Thomas J. Pshak

The computerized rounding report: implementation of a model system to support transitions of care.

OBJECTIVES In response to ACGME work-hour restrictions, residency programs that require continuous inpatient clinical care for educational objectives will be forced to increase the proportion of junior resident experience involved in shift work. Maintaining the balance of education over service at these levels will be a challenge, where a considerable amount of time must be spent gathering data for morning rounds and signing out patients at shift change. Patient safety is an issue with this new paradigm. We hypothesized that computerized sign-out would improve resident efficiency. MATERIALS AND METHODS A multidisciplinary clinical team collaborated to design a computerized rounding and sign-out (CSO) program to automate collection of clinical information in addition to a brief narrative describing ongoing care issues. Residents returned a self-administered questionnaire before (n = 168) and after implementation (n = 83) examining: pre-rounding time, missed patients, handoff quality, and duty hours. RESULTS Residents reported spending 11 fewer min/d pre-rounding (P = 0.006). After implementation, residents missed fewer patients on rounds (P = 0.01). A majority (70%) of responders stated that the new program helped them with duty hours. CONCLUSION The current study demonstrates the reproducibility of the University of Washington model system for rounding and sign-out at an independent site, using basic infrastructure and leadership common to all residency programs. Developing a CSO was associated with a modest reduction in pre-rounding time and fewer patients missed on rounds. Although automating resident tasks may improve workflow in an increasingly complex hospital environment, structured handoff education and other institutional changes are necessary.

Is Tissue Interposition Always Necessary in Transvaginal Repair of Benign, Recurrent Vesicovaginal Fistulae?

OBJECTIVE To evaluate and compare the outcomes of transvaginal repair of benign, primary, and recurrent vesicovaginal fistulas (VVFs) treated without tissue interposition because, historically, tissue interposition with a vascularized flap has been advocated in both transabdominal and transvaginal repairs of recurrent VVFs. METHODS A retrospective chart review was conducted of 73 consecutive women with VVF and treated by a single surgeon (B.J.F.) between January 2003 and May 2012. Patients with a malignant etiology and/or prior irradiation were excluded as they required a more complex repair. All included VVFs were treated by a transvaginal approach with partial vaginal cuff excision without a tissue interposition. Patients were followed in our clinic postoperatively for 1 year and by telephone survey thereafter. RESULTS Forty-nine patients met inclusion criteria: 25 primary and 24 recurrent. There was no statistical difference in patient age, fistula size, time to repair, or fistula etiology between the 2 groups. There has been no fistula recurrence in either group. Forty-one of 49 patients (84%) were discharged the same day as their surgery. CONCLUSION Benign, recurrent VVFs are not synonymous with other complex fistulas that typically require tissue interposition. Our study demonstrates that transvaginal repair of benign, recurrent VVFs without tissue interposition can be equally successful as primary repairs without tissue interposition. The number of prior repairs should not be an independent factor in the use of tissue interposition, as previously suggested. We advocate an individualized approach to each VVF, only using tissue interposition when appropriate.

Oxalate upregulates expression of IL-2Rβ and activates IL-2R signaling in HK-2 cells, a line of human renal epithelial cells

The role of inflammation in oxalate-induced nephrolithiasis is debated. Our gene expression study indicated an increase in interleukin-2 receptor β (IL-2Rβ) mRNA in response to oxalate (Koul S, Khandrika L, Meacham RB, Koul HK. PLoS ONE 7: e43886, 2012). Herein, we evaluated IL-2Rβ expression and its downstream signaling pathway in HK-2 cells in an effort to understand the mechanisms of oxalate nephrotoxicity. HK-2 cells were exposed to oxalate for various time points in the presence or absence of SB203580, a specific p38 MAPK inhibitor. Gene expression data were analyzed by Ingenuity Pathway Analysis software. mRNA expression was quantitated via real-time PCR, and changes in protein expression/kinase activation were analyzed by Western blotting. Exposure of HK-2 cells to oxalate resulted in increased transcription of IL-2Rβ mRNA and increased protein levels. Oxalate treatment also activated the IL-2Rβ signaling pathway (JAK1/STAT5 phosphorylation). Moreover, the increase in IL-2Rβ protein was dependent upon p38 MAPK activity. These results suggest that oxalate-induced activation of the IL-2Rβ pathway may lead to a plethora of cellular changes, the most common of which is the induction of inflammation. These results suggest a central role for the p38 MAPK pathway in mediating the effects of oxalate in renal cells, and additional studies may provide the key to unlocking novel biochemical targets in stone disease.

313 OXLATE-INDUCED CHANGES IN GENE EXPRESSION IN HUMAN RENAL EPITHELIAL CELLS: IDENTIFICATION OF GENES INDUCED BY OXALATE.

Kidney stones affect about 10% of the US population and have an economic impact of 2 to 4 billion US

Correlation between CT-estimated tumor volume, pathologic tumor volume, and final pathologic specimen weight in children with Wilms' tumor

anually. The majority (≈80%) of kidney stones are composed of calcium oxalate crystals. Increased urinary oxalate is an established risk factor for nephrolithiasis. Our laboratory was the first to demonstrate that oxalate is nephrotoxic, and oxalate interactions with the renal ells result in a plethora of changes, including cell growth, death, and altered gene expression. Recently, we evaluated oxalate-induced global changes in gene expression in the renal epithelial (HK2) cells by DNA microarray chip that represented 11 independent replicate probe sets for each message. These studies identified several genes whose expression was either up- or down-regulated by oxalate. In the present study, the most strongly up- and down-regulated genes were confirmed using polymerase chain reaction (PCR) in new experiments, where renal epithelial cells (HK2) were exposed to oxalate. We also extended our studies to define time course (1-24 h) of gene expression changes upon oxalate exposure. Results of our current studies confirmed that oxalate-induced time dependent expression of the beta-adrenergic receptor, beta subunit of the IL-2 receptor, and the transcript of a protein whose function is currently unknown. These exciting observations suggest that oxalate may regulate its actions by turning on additional (previously unknown) intracellular pathways that may be involved in stone pathogenesis. Additional studies into these pathways may provide the key to unlocking a biochemical target in stone disease and are currently under way in our laboratory.