Smartphone Technology: Impact on Interprofessional Working Relations between Doctors and Nurses.

BACKGROUND: For decades, the main communication technology in hospitals has been the paging system. In the era of digital communication, smartphones have been adopted by hospitals seeking to modernize processes and offer real-time, two-way communication to increase efficiency. OBJECTIVE: The aim of this study was to explore physicians' and nurses' perceptions of the impact of smartphones on communication and efficiency. METHODS: Mann-Whitney U-tests were used to compare differences in item scores between physicians and nurses on 17 questionnaire items relating to smartphone impact on interpersonal relationships and communication, efficiency and reliability. An open-ended question was used to elicit additional feedback. RESULTS: In total, 43 nurses and 27 physicians participated in the study. Nurses' ratings were significantly higher than physicians' on a number of questionnaire items, including the following: smartphones have a positive impact on efficiency (Mdn = 4.0 vs. 3.0, U = 321.0, p = 0.027, r = .33), smartphones increase my accessibility to physicians (Mdn = 5.0 vs. 3.0, U = 277.0, p = 0.009, r = 0.42) and smartphones reduce interruptions versus pagers (Mdn = 4.0 vs. 2.0, U = 224.0, p > 0.0001, r = 0.47). CONCLUSION: The findings suggest that smartphone technology may reduce the locus of control for physicians, potentially limiting their ability to prioritize patients' needs and manage workflow efficiently.

Fibrinogen-beta gene haplotype is associated with mortality in sepsis.

OBJECTIVES: Fibrinogen plays a key role in coagulation and inflammation. Transcription of the fibrinogen-beta gene (FGB) is the rate-limiting step in fibrinogen production. Our aim was to determine whether haplotypes of FGB are associated with mortality and organ dysfunction in a cohort of patients with sepsis. METHODS: A prospective cohort of 631 consecutive Caucasian patients with sepsis from a tertiary care medical-surgical ICU were enrolled in a gene association study. Patients were genotyped for three polymorphisms in FGB: -854 G/A, -455 G/A, and +9006 G/A. Haplotypes were inferred using PHASE. The primary outcome was mortality. Secondary outcomes were severity of organ dysfunction as measured by days alive and free (DAF) of organ dysfunction. RESULTS: Haplotype GAA was associated with a significantly lower 28-day mortality (28.9% vs. 36.9% for all other haplotypes, p=0.03). Carriers of two copies of haplotype GAA (vs. one and zero copies) had more DAF of organ dysfunction. In a multivariate analysis, haplotype GAA was an independent predictor for lower mortality (OR=0.66, 95% CI=0.46-0.94, p=0.02). CONCLUSIONS: Haplotype GAA in FGB is associated with lower mortality and lower severity of organ dysfunction. Haplotype GAA encompasses a previously described haplotype -1420A/-854G/-455A/-249C/-148T/+1690G that is associated with higher fibrinogen levels.

Inhaled beta-2 agonist salbutamol and acute lung injury: an association with improvement in acute lung injury.

INTRODUCTION: Beta2 agonists have several properties that could be beneficial in acute lung injury (ALI). We therefore chose to study the effect of inhaled beta2 agonist use (salbutamol) on duration and severity of ALI. METHODS: We undertook a retrospective chart review of 86 consecutive mechanically ventilated patients with ALI, who had varying exposure to inhaled salbutamol. The cohort was divided into two groups according to the average daily dose of inhaled salbutamol they received ('high dose' > or = 2.2 mg/day and 'low dose' < 2.2 mg/day). Severity of ALI and non-pulmonary organ dysfunction was compared between the groups by calculating the days alive and free of ALI and other organ dysfunctions. RESULTS: The high dose and low dose groups received a mean of 3.72 mg and 0.64 mg salbutamol per day, respectively. The high dose salbutamol group had significantly more days alive and free of ALI than the low dose group (12.2 +/- 4.4 days versus 7.6 +/- 1.9 days, p = 0.02). There were no associations between dose of beta agonist and non-pulmonary organ dysfunctions. High dose salbutamol (p = 0.04), APACHE II score (p = 0.02), and cause of ALI (p = 0.02) were independent variables associated with number of days alive and free of ALI in a multivariate linear regression model. CONCLUSION: Our retrospective study suggests that salbutamol, an inhaled beta2 agonist, is associated with a shorter duration and lower severity of ALI. A dose greater than 2.2 mg/day of inhaled salbutamol could be a minimal effective dose to evaluate in a randomized controlled trial.

