Smartphones in medicine: emerging practices in an academic medical center.

Advances in mobile phone technology now provide a myriad of resources to physicians' fingertips. However, the medical profession continues to struggle with potential for misuse of these devices. There is a need for better understanding of physicians' uses of smartphones in order to establish guidelines for appropriate and professional behavior. The purpose of the current study was to survey physicians' and medical students' practices concerning smartphone use in the healthcare setting. Physicians and medical students were asked to complete anonymous surveys regarding uses of smartphones within the past month in various healthcare settings. Overall, the participants reported distinctly different patterns in the uses they made of their phones in different settings (P<.001), with most individuals engaging in most behaviors while on break but few using their smartphones while with patients or during procedures. It appears that physicians and medical students make decisions about using their smartphones according to some combination of three considerations: degree of relevance to patient care, the appropriateness of the behavior in front of patients, and the issue of how disruptive that behavior may be.

Lack of T cells in Act1-deficient mice results in elevated IgM-specific autoantibodies but reduced lupus-like disease.

Act1 is a negative regulator of B-cell activation factor of the TNF family (BAFF) and CD40L-induced signaling. BALB/C mice lacking Act1 develop systemic autoimmunity resembling systemic lupus erythematosus (SLE) and Sjögren's syndrome (SjS). SLE and SjS are characterized by anti-nuclear IgG autoantibody (ANA-IgG) production and inflammation of peripheral tissues. As autoantibody production can occur in a T-cell dependent or T-cell independent manner, we investigated the role of T-cell help during Act1-mediated autoimmunity. Act1-deficiency was bred onto C57Bl/6 (B6.Act1(-/-) ) mice and B6.TCRß(-/-) TCRδ(-/-) Act1(-/-) (TKO) mice were generated. While TCRß/δ-sufficient B6.Act1(-/-) mice developed splenomegaly and lymphadenopathy, hypergammaglobulinemia, elevated levels of ANA-IgG, and kidney pathology, TKO mice failed to develop any such signs of disease. Neither B6.Act1(-/-) nor TKO mice developed SjS-like disease, suggesting that epigenetic interactions on the BALB/C background are responsible for this phenotype in BALB/C.Act1(-/-) mice. Interestingly, BAFF-driven transitional B-cell abnormalities, previously reported in BALB/C.Act1(-/-) mice, were intact in B6.Act1(-/-) mice and largely independent of T cells. In conclusion, T cells are necessary for the development of SLE-like disease in B6.Act1(-/-) mice, but not BAFF-driven transitional B-cell differentiation.

Acute lithium intoxication: properly directing an index of suspicion.

Lithium is known for its efficacy and toxicity. Toxic effects have been characterized even with therapeutic levels. Most physicians will at some point be faced with a patient with altered mental status and no records of his or her history. The differential diagnosis of altered mental status is long, and further lengthens in a patient with a psychiatric history. Since several life-threatening complications of psychotropic medications exist, physicians must be astute with their diagnoses. Lithium toxicity, neuroleptic malignant syndrome, and the serotonin syndrome can present similarly and require rapid recognition. We present a case of lithium toxicity in a patient who presented with altered mental status and a paucity of history information.

Improving Patient Safety Communication in Residency Programs by Incorporating Patient Safety Discussions Into Rounds.

BACKGROUND: Engaging residents in patient safety and quality improvement initiatives is sometimes difficult. The primary goal of the current study was to develop a standardized learning experience designed to facilitate patient safety discussions during rounds. METHODS: Residents who were on inpatient rotations during a 2-month period in 2014 were exposed to patient safety discussions on rounds. Residents who were not on inpatient rotations served as a control group. Faculty received weekly text reminders with 3 questions designed to engage residents in patient safety discussions. Before and after the intervention, residents were asked to complete a modified Agency for Healthcare Research and Quality Hospital Survey on Patient Safety Culture. Faculty members were asked to complete a brief survey designed by the study investigators. RESULTS: Of the 160 residents who participated in the study, 49 responded to both the preintervention and postintervention surveys (31%). Residents who participated in patient safety discussions during rounds reported higher frequencies of safety events reported compared to the control group (P<0.05). Both groups of residents reported better communication (P<0.01) and an increased number of safety events reported (P<0.01) at the end of the intervention. Twenty-two faculty were surveyed, and 19 responded (86%). Most faculty felt incorporating patient safety discussions on rounds was constructive and that the residents were responsive. Few faculty members felt the patient safety discussions were burdensome. CONCLUSION: Using weekly text reminders with 3 prompts to incorporate patient safety discussions into rounds was well received by faculty and residents and had an impact on communication and error reporting.

Graduate Medical Education as a Lever for Collaborative Change: One Institution's Experience with a Campuswide Patient Safety Initiative.

