The relationship between diabetes mellitus and 30-day readmission rates

Abstract Background It is estimated that 9.3% of the population in the United States have diabetes mellitus (DM), 28% of which are undiagnosed. The high prevalence of DM makes it a common comorbid condition in hospitalized patients. In recent years, government agencies and healthcare systems have increasingly focused on 30-day readmission rates to determine the complexity of their patient populations and to improve quality. Thirty-day readmission rates for hospitalized patients with DM are reported to be between 14.4 and 22.7%, much higher than the rate for all hospitalized patients (8.5–13.5%). The objectives of this study were to (1) determine the incidence and causes of 30-day readmission rates for patients with diabetes listed as either the primary reason for the index admission or with diabetes listed as a secondary diagnosis compared to those without DM and (2) evaluate the impact on readmission of two specialized inpatient DM services: the Hyperglycemic Intensive Insulin Program (HIIP) and Endocrine Consults (ENDO). Methods For this study, DM was defined as any ICD-9 discharge diagnosis (principal or secondary) of 250.xx. Readmissions were defined as any unscheduled inpatient admission, emergency department (ED) visit, or observation unit stay. We analyzed two separate sets of patient data. The first pilot study was a retrospective chart review of all patients with a principle or secondary admission diagnosis of diabetes admitted to any adult service within the University of Michigan Health System (UMHS) between October 1, 2013 and December 31, 2013. We then did further uncontrolled analysis of the patients with a principal admitting diagnosis of diabetes. The second larger retrospective study included all adults discharged from UMHS between October 1, 2013 and September 30, 2014 with principal or secondary discharge diagnosis of DM (ICD-9-CM: 250.xx). Results In the pilot study of 7763 admissions, the readmission rate was 26% for patients with DM and 22% for patients without DM. In patients with a primary diagnosis of DM on index admission, the most common cause for readmission was DM-related. In the larger study were 37,702 adult inpatient discharges between October 1, 2013 and September 30, 2014. Of these, 20.9% had DM listed as an encounter diagnosis. Rates for all encounters (inpatient, ED and Observation care) were 24.3% in patients with DM compared to 17.7% in those without DM (p < 0.001). The most common cause for readmission in patients with DM as a secondary diagnosis to the index admission was infection-related. During the index hospital stay, only a small proportion of patients with DM (approximately 12%) received any DM service consult. Those who received a DM consult had a higher case mix index compared to those who did not. Despite the higher acuity, there was a lower rate of ED /observation readmission in patients followed by the DM services (6.6% HIIP or ENDO vs. 9.6% no HIIP or ENDO, p = 0.0012), though no difference in the inpatient readmission rates (17.6% HIIP or ENDO vs. 17.4% no HIIP or ENDO, p = 0.89) was noted. Conclusions Patients with both a primary or secondary diagnosis of DM have higher readmission rates. The reasons for readmission vary; patients with a principal diagnosis of DM have more DM related readmissions and those with secondary diagnosis having more infection-related readmissions. DM services were used in a small proportion of patients and may have contributed to lower DM related ED revisits. Further prospective studies evaluating the role of these services in terms of glucose management, patient education and outpatient follow up on readmission are needed to identify interventions important to reducing readmission rates.https://deepblue.lib.umich.edu/bitstream/2027.42/136189/1/40842_2016_Article_40.pd

Cell cycle stage-specific roles of Rad18 in tolerance and repair of oxidative DNA damage

The E3 ubiquitin ligase Rad18 mediates tolerance of replication fork-stalling bulky DNA lesions, but whether Rad18 mediates tolerance of bulky DNA lesions acquired outside S-phase is unclear. Using synchronized cultures of primary human cells, we defined cell cycle stage-specific contributions of Rad18 to genome maintenance in response to ultraviolet C (UVC) and H(2)O(2)-induced DNA damage. UVC and H(2)O(2) treatments both induced Rad18-mediated proliferating cell nuclear antigen mono-ubiquitination during G(0), G(1) and S-phase. Rad18 was important for repressing H(2)O(2)-induced (but not ultraviolet-induced) double strand break (DSB) accumulation and ATM S1981 phosphorylation only during G(1), indicating a specific role for Rad18 in processing of oxidative DNA lesions outside S-phase. However, H(2)O(2)-induced DSB formation in Rad18-depleted G1 cells was not associated with increased genotoxin sensitivity, indicating that back-up DSB repair mechanisms compensate for Rad18 deficiency. Indeed, in DNA LigIV-deficient cells Rad18-depletion conferred H(2)O(2)-sensitivity, demonstrating functional redundancy between Rad18 and non-homologous end joining for tolerance of oxidative DNA damage acquired during G(1). In contrast with G(1)-synchronized cultures, S-phase cells were H(2)O(2)-sensitive following Rad18-depletion. We conclude that although Rad18 pathway activation by oxidative lesions is not restricted to S-phase, Rad18-mediated trans-lesion synthesis by Polη is dispensable for damage-tolerance in G(1) (because of back-up non-homologous end joining-mediated DSB repair), yet Rad18 is necessary for damage tolerance during S-phase