Getting Performance Metrics Right: A Qualitative Study of Staff Experiences Implementing and Measuring Practice Transformation

BACKGROUND

Quality improvement is a central goal of the patient-centered medical home (PCMH) model, and requires the use of relevant performance measures that can effectively guide comprehensive care improvements. Existing literature suggests performance measurement can lead to improvements in care quality, but may also promote practices that are detrimental to patient care. Staff perceptions of performance metric implementation have not been well-researched in medical home settings.

OBJECTIVE

To describe primary care staff (clinicians and other staff) experiences with the use of performance metrics during the implementation of the Veterans Health Administration’s (VHA) Patient Aligned Care Team (PACT) model of care.

DESIGN

Observational qualitative study; data collection using role-stratified focus groups and semi-structured interviews.

PARTICIPANTS

Two hundred and forty-one of 337 (72 %) identified primary care clinic staff in PACT team and clinic administrative/other roles, from 15 VHA clinics in Oregon and Washington.

APPROACH

Data coded and analyzed using conventional content analysis techniques.

KEY RESULTS

Primary care staff perceived that performance metrics: 1) led to delivery changes that were not always aligned with PACT principles, 2) did not accurately reflect patient-priorities, 3) represented an opportunity cost, 4) were imposed with little communication or transparency, and 5) were not well-adapted to team-based care.

CONCLUSIONS

Primary care staff perceived responding to performance metrics as time-consuming and not consistently aligned with PACT principles of care. The gaps between the theory and reality of performance metric implementation highlighted by PACT team members are important to consider as the medical home model is more widely implemented.

     

Coronary CT angiography versus standard of care strategies to evaluate patients with potential coronary artery disease; effect on long term clinical outcomes

Background: Previous studies have shown that computed tomography coronary angiography (CTA) in patients with suspected coronary artery disease (CAD) predicts short term adverse events. However, there is no current data on whether identifying atherosclerosis on CTA impacts outcomes. We performed a case–control study to assess whether information from CTA can improve outcomes. Methods: 4244 symptomatic patients (mean age 58 ± 9, 62.5% male) without known CAD who underwent CTA (n = 2538) to rule out CAD were matched to 1706 patients who underwent standard of care in an academic cardiology clinic. Patients were propensity-matched by gender, age, ethnicity, CAD risk factors and follow-up duration. The primary outcome measure was all-cause mortality. Multivariable Cox proportional hazards models incorporated age, gender and traditional risk factors for coronary disease as well as pre-test probability of CAD. Results: There were no significant differences in age, gender, conventional risk factors between groups (p > 0.05). During a mean follow up of 80 ± 11 months, the overall death rate was 6.3% (270 deaths). Death rate was significantly lower in CTA group (n = 106, 4.2%) as compared to the control group (n = 184, 10.8%, p = 0.001). Event free survival was 95.8% and 89.2% in CTA and standard of care groups, respectively. Risk-adjusted hazard ratio of death were 2.5 (95%CI: 1.6–6.7, p = 0.003) in standard of care cohort as compared to CTA group. Multivariate analysis demonstrated that undergoing coronary CTA resulted in a risk reduction of 32%, p = 0·0001. Conclusions: Improved knowledge of atherosclerosis or increased anti-atherosclerotic therapies among those undergoing CTA may have contributed to improved survival. Our results provide evidence of potential benefit from scanning for atherosclerosis with CTA in symptomatic patients. Large randomized trials are warranted.     

Prostate cancer derived prostatic acid phosphatase promotes an osteoblastic response in the bone microenvironment

