National Patterns of Risk-Standardized Mortality and Readmission After Hospitalization for Acute Myocardial Infarction,Heart Failure,and Pneumonia: Update on Publicly Reported Outcomes Measures Based on the 2013 Release

BACKGROUND

The Centers for Medicare & Medicaid Services publicly reports risk-standardized mortality rates (RSMRs) within 30-days of admission and, in 2013, risk-standardized unplanned readmission rates (RSRRs) within 30-days of discharge for patients hospitalized with acute myocardial infarction (AMI), heart failure (HF), and pneumonia. Current publicly reported data do not focus on variation in national results or annual changes.

OBJECTIVE

Describe U.S. hospital performance on AMI, HF, and pneumonia mortality and updated readmission measures to provide perspective on national performance variation.

DESIGN

To identify recent changes and variation in national hospital-level mortality and readmission for AMI, HF, and pneumonia, we performed cross-sectional panel analyses of national hospital performance on publicly reported measures.

PARTICIPANTS

Fee-for-service Medicare and Veterans Health Administration beneficiaries, 65 years or older, hospitalized with principal discharge diagnoses of AMI, HF, or pneumonia between July 2009 and June 2012. RSMRs/RSRRs were calculated using hierarchical logistic models risk-adjusted for age, sex, comorbidities, and patients’ clustering among hospitals.

Results

Median (range) RSMRs for AMI, HF, and pneumonia were 15.1% (9.4–21.0%), 11.3% (6.4–17.9%), and 11.4% (6.5–24.5%), respectively. Median (range) RSRRs for AMI, HF, and pneumonia were 18.2% (14.4–24.3%), 22.9% (17.1–30.7%), and 17.5% (13.6–24.0%), respectively. Median RSMRs declined for AMI (15.5% in 2009–2010, 15.4% in 2010–2011, 14.7% in 2011–2012) and remained similar for HF (11.5% in 2009–2010, 11.9% in 2010–2011, 11.7% in 2011–2012) and pneumonia (11.8% in 2009–2010, 11.9% in 2010–2011, 11.6% in 2011–2012). Median hospital-level RSRRs declined: AMI (18.5% in 2009–2010, 18.5% in 2010–2011, 17.7% in 2011–2012), HF (23.3% in 2009–2010, 23.1% in 2010–2011, 22.5% in 2011–2012), and pneumonia (17.7% in 2009–2010, 17.6% in 2010–2011, 17.3% in 2011–2012).

Conclusions

We report the first national unplanned readmission results demonstrating declining rates for all three conditions between 2009–2012. Simultaneously, AMI mortality continued to decline, pneumonia mortality was stable, and HF mortality experienced a small increase.     

Defective Bone Microstructure in Hydronephrotic Mice: A Histomorphometric Study in ICR/Mlac‐hydro Mice

Chronic renal impairment can lead to bone deterioration and abnormal bone morphology, but whether hydronephrosis is associated with bone loss remains unclear. Herein, we aimed to use computer‐assisted bone histomorphometric technique to investigate microstructural bone changes in Imprinting Control Region (ICR) mice with a spontaneous mutation that was associated with bilateral nonobstructive hydronephrosis (ICR/Mlac‐hydro). The results showed that 8‐week‐old ICR/Mlac‐hydro mice manifested decreases in trabecular bone number and thickness, and an increased trabecular separation, thereby leading to a reduction in trabecular bone volume compared with the wild‐type mice. Furthermore, histomorphometric parameters related to both bone resorption and formation, that is, eroded surface, osteoclast surface, and osteoblast surface, were much lower in ICR/Mlac‐hydro mice than in the wild type. A decrease in moment of inertia was found in ICR/Mlac‐hydro mice, indicating a decrease in bone strength. In conclusion, ICR/Mlac‐hydro mice exhibited trabecular bone loss, presumably caused by marked decreases in both osteoblast and osteoclast activities, which together reflected abnormally low bone turnover. Thus, this mouse strain appeared to be a valuable model for studying the hydronephrosis‐associated bone disease. Anat Rec, 297:208–214, 2014. © 2013 Wiley Periodicals, Inc.     

No evidence of chikungunya virus and antibodies shortly before the outbreak on Sri Lanka

A massive outbreak of chikungunya disease occurred on Sri Lanka in 2006. Reasons for the explosive nature of the epidemic are being intensively discussed. According to recognised and anecdotal concepts, absence of human population immunity against chikungunya virus (CHIKV) might have supported virus amplification. However, formal proof of concept is lacking. This study determined the prevalence of anti-CHIKV IgG antibodies as well as CHIKV RNA shortly before the outbreak. Two hundred and six human sera were collected from patients with acute febrile illness in 2004/2005. Validated indirect immunofluorescence and real-time RT-PCR assays for dengue as well as CHIKV were employed. Laboratory evidence of dengue virus infection was seen in 67% of patients, indicating virus activity and exposure to Aedes spp. vectors. These vectors are the same as for chikungunya. However, no evidence of acute or previous chikungunya infection could be demonstrated in the same cohort. This study gives formal evidence that the absence of human population immunity correlated with a large chikungunya epidemic. M. Panning and D. Wichmann contributed equally to this work.     

