Barriers to Early Hospital Discharge: A Cross-Sectional Study at Five Academic Hospitals.

BACKGROUND: Understanding the issues delaying hospital discharges may inform efforts to improve hospital throughput. OBJECTIVE: This study was conducted to identify and determine the frequency of barriers contributing to delays in placing discharge orders. DESIGN: This was a prospective, cross-sectional study. Physicians were surveyed at approximately 8:00 AM, 12:00 PM, and 3:00 PM and were asked to identify patients that were "definite" or "possible" discharges and to describe the specific barriers to writing discharge orders. SETTING: This study was conducted at five hospitals in the United States. PARTICIPANTS: The study participants were attending and housestaff physicians on general medicine services. PRIMARY OUTCOMES AND MEASURES: Specific barriers to writing discharge orders were the primary outcomes; the secondary outcomes included discharge order time for high versus low team census, teaching versus nonteaching services, and rounding style. RESULTS: Among 1,584 patient evaluations, the most common delays for patients identified as "definite" discharges (n = 949) were related to caring for other patients on the team or waiting to staff patients with attendings. The most common barriers for patients identified as "possible" discharges (n = 1,237) were awaiting patient improvement and for ancillary services to complete care. Discharge orders were written a median of 43-58 minutes earlier for patients on teams with a smaller versus larger census, on nonteaching versus teaching services, and when rounding on patients likely to be discharged first (all P < .003). CONCLUSIONS: Discharge orders for patients ready for discharge are most commonly delayed because physicians are caring for other patients. Discharges of patients awaiting care completion are most commonly delayed because of imbalances between availability and demand for ancillary services. Team census, rounding style, and teaching teams affect discharge times.

Prospective comparison of curbside versus formal consultations.

BACKGROUND: Curbside consultations are commonly requested during the care of hospitalized patients, but physicians perceive that the recommendations provided may be based on inaccurate or incomplete information. OBJECTIVE: To compare the accuracy and completeness of the information received from providers requesting a curbside consultation of hospitalists with that obtained in a formal consultation on the same patients, and to examine whether the recommendations offered in the 2 consultations differed. DESIGN: Prospective cohort. SETTING: University-affiliated, urban safety net hospital. MAIN OUTCOME MEASURES: Proportion of curbside consultations with inaccurate or incomplete information; frequency with which recommendations in the formal consultation differed from those in the curbside consultation. RESULTS: Curbside consultations were requested for 50 patients, 47 of which were also evaluated in a formal consultation performed on the same day by a hospitalist other than the one performing the curbside consultation. Based on information collected in the formal consultation, information was either inaccurate or incomplete in 24/47 (51%) of the curbside consultations. Management advice after formal consultation differed from that given in the curbside consultation for 28/47 patients (60%). When inaccurate or incomplete information was received, the advice provided in the formal versus the curbside consultation differed in 22/24 patients (92%, P < 0.0001). CONCLUSIONS: Information presented during inpatient curbside consultations of hospitalists is often inaccurate or incomplete, and this often results in inaccurate management advice.

Rheumatoid arthritis synoviocyte survival is dependent on Stat3.

Rheumatoid arthritis (RA) synovial fibroblasts (SFs) are relatively resistant to apoptosis and exhibit dysregulated growth secondary to production of autocrine-acting growth factors and the accumulation of cell-autonomous defects. Many of the cytokines and growth factors expressed during RA synovitis, including IL-6, epidermal growth factor (EGF), and platelet-derived growth factor, activate the transcription factor Stat3 that has been implicated in promoting cell growth and survival. We analyzed the role of Stat3 in mediating the abnormal growth and survival properties of RA synoviocytes using retroviral-mediated gene transfer of a dominant negative mutant of Stat3, termed Stat3-YF. Approximately 3- to 5-fold overexpression of Stat3-YF effectively blocked endogenous Stat3 activation and Stat3-dependent gene expression, including expression of the socs3 and myc genes. Stat3-YF-transduced RA synoviocytes failed to grow in culture, exhibited markedly diminished [(3)H]thymidine incorporation (>90% decreased), and died spontaneously. Cell death occurred by apoptosis, as confirmed by annexin V staining, propidium iodide exclusion, and identification of cells with subdiploid levels of DNA. In marked contrast to control cells, EGF accelerated death of Stat3-YF-transduced SFs, such that >90% of cells were dead within 24-48 h of transduction. These results indicate that ablation of Stat3 function converts EGF from a growth/survival factor for RA synoviocytes to a death factor. Stat3-YF also induced apoptosis in osteoarthritis synoviocytes, and levels of apoptosis were increased by exogenous EGF. Apoptosis in Stat3-YF-transduced osteoarthritis synoviocytes was suppressed when Stat1 activity was blocked using a dominant negative Stat1 mutant. Our results identify Stat3 as an important molecule for RA SF survival, and suggest that Stat3 may represent a good target for gene therapy.