The Impact of Bedside Interdisciplinary Rounds on Length of Stay and Complications.

BACKGROUND: Communication among team members within hospitals is typically fragmented. Bedside interdisciplinary rounds (IDR) have the potential to improve communication and outcomes through enhanced structure and patient engagement. OBJECTIVE: To decrease length of stay (LOS) and complications through the transformation of daily IDR to a bedside model. DESIGN: Controlled trial. SETTING: 2 geographic areas of a medical unit using a clinical microsystem structure. PATIENTS: 2005 hospitalizations over a 12-month period. INTERVENTIONS: A bedside model (mobile interdisciplinary care rounds [MICRO]) was developed. MICRO featured a defined structure, scripting, patient engagement, and a patient safety checklist. MEASUREMENTS: The primary outcomes were clinical deterioration (composite of death, transfer to a higher level of care, or development of a hospital-acquired complication) and length of stay (LOS). Patient safety culture and perceptions of bedside interdisciplinary rounding were assessed pre- and postimplementation.. RESULTS: There was no difference in LOS (6.6 vs 7.0 days, P = 0.17, for the MICRO and control groups, respectively) or clinical deterioration (7.7% vs 9.3%, P = 0.46). LOS was reduced for patients transferred to the study unit (10.4 vs 14.0 days, P = 0.02, for the MICRO and control groups, respectively). Nurses and hospitalists gave significantly higher scores for patient safety climate and the efficiency of rounds after implementation of the MICRO model. LIMITATIONS: The trial was performed at a single hospital. CONCLUSIONS: Bedside IDR did not reduce overall LOS or clinical deterioration. Future studies should examine whether comprehensive transformation of medical units, including co-leadership, geographic cohorting of teams, and bedside interdisciplinary rounding, improves clinical outcomes compared to units without these features. Journal of Hospital Medicine 2017;12:137-142.

Data-Driven Identification of Risk Factors of Patient Satisfaction at a Large Urban Academic Medical Center.

BACKGROUND: The Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey is the first publicly reported nationwide survey to evaluate and compare hospitals. Increasing patient satisfaction is an important goal as it aims to achieve a more effective and efficient healthcare delivery system. In this study, we develop and apply an integrative, data-driven approach to identify clinical risk factors that associate with patient satisfaction outcomes. METHODS: We included 1,771 unique adult patients who completed the HCAHPS survey and were discharged from the inpatient Medicine service from 2010 to 2012. We collected 266 clinical features including patient demographics, lab measurements, medications, disease categories, and procedures. We developed and applied a data-driven approach to identify risk factors that associate with patient satisfaction outcomes. FINDINGS: We identify 102 significant risk factors associating with 18 surveyed questions. The most significantly recurrent clinical risk factors were: self-evaluation of health, education level, Asian, White, treatment in BMT oncology division, being prescribed a new medication. Patients who were prescribed pregabalin were less satisfied particularly in relation to communication with nurses and pain management. Explanation of medication usage was associated with communication with nurses (q = 0.001); however, explanation of medication side effects was associated with communication with doctors (q = 0.003). Overall hospital rating was associated with hospital environment, communication with doctors, and communication about medicines. However, patient likelihood to recommend hospital was associated with hospital environment, communication about medicines, pain management, and communication with nurse. CONCLUSIONS: Our study identified a number of putatively novel clinical risk factors for patient satisfaction that suggest new opportunities to better understand and manage patient satisfaction. Hospitals can use a data-driven approach to identify clinical risk factors for poor patient satisfaction to support development of specific interventions to improve patients' experience of care.

Effect of cholecalciferol supplementation on inflammation and cellular alloimmunity in hemodialysis patients: data from a randomized controlled pilot trial.

BACKGROUND: Memory T-cells are mediators of transplant injury, and no therapy is known to prevent the development of cross-reactive memory alloimmunity. Activated vitamin D is immunomodulatory, and vitamin D deficiency, common in hemodialysis patients awaiting transplantation, is associated with a heightened alloimmune response. Thus, we tested the hypothesis that vitamin D3 supplementation would prevent alloreactive T-cell memory formation in vitamin D-deficient hemodialysis patients. METHODS AND FINDINGS: We performed a 12-month single-center pilot randomized, controlled trial of 50,000 IU/week of cholecalciferol (D3) versus no supplementation in 96 hemodialysis patients with serum 25(OH)D<25 ng/mL, measuring effects on serum 25(OH)D and phenotypic and functional properties of T-cells. Participants were randomized 2:1 to active treatment versus control. D3 supplementation increased serum 25(OH)D at 6 weeks (13.5 [11.2] ng/mL to 42.5 [18.5] ng/mL, p<0.001) and for the duration of the study. No episodes of sustained hypercalcemia occurred in either group. Results of IFNγ ELISPOT-based panel of reactive T-cell assays (PRT), quantifying alloreactive memory, demonstrated greater increases in the controls over 1 year compared to the treatment group (delta PRT in treatment 104.8+/-330.8 vs 252.9+/-431.3 in control), but these changes in PRT between groups did not reach statistical significance (p = 0.25). CONCLUSIONS: D3 supplements are safe, effective at treating vitamin D deficiency, and may prevent time-dependent increases in T-cell alloimmunity in hemodialysis patients, but their effects on alloimmunity need to be confirmed in larger studies. These findings support the routine supplementation of vitamin D-deficient transplant candidates on hemodialysis and highlight the need for large-scale prospective studies of vitamin D supplementation in transplant candidates and recipients. TRIAL REGISTRATION: Clinicaltrials.gov NCT01175798.