BACKGROUND: The 2013 closure of a public hospital in Baton Rouge, LA transformed graduate medical education (GME) at Our Lady of the Lake Regional Medical Center (OLOL). Administrators were tasked with incorporating residents into patient safety and quality improvement initiatives to fulfill regulatory obligations. This report outlines our experiences as we built these patient safety and quality improvement initiatives in a rapidly expanding independent academic medical center. METHODS: We joined the Alliance of Independent Academic Medical Centers (AIAMC) to meet and learn from national peers. To fulfill the scholarly activity requirement of the AIAMC's National Initiative IV, we formed a multidisciplinary team to develop a patient safety education project. Prioritized monthly team meetings allowed for project successes to be celebrated and circulated within the organization. RESULTS: The public-private partnership that more than quadrupled the historic size of GME at OLOL has, in the past 2 years, led to the development of an interdisciplinary team. This team has expanded to accommodate residency program leadership from across the campus. Our National Initiative IV project won a national award and inspired several follow-up initiatives. In addition, this work led to the formation of a Patient Safety and Clinical Quality Improvement fellowship that matched its first fellow in 2015. CONCLUSION: Through the commitment and support of hospital and medical education leaders, as well as a focus on promoting cultural change through scholarly activity, we were able to greatly expand patient safety and quality improvement efforts in our institution.

Activation of toll-like receptor (TLR)2, TLR4, and TLR9 in the mammalian cornea induces MyD88-dependent corneal inflammation.

PURPOSE: Toll-like receptors (TLRs), which recognize microbial products, have an important role in the host innate immune response. The purpose of the present study was to determine whether activation of these receptors leads to development of keratitis and to assess the role of the common adaptor molecule myeloid differentiation factor-88 (MyD88). METHODS: Corneal epithelium of C57BL/6, TLR2(-/-), TLR9(-/-), and MyD88(-/-) mice was abraded and treated with Pam(3)Cys, LPS, or CpG DNA, which bind TLR2, -4, and -9, respectively, and neutrophil recruitment to the corneal stroma, development of corneal haze, and chemokine production were measured. RESULTS: Activation of TLR2 and -9 stimulated neutrophil recruitment to the corneal stroma of C57BL/6 mice, but not TLR2(-/-) or -9(-/-) mice, respectively. In marked contrast, neutrophil migration to the corneal stroma of MyD88(-/-) mice challenged with Pam(3)Cys, LPS, or CpG DNA was completely ablated. Activation of TLR2, -4, and -9 also caused a significant increase in corneal thickness and haze, indicative of disruption of corneal clarity; however, this response was ablated in MyD88(-/-) mice, which were not significantly different from untreated corneas. Production of CXC chemokines MIP-2 and KC, which mediate neutrophil recruitment to the corneal stroma, was elevated in the corneal epithelium and stroma of control, but not MyD88(-/-) mice. CONCLUSIONS: Together, these findings demonstrate that the corneal epithelium has functional TLR2 and -9, and that TLR2, -4, and -9 signal through MyD88. This pathway is therefore likely to have an important role in the early events leading to microbial keratitis.

MyD88 functions as a negative regulator of TLR3/TRIF-induced corneal inflammation by inhibiting activation of c-Jun N-terminal kinase.

The adaptor molecule MyD88 is necessary for responses to all Toll-like receptors except TLR3 and a subset of TLR4 signaling events, which are mediated by the adaptor molecule TRIF. To determine the role of TRIF in host inflammatory responses, corneal epithelium of C57BL/6, TLR3(-/-), TRIF(-/-), and MyD88(-/-) mice was abraded and stimulated with the synthetic TLR3 ligand poly(I:C). We found that poly(I:C) induced a pronounced cellular infiltration into the corneal stroma, which was TLR3- and TRIF-dependent. Unexpectedly, the inflammatory response was exacerbated in MyD88(-/-) mice, with enhanced neutrophil and F4/80(+) cell infiltration into the corneal stroma and elevated corneal haze, which is an indicator of loss of corneal transparency. To determine whether MyD88-dependent inhibition of TLR3/TRIF responses is a general phenomenon, we examined cytokine production by MyD88(-/-) bone marrow-derived macrophages; however, no significant difference was observed between MyD88(+/+) or MyD88(-/-) macrophages. In contrast, human corneal epithelial cells (HCECs) transfected with MyD88 small interfering RNA had significantly increased (2.5-fold) CCL5/RANTES production compared with control HCECs, demonstrating a negative regulatory role for MyD88 in TLR3/TRIF responses in these cells. Finally, knockdown of MyD88 in HCECs resulted in increased phosphorylation of c-Jun N-terminal kinase (JNK), but not p38, IRF-3, or NF-kappaB. Consistent with this finding, the JNK inhibitor SP600125, but not p38 inhibitor SB203580, ablated this response. Taken together, these findings demonstrate a novel JNK-dependent inhibitory role for MyD88 in the TLR3/TRIF activation pathway.