Mccarthythompson1761

Objectives To provide national estimates of the number and clinical and economic burden of medication errors in the National Health Service (NHS) in England. Methods We used UK-based prevalence of medication errors (in prescribing, dispensing, administration and monitoring) in primary care, secondary care and care home settings, and associated healthcare resource use, to estimate annual number and burden of errors to the NHS. Burden (healthcare resource use and deaths) was estimated from harm associated with avoidable adverse drug events (ADEs). Results We estimated that 237 million medication errors occur at some point in the medication process in England annually, 38.4% occurring in primary care; 72% have little/no potential for harm and 66 million are potentially clinically significant. Prescribing in primary care accounts for 34% of all potentially clinically significant errors. Definitely avoidable ADEs are estimated to cost the NHS £98 462 582 per year, consuming 181 626 bed-days, and causing/contributing to 1708 deaths. This comprises primary care ADEs leading to hospital admission (£83.7 million; causing 627 deaths), and secondary care ADEs leading to longer hospital stay (£14.8 million; causing or contributing to 1081 deaths). Conclusions Ubiquitous medicines use in health care leads unsurprisingly to high numbers of medication errors, although most are not clinically important. There is significant uncertainty around estimates due to the assumption that avoidable ADEs correspond to medication errors, data quality, and lack of data around longer-term impacts of errors. Data linkage between errors and patient outcomes is essential to progress understanding in this area.Background The 2-week wait referral pathway for suspected colorectal cancer was introduced in England to improve time from referral from a general practitioner (GP) to diagnosis and treatment. Patients are required to be seen by a hospital clinician within 2 weeks if their symptoms meet the criteria set by the National Institute for Health and Care Excellence (NICE) and to start cancer treatment within 62 days. To achieve this, many hospitals have introduced a straight-to-test (STT) strategy requiring hospital-based triage of referrals. selleck inhibitor We describe the impact and learning from a new pathway which has removed triage and moved the process of requesting tests from hospital to GPs in primary care. Method An electronic STT pathway was introduced allowing GPs to book tests supported by a decision aid based on NICE guidance eliminating the need for a standard referral form or triage process. The hospital identified referrals as being on a cancer pathway and dealt with all ongoing management. Routinely collected cancer data were used to identify time to cancer diagnosis compared with national data RESULTS 11357 patients were referred via the new pathway over 3 years. Time from referral to diagnosis reduced from 39 to 21 days and led to a dramatic improvement in patients starting treatment within 62 days. Challenges included adapting to a change in referral criteria and developing a robust hospital system to monitor the pathway. Conclusion We have changed the way patients with suspected colorectal cancer are managed within the National Health Service by giving GPs the ability to order tests electronically within a monitored cancer pathway halving time from referral to diagnosis.Optimal care occurs when patients possess the skills, knowledge, and confidence needed to effectively manage their health. Promoting such patient activation in kidney disease care is increasingly being prioritized, and patient activation has recently emerged as central to kidney disease legislative policy in the United States. Two options of the Centers for Medicare and Medicaid Services Kidney Care Choices model-the Kidney Care First option and the Comprehensive Kidney Care Contracting option-now include patient activation as a quality metric; both models specifically name the patient activation measure (PAM) as the patient-reported outcome to use when assessing activation in kidney disease. Because nephrology practices participating in these models will receive capitated payments according to changes in patients' PAM scores, it is time to more critically evaluate this measure as it applies to patients with kidney disease. In this review, we raise important issues related to the PAM's applicability to kidney health, review and summarize existing literature that applies this measure to patients with kidney disease, and outline key elements to consider when implementing the PAM into practice and policy. Our aim is to spur further dialogue regarding how to assess and address patient activation in kidney disease to facilitate best practices for supporting patients in the successful management of their kidney health.Cardiac hypertrophy is a common feature in patients with CKD. Recent studies revealed that two phosphate regulators, fibroblast growth factor-23 and α-Klotho, are highly involved in the pathophysiologic process of CKD-induced cardiac hypertrophy. With decreasing renal function, elevated fibroblast growth factor-23 and decreased α-Klotho may contribute to cardiac hypertrophy by targeting the heart directly or by inducing systemic changes, such as vascular injury, hemodynamic disorders, and inflammation. However, several studies have demonstrated that disturbances in the fibroblast growth factor-23/α-Klotho axis do not lead to cardiac hypertrophy. In this review, we describe the cardiac effects of the fibroblast growth factor-23/α-Klotho axis and summarize recent progress in this field. In addition, we present not only the main controversies in this field but also provide possible directions to resolve these disputes.Background Uremic toxicity may play a role in the elevated risk of developing cognitive impairment found among patients with CKD. Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous system and which we previously identified as the receptor of indoxyl sulfate in endothelial cells. Methods To characterize involvement of uremic toxins in cerebral and neurobehavioral abnormalities in three rat models of CKD, we induced CKD in rats by an adenine-rich diet or by 5/6 nephrectomy; we also used AhR-/- knockout mice overloaded with indoxyl sulfate in drinking water. We assessed neurologic deficits by neurobehavioral tests and blood-brain barrier disruption by SPECT/CT imaging after injection of 99mTc-DTPA, an imaging marker of blood-brain barrier permeability. Results In CKD rats, we found cognitive impairment in the novel object recognition test, the object location task, and social memory tests and an increase of blood-brain barrier permeability associated with renal dysfunction.