Unintended consequences of policy change to watchful waiting for asymptomatic inguinal hernias

Introduction

In 2009 the Department of Health instructed McKinsey & Company to provide advice on how commissioners might achieve world class National Health Service productivity. Asymptomatic inguinal hernia repair was identified as a potentially cosmetic procedure, with limited clinical benefit. The Birmingham and Solihull primary care trust cluster introduced a policy of watchful waiting for asymptomatic inguinal hernia, which was implemented across the health economy in December 2010. This retrospective cohort study aimed to examine the effect of a change in clinical commissioning policy concerning elective surgical repair of asymptomatic inguinal hernias.

Methods

A total of 1,032 patients undergoing inguinal hernia repair in the 16 months after the policy change were compared with 978 patients in the 16 months before. The main outcome measure was relative proportion of emergency repair in groups before and after the policy change. Multivariate binary logistic regression was used to adjust the main outcome for age, sex and hernia type.

Results

The period after the policy change was associated with 59% higher odds of emergency repair (3.6% vs 5.5%, adjusted odds ratio [OR]: 1.59, 95% confidence interval [CI]: 1.03–2.47). In turn, emergency repair was associated with higher odds of adverse events (4.7% vs 18.5%, adjusted OR: 3.68, 95% CI: 2.04–6.63) and mortality (0.1% vs 5.4%, p<0.001, Fisher’s exact test).

Conclusions

Introduction of a watchful waiting policy for asymptomatic inguinal hernias was associated with a significant increase in need for emergency repair, which was in turn associated with an increased risk of adverse events. Current policies may be placing patients at risk.     

对QT离散度实质的探讨

为探讨ＱＴ离散度（ＱＴｄ）的真实意义，观察１３９例急性心肌梗死（ＡＭＩ，ＡＭＩ组）及１０９例正常人（对照组）的最长ＱＴ间期（ＱＴｍａｘ）、校正ＱＴｍａｘ（ＱＴｃｍａｘ）及ＱＴｄ的变化。结果：①ＡＭＩ组的ＱＴｍａｘ、ＱＴｃｍａｘ和ＱＴｄ均显著高于对照组（分别为４２２．６０±３０．５１ｍｓｖｓ３８２．４６±２３．４０ｍｓ、４６０．２１±２８．９６ｍｓｖｓ３８８．５１±２０．１５ｍｓ、５９．８０±２８．４０ｍｓｖｓ３９．４３±１２．２１ｍｓ，Ｐ均＜０．００１）。②ＡＭＩ组中发生严重室性心律失常（ＶＡ）患者（１１４例）的ＱＴｍａｘ、ＱＴｃｍａｘ、ＱＴｄ与无ＶＡ的患者（２５例）相比，均有显著差异（分别为４４８．５８±３３．４０ｍｓｖｓ４１６．１０±３５．３０ｍｓ、４８１．４３±３５．１７ｍｓｖｓ４３９．６０±２７．１０ｍｓ、６６．９０±２０．７２ｍｓｖｓ４８．３２±２３．６１ｍｓ，Ｐ均＜０．００１）。认为ＡＭＩ时ＱＴｄ系Ｔ向量环在不同导联上的“投影”差异所引起的，其异常的本质是ＱＴ间期延长     

急性心肌梗死后CD34+干细胞自体动员的意义

目的:已有理论提出急性心肌梗死后骨髓和外周血中的CD34 干细胞具有自身动员的潜能,观察这一潜能的变化特征及其对心肌梗死组织再生能力的影响。方法:实验于2004-09/2005-02在阜外心血管病医院完成。①实验动物:雄性SD大鼠40只,随机数字表法分为心肌梗死组、假手术组,20只/组。②实验方法:心肌梗死组大鼠采用冠状动脉结扎法建立心肌梗死模型。心电图ST段抬高或有室性心律出现,前壁心肌呈苍白色为造模成功。假手术组仅作开胸手术,前降支不予结扎。③实验评估:于心肌梗死后3,7,14,28d,流式细胞仪检测骨髓和外周血中CD34 干细胞的含量。用免疫组化方法检测梗死心肌组织中的Ki67细胞和毛细血管数量。结果:①外周血及骨髓CD34 干细胞含量的变化:心肌梗死组外周血中的CD34 干细胞数量于造模后3d开始上升,7d后明显高于假手术组(P<0.01),至14,28d时逐渐回落至假手术组水平(P>0.05)。心肌梗死组骨髓中的CD34 干细胞数量于造模后各时间点始终无明显变化(P>0.05)。②组织学评定:心肌梗死组梗死区Ki67细胞和毛细血管数量于造模后3d开始增多,7d时明显多于非梗死区(P<0.05);至14,28d梗死区Ki67细胞数量明显少于造模后7d(P<0.05),毛细血管数量的减少不明显(P>0.05)。免疫组化染色显示少数Ki67细胞分化为血管内皮细胞,未见向心肌细胞分化。③相关性分析:梗死区Ki67细胞、毛细血管数量于造模后7d与外周血中CD34 干细胞数量呈显著正相关(r=0.913,P=0.021;r=0.887,P=0.035)。结论:机体CD34 干细胞的自体动员、增殖反应的潜能随急性心肌梗死时间的延长而逐渐减弱,自体动员的干细胞功能尚不足以达到修复梗死心肌组织的效果。     

