Anesthesia personnel’s visual attention regarding patient monitoring in simulated non-critical and critical situations, an eye-tracking study

Background: Cognitive ergonomics design of patient monitoring may reduce human factor errors in high-stress environments. Eye-tracking is a suitable tool to gain insight into the distribution of visual attention of healthcare professionals with patient monitors, which may facilitate their further development. Methods: This prospective, exploratory, high-fidelity simulation study compared anesthesia personnel's visual attention (fixation count and dwell-time) to 15 areas of interest on the patient monitor during non-critical and critical anesthesia situations. Furthermore, we examined the extent to which participants' experience influenced visual attention and which vital signs displayed on the patient monitor received the most visual attention. We used mixed zero-inflated Poisson regression and mixed linear models to analyze the data. Results: Analyzing 23 ten-minute scenarios, we found significantly more fixations to the areas of interest on the patient monitor during critical than non-critical situations (rate ratio of 1.45; 95% CI 1.33 to 1.59; p < 0.001). However, the dwell-time on the areas of interest did not significantly differ between the non-critical and critical situations (coefficient of - 1.667; 95% CI - 4.549 to 1.229; p = 0.27). The professional experience did not significantly influence the visual attention (fixation: rate ratio of 0.88; 95% CI 0.54 to 1.43; p = 0.61 and dwell-time: coefficient of 0.889; 95% CI - 1.465 to 3.229; p = 0.27). Over all situations, anesthesia personnel paid the most attention to the vital signs blood pressure (fixation: mean [SD] of 108 [74.83]; dwell-time: mean [SD] of 27 [15.90] seconds), end-expiratory carbon dioxide (fixation: mean [SD] of 59 [47.39]; dwell-time: mean [SD] of 30 [21.51] seconds), and the electrocardiogram (fixation: mean [SD] of 58 [64.70]; dwell-time: mean [SD] of 15 [14.95] seconds). Conclusions: Critical anesthesia situations increased anesthesia personnel's visual interaction with the patient monitor. Furthermore, we found that their visual attention focused mainly on a few vital signs. To assist clinicians in critical situations, manufacturers should optimize monitors to convey necessary information as easily and quickly as possible and optimize the visibility of less frequently observed but equally critical vital signs, especially when they are in an abnormal range. Keywords: Anesthesia, general; Eye-tracking technology; Patient monitoring; Patient simulation; Situation awareness; Visual attention

Dimethylarginine Dimethylaminohydrolase-1 Transgenic Mice Are Not Protected from Ischemic Stroke

Methylated arginines are endogenous analogues of L-arginine, the substrate for nitric oxide (NO) synthase. Asymmetric dimethylarginine (ADMA) interferes with NO formation, causing endothelial dysfunction. ADMA is a predictor of cardiovascular events and mortality in humans. It is eliminated primarily by enzymatic activity of dimethylarginine dimethylaminohydrolase (DDAH).We investigated whether human DDAH-1 (hDDAH-1) transgenicity protects from ischemic tissue damage in temporary middle cerebral artery occlusion (tMCAO) in mice. Infarct sizes did not significantly differ between hDDAH-1 transgenic (TG) mice and wild-type littermates (WT). As expected, ADMA plasma concentrations were significantly decreased, cerebral hDDAH expression and protein significantly increased in transgenic animals. Interestingly, neither brain tissue DDAH activity nor ADMA concentrations were different between TG and WT mice. In contrast, muscular DDAH activity was generally lower than in brain but significantly increased in TG mice.Our study demonstrates that hDDAH-1 transgenic mice are not protected from ischemic cerebral tissue damage in tMCAO. This lack of protection is due to high basal cerebral DDAH activity, which is not further increasable by transgenic overexpression of DDAH

Focal brain trauma in the cryogenic lesion model in mice

The method to induce unilateral cryogenic lesions was first described in 1958 by Klatzo. We describe here an adaptation of this model that allows reliable measurement of lesion volume and vasogenic edema by 2, 3, 5-triphenyltetrazolium chloride-staining and Evans blue extravasation in mice. A copper or aluminium cylinder with a tip diameter of 2.5 mm is cooled with liquid nitrogen and placed on the exposed skull bone over the parietal cortex (coordinates from bregma: 1.5 mm posterior, 1.5 mm lateral). The tip diameter and the contact time between the tip and the parietal skull determine the extent of cryolesion. Due to an early damage of the blood brain barrier, the cryogenic cortical injury is characterized by vasogenic edema, marked brain swelling, and inflammation. The lesion grows during the first 24 hours, a process involving complex interactions between endothelial cells, immune cells, cerebral blood flow, and the intracranial pressure. These contribute substantially to the damage from the initial injury. The major advantage of the cryogenic lesion model is the circumscribed and highly reproducible lesion size and location

The Relationship Between Therapist Effects and Therapy Delivery Factors: Therapy Modality, Dosage, and Non-completion.

To consider the relationships between, therapist variability, therapy modality, therapeutic dose and therapy ending type and assess their effects on the variability of patient outcomes. Multilevel modeling was used to analyse a large sample of routinely collected data. Model residuals identified more and less effective therapists, controlling for case-mix. After controlling for case mix, 5.8 % of the variance in outcome was due to therapists. More sessions generally improved outcomes, by about half a point on the PHQ-9 for each additional session, while non-completion of therapy reduced the amount of pre-post change by six points. Therapy modality had little effect on outcome. Patient and service outcomes may be improved by greater focus on the variability between therapists and in keeping patients in therapy to completion

SYNGAP1 encephalopathy:A distinctive generalized developmental and epileptic encephalopathy

Objective To delineate the epileptology, a key part of the SYNGAP1 phenotypic spectrum, in a large patient cohort. Methods Patients were recruited via investigators' practices or social media. We included patients with (likely) pathogenic SYNGAP1 variants or chromosome 6p21.32 microdeletions incorporating SYNGAP1. We analyzed patients' phenotypes using a standardized epilepsy questionnaire, medical records, EEG, MRI, and seizure videos. Results We included 57 patients (53% male, median age 8 years) with SYNGAP1 mutations (n = 53) or microdeletions (n = 4). Of the 57 patients, 56 had epilepsy: generalized in 55, with focal seizures in 7 and infantile spasms in 1. Median seizure onset age was 2 years. A novel type of drop attack was identified comprising eyelid myoclonia evolving to a myoclonic-atonic (n = 5) or atonic (n = 8) seizure. Seizure types included eyelid myoclonia with absences (65%), myoclonic seizures (34%), atypical (20%) and typical (18%) absences, and atonic seizures (14%), triggered by eating in 25%. Developmental delay preceded seizure onset in 54 of 56 (96%) patients for whom early developmental history was available. Developmental plateauing or regression occurred with seizures in 56 in the context of a developmental and epileptic encephalopathy (DEE). Fifty-five of 57 patients had intellectual disability, which was moderate to severe in 50. Other common features included behavioral problems (73%); high pain threshold (72%); eating problems, including oral aversion (68%); hypotonia (67%); sleeping problems (62%); autism spectrum disorder (54%); and ataxia or gait abnormalities (51%). Conclusions SYNGAP1 mutations cause a generalized DEE with a distinctive syndrome combining epilepsy with eyelid myoclonia with absences and myoclonic-atonic seizures, as well as a predilection to seizures triggered by eating.</p

Building on Progress Towards Fair Access : annual report 2019

Supplementary Table 3: Anti-epileptic drug use in patients with SYNGAP1 mutations or deletion