Implementing a Hospitalist Program in a Critical Access Hospital.

PURPOSE: The hospitalist model of inpatient care has rapidly expanded, but little is known about hospitalist care in critical access hospitals (CAHs). We aimed to determine the impact of a hospitalist model of care on staff satisfaction, patient volumes, patient satisfaction, length of stay, and care quality in a CAH. METHODS: We initiated a hybrid rotating hospitalist program in September 2008 at Winneshiek Medical Center (Decorah, Iowa), a 25-bed rural CAH. We reviewed patient volumes, Centers for Medicare and Medicaid Services core quality measures, acute length of stay, and staff satisfaction for primary care-hospitalist physicians and inpatient and clinic nurses. Patient volume and length of stay were compared with CAH data reported by the Iowa Hospital Association. FINDINGS: Patient volumes (acute, skilled, and observation) increased by 15% compared with a 17% decrease for statewide CAHs. Length of stay decreased from 2.88 to 2.75 days and remained lower than the average stay for Iowa CAHs (3.05 days). In the year after implementation, we observed no deterioration in core quality measures (range, 93%-100%) or patient satisfaction (86th percentile). Inpatient nurse satisfaction and primary care-hospitalist satisfaction improved. Early clinic nurse skepticism showed improved satisfaction at the 5-year review. CONCLUSIONS: Hospitalist care contributed to ongoing delivery of high-quality care and satisfactory patient experiences while supporting the mission of a CAH in rural Iowa. Implementation required careful consideration of its effects on the outpatient practice. Broader implementation of this model in CAHs may be warranted.

Mystixin peptides reduce hyaluronan deposition and edema formation.

Hyaluronan and its associated water of hydration are the basis of the swelling and edema of acute inflammation. Mystixins are small, synthetic peptides that suppress the acute inflammatory response. Mystixin-7, a prototype of these peptides, has the structure p-anisoyl-Arg-Lys-Leu-Leu-D-Thi-Ile-D-Leu-NH(2). As shown previously by this laboratory, the mystixin-7 peptide inhibits edema formation in vivo following intravenous administration at doses of less than 1.0 mg/kg. Mechanisms by which this peptide might suppress edema were examined here in vitro using cultured cells. Normal human dermal fibroblasts normally secrete large quantities of hyaluronan in response to inflammatory stimuli. Mystixin-7 reduced hyaluronan deposition by up to 80% in such cultures. Stimulation of hyaluronidase activity was observed. Mystixins represent a novel class of anti-inflammatory peptides that suppress the edema associated with inflammation. We propose that stimulation of hyaluronidase activity, with a decrease in net hyaluronan deposition and its associated water of hydration, is among the mechanisms of the anti-inflammatory effect of mystixin peptides.

Differential effects of mu-opioid receptor ligands on Ca(2+) signaling.

Activation of mu-opioid receptors (MORs) transfected into human embryonic kidney 293 cells, caused a multiphasic increase in cytosolic free Ca(2+) levels (Ca(2+)i). The first Ca(2+)i maximum (peak 1) between 5 and 7 s depended on the presence of extracellular Ca(2+) (Ca(2+)e). The second phase peaking at approximately 15 s (peak 2) was independent of Ca(2+)e and thus represents Ca(2+) release from intracellular stores. A decrease in temperature from 37 to 25 degrees C also caused reduction of peak 1 but not peak 2, suggesting that the two responses arise from mechanistically distinct pathways. A delayed Ca(2+)e-dependent third response phase is thought to represent capacitative Ca(2+)e influx evoked after release of Ca(2+) from internal stores. Agonists and antagonists of two major classes of opioid ligands, oxymorphinans (morphine and naloxone) and oripavines (etorphine and diprenorphine), had differential effects on Ca(2+) currents. Although morphine activated both phases with equal potency, etorphine was 20-fold less potent at stimulating peak 1 over peak 2. Similarly, the antagonists, naloxone and diprenorphine, blocked the Ca(2+) response to each agonist with greatly varying potencies. Specifically, concomitant injection of diprenorphine failed to affect peak 1 (thought to represent rapid Ca(2+)e influx) stimulated by morphine while fully blocking peak 2 (intracellular Ca(2+) release). However, diprenorphine potently inhibited peak 1 as well when added to the cells before morphine, indicating limited or slow access of diprenorphine to these morphine binding sites. The existence of multiple, functionally distinct binding site conformations could account for these findings. In conclusion, different opioid ligands can differentially affect Ca(2+) response patterns resulting from MOR activation.