Mount Sinai Journal of Medicine最新文献

The purpose of this article is to briefly review the history of how quality and safety have been addressed in the United States by those who have been teaching medical students and residents, and then discuss why and how this training must change in the future to more effectively address the problems of improving healthcare quality and safety. Although it has become clear that the curriculum in medical schools should encompass quality and safety training, medical schools have been very slow to implement the reforms that are necessary to accomplish such a goal. These changes, although desirable from a rational perspective, involve basic changes in the culture of medical schools and teaching hospitals. Moreover, the cost of implementing these changes would be very large, and, if imposed by outside agencies, would likely constitute an unfunded mandate. It should also be noted that at the present time there are very few people who are well trained to develop and teach these classes. In order to accomplish the goal of improving patient safety, it is essential that we provide much more training and knowledge regarding patient safety to medical students, including knowledge of interventions known to be effective in preventing errors; education in technical performance; information about organizational and team issues; and training in disclosing errors to patients. This training should occur early in the training of professionals, preferably while they are still in school, if such training is to change the culture of medicine. Some suggestions and plans for implementation are discussed, using some innovative programs as examples.

Detection of small pulmonary nodules has markedly increased as computed tomography (CT) technology has advanced and interpretation evolved from viewing small CT images on film to magnified images on large, high-resolution computer monitors. Despite these advances, determining the etiology of a lung nodule short of major surgery remains problematic. Initial nodule size is a major criterion in evaluating the risk for malignancy, and the majority of CT detected nodules are <10 mm in diameter. Also, the likelihood that the nodule is a lung cancer increases with increasing age and smoking history, and such clinical information needs to be integrated into algorithms that guide the workup of such nodules. Baseline and annual repeat screening results are also very helpful in developing and assessing the usefulness of such algorithms. Based on CT morphology, subtypes of nodules have been identified; today nodules are routinely classified as being solid, part-solid, or nonsolid. It has been shown that part-solid nodules have a higher frequency of being malignant than solid or nonsolid ones. Other nodule characteristics such as spiculation are useful, although granulomas and fibrosis also have such features, so these characteristics have not been as useful as nodule-growth assessment. Depending on the aggressiveness of the lung cancer and the size of the nodule when it is initially seen, a follow-up CT scan 1-3 months after the first CT scan can identify those nodules with growth at a malignant rate. Software has been developed by all CT scanner manufacturers for such growth assessment, but the inherent variability of such assessments needs further development. Nodule-growth assessment based on 2-dimensional approaches is limited; therefore, software has been developed for the 3-dimensional assessment of growth. Different approaches for such growth assessment have been developed, either using automated computer segmentation techniques or hybrid methods that allow the radiologist to adjust such segmentation. There are, however, inherent reasons for variability in such measurements that need to be carefully considered, and this, together with continued technologic advances and integration of the relevant clinical information, will allow for individualization of the algorithms for the workup of small pulmonary nodules.

In the decade since the Institute of Medicine released To Err Is Human, patient harm from medical errors is still widespread. Healthcare has not undergone the transformative change that is needed to reduce medical errors and improve quality. This article discusses patient-centeredness as an organizing principle for transforming healthcare. We also describe important efforts that depict the shift from a provider-focused system to one that is more patient-centered. Finally, the article discusses challenges for the future and the importance of involving patients in the quest to deliver safe, quality care.

The phrase "patient safety" represents freedom from accidental or preventable harm due to events occurring in the healthcare setting. Practitioners aim to reduce, if not prevent, medical errors and adverse outcomes. Yet studies performed from many perspectives show that medical error constitutes a serious worldwide problem. Transfusion medicine, with its interdisciplinary intricacies and the danger of fatal outcomes, serves as an exemplar of lessons learned. Opportunity for error in complex systems is vast, and although errors are traditionally blamed on humans, they are often set up by preexisting factors. Transfusion has inherent hazards such as clinical vulnerabilities (eg, contracting an infectious agent or experiencing a transfusion reaction), but there also exists the possibility of hazards associated with process errors. Sample collection errors, or preanalytic errors, may occur when samples are drawn from donors during blood donation, as well as when drawn from patients prior to transfusion-related testing, and account for approximately one-third of events in transfusion. Errors in the analytic phase of the transfusion chain, slips and errors in the laboratory, comprise close to one-third of patient safety-related transfusion events. As many as 40% of mistransfusions are due to errors in the postanalytic phase: often failures in the final check of the right blood and the right patient at the bedside. Bar-code labels, radiofrequency identification tags, and even palm vein-scanning technology are increasingly being utilized in patient identification. The last phase of transfusion, careful monitoring of the recipient for adverse signs or symptoms, when performed diligently can help prevent or manage a potentially fatal reaction caused by an earlier process error or an unavoidable physiologic condition. Ways in which we can and do deal with potential hazards of transfusion are discussed, including a method of hazard reduction termed inherently safer design. This approach aims to lessen risk, with elimination of a hazard or the reduction of its occurrence as primary. In blood transfusion, elimination and marked reduction of some hazards has been employed to good effect. However, there is still a heavy reliance on procedural methods in the essentially manual steps constituting the phases of the transfusion chain. Some hospitals have created a new role of transfusion safety officer to assist in the effort of monitoring, identifying, and resolving conditions that may lessen safety.