Interleukin-10 haplotype associated with increased mortality in critically ill patients with sepsis from pneumonia but not in patients with extrapulmonary sepsis.

STUDY OBJECTIVE: To test the hypothesis that haplotypes of the interleukin (IL)-10 gene are associated with clinical outcomes, comparing critically ill patients with sepsis from pneumonia vs those with extrapulmonary sepsis. DESIGN: Genetic association study. SETTING: Medical/surgical ICUs in a tertiary-care, university-affiliated teaching hospital. PATIENTS: Of 550 white patients with sepsis, 158 had pneumonia as the principle cause of their sepsis and 392 had an extrapulmonary source of sepsis. MEASUREMENTS: Haplotypes of the IL-10 gene were defined by measurement of haplotype tag single-nucleotide polymorphisms (SNPs). Primary outcome was 28-day survival. Secondary outcomes were days alive and free of organ dysfunction. RESULTS: Three SNPs in the IL-10 gene (-592 C/A, +734 G/T, and +3367 G/A) identified four major haplotypes: CGG, AGG, CTA, and CTG. Patients with pneumonia who carried one or two copies of the CGG haplotype had greater 28-day mortality (51.4%) than patients who did not carry this haplotype (29.1%, p = 0.007). Carriers of CGG had significantly more cardiovascular dysfunction (and use of vasopressors), renal dysfunction (and requirement of dialysis), hepatic dysfunction, and hematologic dysfunction (p < 0.05 in each case). In contrast, in patients with an extrapulmonary source of infection there was no significant association of the CGG haplotype (or any measured IL-10 genotype) with 28-day mortality or organ dysfunction. CONCLUSIONS: The IL-10 haplotype - 592C/734G/3367G is associated with increased mortality and organ dysfunction in critically ill patients with pulmonary sepsis but not in similarly ill patients with extrapulmonary sepsis. Therefore, polymorphisms within the IL-10 gene may be predictors of outcome in patients with sepsis from pneumonia.

The association of interleukin 6 haplotype clades with mortality in critically ill adults.

BACKGROUND: Interleukin 6 (IL-6) is a key proinflammatory cytokine in the systemic inflammatory response syndrome (SIRS). A G-->C polymorphism at position -174 of the IL-6 gene is associated with an adverse outcome in a number of inflammatory diseases, although its association with sepsis as an outcome remains unclear. We tested the hypothesis that specific haplotype clades of IL-6 may be associated with an outcome of SIRS. METHODS: We studied a cohort of 228 critically ill white patients who met at least 2 of 4 SIRS criteria. Clinical data were collected over 28 days after hospital admission. Haplotypes of IL-6 were inferred from publicly available data using PHASE (software for haplotype reconstruction and recombination rate estimation from population data), and cladistic structure was determined using Molecular Evolutionary Genetic Analyses (MEGA2) software. Then, a minimum set of "haplotype tag" single nucleotide polymorphisms (-174G/C, 1753C/G, and 2954G/C) that defined all 4 major haplotype clades of the IL-6 gene was chosen for further genotyping. RESULTS: Patients who had 2 copies of haplotypes from within the haplotype clades -174C/1753C/2954G (C/C/G), G/G/G, or G/C/C had a greater 28-day mortality compared with patients who carried 1 or no copies of these haplotypes (40.0% vs 26.0%; P = .02). These patients also had fewer days alive and free of multiple system organ dysfunction (P<.05). There were no associations between individual single nucleotide polymorphisms (including -174G/C) and survival or organ dysfunction. CONCLUSIONS: The C/C/G, G/G/G, and G/C/C haplotype clades of IL-6 were strongly associated with increased mortality and more organ dysfunction in a cohort of critically ill patients who had SIRS. Haplotype-based analysis succeeded in identifying this association, whereas individual single nucleotide polymorphism-based analysis failed.

Mechanisms of beta-receptor stimulation-induced improvement of acute lung injury and pulmonary edema.

