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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Relative Nephroprotection During Escherichia coli O157:H7 Infections: Association With Intravenous Volume Expansion
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Relative Nephroprotection During Escherichia coli O157:H7 Infections: Association With Intravenous Volume Expansion

机译:大肠杆菌O157:H7感染过程中的相对肾保护作用:与静脉内容积扩张相关

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Objective. The hemolytic uremic syndrome (HUS) consists of hemolytic anemia, thrombocytopenia, and renal failure. HUS is often precipitated by gastrointestinal infection with Shiga toxin–producing Escherichia coli and is characterized by a variety of prothrombotic host abnormalities. In much of the world, E coli O157:H7 is the major cause of HUS. HUS can be categorized as either oligoanuric (which probably signifies acute tubular necrosis) or nonoligoanuric. Children with oligoanuric renal failure during HUS generally require dialysis, have more complicated courses, and are probably at increased risk for chronic sequelae than are children who experience nonoligoanuric HUS. Oligoanuric HUS should be avoided, if possible. The presentation to medical care of a child with definite or possible E coli O157:H7 infections but before HUS ensues affords a potential opportunity to ameliorate the course of the subsequent renal failure. However, it is not known whether events that occur early in E coli O157:H7 infections, particularly measures to expand circulating volume, affect the likelihood of experiencing oligoanuric HUS if renal failure develops. We attempted to assess whether pre-HUS interventions and events, especially the volume and sodium content of intravenous fluids administered early in illness, affect the risk for developing oligoanuric HUS after E coli O157:H7 infections.Methods. We performed a prospective cohort study of 29 children with HUS that was confirmed microbiologically to be caused by E coli O157:H7. Infected children were enrolled when they presented with acute bloody diarrhea or as contacts of patients who were known to be infected with E coli O157:H7, or if they had culture-confirmed infection, or if they presented with HUS. HUS was defined as hemolytic anemia (hematocrit 30%, with fragmented erythrocytes on peripheral-blood smear), thrombocytopenia (platelet count of 150000/mm3), and renal insufficiency (serum creatinine concentration that exceeded the upper limit of normal for age). A wide range of pre-HUS variables, including demographic factors, clinical history, medications given, initial laboratory values, and volume and content of parenteral fluid administered, were recorded and entered into analysis. Estimates of odds ratios were adjusted for possible confounding effects using logistic regression analysis. Twenty-nine children who were 10 years old, had HUS confirmed to be caused by E coli O157:H7, and were hospitalized at the Children's Hospital and Regional Medical Center, Seattle, were studied. The main outcome measured was development of oligoanuric renal failure. Oligoanuria was defined as a urine output 0.5 mL/kg per hour for at least 24 consecutive hours.Results. As a group, the children with oligoanuric renal failure presented to medical attention and were evaluated with laboratory testing later than the children with nonoligoanuric renal failure. On initial assessments, the children with oligoanuric outcomes