Approximately 90 % of patients who die of prostate cancer (PCa) have bone metastases, often promoting osteoblastic lesions. We observed that 88 % of castration-resistant PCa (CRPC) bone metastases express prostatic acid phosphatase (PAP), a soluble secreted protein expressed by prostate epithelial cells in predominately osteoblastic (n = 18) or osteolytic (n = 15) lesions. Additionally, conditioned media (CM) of an osteoblastic PCa xenograft LuCaP 23.1 contained significant levels of PAP and promoted mineralization in mouse and human calvaria-derived cells (MC3T3-E1 and HCO). To demonstrate that PAP promotes mineralization, we stimulated MC3T3-E1 cells with PAP and observed increased mineralization, which could be blocked with the specific PAP inhibitor, phosphonic acid. Furthermore, the mineralization promoted by LuCaP 23.1 CM was also blocked by phosphonic acid, suggesting PAP is responsible for the mineralization promoting activity of LuCaP 23.1. In addition, gene expression arrays comparing osteoblastic to osteolytic CRPC (n = 14) identified betacellulin (BTC) as a gene upregulated during the osteoblastic response in osteoblasts during new bone formation. Moreover, BTC levels were increased in bone marrow stromal cells in response to LuCaP 23.1 CM in vitro. Because new bone formation does occur in osteoblastic and can occur in osteolytic CRPC bone metastases, we confirmed by immunohistochemistry (n = 36) that BTC was highly expressed in osteoblasts involved in new bone formation occurring in both osteoblastic and osteolytic sites. These studies suggest a role for PAP in promoting the osteoblastic reaction in CRPC bone metastases and identify BTC as a novel downstream protein expressed in osteoblasts during new bone formation.     

Sonography of the penis/erectile dysfunction

Abdominal Radiology - Erectile dysfunction (ED) is defined as the persistent inability to achieve and/or maintain an erection for a satisfactory sexual activity. It is secondary to several organic,...     

Tooth eruption: Theories and facts

The mechanisms of tooth eruption (i.e., the answer to the question of how and why teeth erupt) has been a matter of long historical debate. This review focuses on human and other mammalian teeth with a time- and spacewise limited period of eruption and analyzes recent observations and experimental data on dogs, rats, primates, and humans in a framework of basic biological parameters to formulate a guiding theory of tooth eruption. Acknowledging basic parameters (i.e., that teeth move in three-dimensional space, erupt with varying speed, and arrive at a functional position that in inheritable) eliminates a number of previously held theories and favors those that accommodate basic parameters, such as alveolar bone remodeling in association with root elongation, with possible correction factors in the form of cementum apposition and periodontal ligament formation. We have critically analyzed, summarized, and integrated recent findings associated with preeruptive movements of developing teeth, the intraosseous stage of premolar eruption in dogs, molar eruption in rodents, and premolar and molar eruption in primates. The variable speeds of eruption are particularly important. We conclude with basic principles of tooth eruption—that is, the type of signals generated by the dental follicle proper, the conditions under which teeth are moved and the clinical understanding to be derived from this knowledge. © 1996 Wiley-Liss, Inc.     

Inhibitory neuronal changes following a mixed diffuse-focal model of traumatic brain injury

Traumatic brain injury (TBI) can result in excitation: inhibition imbalance, as well as a range of chronic neurological deficits. However, how TBI affects different interneurons, and how this relates to behavioral abnormalities, remains poorly understood. This study examined the effects of a mixed diffuse-focal model of TBI, the lateral fluid percussion injury (LFPI), on interneurons, 8 weeks post-TBI in rats. Brains were labeled with antibodies against calbindin, parvalbumin, calretinin, neuropeptide Y, and somatostatin, and the number of interneurons were assessed in the cortex and hippocampus following LFPI. LFPI caused a reduction in the numbers of interneurons mediating both perisomatic and dendritic inhibition in the somatosensory cortex. In hippocampus, there were heterogenous changes in the number of interneurons while motor cortex, showed no obvious loss in any of the subsets of interneurons after TBI. In parallel to the investigations of changes in the number of interneurons, we also investigated the long-term behavioral consequences of LFPI. Behaviorally, rats given an LFPI displayed transient reduction in performance in motor tasks and were significantly impaired in reversal learning in the water maze task post-TBI. We also report here progressive neurodegeneration in cortex and hippocampus indicated by Fluoro-Jade C in the different brain areas examined after injury. Our findings suggest differential vulnerability of inhibitory neurons to LFPI in the different brain areas examined after injury. These data will aid in evaluation of new treatments for TBI and help target specific neuronal subtypes as a function of injury time and type.     

A roleplaying test for the assessment of interpresonal styles

The Improvisation Test for Individuals (Impro-I) consists of 12 roleplays that represent a variety of interpersonal situations. Performance is evaluated by observers. Forty-seven Ss were examined by two test teams in order to evaluate the reactions of the Ss to the roleplays and to determine interrater reliabilities. Ss found the roleplays generally realistic and their own performances lifelike. Interrater reliabilities were moderate to high.