Monitoring Nutrition and Glucose in Acute Brain Injury

The metabolic response to injury is well described; however, very little is understood about optimal markers to measure this response. This summary will address the current evidence about monitoring nutritional status including blood glucose after acute brain injury (ABI). An electronic literature search was conducted for English language articles describing the testing, utility, and optimal methods to measure nutritional status and blood glucose levels in the neurocritical care population. A total of 45 articles were included in this review. Providing adequate and timely nutritional support can help improve outcome after ABI. However, the optimal content and total nutrition requirements remain unclear. In addition, how best to monitor the nutritional status in ABI is still being elucidated, and at present, there is no validated optimal method to monitor the global response to nutritional support on a day-to-day basis in ABI patients. Nitrogen balance may be monitored to assess the adequacy of caloric intake as it relates to protein energy metabolism, but indirect calorimetry, anthropometric measurement, or serum biomarker requires further validation. The adverse effects of hyperglycemia in ABI are well described, and data indicate that blood glucose should be carefully controlled in critically ill patients. However, the optimal frequency or duration for blood glucose monitoring after ABI remains poorly defined. There are significant knowledge gaps about monitoring nutritional status and response to nutritional interventions in ABI; these need to be addressed and hence few recommendations can be made. The optimal frequency and duration of blood glucose monitoring need further study.     

Multimodality Monitoring: Informatics,Integration Data Display and Analysis

The goal of multimodality neuromonitoring is to provide continuous, real-time assessment of brain physiology to prevent, detect, and attenuate secondary brain injury. Clinical informatics deals with biomedical data, information, and knowledge including their acquisition, storage, retrieval, and optimal use for clinical decision-making. An electronic literature search was conducted for English language articles describing the use of informatics in the intensive care unit setting from January 1990 to August 2013. A total of 64 studies were included in this review. Clinical informatics infrastructure should be adopted that enables a wide range of linear and nonlinear analytical methods be applied to patient data. Specific time epochs of clinical interest should be reviewable. Analysis strategies of monitor alarms may help address alarm fatigue. Ergonomic data display that present results from analyses with clinical information in a sensible uncomplicated manner improve clinical decision-making. Collecting and archiving the highest resolution physiologic and phenotypic data in a comprehensive open format data warehouse is a crucial first step toward information management and two-way translational research for multimodality monitoring. The infrastructure required is largely the same as that needed for telemedicine intensive care applications, which under the right circumstances improves care quality while reducing cost.     

Intracranial Pressure Monitoring: Fundamental Considerations and Rationale for Monitoring

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. In large part critical care for TBI is focused on the identification and management of secondary brain injury. This requires effective neuromonitoring that traditionally has centered on intracranial pressure (ICP). The purpose of this paper is to review the fundamental literature relative to the clinical application of ICP monitoring in TBI critical care and to provide recommendations on how the technique maybe applied to help patient management and enhance outcome. A PubMed search between 1980 and September 2013 identified 2,253 articles; 244 of which were reviewed in detail to prepare this report and the evidentiary tables. Several important concepts emerge from this review. ICP monitoring is safe and is best performed using a parenchymal monitor or ventricular catheter. While the indications for ICP monitoring are well established, there remains great variability in its use. Increased ICP, particularly the pattern of the increase and ICP refractory to treatment is associated with increased mortality. Class I evidence is lacking on how monitoring and management of ICP influences outcome. However, a large body of observational data suggests that ICP management has the potential to influence outcome, particularly when care is targeted and individualized and supplemented with data from other monitors including the clinical examination and imaging.     

Association of stressful life events with accelerated bone loss in older men: the osteoporotic fractures in men (MrOS) study

Summary

Prior studies suggest an association between stressful life events and fractures that may be mediated by BMD. In the current study, risk of accelerated hip BMD loss was higher in older men with any type of stressful life event and increased with the number of types of stressful life events.

Introduction

Prior studies suggest that stressful life events may increase adverse health outcomes, including falls and possibly fractures. The current study builds on these findings and examines whether stressful life events are associated with increased bone loss.

Methods

Four thousand three hundred eighty-eight men aged ≥65 years in the Osteoporotic Fractures in Men study completed total hip bone mineral density (BMD) measures at baseline and visit 2, approximately 4.6 years later, and self-reported stressful life events data mid-way between baseline and visit 2, and at visit 2. We used linear regression to model the association of stressful life events with concurrent annualized total hip BMD loss, and log binomial regression or Poisson regression to model risk of concurrent accelerated BMD loss (>1 SD more than mean annualized change).

