Hospital providers often use workarounds to circumvent processes so that patients can receive care. Workarounds in response to operational failures enable care to continue and therefore may be indicative of workers' commitment. On the other hand, workarounds in the absence of operational failures may signal an ineffective approach associated with lower quality of care and worse patient outcomes. Working closely with healthcare providers, we developed a survey to measure workaround behaviors and operational failures on medical/surgical units. The lead author surveyed over 4,000 nurses from 63 hospitals throughout the United States. We matched this data with audit data on the incidence of pressure injuries among over 21,000 patients on 262 nursing units in 56 survey hospitals. Hospital‐acquired pressure injuries are a significant risk to patient health and hospital costs. We do not find support for our hypothesis that workarounds are associated with a higher rate of hospital‐acquired pressure injuries. However, when we take into account the moderating role of operational failures on the relationship between workarounds and pressure injuries, we find significant results. When nursing units have lower levels of operational failures, workarounds are associated with higher rates of hospital‐acquired pressure injuries. Our results provide evidence that workarounds may be associated with negative patient outcomes, if they stem from a process‐avoiding approach. The best results can be achieved by reducing both operational failures and workarounds via instilling a process‐focused approach.

Among clinical studies used to support FDA approval of high-risk medical device modifications, fewer than half were randomized, blinded, or controlled, and most primary outcomes were based on surrogate end points. These findings suggest that the quality of studies and data evaluated to support approval by the FDA of modifications of high-risk devices should be improved.

Homeostatic maintenance of corneal endothelial cells is essential for maintenance of corneal deturgescence and transparency. in fuchs endothelial corneal dystrophy (fecD), an accelerated loss and dysfunction of endothelial cells leads to progressively severe visual impairment. An abnormal accumulation of extracellular matrix (ecM) is a distinctive hallmark of the disease, however the molecular pathogenic mechanisms underlying this phenomenon are not fully understood. Here, we investigate genome-wide and sequence-specific DNA methylation changes of miRNA genes in corneal endothelial samples from fecD patients. We discover that miRnA gene promoters are frequent targets of aberrant DNA methylation in FECD. More specifically, miR-199B is extensively hypermethylated and its mature transcript miR-199b-5p was previously found to be almost completely silenced in FECD. Furthermore, we find that miR-199b-5p directly and negatively regulates Snai1 and ZEB1, two zinc finger transcription factors that lead to increased ECM deposition in FECD. Taken together, these findings suggest a novel epigenetic regulatory mechanism of matrix protein production by corneal endothelial cells in which miR-199B hypermethylation leads to miR-199b-5p downregulation and thereby the increased expression of its target genes, including Snai1 and ZEB1. our results support miR-199b-5p as a potential therapeutic target to prevent or slow down the progression of FECD disease. Corneal transparency is critical for good visual acuity. The corneal endothelium regulates the hydration status of the cornea and has an essential role in maintaining corneal deturgescence and preventing edema that can degrade corneal transparency. It is the innermost layer of the cornea and is composed of a single layer of cells that pump excess fluid out of the cornea through active ion-transport processes 1,2. Fuchs endothelial corneal dystrophy (FECD) is a bilateral, slowly progressive disorder in which the corneal endothelial cells are diseased and become less efficient at removing fluid. As a result, the highly ordered arrangement of collagen fibers in the corneal stromal layer become disrupted, leading to corneal opacification and vision loss 3. Other clinical phenotypic changes that occur in FECD include an excessive accumulation of extracellular matrix (ECM), formation of central excrescences (corneal guttae), thickening of Descemet's membrane, and corneal scarring 4. At earlier stages of FECD, the formation of corneal guttae can cause light scatter and optical aberrations that can impair vision, even in the absence of overt corneal edema. In later FECD, overt endothelial dysfunction and resultant corneal edema contribute significantly to visual loss. Corneal endothelial cells are largely non-regenerative in vivo and their loss is often irreversible 5. Medical management is often inadequate and corneal endothelial transplantation remains the main therapeutic option to restore vision in patients with advanced FECD. FECD is a leading indication for corneal transplantation i...

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The case of a patient with recurrent esthesioneuroblastoma complicated by ectopic adrenocorticotropic hormone production is presented, including the workup and management of this uncommon complication of an uncommon disease. The Oncologist 2010;15: 51-58 CASE PRESENTATIONIn 1992, a 55-year-old white man presented with epistaxis and was diagnosed with esthesioneuroblastoma. He underwent a craniofacial resection with postoperative radiation therapy to his tumor site. In 1996, he relapsed in the cervical lymph nodes and underwent a bilateral cervical lymph node dissection. In total, eight positive lymph nodes were removed. He was then treated with chemotherapy with etoposide and cisplatin for four cycles. Although radiation therapy to the neck was recommended, the patient refused. In 1998, he relapsed again in the left submandibular area, and two involved lymph nodes were resected. He then agreed to and received radiation therapy to both sides of the neck. In 2002, he had evidence of further disease progression in the posterior nasopharynx and a left preauricular node. In 2004, he was treated with etoposide and carboplatin for four cycles with a minor response. Following that, he was observed without further therapy, given the indolent nature of his disease and minimal symptoms. He did, however, experience focal seizures, occasional epistaxis, hyponatremia, hypothyroidism, and an episode of pneumococcal meningitis.In August 2007, he developed fatigue, confusion, severe hypertension, and proximal muscle weakness. Laboratory studies revealed a serum glucose level of 228 mg/dl (normal, 70 -99 mg/dl), serum potassium of 2.9 mmol/l (normal, 3.5-5.1 mmol/l), pH of 7.570 (normal, 7.350 -7.450