失眠的评价

失眠的定义失眠分为急性和慢性失眠.急性失眠通常持续时间不超过2 w,与应激状态有关,例如上班、搬家、婚姻或亲人朋友的去世等.而慢性失眠则是失眠持续超过3 w以上,或者不充足睡眠伴随着日间睡意和抑郁,且持续时间不少于1个月.     

Incidence and mortality of venous thrombosis: a population-based study

Background: Estimates of the incidence of venous thrombosis (VT) vary, and data on mortality are limited. Objectives: We estimated the incidence and mortality of a first VT event in a general population. Methods: From the residents of Nord‐Trøndelag county in Norway aged 20 years and older (n = 94 194), we identified all cases with an objectively verified diagnosis of VT that occurred between 1995 and 2001. Patients and diagnosis characteristics were retrieved from medical records. Results: Seven hundred and forty patients were identified with a first diagnosis of VT during 516 405 person‐years of follow‐up. The incidence rate for all first VT events was 1.43 per 1000 person‐years [95% confidence interval (CI): 1.33–1.54], that for deep‐vein thrombosis (DVT) was 0.93 per 1000 person‐years (95% CI: 0.85–1.02), and that for pulmonary embolism (PE) was 0.50 per 1000 person‐years (95% CI: 0.44–0.56). The incidence rates increased exponentially with age, and were slightly higher in women than in men. The 30‐day case‐fatality rate was higher in patients with PE than in those with DVT [9.7% vs. 4.6%, risk ratio 2.1 (95% CI: 1.2–3.7)]; it was also higher in patients with cancer than in patients without cancer [19.1% vs. 3.6%, risk ratio 3.8 (95% CI 1.6–9.2)]. The risk of dying was highest in the first months subsequent to the VT, after which it gradually approached the mortality rate in the general population. Conclusions: This study provides estimates of incidence and mortality of a first VT event in the general population.     

Reversible oxidant-induced increases in albumin transfer across cultured endothelium: alterations in cell shape and calcium homeostasis

To determine whether reactive oxygen molecules could directly and reversibly increase the transfer of albumin across an endothelial barrier, we measured albumin transfer across monolayers of endothelium cultured on micropore filters before and after exposure to xanthine and xanthine oxidase. Xanthine and xanthine oxidase increased endothelial albumin transfer in a dose-dependent fashion. Parallel phase contrast and fluorescence microscopy demonstrated retraction of adjacent cells from one another and disruption of the actin filaments. The oxidant- induced increases in albumin transfer and changes in cell shape were reversed by removing xanthine oxidase and then incubating the monolayers for 3 1/2 hours in tissue culture media enriched with fetal bovine serum. However, incubation in tissue culture media without serum resulted in progressive injury and cell death. Hence, the brief exposure to oxidants initiated a progressive injury process that was reversed by incubation in serum. Because intracellular and extracellular calcium are important determinants of cell shape, and because some oxidized membrane lipids act as calcium ionophores, we asked whether oxidants altered endothelial calcium homeostasis. Xanthine-xanthine oxidase increased release of 45Ca++ from preloaded cells. The calcium antagonist lanthanum chloride prevented xanthine- xanthine oxidase increases in endothelial albumin transfer and prevented the changes in cell shape; chelation of extracellular calcium inhibited lysis of endothelium by xanthine-xanthine oxidase; and the calcium ionophore A23187 increased endothelial albumin transfer and mimicked the oxidant-induced changes in cell shape. Lanthanum chloride inhibited these effects of A23187. These data suggest that oxygen radicals can reversibly increase endothelial permeability to macromolecules, that this is associated with reversible changes in endothelial cell shape and actin filaments, and that the changes in cell shape are related to oxidant-induced changes in endothelial calcium homeostasis.