Evaluation of the BACTEC MGIT 960 system for the recovery of mycobacteria

We evaluated the BACTEC MGIT 960 system, which is a fully automated, non-invasive, continuous monitoring system for the growth and detection of mycobacteria. Including respiratory and other specimens, 1,742 specimens were processed and inoculated into the BACTEC MGIT 960 and the BACTEC 460 TB Systems, as well as onto Lowenstein-Jensen (L-J) media. A total of 104 isolates of mycobacteria were recovered from all culture systems. This included Mycobacterium tuberculosis complex, Mycobacterium avium-intracellulare (MAI) complex and other mycobacteria (MOTT). The isolation rates for M. tuberculosis complex and MAI complex were comparable for the BACTEC 460 (54.8% and 13.5%) and the BACTEC MGIT 960 (51.9% and 13.5%). The overall isolation rate was less for BACTEC MGIT 960 (76.9%) which was due to lesser number of MOTT isolates recovered from this system. The mean times to detection (TTD) for all mycobacteria were 9.3 days for the BACTEC MGIT, 14.6 days for the BACTEC 460 and 21.6 days for L-J. A significant difference was observed when TTD was tested in relation to degree of positivity in smears, with the BACTEC MGIT maintaining the short TTD even with less number of bacilli in the smear. The contamination rates were, 6.4% for BACTEC MGIT, 2.9% for BACTEC 460 and 12.1% for L-J medium. The BACTEC MGIT 960 system shows performances comparable to the BACTEC 460 and seems to be a dependable, user friendly system.     

Routine blood counts in children with acute lymphoblastic leukaemia after completion of therapy: are they necessary?

Children who have completed treatment for acute lymphoblastic leukaemia (ALL) are commonly followed up for the first 5 years with regular full blood counts (FBCs) to monitor for relapse of disease. There is little evidence to suggest that this practice improves the detection rate of unexpected relapse. Surveillance FBCs, performed on 43 children with relapsed ALL between 1990 and 1999, were analysed. Of the 42 relapses in children off therapy, only two were detected by an abnormal FBC. Routine FBCs in asymptomatic children off therapy lacks specificity in detecting unexpected relapses and maybe safely discontinued.     

AQP1 and AQP3, psoriasin, and nitric oxide synthases 1-3 are inflammatory mediators in erythema toxicum neonatorum

Erythema toxicum neonatorum is a common, inflammatory skin reaction in healthy newborn infants characterized by an accumulation of activated immune cells in the lesions. Its etiology and physiologic significance are still unclear. The purpose of this study was to extend the search for possible inflammatory mediators of the rash. We performed immunohistochemistry on punch biopsy cryosections from lesions of four, 1-day-old infants and from four matched controls without rash, using antibodies against the water channel proteins aquaporin-1 (AQP1) and aquaporin-3 (AQP3), psoriasin, and the nitric oxide synthase (NOS) enzymes, neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). All sections from the lesions showed a dense, nodular cellular infiltrate located near the hair follicle. The vessels in the dermis showed a high incidence of AQP1 and eNOS. Strong staining for AQP1, AQP3, and psoriasin, as well as nNOS, iNOS, and eNOS were seen in the entire epidermal layer. The infiltrate in the dermis contained numerous cells expressing AQP1, AQP3, nNOS, iNOS, and eNOS. Double immunofluorescence staining showed that AQP3 was located in CD1a-expressing Langerhans cells and other dendritic cells in the dermis, as well as in CD14-expressing macrophages, CD15-expressing neutrophils, and EG2-expressing eosinophils surrounding the hair follicle. Our findings show that AQP1 and AQP3, psoriasin, and NOSs are involved in the activation of the skin immune system at birth.     

Endosonographic characteristics of the anal sphincter complex in primigravid Sri Lankan women

OBJECTIVE: To determine the endosonographic anatomy of the anal sphincter complex in primigravid Sri Lankan women. METHOD: This is an observational study of 95 primigravid women admitted to an antenatal ward. They were examined using anal endosonography and data from subjects without sphincter injury were analyzed to describe anal sphincter morphology. Individual anal canal components were measured at defined levels, and the relationship of individual measurements with age and body mass index was calculated. RESULTS: Ninety-three of 95 women had no anal sphincter damage. The puborectalis sling (mean 5.5 mm, S.D. 0.77) forms the upper most border of the sphincter complex. The mean width of the deep external sphincter was 4.3 mm (S.D. 0.61); that of the superficial external sphincter was 4.5 mm (S.D. 0.56); and that of the internal anal sphincter at the mid anal canal was 2.1 mm (S.D. 0.21). The intersphincteric space (mean 2.1 mm, S.D. 0.26) could be distinguished sonographically in all subjects. The mean width of the anterior ring of the subcutaneous component was 3.8 mm (S.D. 1.01). The perineal body was sonographically identified in 60%. CONCLUSION: A set of normal values for the anal sphincter components in Sri Lankan primigravid women was established.