A scientometric analysis of fairness in health AI literature.

Artificial intelligence (AI) and machine learning are central components of today's medical environment. The fairness of AI, i.e. the ability of AI to be free from bias, has repeatedly come into question. This study investigates the diversity of members of academia whose scholarship poses questions about the fairness of AI. The articles that combine the topics of fairness, artificial intelligence, and medicine were selected from Pubmed, Google Scholar, and Embase using keywords. Eligibility and data extraction from the articles were done manually and cross-checked by another author for accuracy. Articles were selected for further analysis, cleaned, and organized in Microsoft Excel; spatial diagrams were generated using Public Tableau. Additional graphs were generated using Matplotlib and Seaborn. Linear and logistic regressions were conducted using Python to measure the relationship between funding status, number of citations, and the gender demographics of the authorship team. We identified 375 eligible publications, including research and review articles concerning AI and fairness in healthcare. Analysis of the bibliographic data revealed that there is an overrepresentation of authors that are white, male, and are from high-income countries, especially in the roles of first and last author. Additionally, analysis showed that papers whose authors are based in higher-income countries were more likely to be cited more often and published in higher impact journals. These findings highlight the lack of diversity among the authors in the AI fairness community whose work gains the largest readership, potentially compromising the very impartiality that the AI fairness community is working towards.

Ingestion and surgical retrieval of an endodontic file: a case report.

Ingestions and aspirations of foreign bodies are rare, but do occasionally occur during dental treatment. Although reports exist, few include photos demonstrating the extensive surgical intervention that may be necessary to manage such events. Perhaps this lack of visualization, and associated lack of awareness, is one of the reasons some clinicians still provide non-surgical root canal therapy (NSRCT) without a rubber dam. This case report outlines the medical treatment of a 30-year-old male who initially presented to a general dentist's office (not associated with the authors) for NSRCT of their mandibular right first molar. A rubber dam was not used for this procedure, during which the accidental ingestion of an endodontic K-file occurred. The patient was subsequently hospitalized for evaluation and treatment, consisting of numerous imaging studies, endoscopic evaluation, and surgical removal of the file from his small intestine. The ingestion of foreign bodies, and the associated complications, can be reduced through the routine use of a rubber dam, which is considered the standard of care for NSRCT. This case graphically illustrates the potential consequences associated with deviating from the standard of care and should remind clinicians that a rubber dam is necessary for all cases of NSRCT.

Effect of Protocolized Sedation on Clinical Outcomes in Mechanically Ventilated Intensive Care Unit Patients: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

OBJECTIVE: To assess the effects of protocolized sedation (algorithm or daily interruption) compared with usual care without protocolized sedation on clinical outcomes in mechanically ventilated adult intensive care unit (ICU) patients via a systematic review and meta-analysis of randomized controlled trials (RCTs). METHODS: We searched Ovid MEDLINE, EMBASE, Cochrane CENTRAL, Web of Science, and ClinicalTrials.gov from their inception to February 28, 2013. A random-effects model was used to synthesize risk ratios (RRs) and weighted mean differences (WMDs). RESULTS: Of 4782 records screened, 6 RCTs including 1243 patients met the inclusion criteria. Protocolized sedation was associated with significant reductions in overall mortality (RR, 0.85; 95% CI, 0.74 to 0.97; P=.02; number needed to treat, 20; P=.11), ICU length of stay (WMD, -1.73 days; 95% CI, -3.32 to -0.14 days; P=.03), hospital length of stay (WMD, -3.55 days; 95% CI, -5.98 to -1.12 days; P=.004), and tracheostomy (RR, 0.69; 95% CI, 0.50 to 0.96; P=.03; number needed to treat, 16.6; P=.04; 5 RCTs) compared with usual care. Protocolized sedation produced no significant differences in duration of mechanical ventilation (WMD, -1.04 days; 95% CI, -2.54 to 0.47 days; P=.18), reintubation (RR, 0.78; 95% CI, 0.52 to 1.15; P=.21; 3 RCTs), and self-extubation (RR, 1.49; 95% CI, 0.46 to 4.82; P=.51; 4 RCTs) compared with usual care. Included studies did not report delirium incidence. CONCLUSION: In mechanically ventilated adults in closed, nonspecialty ICUs, protocolized sedation seems to decrease overall mortality (15%), ICU and hospital lengths of stay (1.73 and 3.55 days, respectively), and tracheostomy (31%) compared with usual care without protocolized sedation.

