural and functional characteristics of the myopathy, and how the improvements can be quantitatively expressed. In transgenic mice, deficient in dystrophin, but overexpressing large quantities of utrophin, the latter is found on structures where dystrophin is normally located, histological signs of necrosis disappear and the recovery of functional disorders, specially affecting the mechanical properties of the muscle fibres, can be complete. The review examines also several ways of obtaining overexpression of utrophin in adult mdx mice, such as conditioned expression of the utrophin transgene (using a tetracycline-sensitive transactivator), transfection with viral vectors containing the utrophin cDNA (complete or truncated), actions on factor(s) controlling utrophin expression at the neuromuscular junction (heregulin, 4 N-acetylgalactosamine), and pharmacological ways of inducing expression (NO, arginine). Though partial improvements of the myopathy status have been obtained by these various approaches, they remain limited by their localized action and/or by the moderate level of utrophin expression obtained. Further researchs to overcome these limitations are urgently needed in order to transform the very promising effect of utrophin overexpression into a real treatment of Duchenne myopathy.

Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle.

Deletion of murine Smn exon 7, the most frequent mutation found in spinal muscular atrophy, has been directed to either both satellite cells, the muscle progenitor cells and fused myotubes, or fused myotubes only. When satellite cells were mutated, mutant mice develop severe myopathic process, progressive motor paralysis, and early death at 1 mo of age (severe mutant). Impaired muscle regeneration of severe mutants correlated with defect of myogenic precursor cells both in vitro and in vivo. In contrast, when satellite cells remained intact, mutant mice develop similar myopathic process but exhibit mild phenotype with median survival of 8 mo and motor performance similar to that of controls (mild mutant). High proportion of regenerating myofibers expressing SMN was observed in mild mutants compensating for progressive loss of mature myofibers within the first 6 mo of age. Then, in spite of normal contractile properties of myofibers, mild mutants develop reduction of muscle force and mass. Progressive decline of muscle regeneration process was no more able to counterbalance muscle degeneration leading to dramatic loss of myofibers. These data indicate that intact satellite cells remarkably improve the survival and motor performance of mutant mice suffering from chronic myopathy, and suggest a limited potential of satellite cells to regenerate skeletal muscle.

Multivariate evaluation of the functional recovery obtained by the overexpression of utrophin in skeletal muscles of the mdx mouse.

This paper summarizes the various aspects of functional recovery obtained in dystrophin-deficient muscles of the mdx mice where utrophin was overexpressed. This includes preliminary results on tetracycline-controlled expression of utrophin. It is shown that overexpression of utrophin leads to major functional improvements and that full-length utrophin is more efficient than truncated utrophin, missing a part of the central rod-segment. A generalized way of presenting improvements obtained by any treatment in the form of a 'recovery score' is emphasized. The quantitative aspect of the replacement of dystrophin by utrophin is discussed.