Comparison Between a Color-only Method and a Food and Drug Administration-approved Validation Method for a Pediatric Color-coded Syringe Using Midazolam: A Randomized Crossover Trial.

OBJECTIVE: The objective of this study was to assess the use of a color-only method syringe for accuracy and timeliness when administrating midazolam. This method was compared with a U.S. Food and Drug Administration (FDA)-approved validation method. METHODS: A prospective, randomized, crossover trial was conducted to compare the dosing accuracy and timeliness of the color-only syringe method versus the validation method. Twenty-five participants prepared pediatric midazolam doses according to their preferred method, a FDA-approved validation method, and a color-only method. Primary endpoints included dosing accuracy and time to medication administration. RESULTS: The preferred 3-kg calculations had a median margin of error of 5.6% and a median time to completion of 55.6 seconds. The color-only method took less time to complete than the validation method (median time: 29.5 seconds vs 58.2 seconds). There was no statistically significant difference in errors between the color-only method and the validation method. None of the participants reported a mistake using the color-only method, whereas 25% (5/20) reported a mistake using the validation method. Only 20% (4/20) of participants believed that the validation method found or eliminated any mistakes. There were 8 medication errors identified when participants used the method of choice, 4 with the validation method, and 1 with the color-only method. CONCLUSIONS: There was no significant difference in dosing errors between the FDA-approved validation method and the color-only method. Use of a color-only method did reduced time to medication administration when compared with a preferred method and an FDA-approved validation method.

Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overload.

Coenzyme A (CoA) is an essential cofactor required for intermediary metabolism. Perturbations in homeostasis of CoA have been implicated in various pathologies; however, whether CoA homeostasis is changed and the extent to which CoA levels contribute to ventricular function and remodeling during pressure overload has not been explored. In this study, we sought to assess changes in CoA biosynthetic pathway during pressure overload and determine the impact of limiting CoA on cardiac function. We limited cardiac CoA levels by deleting the rate-limiting enzyme in CoA biosynthesis, pantothenate kinase 1 (Pank1). We found that constitutive, cardiomyocyte-specific Pank1 deletion (cmPank1-/-) significantly reduced PANK1 mRNA, PANK1 protein, and CoA levels compared with Pank1-sufficient littermates (cmPank1+/+) but exerted no obvious deleterious impact on the mice at baseline. We then subjected both groups of mice to pressure overload-induced heart failure. Interestingly, there was more ventricular dilation in cmPank1-/- during the pressure overload. To explore potential mechanisms contributing to this phenotype, we performed transcriptomic profiling, which suggested a role for Pank1 in regulating fibrotic and metabolic processes during the pressure overload. Indeed, Pank1 deletion exacerbated cardiac fibrosis following pressure overload. Because we were interested in the possibility of early metabolic impacts in response to pressure overload, we performed untargeted metabolomics, which indicated significant changes to metabolites involved in fatty acid and ketone metabolism, among other pathways. Collectively, our study underscores the role of elevated CoA levels in supporting fatty acid and ketone body oxidation, which may be more important than CoA-driven, enzyme-independent acetylation in the failing heart.NEW & NOTEWORTHY Changes in CoA homeostasis have been implicated in a variety of metabolic diseases; however, the extent to which changes in CoA homeostasis impacts remodeling has not been explored. We show that limiting cardiac CoA levels via PANK deletion exacerbated ventricular remodeling during pressure overload. Our results suggest that metabolic alterations, rather than structural alterations, associated with Pank1 deletion may underlie the exacerbated cardiac phenotype during pressure overload.

Making Use of Your Assets: Clinical Use of EOD Radiography in the Forward-Deployed Setting.

Ultrasonography is currently the primary means of imaging for forward surgical teams/forward resuscitative surgical teams (FSTs/FRSTs). As FSTs/FRSTs are pushed farther forward into more austere environments, access to other imaging modalities may be limited, potentially affecting resources. On a recent deployment, the 126th FRST was able to use radiography equipment from a co-located explosive ordnance disposal (EOD) team to assist in the diagnosis and treatment of medical and surgical patients, thereby saving time and resources. We provide three case examples in which using EOD radiography assisted in clinical decision making. Although the safety profile has not been assessed for clinical use in humans, EOD radiography can be a useful technique to aid in time-sensitive decision making in resource-constrained operational areas.

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.

Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals, and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, and 6 weeks) or high-efficiency particulate absorbing-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone, and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5- to 2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.

The association between preoperative spinal cord rotation and postoperative C5 nerve palsy.

BACKGROUND: C5 nerve palsy is a known complication of cervical spine surgery. The development and etiology of this complication are not completely understood. The purpose of the present study was to determine whether rotation of the cervical spinal cord predicts the development of a C5 palsy. METHODS: We performed a retrospective review of prospectively collected spine registry data as well as magnetic resonance images. We reviewed the records for 176 patients with degenerative disorders of the cervical spine who underwent anterior cervical decompression or corpectomy within the C4 to C6 levels. Our measurements included area for the spinal cord, space available for the cord, and rotation of the cord with respect to the vertebral body. RESULTS: There was a 6.8% prevalence of postoperative C5 nerve palsy as defined by deltoid motor strength of ≤ 3 of 5. The average rotation of the spinal cord (and standard deviation) was 2.8° ± 3.0°. A significant association was detected between the degree of rotation (0° to 5° versus 6° to 10° versus ≥ 11°) and palsy (point-biserial correlation = 0.94; p < 0.001). A diagnostic criterion of 6° of rotation could identify patients who had a C5 palsy (sensitivity = 1.00 [95% confidence interval, 0.70 to 1.00], specificity = 0.97 [95% confidence interval, 0.93 to 0.99], positive predictive value = 0.71 [95% confidence interval, 0.44 to 0.89], negative predictive value = 1.00 [95% confidence interval, 0.97 to 1.00]). CONCLUSIONS: Our evidence suggests that spinal cord rotation is a strong and significant predictor of C5 palsy postoperatively. Patients can be classified into three types, with Type 1 representing mild rotation (0° to 5°), Type 2 representing moderate rotation (6° to 10°), and Type 3 representing severe rotation (≥ 11°). The rate of C5 palsy was zero of 159 in the Type-1 group, eight of thirteen in the Type-2 group, and four of four in the Type-3 group. This information may be valuable for surgeons and patients considering anterior surgery in the C4 to C6 levels.