Deployment of a Digital Advance Care Planning Platform at an Accountable Care Organization.

BACKGROUND: Advance care planning (ACP), a process of sharing one's values and preferences for future medical treatments, can improve quality of life, reduce loved ones' anxiety, and decrease unwanted medical utilization and costs. Despite benefits to patients and health care systems, ACP uptake often remains low, due partially to lack of knowledge and difficulty initiating discussions. Digital tools may help reduce these barriers to entry. METHODS: We retrospectively examined data from pilot deployment of Koda Health patient-facing ACP among Houston Methodist Coordinated Care patients, for quality improvement (QI) purposes. Patients referred by nurse navigators could access Koda's digital platform, complete ACP, and share the legal documentation generated. Analyzed measures include usage rates and ACP-related decisions within the platform. RESULTS: Of eligible patients (n = 203), 52.7% voluntarily completed their plan. Engagement and completion rates were similar across demographics. Patients indicated majority preference (66.4%) toward spending the last days of life at home. Most patients indicated wanting no life-support intervention if quality of life became unacceptable (51 to 71% across 4 treatments). Life-support decisions were similar between demographic categories, excepting CPR and dialysis, wherein a greater portion of Black patients than White patients preferred at least trial intervention, rather than none. CONCLUSIONS: As an observational QI analysis, limitations include bounded geographical reach and lack of data on ACP impacts to subsequent health care utilization, which future studies will address. Findings suggest that digital health tools like Koda can effectively facilitate equitable ACP access and may help support health systems and providers in offering comprehensive ACP.

Age and ethnicity in cirrhosis.

BACKGROUND: Cirrhosis is diagnosed in patients of all ages and is the end result of many different diseases. The aim of this study was to characterize clinical and ethnic features of adult patients who were admitted to the hospital at different (young/old) ages and examine associations between age and ethnicity within these groups. METHODS: In this retrospective analysis of a diverse cohort of 2017 patients with a clinical diagnosis of cirrhosis between January 2001 and December 2011, we focused on age, ethnicity, and outcome of patients with cirrhosis. RESULTS: We identified 219 patients younger than the age of 40 years, including 87 (11%) of 802 white, 31 (6%) of 550 African American, and 89 (16%) of 550 Hispanic patients (P < 0.001). Ethnicity and causes of cirrhosis were found to have a significant correlation with age. Overall, Hispanic and white patients together were more than twice as likely to be diagnosed with cirrhosis at an age younger than 40 years compared with African American patients (P < 0.001). Autoimmune hepatitis caused cirrhosis at a younger age regardless of ethnicity (P < 0.001), whereas cryptogenic/nonalcoholic fatty liver disease/nonalcoholic steatohepatitis was more likely identified at an older age (P = 0.008). African American patients with cirrhosis due to either alcohol or hepatitis C virus were older than Hispanic (P < 0.001 and P = 0.003, respectively) and white patients (P < 0.001 and P < 0.001, respectively) at presentation. Finally, younger patients admitted with cirrhosis had a higher in-hospital mortality rate (P < 0.001). CONCLUSIONS: The data suggest an association between ethnicity and age of cirrhosis diagnosis, both overall and in patients with certain cirrhosis etiologies. This work raises the possibility of an ethnic and/or genetic basis for cirrhosis.

Reduction in ovulation or male sex phenotype increases long-term anoxia survival in a daf-16-independent manner in Caenorhabditis elegans.

Identifying genotypes and phenotypes that enhance an organism's ability to survive stress is of interest. We used Caenorhabditis elegans mutants, RNA interference (RNAi), and the chemical 5-fluorodeoxyuridine (FUDR) to test the hypothesis that a reduction in progeny would increase oxygen deprivation (anoxia) survival. In the hermaphrodite gonad, germ line processes such as spermatogenesis and oogenesis can be simultaneously as well as independently disrupted by genetic mutations. We analyzed genetic mutants [glp-1(q158), glp-4(bn2ts), plc-1(rx1), ksr-1(ku68), fog-2(q71), fem-3(q20), spe-9(hc52ts), fer-15(hc15ts)] with reduced progeny production due to various reproductive defects. Furthermore, we used RNAi to inhibit the function of gene products in the RTK/Ras/MAPK signaling pathway, which is known to be involved in a variety of developmental processes including gonad function. We determined that reduced progeny production or complete sterility enhanced anoxia survival except in the case of sterile hermaphrodites [spe-9(hc52ts), fer-15(hc15ts)] undergoing oocyte maturation and ovulation as exhibited by the presence of laid unfertilized oocytes. Furthermore, the fog-2(q71) long-term anoxia survival phenotype was suppressed when oocyte maturation and ovulation were induced by mating with males that have functional or nonfunctional sperm. The mutants with a reduced progeny production survive long-term anoxia in a daf-16- and hif-1-independent manner. Finally, we determined that wild-type males were able to survive long-term anoxia in a daf-16-independent manner. Together, these results suggest that the insulin signaling pathway is not the only mechanism to survive oxygen deprivation and that altering gonad function, in particular oocyte maturation and ovulation, leads to a physiological state conducive for oxygen deprivation survival.