The surgical management of renal hyperparathyroidism.

Secondary and tertiary hyperparathyroidism (HPT) develop in patients with renal failure due to a variety of mechanisms including increased phosphorus and fibroblast growth factor 23 (FGF23), and decreased calcium and 1,25-dihydroxy vitamin D levels. Patients present with various bone disorders, cardiovascular disease, and typical laboratory abnormalities. Medical treatment consists of controlling hyperphosphatemia, vitamin D/analog and calcium administration, and calcimimetic agents. Improved medical therapies have led to a decrease in the use of parathyroidectomy (PTX). The surgical indications include parathyroid hormone (PTH) levels >800 pg/ml associated with hypercalcemia and/or hyperphosphatemia despite medical therapy. Other indications include calciphylaxis, fractures, bone pain or pruritis. Transplant recipients often show decreased PTH, calcium and phosphorus levels, but some will have persistent HPT. Evidence suggests that PTX may cause deterioration in renal graft function in the short-term calling into the question the indications for PTX in these patients. Pre-operative imaging is only occasionally helpful except in re-operative PTX. Operative approaches include subtotal PTX, total PTX with or without autotransplantation, and possible thymectomy. Each approach has its proponents, advantages and disadvantages which are discussed. Intraoperative PTH monitoring has a high positive predictive value of cure but a poor negative predictive value and therefore is of limited utility. Hypocalcemia is the most common complication requiring aggressive calcium administration. Benefits of surgery may include improved survival, bone mineral density and alleviation of symptoms.

Clinical and molecular epidemiology of methicillin-resistant Staphylococcus aureus among patients in an ambulatory hemodialysis center.

OBJECTIVE: To describe the epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) carriage and transmission in an ambulatory hemodialysis population. DESIGN: Prospective cohort study. SETTING: Outpatient hemodialysis facility affiliated with a large academic medical center. PARTICIPANTS: Of the 170 facility patients, 103 (61%) participated in the study. METHODS: Swab specimens of the nares, axillae, and vascular access site were collected from participants weekly for 3 weeks and then monthly for 5 months. Demographic and clinical data were collected monthly for 12 months. Molecular analysis of MRSA isolates was performed. RESULTS: The baseline MRSA carriage prevalence was 12%. Factors associated with MRSA carriage included a history of MRSA; failed renal transplantation; hospital admission within 6 months; and receipt of a first-generation cephalosporin, cefepime, or vancomycin. Six subjects acquired MRSA after enrollment (incidence, 1.2 per 100 patient-months at-risk; overall prevalence, 18%). Molecular analysis suggested that transmission occurred within the facility. The incidence of MRSA infection among carriers was 1.76 per 100 patient-months. Community-associated strains (ie, USA300) were isolated from 28% of carriers and at least 25% of infections. CONCLUSIONS: The prevalence of MRSA carriage and the incidence of infection among carriers were high among ambulatory hemodialysis patients, and community-associated MRSA was responsible for a large portion of the MRSA burden. A relatively high rate of MRSA acquisition was observed, with indirect evidence of intrafacility transmission. Additional studies are needed to confirm these findings and to identify effective and feasible methods to prevent MRSA transmission and infection among hemodialysis patients.

Loss of matrix metalloproteinase-2 amplifies murine toxin-induced liver fibrosis by upregulating collagen I expression.

BACKGROUND AND AIMS: Matrix metalloproteinase-2 (MMP-2), a type IV collagenase secreted by activated hepatic stellate cells (HSCs), is upregulated in chronic liver disease and is considered a profibrotic mediator due to its proliferative effect on cultured HSCs and ability to degrade normal liver matrix. Although associative studies and cell culture findings suggest that MMP-2 promotes hepatic fibrogenesis, no in vivo model has definitively established a pathologic role for MMP-2 in the development and progression of liver fibrosis. We therefore examined the impact of MMP-2 deficiency on liver fibrosis development during chronic CCl(4) liver injury and explored the effect of MMP-2 deficiency and overexpression on collagen I expression. METHODS: Following chronic CCl(4) administration, liver fibrosis was analyzed using Sirius Red staining with quantitative morphometry and real-time polymerase chain reaction (PCR) in MMP-2-/- mice and age-matched MMP-2+/+ controls. These studies were complemented by analyses of cultured human stellate cells. RESULTS: MMP-2-/- mice demonstrated an almost twofold increase in fibrosis which was not secondary to significant differences in hepatocellular injury, HSC activation or type I collagenase activity; however, type I collagen messenger RNA (mRNA) expression was increased threefold in the MMP-2-/- group by real-time PCR. Furthermore, targeted reduction of MMP-2 in cultured HSCs using RNA interference significantly increased collagen I mRNA and protein, while overexpression of MMP-2 resulted in decreased collagen I mRNA. CONCLUSIONS: These findings suggest that increased MMP-2 during the progression of liver fibrosis may be an important mechanism for inhibiting type I collagen synthesis by activated HSCs, thereby providing a protective rather than pathologic role.

