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Background Hospital medicine groups (HMGs) typically receive financial support from hospitals. Determining a fair amount of financial support requires negotiation between HMG and hospital leaders. As the hospital medicine care model evolves, hospital leaders may regularly challenge HMGs to demonstrate the financial value of activities that do not directly generate revenue. Objective To describe current attitudes and beliefs of hospital executives regarding the value of contributions made by HMGs. Design Thematic content analysis of key informant interviews. Participants Twenty-four healthcare institutional leaders, including hospital presidents, chief medical officers, chief executive officers, and chief financial officers. Participants comprised a diverse sample from all regions in the United States, including rural, suburban, and urban locations, and academic and nonacademic institutions. Results Executives highly valued hospitalist groups that demonstrate alignment with hospital priorities, and often used this concept to summarize the HMG's success across several value domains. Most executives evaluated only a few key HMG metrics, but almost no executives reported calculating the HMG return on investment by summing pertinent quantitative contributions. Respondents described an evolving concept of hospitalist value and believed that HMGs generate substantial value that is difficult to measure financially. Conclusions Hospital executives appear to make financial support decisions based on a small number of basic financial or care quality metrics combined with a subjective assessment of the HMG's broader alignment with hospital priorities. HMG leaders should focus on building relationships that facilitate dialog about alignment with hospital needs.

Pseudomonas aeruginosa bacteremia is a serious and life-threatening infection associated with high mortality. Among the multitude of virulence determinants possessed by P. aeruginosa, the type 3 secretion system has been implicated with more acute and invasive infection in respiratory diseases. However, the relationship between the type 3 secretion system and clinical outcomes in P. aeruginosa bacteremia has not been investigated.To determine the association between the type 3 secretion system virulence factor in P. aeruginosa bloodstream infection and 30-day mortality.Retrospective analysis of 85 cases of P. aeruginosa bacteremia.Tertiary care hospital.Bacterial isolates were assayed in vitro for secretion of type 3 exotoxins (ExoU, ExoT, and ExoS). Strain relatedness was analyzed using randomly amplified polymorphic DNA polymerase chain reaction genotyping. Antimicrobial susceptibilities were determined by means of the Kirby-Bauer disk-diffusion test.At least one of the type 3 secretion system proteins was detected in 37 out of the 85 isolates (44%). Septic shock was identified in 43% of bacteremic patients with type 3 secretion system+ isolates compared to 23% of patients with type 3 secretion system- isolates (p = .12). A high frequency of resistance in the type 3 secretion system+ isolates was observed to ciprofloxacin (59%), cefepime (35%), and gentamicin (38%). There was a significant difference in the 30-day cumulative probability of death after bacteremia between secretors and nonsecretors (p = .02). None of the type 3 secretion system+ patients who survived the first 30 days had a P. aeruginosa isolate which exhibited ExoU phenotype.The expression of type 3 secretion system exotoxins in bacteremic isolates of P. aeruginosa confers poor clinical outcomes independent of antibiotic susceptibility profile.

To assess the predictive accuracy of serum procalcitonin in distinguishing bacterial aspiration pneumonia from aspiration pneumonitis.Prospective observational study.Intensive care unit of a university-affiliated hospital.Sixty-five consecutive patients admitted with pulmonary aspiration and seven control subjects intubated for airway protection.None.Quantitative cultures from bronchoalveolar lavage fluid were conducted on all participants at the time of admission. Serial serum procalcitonin levels were measured on day 1 and day 3 using the procalcitonin enzyme-linked fluorescent assay. There were no differences in the median serum concentrations of procalcitonin between patients with positive bronchoalveolar lavage cultures (n = 32) and patients with negative bronchoalveolar lavage cultures (n = 33) on either day 1 or day 3 postadmission. The areas under the receiver operator characteristic curves were 0.59 (95% confidence interval, 0.47-0.72) and 0.63 (95% confidence interval, 0.5-0.75), respectively (p = .74). However, duration of mechanical ventilation and antibiotic therapy were shorter in those who had a decrease in their procalcitonin levels on day 3 from baseline compared with those who did not (6.7 ± 7.1 days and 11.1 ± 13.5 days, p = .03; and 8.2 ± 2.6 days vs. 12.8 ± 4.6 days; p.001, respectively). Hospital mortality was associated with radiographic multilobar disease (adjusted odds ratio, 1.14; 95% confidence interval, 1.01-1.31; p = .04) and increasing procalcitonin levels (adjusted odds ratio, 5.63; 95% confidence interval, 1.56-20.29; p = .008).Serum procalcitonin levels had poor diagnostic value in separating bacterial aspiration pneumonia from aspiration pneumonitis based on quantitative bronchoalveolar lavage culture. However, serial measurements of serum procalcitonin may be helpful in predicting survival from pulmonary aspiration.

The development of adjunctive therapies which attenuate adverse remodeling and improve LV function post myocardial infarction (MI) is of significant clinical interest. Previously, we have shown that targeted delivery of therapeutic vascular endothelial growth factor (VEGF) to the infarct border zone significantly increases vascular perfusion and results in improvements in LV function. In this study, we tested the hypothesis that improvements in cardiac function observed with this novel targeted drug delivery system strongly correlate with reductions in collagen deposition in the scar tissue after an MI. Rats received anti-P-selectin conjugated immunoliposomes containing VEGF immediately post-MI. Over 4 weeks, evolutionary changes in LV geometry and function were correlated with collagen deposition and infarct size quantified by Gomori's trichrome and picrosirius red staining. Targeted VEGF treated hearts showed a 37% decrease in collagen deposition in the anterior wall, as well as significant improvements in LV filling pressures. Multi-regression analysis showed that the extent of collagen deposition post MI can be predicted by a linear combination of normalized LV mass and ejection fraction. Targeted delivery of VEGF post-MI results in significant decreases in collagen deposition and adverse remodeling. Improvements in cardiac function in this model are related to degree of collagen deposition and extent of scar formation.