had higher white blood cell counts, lower platelet counts and hematocrits, and higher creatinine concentrations than the children with nonoligoanuric outcomes, but these determinations probably reflect later points of these initial determinations, often when HUS was already developing. Stool cultures were obtained (medians of 3 vs 2 days, respectively) and positive (medians of 7 vs 4 days, respectively) at later points in illness in the children in the oligoanuric than in the nonoligoanuric group. Intravenous volume expansion began later in illness in the children who subsequently developed oligoanuric renal failure than in those whose renal failure was nonoligoanuric (medians: 4.5 vs 3.0 days, respectively). Moreover, the 13 patients with nonoligoanuric renal failure received more intravenous fluid and sodium before HUS developed (1.7- and 2.5-fold differences, respectively, between medians) than the 16 patients with oligoanuric renal failure. These differences were even greater when the first 4 days of illness were examined, with 17.1- and 21.8-fold differences, respectively, between medians. In a multivariate analysis adjusted for age, gender, antibiotic use, and free water volume administered intravenously to these children during the first 4 days of illness, the amount of sodium infused remained associated with protection against developing oligoanuric HUS. Dialysis was used in each of the children with oligoanuric renal failure and in none of the children with nonoligoanuric renal failure. The median length of stay in hospital after the diagnosis of HUS was 12 days in the oligoanuric group and 6 days in the nonoligoanuric group.Conclusions. Early recognition of and parenteral volume expansion during E coli O157:H7 infections, well before HUS develops, is associated with attenuated renal injury failure. Parenteral hydration in children who are possibly infected with E coli O157:H7, at the time of presentation with bloody diarrhea and in advance of cu
机译:目的。溶血性尿毒症综合征(HUS)由溶血性贫血,血小板减少和肾衰竭组成。 HUS通常由产生志贺毒素的大肠杆菌经胃肠道感染而沉淀,其特征是多种血栓形成前的宿主异常。在世界许多地方,大肠杆菌O157:H7是HUS的主要原因。 HUS可分为少尿性尿酸(可能表示急性肾小管坏死)或非少尿性尿酸。 HUS期间少尿性肾功能衰竭的儿童通常需要透析,病程较复杂,并且可能比非尿性无尿HUS的儿童患慢性后遗症的风险更高。如果可能,应避免低尿酸尿毒症。在HUS发生之前在确诊或可能感染O157:H7大肠埃希氏菌的儿童中就诊提供了可能的机会,以改善随后的肾衰竭的进程。但是,尚不知道在大肠杆菌O157:H7感染早期发生的事件(尤其是扩大循环量的措施)是否会在肾衰竭发生时影响发生少尿性尿道感染的可能性。我们试图评估HUS之前的干预措施和事件,尤其是疾病早期给予的静脉输液的量和钠含量,是否会影响大肠杆菌O157:H7感染后发展为少尿性尿道感染的风险。我们对29名HUS儿童进行了一项前瞻性队列研究,该研究在微生物学上被确认是由大肠杆菌O157:H7引起的。当感染的儿童表现出急性血性腹泻或与已知感染了O157:H7大肠杆菌的患者接触时,或者他们是否经培养证实的感染,或者是否表现出HUS时,就入组。 HUS定义为溶血性贫血(血细胞比容<30%,外周血涂片上有红细胞碎裂),血小板减少症(血小板计数<150000 / mm3)和肾功能不全(血清肌酐浓度超过正常年龄的上限) 。记录广泛的HUS前变量,包括人口统计学因素,临床病史,所用药物,初始实验室值以及所用肠胃外液体的量和含量,并进行分析。使用Logistic回归分析对优势比的估计值进行了调整,以考虑可能的混杂效应。研究对象有29名年龄在10岁以下的儿童,他们已确认HUS由大肠杆菌O157:H7引起,并在西雅图儿童医院和地区医疗中心住院。测得的主要结局是少尿性肾功能衰竭的发展。少尿症定义为连续至少24小时每小时尿量<0.5 mL / kg。作为一个小组,少尿尿性肾衰竭的儿童受到医疗的关注,并且比非少尿性尿酸肾衰竭的儿童接受了实验室检查的评估晚。在初步评估中,少尿尿结局患儿的白细胞计数较高,血小板计数和血细胞比容较低,肌酐浓度较高,但非尿尿无尿结局的患儿较早,但通常是在HUS出现时发展。少尿尿症患儿的患病率比非少尿尿症患儿的粪便培养物(中位数分别为3天和2天)和阳性(中位数分别为7天和4天)。后来发生少尿性神经衰弱的儿童患病的静脉血容量开始较那些患非少尿性神经衰弱的儿童(中位数分别为4.5天和3.0天)更晚。此外,与16个少尿尿性尿道衰竭的患者相比,13个非尿尿性尿道衰竭的患者在HUS出现之前接受了更多的静脉输液和钠盐治疗(中位数之间分别相差1.7和2.5倍)。当检查疾病的前4天时,这些差异甚至更大,中位数之间分别有17.1和21.8倍的差异。在对年龄,性别,抗生素的使用以及患病的前4天静脉注射这些孩子的自由水量进行多因素分析后,注入的钠量仍与预防发展为少尿性尿道出血的HUS有关。透析用于每个少尿性尿道肾衰竭的儿童,而没有一个用于非少尿性尿道肾衰竭的儿童。尿少尿症组确诊为HUS后住院时间的中位数为12天,非尿少尿症组为6天。大肠杆菌O157:H7感染期间(在HUS发生之前)就及早认识到肠胃外容量的增加,这与减轻的肾损伤衰竭有关。在出现腹泻和血尿之前,可能被大肠杆菌O157:H7感染的儿童的肠胃外补液

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