A Survey of Burnout Among Neurocritical Care Practitioners.

BACKGROUND: Burnout is a growing problem among medical professionals, reaching a crisis proportion. It is defined by emotional exhaustion, cynicism, and career dissatisfaction and is triggered by a mismatch between the values of the person and the demands of the workplace. Burnout has not previously been examined thoroughly in the Neurocritical Care Society (NCS). The purpose of this study is to assess the prevalence, contributing factors, and potential interventions to reduce burnout within the NCS. METHODS: A cross-sectional study of burnout was conducted using a survey distributed to members of the NCS. The electronic survey included personal and professional characteristic questions and the Maslach Burnout Inventory Human Services Survey for Medical Personnel (MBI). This validated measure assesses for emotional exhaustion (EE), depersonalization (DP), and personal achievement (PA). These subscales are scored as high, moderate, or low. Burnout (MBI) was defined as a high score in either EE or DP or a low score in PA. A Likert scale (0-6) was added to the MBI (which contained 22 questions) to provide summary data for the frequencies of each particular feeling. Categorical variables were compared using χ2 tests, and continuous variables were compared using t-tests. RESULTS: A total of 82% (204 of 248) of participants completed the entire questionnaire; 61% (124 of 204) were burned out by MBI criteria. A high score in EE was present in 46% (94 of 204), a high score in DP was present in 42% (85 of 204), and a low score in PA was present in 29% (60 of 204). The variables feeling burned out now, feeling burned out in the past, not having an effective/responsive supervisor, thinking about leaving one's job due to burnout, and leaving one's job due to burnout were significantly associated with burnout (MBI) (p < 0.05). Burnout (MBI) was also higher among respondents early in practice (currently training/post training 0-5 years) than among respondents post training 21 or more years. In addition, insufficient support staff contributed to burnout, whereas improved workplace autonomy was the most protective factor. CONCLUSIONS: Our study is the first to characterize burnout among a cross-section of physicians, pharmacists, nurses, and other practitioners in the NCS. A call to action and a genuine commitment by the hospital, organizational, local, and federal governmental leaders and society as a whole is essential to advocate for interventions to ameliorate burnout and care for our health care professionals.

Exploiting telerobotics for sensorimotor rehabilitation: a locomotor embodiment.

BACKGROUND: Manual treadmill training is used for rehabilitating locomotor impairments but can be physically demanding for trainers. This has been addressed by enlisting robots, but in doing so, the ability of trainers to use their experience and judgment to modulate locomotor assistance on the fly has been lost. This paper explores the feasibility of a telerobotics approach for locomotor training that allows patients to receive remote physical assistance from trainers. METHODS: In the approach, a trainer holds a small robotic manipulandum that shadows the motion of a large robotic arm magnetically attached to a locomoting patient's leg. When the trainer deflects the manipulandum, the robotic arm applies a proportional force to the patient. An initial evaluation of the telerobotic system's transparency (ability to follow the leg during unassisted locomotion) was performed with two unimpaired participants. Transparency was quantified by the magnitude of unwanted robot interaction forces. In a small six-session feasibility study, six individuals who had prior strokes telerobotically interacted with two trainers (separately), who assisted in altering a targeted gait feature: an increase in the affected leg's swing length. RESULTS: During unassisted walking, unwanted robot interaction forces averaged 3-4 N (swing-stance) for unimpaired individuals and 2-3 N for the patients who survived strokes. Transients averaging about 10 N were sometimes present at heel-strike/toe-off. For five of six patients, these forces increased with treadmill speed during stance (R2 = .99; p < 0.001) and increased with patient height during swing (R2 = .71; p = 0.073). During assisted walking, the trainers applied 3.0 ± 2.8 N (mean ± standard deviation across patients) and 14.1 ± 3.4 N of force anteriorly and upwards, respectively. The patients exhibited a 20 ± 21% increase in unassisted swing length between Days 1-6 (p = 0.058). CONCLUSIONS: The results support the feasibility of locomotor assistance with a telerobotics approach. Simultaneous measurement of trainer manipulative actions, patient motor responses, and the forces associated with these interactions may prove useful for testing sensorimotor rehabilitation hypotheses. Further research with clinicians as operators and randomized controlled trials are needed before conclusions regarding efficacy can be made.

Tocilizumab in the treatment of twelve cases with aa amyloidosis secondary to familial mediterranean fever.