Retained catheter fragment from a fractured tunneled catheter--a rare and potentially lethal complication.

Despite efforts to curtail central vein catheter use for dialysis catheters are frequently used in the treatment of end-stage renal disease (ESRD). In 2006, 82% of patients in the USA initiated dialysis via a catheter. The overall of tunnelled cuffed catheter (TCC) use was 35% greater in 2005 compared with 1996. Dialysis catheter tip fracture is a rare and potentially serious complication. Herein, we present the case of an incidental finding of a retained catheter fragment from a fractured TCC in the right atrium. Fragment retrieval (via snare technique) and subsequent placement of a new central venous catheter are outlined.

Protein kinase-X interacts with Pin-1 and Polycystin-1 during mouse kidney development.

The regulation of epithelial branching morphogenesis by bone morphogenetic protein-7 depends, in part, on functionally defined cyclic adenosine monophosphate (cAMP)-dependent protein kinases. We previously identified protein kinase-X (PRKX), a cAMP-dependent kinase, as a regulator of epithelial morphogenesis during kidney development and found that it binds to and phosphorylates Polycystin-1. Overexpression of PRKX stimulates renal epithelial cell migration, tubulogenesis, ureteric bud branching, and glomerular induction in embryonic mouse kidney explants in organ cultures. Here we determined the physiological functions of endogenous PRKX. Knockdown by siRNA of PRKX gene expression in a human fetal collecting tubule (HFCT) cell line exceeded 70% and resulted in decreased cell migration and increased adhesion of the cells to a collagen I matrix. In embryonic mouse kidney explants, the same degree of knockdown decreased ureteric bud branching and glomerular induction. Because PRKX BAG-3 PIN-1 and MAGI-1 are all expressed in ureteric bud derivatives, we tested for interactions among them and found that PRKX binds to all three proteins through its WW domain as determined by TransSignal domain arrays, and it coimmunoprecipitated with Pin-1 in HFCT cell lysates. These studies suggest that Polycystin-1 and Pin-1 may mediate the function of PRKX in kidney development.

Rationale and strategies for early detection and management of diabetic kidney disease.

Diabetic kidney disease (DKD) occurs in 20% to 40% of patients with diabetes mellitus and is the leading cause of chronic kidney disease and end-stage renal disease in the United States. Despite the American Diabetes Association and the National Kidney Foundation advocating annual screening of diabetic patients, DKD remains underdiagnosed in the diabetic population. Early recognition of diabetic nephropathy by health care professionals is vital for proper management. The presence of microalbuminuria is particularly important as even low levels of dipstick-negative albuminuria indicate early disease long before a diminished glomerular filtration rate and are associated with an elevated cardiovascular disease risk. Like all forms of chronic kidney disease, DKD causes a progressive decline in renal function that, despite current treatment strategies, is largely irreversible. Many patients with DKD might be expected to develop end-stage renal disease, but many more patients will likely die of a cardiovascular event before renal replacement therapy is needed. Therefore, a renewed focus on cardiovascular risk factor reduction and a timely nephrology consultation with an emphasis on patient education is essential to proper DKD management.

Interleukin-6 protects hepatocytes from CCl4-mediated necrosis and apoptosis in mice by reducing MMP-2 expression.

BACKGROUND/AIMS: Interleukin-6 stimulates liver regeneration and promotes hepatoprotection following experimental liver injury, but underlying mechanisms have not been fully characterized. Because studies suggest matrix metalloproteinase-2 (MMP-2) may promote liver injury, we examined whether IL-6 exerted its protective effects via regulation of MMP-2. METHODS: MMP-2 was analyzed in livers of IL-6-/- and IL-6+/+ mice following CCl(4) administration. IL-6-/- mice were pretreated with IL-6 and liver histology and MMP-2 expression were examined after liver injury. IL-6-/- mice were treated with an MMP-2 inhibitor and assessment of injury (histology and serum ALT levels), apoptosis by TUNEL assay, and hepatocyte proliferation by BRDU-labeling was performed. These studies were complemented by analysis of cultured stellate cells. RESULTS: MMP-2 mRNA, protein, and activity was increased in IL-6-/- livers. Restoration of IL-6 signaling in IL-6-/- mice rescued injury and restored MMP-2 expression to wild-type levels. Furthermore, pharmacologic inhibition of MMP-2 decreased hepatocellular injury and apoptosis in IL-6-/- mice. In cultured stellate cells, recombinant IL-6 suppressed endogenous MMP-2 mRNA and protein expression. CONCLUSIONS: IL-6 may be hepatoprotective in acute injury through down-regulation of MMP-2. These findings suggest a role for MMP-2 in amplifying liver injury in vivo.