Results

Men (75.3 %) reported ≥1 type of stressful life event, including 43.3 % with ≥2 types of stressful life events. Mean annualized BMD loss was ?0.36 % (SD 0.88), and 13.9 % of men were categorized with accelerated BMD loss (about 5.7 % or more total loss). Rate of annualized BMD loss increased with the number of types of stressful life events after adjustment for age (p?p?=?0.07). Multivariable-adjusted risk of accelerated BMD loss increased with the number of types of stressful life events (RR, 1.10 [95 % confidence interval (CI), 1.04–1.16]) per increase of one type of stressful life event). Fracture risk was not significantly different between stressful life event-accelerated bone loss subgroups (p?=?0.08).

Conclusions

In these older men, stressful life events were associated with a small, dose-related increase in risk of concurrent accelerated hip bone loss. Low frequency of fractures limited assessment of whether rapid bone loss mediates any association of stressful life events with incident fractures. Future studies are needed to confirm these findings and to investigate the mechanism that may underlie this association.     

Resistance to macrolides, clindamycin and telithromycin in Streptococcus pyogenes isolated in Spain during 2004

OBJECTIVES: To study the antimicrobial susceptibility and prevalence of the different phenotypes and genotypes of macrolide resistance in group A streptococci isolated in Spain in 2004, and to compare the results with those obtained in 1998 and 2001 using the same methodology and centres. METHODS: A total of 530 unique isolates of Streptococcus pyogenes collected in 21 laboratories from 16 geographic areas (regions) in Spain were used. Antimicrobial susceptibility testing was performed using the agar dilution method. Discs containing erythromycin or clindamycin were used to recognize the phenotypes of macrolide-lincosamide-streptogramin (MLS) resistance. Genes encoding macrolide-lincosamide resistance were detected by PCR. RESULTS: Resistance to erythromycin was 21.7% [95% confidence interval (CI) 16.5-26.3]. The resistance to azithromycin was 21.5%, whereas the resistance to miocamycin and to clindamycin was 6.6% (95% CI 3.0-8.9). Thirty-one (5.8%) of the isolates were resistant to telithromycin. Of the 115 erythromycin-resistant isolates, 67.8% had the M phenotype, representing 14.7% of all the isolates tested. Thirty-five isolates (30.5% of the erythromycin-resistant strains and 6.6% of all the isolates) had the MLS(B) constitutive phenotype. There was a high prevalence of resistance to telithromycin (88.6%) among the 35 strains with the MLS(B) constitutive phenotype. When we compared these results with those from previous studies (1998 and 2001), we found a significant increase in the MLS(B) constitutive phenotype (P < 0.001), and a significant decrease in the M phenotype (P < 0.005) was noted. CONCLUSIONS: The significant increase in the prevalence of resistance to clindamycin and miocamycin, and the prevalence of resistance to telithromycin reached in a short period of time from the introduction of its use, underscore the need for continuous surveillance of antimicrobial resistance in S. pyogenes in Spain.     

Tideglusib reduces progression of brain atrophy in progressive supranuclear palsy in a randomized trial

It is believed that glycogen synthase kinase‐3 hyperphosphorylates tau protein in progressive supranuclear palsy (PSP). The Tau Restoration on PSP (TAUROS) trial assessed the glycogen synthase kinase‐3 inhibitor tideglusib as potential treatment. For the magnetic resonance imaging (MRI) substudy reported here, we assessed the progression of brain atrophy. TAUROS was a multinational, phase 2, double‐blind, placebo‐controlled trial in patients with mild‐to‐moderate PSP who were treated with oral tideglusib (600 mg or 800 mg daily) or with placebo for 1 year. A subset of patients underwent baseline and 52‐week MRI. Automated, observer‐independent, atlas‐based, and mask‐based volumetry was done on high‐resolution, T1‐weighted, three‐dimensional data. For primary outcomes, progression of atrophy was compared both globally (brain, cerebrum) and regionally (third ventricle, midbrain, pons) between the active and placebo groups (Bonferroni correction). For secondary outcomes, 15 additional brain structures were explored (Benjamini & Yekutieli correction). In total, MRIs from 37 patient were studied (placebo group, N = 9; tideglusib 600 mg group, N = 19; tideglusib 800 mg group, N = 9). The groups compared well in their demographic characteristics. Clinical results showed no effect of tideglusib over placebo. Progression of atrophy was significantly lower in the active group than in the placebo group for the brain (mean ± standard error of the mean: ?1.3% ± 1.4% vs. ?3.1% ± 2.3%, respectively), cerebrum (?1.3% ± 1.5% vs. ?3.2% ± 2.1%, respectively), parietal lobe (?1.6% ± 1.9% vs. ?4.1% ± 3.0%, respectively), and occipital lobe (?0.3% ± 1.8% vs. ?2.7% ± 3.2%, respectively). A trend toward reduced atrophy also was observed in the frontal lobe, hippocampus, caudate nucleus, midbrain, and brainstem. In patients with PSP, tideglusib reduced the progression of atrophy in the whole brain, particularly in the parietal and occipital lobes. © 2014 International Parkinson and Movement Disorder Society