The resident experience on trauma: declining surgical opportunities and career incentives? Analysis of data from a large multi-institutional study

PURPOSE: The surgical resident experience with trauma has changed. Many residents are exposed to predominantly nonoperative patient care experiences while on trauma rotations. Data from a large multicenter study were analyzed to estimate surgical resident exposure to trauma laparotomy, diagnostic peritoneal lavage (DPL), and focused abdominal sonography for trauma (U/S). METHODS: Centers completed a self-report questionnaire on their institutional demographics, admissions, and procedure for a 2-year period (1998-1999). RESULTS: A total of 82 trauma centers that provide resident teaching were included. The included centers represent over 247,000 trauma admissions. The majority of trauma centers (65.9%) had > 80% blunt injury. Although all centers performed laparotomies, other results were more variable. For U/S, 24.2% performed none at all and 47.0% performed fewer than two U/S examinations per month. For DPLs, 3.8% performed none and 66.7% performed fewer than two per month. Assuming 1 night of 4 on call, the average surgical resident training at a trauma center performing > 80% blunt trauma has the potential to participate in only 15 trauma laparotomies, 6 diagnostic peritoneal lavages, and 45 ultrasound examinations per year. In addition, the resident will care for an average of 500 blunt trauma patients before performing a splenectomy or liver repair. CONCLUSION: Surgical resident experience on most trauma services is heavily weighted to nonoperative management, with a relatively low number of procedures, little experience with DPL, and highly variable experience with ultrasound. These data have serious implications for resident training and recruitment into the specialty.     

Half the burden of fragility fractures in the community occur in women without osteoporosis. When is fracture prevention cost-effective?

To determine the age- and BMD-specific burden of fractures in the community and the cost-effectiveness of targeted drug therapy, we studied a demographically well-categorized population with a single main health provider. Of 1224 women over 50 years of age sustaining fractures during 2 years, the distribution of all fractures was 11%, 20%, 33%, and 36% in those aged 50-59, 60-69, 70-79, and 80+ years, respectively. Osteoporosis (T score < -2.5) was present in 20%, 46%, 59%, and 69% in the respective age groups. Based on this sample and census data for the whole country, treating all women over 50 years of age in Australia with a drug that halves fracture risk in osteoporotic women and reduces fractures in those without osteoporosis by 20%, was estimated to prevent 18,000 or 36% of the 50,000 fractures per year at a total cost of $573 million (AUD). Screening using a bone mineral density of T score of -2.5 as a cutoff, misses 80%, 54%, 41%, and 31% of fractures in women in the respective age groups. An analysis of cost per averted fracture by age group suggests that treating women in the 50- to 59-year age group with osteoporosis alone costs $156,400 per averted fracture. However, in women aged over 80 years, the cost per averted fracture is $28,500. We infer that treating all women over 50 years of age is not feasible. Using osteoporosis and age (>60 years) as criteria for intervention reduces the population burden of fractures by 28% and is cost-effective but solutions to the prevention of the remaining 72% of fragility fractures remain unavailable.     

Reduction of hepatic and adipose tissue glucocorticoid receptor expression with antisense oligonucleotides improves hyperglycemia and hyperlipidemia in diabetic rodents without causing systemic glucocorticoid antagonism