Trazodone Effects on Obstructive Sleep Apnea and Non-REM Arousal Threshold.

RATIONALE: A low respiratory arousal threshold is a physiological trait involved in obstructive sleep apnea (OSA) pathogenesis. Trazodone may increase arousal threshold without compromising upper airway muscles, which should improve OSA. OBJECTIVES: We aimed to examine how trazodone alters OSA severity and arousal threshold. We hypothesized that trazodone would increase the arousal threshold and improve the apnea/hypopnea index (AHI) in selected patients with OSA. METHODS: Subjects were studied on two separate nights in a randomized crossover design. Fifteen unselected subjects with OSA (AHI ≥ 10/h) underwent a standard polysomnogram plus an epiglottic catheter to measure the arousal threshold. Subjects were studied after receiving trazodone (100 mg) and placebo, with 1 week between conditions. The arousal threshold was calculated as the nadir pressure before electrocortical arousal from approximately 20 spontaneous respiratory events selected randomly. MEASUREMENTS AND MAIN RESULTS: Compared with placebo, trazodone resulted in a significant reduction in AHI (38.7 vs. 28.5 events/h, P = 0.041), without worsening oxygen saturation or respiratory event duration. Trazodone was not associated with a significant change in the non-REM arousal threshold (-20.3 vs. -19.3 cm H2O, P = 0.51) compared with placebo. In subgroup analysis, responders to trazodone spent less time in N1 sleep (20.1% placebo vs. 9.0% trazodone, P = 0.052) and had an accompanying reduction in arousal index, whereas nonresponders were not observed to have a change in sleep parameters. CONCLUSIONS: These findings suggest that trazodone could be effective therapy for patients with OSA without worsening hypoxemia. Future studies should focus on underlying mechanisms and combination therapies to eliminate OSA. Clinical trial registered with www.clinicaltrials.gov (NCT 01817907).

Intraventricular orexin-A improves arousal and early EEG entropy in rats after cardiac arrest.

The recovery of arousal after cardiac arrest (CA) is associated with evolution from electroencephalographic (EEG) burst-suppression to continuous activity. Orexin-A elicits arousal EEG during anesthetic burst-suppression. We hypothesized that orexin-A would improve arousal and EEG entropy after CA. Eighteen Wistar rats were subjected to 7-minute asphyxial CA and resuscitation. Rats were divided into treatment (n=9) and control (n=9) groups. Twenty minutes after resuscitation, the treatment group received 0.1 mL of 1 nM orexin-A intraventricularly, while controls received saline. EEG was quantified using Information Quantity (IQ), a measure of entropy validated for detection of burst-suppression and arousal patterns. IQ values range from 0 to 1.0. Arousal was quantified using the neurological deficit scale (NDS). The ischemic neuronal fraction of hippocampus CA1 and cortex was histologically determined. Baseline and post-resuscitation characteristics were similar between the groups. The NDS score (mean+/-SD) at 4 h was higher in the orexin-A group compared to controls (57.3+/-5.8 vs. 40.7+/-5.9, p<0.02), but scores were similar at 72 h. Burst frequency was similar in both groups but the orexin-A group demonstrated higher IQ values compared to controls beginning within 10 min. IQ values remained significantly higher in the orexin-A group for the first 120 min (p=0.008) and subsequently converged. The ischemic neuronal fraction was similar between groups in cortex (p=0.54) and hippocampus CA1 (p=0.14). In rats resuscitated from CA, orexin-A transiently increased arousal and EEG entropy without worsening ischemic neuronal injury. The role of orexin-A in recovery of arousal after CA deserves further investigation.