The last 25 years have witnessed remarkable advances in our understanding of the etiology and pathogenesis of Parkinson's disease. The ability to undertake detailed biochemical analyses of the Parkinson's disease postmortem brain enabled the identification of defects of mitochondrial and free-radical metabolism. The discovery of the first gene mutation for Parkinson's disease, in alpha-synuclein, ushered in the genetic era for the disease and the subsequent finding of several gene mutations causing parkinsonism, 15 at the time of writing. Technological advances both in sequencing technology and software analysis have allowed association studies of sufficiently large size accurately to describe genes conferring an increased risk for Parkinson's disease. What has been so surprising is the convergence of these 2 separate disciplines (biochemistry and genetics) in terms of reinforcing the importance of the same pathways (ie, mitochondrial dysfunction and free-radical metabolism). Other pathways are also important in pathogenesis, including protein turnover, inflammation, and post-translational modification, particularly protein phosphorylation and ubiquitination. However, even these additional pathways overlap with each other and with those of mitochondrial dysfunction and oxidative stress. This review explores these concepts with particular relevance to mitochondrial involvement.

Seminal plasma hypersensitivity manifests as a spectrum of systemic and/or localized clinical symptoms after exposure to specific protein components in seminal fluid. The prevalence of this disease is largely unknown, but it is believed to affect up to 40,000 women in the United States. Although no definitive risk factors have been confirmed, women with systemic reactions are frequently atopic. Prostate-specific antigen is believed to be the major allergen involved in the disorder, but other proteins are likely involved. Interestingly, up to 40%-50% of both systemic and localized seminal plasma hypersensitivity cases can occur after first-time intercourse. Diagnosis is based on clinical history. The gold standard for diagnosing seminal plasma hypersensitivity is prevention of symptoms with the use of a condom. Patients with seminal plasma hypersensitivity demonstrate positive prick skin test and/or serum-specific immunoglobulin E to whole seminal fluid or fractionated seminal plasma proteins. Treatment of seminal plasma hypersensitivity involves either avoidance with the use of condoms, intravaginal graded challenge using dilutions of whole seminal fluid, or subcutaneous desensitization to relevant fractionated seminal plasma proteins obtained from the woman's sexual partner. In most cases, treatment using one or more of the above approaches has been very successful. Infertility has not been demonstrated to be directly related to seminal plasma hypersensitivity, although women with the condition frequently have difficulty conceiving due to their inability to have unprotected sexual intercourse.

Atopic dermatitis, commonly known as eczema, is a common chronic, relapsing skin disease characterized by pruritus, disrupted epidermal barrier function, and immunoglobulin E-mediated sensitization to food and environmental allergens. Atopic dermatitis is a complex disease that arises from interactions between genes and the environment. Loci on several chromosomes have been identified, including a family of epithelium-related genes called the epidermal differentiation complex on chromosome 1q21. Mutations in filaggrin, a key protein in epidermal differentiation, have also been identified in early-onset and severe atopic dermatitis. There are 3 classical stages of eczema: infantile, childhood, and adulthood. The spectrum of eczema presentation varies widely from a variant that only affect the hand to major forms where a patient presents with erythroderma. The acute and subacute lesions of atopic dermatitis are often characterized by intensely pruritic, erythematous papules and vesicles with excoriations and a serous exudate. Chronic atopic dermatitis is exemplified by lichenified plaques and papules with excoriations. Atopic dermatitis patients are also at higher risk for skin infections, including bacterial and viral superinfections. Conventional therapy includes avoidance of irritants and potential allergens, as well as continued hydration of the skin with thick emollients. Topical corticosteroids and topical immunomodulators are often used primarily. Other therapies including phototherapy, antimicrobials, antihistamines, and systemic immunosuppressives are also options in certain situations.