Glucocorticoids (GCs) increase hepatic gluconeogenesis and play an important role in the regulation of hepatic glucose output. Whereas systemic GC inhibition can alleviate hyperglycemia in rodents and humans, it results in adrenal insufficiency and stimulation of the hypothalamic-pituitary-adrenal axis. In the present study, we used optimized antisense oligonucleotides (ASOs) to cause selective reduction of the glucocorticoid receptor (GCCR) in liver and white adipose tissue (WAT) and evaluated the resultant changes in glucose and lipid metabolism in several rodent models of diabetes. Treatment of ob/ob mice with GCCR ASOs for 4 weeks resulted in approximately 75 and approximately 40% reduction in GCCR mRNA expression in liver and WAT, respectively. This was accompanied by approximately 65% decrease in fed and approximately 30% decrease in fasted glucose levels, a 60% decrease in plasma insulin concentration, and approximately 20 and 35% decrease in plasma resistin and tumor necrosis factor-alpha levels, respectively. Furthermore, GCCR ASO reduced hepatic glucose production and inhibited hepatic gluconeogenesis in liver slices from basal and dexamethasone-treated animals. In db/db mice, a similar reduction in GCCR expression caused approximately 40% decrease in fed and fasted glucose levels and approximately 50% reduction in plasma triglycerides. In ZDF and high-fat diet-fed streptozotocin-treated (HFD-STZ) rats, GCCR ASO treatment caused approximately 60% reduction in GCCR expression in the liver and WAT, which was accompanied by a 40-70% decrease in fasted glucose levels and a robust reduction in plasma triglyceride, cholesterol, and free fatty acids. No change in circulating corticosterone levels was seen in any model after GCCR ASO treatment. To further demonstrate that GCCR ASO does not cause systemic GC antagonism, normal Sprague-Dawley rats were challenged with dexamethasone after treating with GCCR ASO. Dexamethasone increased the expression of GC-responsive genes such as PEPCK in the liver and decreased circulating lymphocytes. GCCR ASO treatment completely inhibited the increase in dexamethasone-induced PEPCK expression in the liver without causing any change in the dexamethasone-induced lymphopenia. These studies demonstrate that tissue-selective GCCR antagonism with ASOs may be a viable therapeutic strategy for the treatment of the metabolic syndrome.     

Venous thromboembolism associated with hip and knee replacement over a ten-year period: a population-based study

This population-based study investigated the incidence and trends in venous thromboembolic disease after total hip and knee arthroplasty over a ten-year period. Death or readmission for venous thromboembolic disease up to two years after surgery for all patients in Scotland was the primary outcome. The incidence of venous thromboembolic disease, including fatal pulmonary embolism, three months after surgery was 2.27% for primary hip arthroplasty and 1.79% for total knee arthroplasty. The incidence of fatal pulmonary embolism within three months was 0.22% for total hip arthroplasty and 0.15% for total knee arthroplasty. The majority of events occurred after hospital discharge, with no apparent trend over the period. The data support current advice that prophylaxis should be continued for at least six weeks following surgery. Despite the increased use of policies for prophylaxis and earlier mobilisation, there has been no change in the incidence of venous thromboembolic disease.     

Effects of Yearly Zoledronic Acid 5 mg on Bone Turnover Markers and Relation of PINP With Fracture Reduction in Postmenopausal Women With Osteoporosis

In patients with osteoporosis treated with antiresorptive agents, reduction in bone turnover explains much of the observed fracture risk reduction. Lower levels of bone turnover markers (BTMs) appear to be associated with a lower risk of fracture in bisphosphonate‐treated patients. BTMs were measured in a subset of subjects in the HORIZON Pivotal Fracture Trial. Annual infusions of zoledronic acid 5 mg significantly reduced BTMs: median decrease of 50% for β‐C‐terminal telopeptides of type 1 collagen (β‐CTX), 30% for bone alkaline phosphatase (ALP), and 56% for procollagen type 1 amino‐terminal propeptide (PINP). The mean level of BTMs decreased in treated patients but remained within the premenopausal range before the next injection. The percentage of zoledronic acid–treated patients with values below the premenopausal reference range at all time points was 1.7%, 17.8%, and 19% for bone ALP, CTX, and PINP, respectively. The third injection of zoledronic acid resulted in 60% reduction of β‐CTX within 9–11 days, followed by a gradual increase, indicating the persistence of osteoclastic bone resorption. The association between changes in BTMs and fracture incidence was assessed in 1132 patients who had PINP measurements at baseline and 1 yr. There was no association between low PINP levels at 1 yr and increased fracture incidence. In summary, (1) annual injections of zoledronic acid reduced BTMs in the premenopausal range, with a significant response persisting after the third infusion; and (2) low levels of PINP were not associated with increased fracture risk.     

Can cost utility evaluations inform decision making about interventions for low back pain?