Acute lung injury (ALI) and the acute respiratory distress syndrome are complex syndromes because both inflammatory and coagulation cascades cause lung injury. Transport of salt and water, repair and remodeling of the lung, apoptosis, and necrosis are additional important mechanisms of injury. Alveolar edema is cleared by active transport of salt and water from the alveoli into the lung interstitium by complex cellular mechanisms. Beta-2 agonists act on the cellular mechanisms of pulmonary edema clearance as well as other pathways relevant to repair in ALI. Numerous studies suggest that the beneficial effects of beta-2 agonists in ALI include at least enhanced fluid clearance from the alveolar space, anti-inflammatory actions, and bronchodilation. The purposes of the present review are to consider the effects of beta agonists on three mechanisms of improvement of lung injury: edema clearance, anti-inflammatory effects, and bronchodilation. This update reviews specifically the evidence on the effects of beta-2 agonists in human ALI and in models of ALI. The available evidence suggests that beta-2 agonists may be efficacious therapy in ALI. Further randomized controlled trials of beta agonists in pulmonary edema and in acute lung injury are necessary.

Severe acute respiratory distress syndrome (SARS): a critical care perspective.

OBJECTIVE: To review the epidemiology, clinical features, etiology, diagnosis, and management of severe acute respiratory syndrome (SARS) from a critical care perspective. DATA SOURCES: A MEDLINE search was performed using the following terms: severe acute respiratory syndrome and SARS virus. Additional information and references were obtained from the Web sites for the Centers for Disease Control and Prevention, World Health Organization, and Health Canada. STUDY SELECTION: Recent case series were used to develop a review of the epidemiology, clinical features, outcomes, and management of patients with SARS from an intensive care unit (ICU) perspective. This was supplemented by epidemiology information obtained from other Web-based sources. Recent published studies describing the etiology of SARS were also included. DATA SYNTHESIS: SARS has rapidly spread from Southeast Asia to numerous countries, including Canada and the United States. A new coronavirus has been isolated and detected from many affected patients. The mortality rate worldwide is approximately 10.5%. From five cohorts, the ICU admission rate ranged from 20% to 38%. Fifty-nine percent to 100% of the ICU patients required mechanical ventilatory support. The mortality rate of SARS patients admitted to the ICU ranged from 5% to 67%. The most common clinical symptoms and signs are fever, cough, dyspnea, myalgias, malaise, and inspiratory crackles. Common laboratory abnormalities included mild leukopenia, lymphopenia, and increased aspartate transaminase, alanine transaminase, lactic dehydrogenase, and creatine kinase. The chest radiograph pattern ranged from focal infiltrates to diffuse airspace disease. Management consisted of isolation, strict respiratory and contact precautions, ventilatory support as needed, empiric broad-spectrum antibiotics, ribavirin, and corticosteroids. Predictors of mortality included advanced age, the presence of comorbidities, and a high lactic dehydrogenase or high neutrophil count at admission. CONCLUSIONS: SARS is a highly contagious, infectious process that can advance to significant hypoxemic respiratory failure requiring ICU monitoring and support. Early recognition is critical for effective management and containment of this disease.

Novel therapies for sepsis: antiendotoxin therapies.

Severe sepsis and septic shock is a common problem encountered in the critical care unit with an estimated incidence in the US of 750,000 cases/year and a mortality rate of 30-50%. Sepsis involves a complex interaction between bacterial factors and the host immune system producing a systemic inflammatory state that may progress to multiple organ failure and death. Endotoxin (a lipopolysaccharide) released from Gram-negative bacteria has been implicated as a potent, prototypical stimulus of the immune response to bacterial infection. Current antiendotoxin strategies utilise various approaches ranging from the prevention of binding to endotoxin receptors with antibodies (monoclonal or polyclonal) against endotoxin or endotoxin receptor/carrier molecules (antiCD14 or antilipopolysaccharide-binding protein antibodies), enhancing clearance or neutralisation (haemoperfusion, lipoproteins, lipopolysaccharide-neutralising proteins) or impairing cellular signalling (lipid A analogues, tyrosine kinase inhibitors). In the future, innovative therapies involving Toll-like receptors and their downstream signalling elements will be developed. This review discusses current knowledge regarding endotoxin signalling, antiendotoxin therapies currently under development, and future areas for research.