Video display terminal use and dry eye: preventive measures and future perspectives

Background Dry eye disease (DED) is a common cause of ocular pain and discomfort. Dry eye disease (DED) stems from a loss-of-tear film homeostasis and is frequently seen in video display terminal (VDT) users. Video display terminal (VDT) use reduces blink rates and increases incomplete blinks, leading to tear film instability and ocular inflammation, promoting DED. Purpose To assess and evaluate the methods for preventing VDT-associated DED and ocular discomfort. Methods Studies were found using PubMed and Embase with the search terms: (digital visual terminal* OR computer use OR screen use OR smartphone OR display OR visual display terminal* OR computer vision syndrome OR tablet OR phone OR screen time) AND (dry eye OR DED). Results Thirty-one relevant articles were found. Ten described single-visit studies, whereas 21 had a prolonged follow-up. Most preventive measures of VDT-associated DED aimed to increase blink rate or directly prevent tear film instability, ocular inflammation, mucin loss or ocular surface damage. Using an adjustable chair and ergonomic training, blink animations and omega-3 supplementation improved signs and symptoms of VDT-associated DED. Taking frequent breaks was associated with fewer symptoms, but no study assessed the commonly suggested 20-20-20 rule. Conclusion Preventive measures, such as blink animation programmes, oral intake of omega-3 fatty acids and improved ergonomics act on different parts of the vicious cycle of dry eye and could supplement each other. A comparison of the efficacy of the different interventions as well as more evidence of the effect of increased humidity, VDT filters and ergonomic practices, are required.publishedVersionPaid open acces

Video display terminal use and dry eye: preventive measures and future perspectives

Background Dry eye disease (DED) is a common cause of ocular pain and discomfort. Dry eye disease (DED) stems from a loss-of-tear film homeostasis and is frequently seen in video display terminal (VDT) users. Video display terminal (VDT) use reduces blink rates and increases incomplete blinks, leading to tear film instability and ocular inflammation, promoting DED. Purpose To assess and evaluate the methods for preventing VDT-associated DED and ocular discomfort. Methods Studies were found using PubMed and Embase with the search terms: (digital visual terminal* OR computer use OR screen use OR smartphone OR display OR visual display terminal* OR computer vision syndrome OR tablet OR phone OR screen time) AND (dry eye OR DED). Results Thirty-one relevant articles were found. Ten described single-visit studies, whereas 21 had a prolonged follow-up. Most preventive measures of VDT-associated DED aimed to increase blink rate or directly prevent tear film instability, ocular inflammation, mucin loss or ocular surface damage. Using an adjustable chair and ergonomic training, blink animations and omega-3 supplementation improved signs and symptoms of VDT-associated DED. Taking frequent breaks was associated with fewer symptoms, but no study assessed the commonly suggested 20-20-20 rule. Conclusion Preventive measures, such as blink animation programmes, oral intake of omega-3 fatty acids and improved ergonomics act on different parts of the vicious cycle of dry eye and could supplement each other. A comparison of the efficacy of the different interventions as well as more evidence of the effect of increased humidity, VDT filters and ergonomic practices, are required.publishedVersio

Review on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye disease

Background: Visual display terminal (VDT) use is a key risk factor for dry eye disease (DED). Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described. Purpose: The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT-associated DED. Methods: A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated. Findings: Fifty-five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development. Conclusion: Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands. Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT-associated DED.publishedVersio

Analysis of Career Stage, Gender, and Personality and Workplace Violence in a 20-Year Nationwide Cohort of Physicians in Norway

Importance Workplace violence (WPV) is a worldwide problem in health services. Several studies have pointed to organizational factors, such as working in psychiatry and work stress. However, there is a lack of long-term longitudinal cohort studies with respect to trends during the career and individual factors among physicians. Objective To investigate WPV trends during Norwegian physicians’ careers and assess individual and work-related factors associated with WPV in a long-term longitudinal study. Design, Setting, and Participants This cohort study involved 2 nationwide medical student cohorts who graduated 6 years apart and were surveyed at graduation (T1: 1993-1994 and 1999) and 4 years later (T2), 10 years later (T3), 15 years later (T4), and 20 years after graduation (T5). Generalized estimated equations were used. Statistical analysis was performed from January to September 2020. Exposures Medical career during 20 years in Norway. Main Outcomes and Measures WPV was measured as threats or acts of violence from a patient or visitor experienced at least twice, at each of the stages after leaving medical school. Individual factors were obtained at T1 and work-related factors at T2 through T5. We analyzed WPV by repeated measures. Results At T1, a total of 893 participants (with a mean [SD] age of 28 (2.83) years; 499 [56%] women) responded to the questionnaire. The prevalence of multiple threats of violence was 20.3% (156 of 769) at T2, 17.1% (118 of 691) at T3, 11.2% (66 of 588) at T4, and 8.6% (46 of 536) at T5; and the prevalence of multiple acts of violence was 4.3% (33 of 763) at T2, 5.2% (36 of 687) at T3, 3.1% (18 of 584) at T4, and 2.2% (12 of 532) at T5. There was a decline from T2 to T5 of both multiple threats (β = −1.06; 95% CI, −1.31 to −0.09; P < .001) and acts of violence (β = −1.13; 95% CI, −1.73 to −0.53; P < .001). In adjusted analysis, factors associated with multiple threats of violence were male gender (odds ratio [OR], 2.76; 95% CI, 1.73 to 4.40; P < .001), vulnerability trait (neuroticism) (OR, 0.90; 95% CI, 0.82 to 0.99; P = .03), young physician cohort (OR, 1.63; 95% CI, 1.04 to 2.58; P = .04), and working in psychiatry (OR, 7.50; 95% CI, 4.42 to 12.71; P < .001). Factors associated with multiple acts of violence in adjusted analysis were male gender (OR, 3.37; 95% CI, 1.45 to 7.84; P = .005), young physician cohort (OR, 6.08; 95% CI, 1.68 to 21.97; P = .006), and working in psychiatry (OR, 12.34; 95% CI, 5.40 to 28.23; P < .001). There were no interactions with gender or cohort in the significant associated factors. Conclusions and Relevance Higher rates of multiple threats and acts of violence were observed during early medical careers, among male physicians, and in psychiatry. Low levels of the vulnerability trait (neuroticism) were associated with the experience of multiple threats. There was an association between the young physician cohort and WPV. Preventive efforts should include early-career and male physicians, with additional emphasis on personality

