The need for caution with topical anesthesia during endoscopic procedures, as liberal use may result in methemoglobinemia

During upper gastrointestinal endoscopy, topical oropharyngeal anesthesia with lidocaine and/or benzocaine is used routinely by many endodscopists. Although such a practice is usually safe, there have been a number of reports of methemoglobinemia induced by topical anesthesia. Early treatment is extremely important as the development of methemoglobinemia is potentially fatal. Methemoglobinemia should be considered when oxygen desaturation occurs without another explanation. In this case series, we report 4 cases of methemoglobinemia that followed the liberal application of Cetacaine for ERCP. All patients recovered after appropriate treatment but these cases serve to highlight the potential problem, the importance of early recognition and treatment, and the most appropriate treatment options.     

004 65岁以上收缩功能正常的心衰者的临床特点

众所周知,充血性心衰(CHF)为老年人较为常见的临床综合征之一.迄今关于左室收缩功能正常的CHF老人的相关临床特点远未清楚,本文特此进行了大样本分析. 对象与方法 4842例老年人,男1922例,女2920例,年龄66～103岁.尔后人均随访1年.旨在分析老年CHF年发病率,以及左室收缩功能正常的CHF老人相关临床特点. 结果随访期内,罹发1次或以上CHF者共425例次(8.8%/年).与未患发CHF老人相比,CHF老人平均年龄更大(79±6岁:77±5岁,P＜0.001),女性居多,尤以高龄女性更多,如85岁以上的高龄女性CHF年发病率约较65～69岁女性高2倍(14%∶6.6%,P＜0.001),AMI史、房颤、高血压、糖尿病、慢性阻塞型肺病、吸烟者均多,血脂及血肌酐亦高.多变量分析表明,罹患CHF与下列因素有关:老年尤其是高龄[年龄每增加5岁的患病奇数率(OR)女性1.2,男性1.1],AMI史(OR7.3),房颤者(OR3.0),糖尿病(OR2.1),肾功能不全(血肌酐≥1.5mg/dl的OR2.0),慢性阻塞肺病(仅老年女性的OR为1.8),以及左房、左室内径增大(内径每递增1cm的OR为2.0),和左室重量增加、左室收缩末期室壁张力增高、早期跨心房血流增多.超声心动图检测结果显示,CHF老人中,左室收缩功能正常者达55%,而仅有左室舒张功能不全,且左室收缩功能正常或轻度减退者高达80%.其中女性左室收缩功能正常者尤较男性多见(67%∶42%,P＜0.001),表现为单纯左室舒张功能不良.而在左室收缩功能正常的CHF老人,常伴有左室内径较小、左室收缩末期室壁张力较低、左室重量较轻、左室收缩末期室壁厚度增加,而左室射血分数正常或仅轻度降低. 讨论以上结果提示,在老年人群中,CHF年发病率相对较高,且随年龄而增加,多数左室收缩功能正常,仅有左室舒张功能障碍,尤其是在高龄女性,亦即高龄女性左室舒张功能不全性CHF更为常见.对此,临床上更应拟出合理的防范措施,来正确诊治老年CHF综合征. (袁志敏摘)     

Idiopathic cholangiopathy in a biliary cast syndrome necessitating liver transplantation following head trauma

The development of total biliary casts is very unusual, especially in patients who have not undergone liver transplantation. The aetiology of these casts is uncertain but several factors are believed to play a role, including periods of fasting, haemolysis, cholangitis and recent surgery. Resultant bile stasis and/or gallbladder hypocontractility promote sludge and subsequent stone formation. Here we present the case of a previously well 66-year-old woman who developed a total biliary cast several weeks after being involved in a road traffic accident during which she sustained head injuries but no obvious liver insult. This cast was removed at laparotomy but the patient had resultant diffuse biliary tree abnormalities and persistent cholestasis and subsequently required a liver transplant. The possible aetiologies of biliary cast formation and subsequently cholangiopathy necessitating transplantation in this patient are described.     

Contrasting roles of NADPH oxidase isoforms in pressure-overload versus angiotensin II-induced cardiac hypertrophy

Increased production of reactive oxygen species (ROS) is implicated in the development of left ventricular hypertrophy (LVH). Phagocyte-type NADPH oxidases are major cardiovascular sources of ROS, and recent data indicate a pivotal role of a gp91phox-containing NADPH oxidase in angiotensin II (Ang II)-induced LVH. We investigated the role of this oxidase in pressure-overload LVH. gp91phox-/- mice and matched controls underwent chronic Ang II infusion or aortic constriction. Ang II-induced increases in NADPH oxidase activity, atrial natriuretic factor (ANF) expression, and cardiac mass were inhibited in gp91phox-/- mice, whereas aortic constriction-induced increases in cardiac mass and ANF expression were not inhibited. However, aortic constriction increased cardiac NADPH oxidase activity in both gp91phox-/- and wild-type mice. Myocardial expression of an alternative gp91phox isoform, Nox4, was upregulated after aortic constriction in gp91phox-/- mice. The antioxidant, N-acetyl-cysteine, inhibited pressure-overload-induced LVH in both gp91phox-/- and wild-type mice. These data suggest a differential response of the cardiac Nox isoforms, gp91phox and Nox4, to Ang II versus pressure overload.