Background contextLow back pain (LBP) is associated with high health-care utilization and lost productivity. Numerous interventions are routinely used, although few are supported by strong evidence. Cost utility analyses (CUAs) may be helpful to inform decision makers.PurposeTo conduct a systematic review of CUAs of interventions for LBP.Study designSystematic review.MethodsA search strategy combining medical subject headings and free text related to LBP and health economic evaluations was executed in MEDLINE. Cost utility analyses combined with randomized controlled trials for LBP were included. Studies that were published before 1998, non-English, decision analyses, and duplicate reports were excluded. Search results were evaluated by two reviewers, who extracted data independently related to clinical study design, economic study design, direct cost components, utility results, cost results, and CUA results.ResultsThe search produced 319 citations, and of these 15 met eligibility criteria. Most were from the United Kingdom (n=8), published in the past 3 years (n=12), studied chronic LBP or radiculopathy (n=13), and had a follow-up >12 months (n=13). Combined, there were 33 study groups who received a mean 2.1 interventions, most commonly education (n=17), exercise therapy (n=13), spinal manipulation therapy (n=7), surgery (n=7), and usual care from a general practitioner (n=7). Mean baseline utility was 0.57, improving to 0.67 at follow-up; the mean difference in utility improvement between study groups was 0.04. Based on available data and converted to US dollars, the cost per quality-adjusted life year ranged from $304 to $579,527, with a median of $13,015.ConclusionsFew CUAs were identified for LBP, and there was heterogeneity in the interventions compared, direct cost components measured, indirect costs, other methods, and results. Reporting quality was mixed. Currently published CUAs do not provide sufficient information to assist decision makers. Future CUAs should attempt to measure all known direct cost components relevant to LBP, estimate indirect costs such as lost productivity, have a follow-up period sufficient to capture meaningful changes, and clearly report methods and results to facilitate interpretation and comparison.     

Merkel Cell Carcinoma Arising from the Subcutaneous Fat of the Arm with Intact Skin

BACKGROUND: Merkel cell carcinoma is a rare malignant neuroendocrine neoplasm characteristically arising from the dermis of sunlight-exposed skin. It rarely arises outside the skin. OBJECTIVE: We present a patient with primary Merkel cell carcinoma arising from subcutaneous fat, with no involvement of the overlying skin. We describe the clinical manifestations and magnetic resonance imaging (MRI) findings. METHODS: We report a 63-year-old woman with a primary lesion of Merkel cell carcinoma that arose from the subcutaneous fat layer of the left arm. The lesion presented as a subcutaneous nodule with intact overlying skin. MRI showed that the nodular lesion was located entirely in the subcutaneous fat layer, with no involvement of the dermis. Peritumoral infiltration around the lesion and enlarged lymph nodes deep to the lesion were noted. The patient received wide excision of the lesion with dissection of the regional lymph nodes and adjuvant radiotherapy and chemotherapy. RESULTS: Histopathologic examination confirmed the diagnosis of Merkel cell carcinoma with local lymphatic metastasis, and the lesion was completely located in the subcutaneous fat, with no involvement of the dermis. These findings were well correlated with MRI findings. CONCLUSION: Primary Merkel cell carcinoma may arise from the subcutaneous fat and present as an entirely subcutaneous lesion with intact skin. MRI is helpful to evaluate the local extension of the lesion and regional lymphatic metastasis.     

Complete genomic screen in Parkinson disease: evidence for multiple genes.