BACKGROUND: There is no established treatment of AA amyloidosis, a long-term complication of various chronic inflammatory diseases associated with increased mortality, such as familial Mediterranian fever (FMF). Recently there are few reports pointing out that tocilizumab(TCZ), an anti IL-6 agent may be effective in AA amyloidosis resistant to conventional treatments. We report our data on the effect of TCZ in patients with FMF complicated with AA amyloidosis. METHODS: FMF patients with histologically proven AA amyloidosis, treated with TCZ (8 mg/kg per month) were followed monthly and the changes in creatinine, creatinine clearance, the amount of 24-hour urinary protein, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were noted throughout the treatment period. Adverse effects of the treatment were closely monitored. RESULTS: TCZ was given to 12 patients (6 F, 6 M) who also continued to receive colchicine (1.9 ± 0.4 mg/day). Coexisting diseases were ankylosing spondylitis(4) and Crohn's disease(1). The mean age was 35.2 ± 10.0 years and the mean follow-up on TCZ was 17.5 ± 14.7 months. The renal functions remained stable (mean creatinine from 1.1 ± 0.9 mg/dl to 1.0 ± 0.6 mg/dl), while a significant decrease in acute phase response (the mean CRP from 18.1 ± 19.5 mg/L to 5.8 ± 7.1 mg/L and ESR from 48.7 ± 31.0 mm/h to 28.7 ± 28.3 mm/h) was observed and the mean 24-hour urinary protein excretion reduced from 6537.6 ± 6526.0 mg/dl to 4745.5 ± 5462.7 mg/dl. Two patients whose renal functions were impaired prior to TCZ therapy improved significantly on this regimen. No infusion reaction was observed. None of the patients experienced any FMF attack under TCZ treatment with the exception of 2, one of whom had less frequent attacks while the other had episodes of erysipelas-like erythema. CONCLUSiON: Tocilizumab improved the acute phase response and the renal function in this group of patients and was generally well tolerated. Besides improving the renal function TCZ seemed to control the recurrence of FMF attacks too. Further studies are warrented to test the efficacy and safety of TCZ in AA amyloidosis secondary to FMF as well as other inflammatory conditions.

Mitochondrial DAMPs increase endothelial permeability through neutrophil dependent and independent pathways.

Trauma and sepsis can cause acute lung injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) in part by triggering neutrophil (PMN)-mediated increases in endothelial cell (EC) permeability. We had shown that mitochondrial (mt) damage-associated molecular patterns (DAMPs) appear in the blood after injury or shock and activate human PMN. So we now hypothesized that mitochondrial DAMPs (MTD) like mitochondrial DNA (mtDNA) and peptides might play a role in increased EC permeability during systemic inflammation and proceeded to evaluate the underlying mechanisms. MtDNA induced changes in EC permeability occurred in two phases: a brief, PMN-independent 'spike' in permeability was followed by a prolonged PMN-dependent increase in permeability. Fragmented mitochondria (MTD) caused PMN-independent increase in EC permeability that were abolished with protease treatment. Exposure to mtDNA caused PMN-EC adherence by activating expression of adherence molecule expression in both cell types. Cellular activation was manifested as an increase in PMN calcium flux and EC MAPK phosphorylation. Permeability and PMN adherence were attenuated by endosomal TLR inhibitors. EC lacked formyl peptide receptors but were nonetheless activated by mt-proteins, showing that non-formylated mt-protein DAMPs can activate EC. Mitochondrial DAMPs can be released into the circulation by many processes that cause cell injury and lead to pathologic endothelial permeability. We show here that mitochondria contain multiple DAMP motifs that can act on EC and/or PMN via multiple pathways. This can enhance PMN adherence to EC, activate PMN-EC interactions and subsequently increase systemic endothelial permeability. Mitochondrial DAMPs may be important therapeutic targets in conditions where inflammation pathologically increases endothelial permeability.

Bacterial DNA induces pulmonary damage via TLR-9 through cross-talk with neutrophils.

Bacterial DNA (bDNA) contains hypomethylated "CpG" repeats that can be recognized by Toll-like receptor 9 (TLR-9) as a pathogen-associated molecular pattern. The ability of bDNA to initiate lung injury via TLR-9 has been inferred on the basis of studies using artificial CpG DNA. But the role of authentic bDNA in lung injury is still unknown. Moreover, the mechanisms by which CpG DNA species can lead to pulmonary injury are unknown, although neutrophils (PMNs) are thought to play a key role in the genesis of septic acute lung injury. We evaluated the effects of bDNA on PMN-endothelial cell (EC) interactions thought critical for initiation of acute lung injury. Using a biocapacitance system to monitor real-time changes in endothelial permeability, we demonstrate here that bDNA causes EC permeability in a dose-dependent manner uniquely in the presence of PMNs. These permeability changes are inhibited by chloroquine, suggesting TLR-9 dependency. When PMNs were preincubated with bDNA and applied to ECs or when bDNA was applied to ECs without PMNs, no permeability changes were detected. To study the underlying mechanisms, we evaluated the effects of bDNA on PMN-EC adherence. Bacterial DNA significantly increased PMN adherence to ECs in association with upregulated adhesion molecules in both cell types. Taken together, our results strongly support the conclusion that bDNA can initiate lung injury by stimulating PMN-EC adhesive interactions predisposing to endothelial permeability. Bacterial DNA stimulation of TLR-9 appears to promote enhanced gene expression of adhesion molecules in both cell types. This leads to PMN-EC cross-talk, which is required for injury to occur.