Video display terminal use and dry eye: preventive measures and future perspectives

Background Dry eye disease (DED) is a common cause of ocular pain and discomfort. Dry eye disease (DED) stems from a loss-of-tear film homeostasis and is frequently seen in video display terminal (VDT) users. Video display terminal (VDT) use reduces blink rates and increases incomplete blinks, leading to tear film instability and ocular inflammation, promoting DED. Purpose To assess and evaluate the methods for preventing VDT-associated DED and ocular discomfort. Methods Studies were found using PubMed and Embase with the search terms: (digital visual terminal* OR computer use OR screen use OR smartphone OR display OR visual display terminal* OR computer vision syndrome OR tablet OR phone OR screen time) AND (dry eye OR DED). Results Thirty-one relevant articles were found. Ten described single-visit studies, whereas 21 had a prolonged follow-up. Most preventive measures of VDT-associated DED aimed to increase blink rate or directly prevent tear film instability, ocular inflammation, mucin loss or ocular surface damage. Using an adjustable chair and ergonomic training, blink animations and omega-3 supplementation improved signs and symptoms of VDT-associated DED. Taking frequent breaks was associated with fewer symptoms, but no study assessed the commonly suggested 20-20-20 rule. Conclusion Preventive measures, such as blink animation programmes, oral intake of omega-3 fatty acids and improved ergonomics act on different parts of the vicious cycle of dry eye and could supplement each other. A comparison of the efficacy of the different interventions as well as more evidence of the effect of increased humidity, VDT filters and ergonomic practices, are required

Sex Effects on Gene Expression in Lacrimal Glands of Mouse Models of Sjögren Syndrome

Purpose: Sjögren syndrome is an autoimmune disease that occurs primarily in women, and is associated with lacrimal gland inflammation and aqueous-deficient dry eye. We hypothesize that sex-associated differences in lacrimal gland gene expression are very important in promoting lymphocyte accumulation in this tissue and contribute to the onset, progression, and/or severity of the inflammatory disease process. To test our hypothesis, we explored the nature and extent of sex-related differences in gene expression in autoimmune lacrimal glands. Methods: Lacrimal glands were collected from age-matched, adult, male and female MRL/MpJ-Tnfrsf6lpr (MRL/lpr) and nonobese diabetic/LtJ (NOD) mice. Glands were processed for the analysis of differentially expressed mRNAs by using CodeLink Bioarrays and Affymetrix GeneChips. Data were evaluated with bioinformatics and statistical software. Results: Our results show that sex significantly influences the expression of thousands of genes in lacrimal glands of MRL/lpr and NOD mice. The immune nature of this glandular response is very dependent on the Sjögren syndrome model. Lacrimal glands of female, as compared with male, MRL/lpr mice contain a significant increase in the expression of genes related to inflammatory responses, antigen processing, and chemokine pathways. In contrast, it is the lacrimal tissue of NOD males, and not females, that presents with a significantly greater expression of immune-related genes. Conclusions: These data support our hypothesis that sex-related differences in gene expression contribute to lacrimal gland disease in Sjögren syndrome. Our findings also suggest that factors in the lacrimal gland microenvironment are critically important in mediating these sex-associated immune effects

Review on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye disease

Background: Visual display terminal (VDT) use is a key risk factor for dry eye disease (DED). Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described. Purpose: The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT-associated DED. Methods: A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated. Findings: Fifty-five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development. Conclusion: Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands. Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT-associated DED

Review on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye disease

Background: Visual display terminal (VDT) use is a key risk factor for dry eye disease (DED). Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described. Purpose: The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT-associated DED. Methods: A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated. Findings: Fifty-five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development. Conclusion: Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands. Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT-associated DED