CONTEXT: The relative contribution of genes vs environment in idiopathic Parkinson disease (PD) is controversial. Although genetic studies have identified 2 genes in which mutations cause rare single-gene variants of PD and observational studies have suggested a genetic component, twin studies have suggested that little genetic contribution exists in the common forms of PD. OBJECTIVE: To identify genetic risk factors for idiopathic PD. DESIGN, SETTING, AND PARTICIPANTS: Genetic linkage study conducted 1995-2000 in which a complete genomic screen (n = 344 markers) was performed in 174 families with multiple individuals diagnosed as having idiopathic PD, identified through probands in 13 clinic populations in the continental United States and Australia. A total of 870 family members were studied: 378 diagnosed as having PD, 379 unaffected by PD, and 113 with unclear status. MAIN OUTCOME MEASURES: Logarithm of odds (lod) scores generated from parametric and nonparametric genetic linkage analysis. RESULTS: Two-point parametric maximum parametric lod score (MLOD) and multipoint nonparametric lod score (LOD) linkage analysis detected significant evidence for linkage to 5 distinct chromosomal regions: chromosome 6 in the parkin gene (MLOD = 5.07; LOD = 5.47) in families with at least 1 individual with PD onset at younger than 40 years, chromosomes 17q (MLOD = 2.28; LOD = 2.62), 8p (MLOD = 2.01; LOD = 2.22), and 5q (MLOD = 2.39; LOD = 1.50) overall and in families with late-onset PD, and chromosome 9q (MLOD = 1.52; LOD = 2.59) in families with both levodopa-responsive and levodopa-nonresponsive patients. CONCLUSIONS: Our data suggest that the parkin gene is important in early-onset PD and that multiple genetic factors may be important in the development of idiopathic late-onset PD.     

Association of single-nucleotide polymorphisms of the tau gene with late-onset Parkinson disease.

CONTEXT: The human tau gene, which promotes assembly of neuronal microtubules, has been associated with several rare neurologic diseases that clinically include parkinsonian features. We recently observed linkage in idiopathic Parkinson disease (PD) to a region on chromosome 17q21 that contains the tau gene. These factors make tau a good candidate for investigation as a susceptibility gene for idiopathic PD, the most common form of the disease. OBJECTIVE: To investigate whether the tau gene is involved in idiopathic PD. DESIGN, SETTING, AND PARTICIPANTS: Among a sample of 1056 individuals from 235 families selected from 13 clinical centers in the United States and Australia and from a family ascertainment core center, we tested 5 single-nucleotide polymorphisms (SNPs) within the tau gene for association with PD, using family-based tests of association. Both affected (n = 426) and unaffected (n = 579) family members were included; 51 individuals had unclear PD status. Analyses were conducted to test individual SNPs and SNP haplotypes within the tau gene. MAIN OUTCOME MEASURE: Family-based tests of association, calculated using asymptotic distributions. RESULTS: Analysis of association between the SNPs and PD yielded significant evidence of association for 3 of the 5 SNPs tested: SNP 3, P =.03; SNP 9i, P =.04; and SNP 11, P =.04. The 2 other SNPs did not show evidence of significant association (SNP 9ii, P =.11, and SNP 9iii, P =.87). Strong evidence of association was found with haplotype analysis, with a positive association with one haplotype (P =.009) and a negative association with another haplotype (P =.007). Substantial linkage disequilibrium (P<.001) was detected between 4 of the 5 SNPs (SNPs 3, 9i, 9ii, and 11). CONCLUSIONS: This integrated approach of genetic linkage and positional association analyses implicates tau as a susceptibility gene for idiopathic PD.     

腹泻标本中同时分离类志贺邻单胞菌和豚鼠气单胞菌1例

0　引言　腹泻标本中同时检出类志贺邻单胞菌和豚鼠气单胞菌 ,在国内尚未见报道 .现报告如下 .1　临床资料　患者 ,女 ,45岁 .主诉于 12 h前因食不洁冷冻鱼类食品后 ,出现腹痛伴腹泻 ,为黄色稀水便转为血水样便 ,9次 / d,每次量约 2 0 0 m L.伴轻度乏力、恶心、里急后重 .腹痛以上腹部及左下腹部为著 ,呈持续隐痛伴有阵发性加重 .于2 0 0 0 - 0 3- 2 7就诊 .体检 :T37.2℃ ,P78次 / min,R16次 /min,BP13/ 8KPa.实验室检查 :WBC10 .8× 10 9· L- 1 ,N0 .84,L 0 .16 .大便常规 :RBC +++/ HP,WBC 3- 9/ HP,便隐血阳性 .取粪便送检做…