Background: Little is known about the risk of in-hospital cardiac arrest (IHCA) among patients with sepsis. We aimed to characterize the incidence and outcome of IHCA among patients with sepsis in a national database. We then determined the major risk factors associated with IHCA among sepsis patients.Methods: We used data from a population-based cohort study based on the National Health Insurance Research Database of Taiwan (NHRID) between 2000 and 2013. We used Martin's implementation that combined the explicit ICD-9 CM codes for sepsis and six major organ dysfunction categories. IHCA among sepsis patients was identified by the presence of cardiopulmonary resuscitation procedures. The survival impact was analyzed with the Cox proportional-hazards model using inverse probability of treatment weighting (IPTW). The risk factors were identified by logistic regression models with 10-fold cross-validation, adjusting for competing risks.Results: We identified a total of 20,022 patients with sepsis, among whom 2,168 developed in-hospital cardiac arrest. Sepsis patients with a higher burden of comorbidities and organ dysfunction were more likely to develop in-hospital cardiac arrest. Acute respiratory failure, hematological dysfunction, renal dysfunction, and hepatic dysfunction were associated with increased risk of IHCA. Regarding the source of infection, patients with respiratory tract infections were at the highest risk, whereas patients with urinary tract infections and primary bacteremia were less likely to develop IHCA. The risk of IHCA correlated well with age and revised cardiac risk index (RCRI). The final competing risk model concluded that acute respiratory failure, male gender, and diabetes are the three strongest predictors for IHCA. The effect of IHCA on survival can last 1 year after hospital discharge, with an IPTW-weighted hazard ratio of 5.19 (95% CI: 5.06, 5.35) compared to patients who did not develop IHCA.Conclusion: IHCA in sepsis patients had a negative effect on both short- and long-term survival. The risk of IHCA among hospitalized sepsis patients was strongly correlated with age and cardiac risk index. The three identified risk factors can help clinicians to identify patients at higher risk for IHCA.

Inspired by the famous Libby Zion case in 1984, which revealed the underlying flaw in the medical system at the time──the exploitation of junior medical staff and the inadequate surveillanceby attending physicians, authors of this systemic review aim to investigate the potential consequence of overworking in medical scenarios. Methods Excerpta medica database (EMBASE) and PubMed had been systematically searched, bibliographies of relevant studies additionally reviewed. Four cohorts and three randomized controlled trials were selected and quality-assessed with Newcastle-Ottawa Scale and the Cochrane risk of bias tool, respectively. Literature were extracted and discussed. Results Two randomized controlled trials have concluded that residents or interns with longer consecutive working hours per shift in the division of internal medicineare prone to more medical errors. One cohort study has shown a significant association between longer weekly working hours and worsened quality of patient care (intensive care unit (ICU) transfer rates and in-hospital mortality) in the setting of internal medicine. However, none of the 3 studies which were conducted in surgical departments suggests a further restriction on weekly working hours or shift length. Conclusion The specialty-specific policy is recommended based on our between-study comparison. Specifically, with respect to the incidence of medical errors or adverse events, weekly hours or shift length are weakly recommended to be regulated in the department of internal medicine, but there is no recommendation to surgical departments. However, one must consider all respects of the impact brought by any alternation of working policy before the actual implementation.

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Until recently, most genetic studies of headache have been conducted on participants with European ancestry. We therefore conducted a large-scale genome-wide association study of self-reported headache in individuals of East Asian ancestry (specifically those who were identified as Han Chinese). In this study, 108,855 participants were enrolled, including 12,026 headache cases from the Taiwan Biobank. For broadly-defined headache phenotype, we identified a locus on chromosome 17, with the lead single nucleotide polymorphism (SNP) rs8072917 (odds ratio 1.08, p = 4.49 × 10–8) mapped to two protein-coding genes RNF213 and ENDOV. For severe headache phenotype, we found a strong association on chromosome 8, with the lead SNP rs13272202 [odds ratio 1.30, p = 1.02 × 10–9], mapped to gene RP11-1101K5.1. We then conducted a conditional analysis and a statistical fine mapping of the broadly-defined headache-associated loci and identified a single credible set of loci with rs8072917 supporting that this lead variant was the true causal variant on RNF213 gene region. RNF213 replicated the result of previous studies and played important roles in the biological mechanism of broadly-defined headache. On the basis of the previous results found in the Taiwan biobank, we conducted phenome-wide association studies for the lead variants using data from the UK biobank, and found that the causal variant (SNP rs8072917) was associated with muscle symptoms, cellulitis and abscess of face and neck, and cardiogenic shock. Our findings foster the genetic architecture of headache in individuals of East Asian ancestry. Our study can be replicated using genomic data linked to electronic health records from a variety of countries, therefore affecting a wide range of ethnicities globally. Our genome-phenome association study may facilitate the development of new genetic tests and novel drug mechanisms.