Systemic inflammatory response syndrome

Despite advances in perinatal care in the past decade, sepsis and its complications continue to present problems for the neonate, remaining a major cause of neonatal morbidity and mortality. Sepsis research is focusing on how the neonate (host) responds to bacteria. The newborn may develop a systemic reaction to bacteria that induces the release of substances known as inflammatory mediators. Termed the systemic inflammatory response syndrome (SIRS), this reaction is believed to be responsible for the signs and symptoms of sepsis. This article introduces the neonatal nurse to SIRS, providing an overview of various inflammatory mediators and cytokines, their clinical consequences, and potential new therapies in the management of SIRS.     

全身炎症反应综合征与脓毒症

全身炎症反应综合征一、定义全身炎症反应综合征(systemic inflammato-ry response syndrome,SIRS)是机体对各种严重损伤,包括感染、创伤、烧伤、缺氧和再灌注等引起的全身反应。机体受到严重打击后引起免疫系统的应激反应,包括多种炎性介质的大量释放,导致抗炎反应与致炎反应系统失衡,若过度的炎症反应继续发展或恶化,可导致急性肺损伤(ALI)、急性呼吸窘迫综合征(ARDS)、多器官障碍综合征(MODS)或MSOF等。SIRS的含义比脓毒症(sepsis)更广泛,更有意义,它不是一种疾病,而是基于对感染、炎症和危重症发生、发展机制深入认识提出的新…     

全身性炎症反应综合征与多器官功能障碍综合征

近年来 ,已认识到危重患儿常与全身炎症反应综合征 (ＳＩＲＳ)有关。但一般感染在免疫功能低下、感染过重或早期处理不当时 ,最终也能发展成ＳＩＲＳ。下面将我院所见 1例上呼吸道感染、颈淋巴结炎发展成ＳＩＲＳ的病例介绍如下 ,以引起同道注意。1　病例摘要　女 ,8 5岁 ,因发热、咽痛、颈淋巴结肿大诊断为上呼吸道感染、颈淋巴结炎在院外医院治疗。据述体温在 38～ 39℃左右 ,给青霉素治疗。第 3天出现皮疹 ,由淡红色渐变为深红色 ,高出皮面 ,易破溃 ,口腔粘膜、眼结膜充血溃烂。第 4天突然呼吸困难、发绀、神志不清 ,急转本院ＰＩＣＵ。…     

危重患儿全身炎症反应综合征与临床应用评价

败血症 (Ｓｅｐｔｉｃｅｍｉａ)是指细菌在血循环 (菌血症ｂａｃｔｅｒｅｍｉａ)中生长繁殖 ,产生毒素造成的全身感染。随着危重病医学的发展 ,人们认识到 ,单纯从机体某系统或器官受损来描述危重病已不能全面反应疾病的本质 ,因机体对致病因素侵袭的反应往往是全身的。这种全身性的炎症反应称为全身炎症反应综合征 (ＳＩＲＳ)。败血症或全身感染只是一种由感染因素引起的ＳＩＲＳ。ＳＩＲＳ一词的提出更新了既往关于急性感染与炎症的概念 ,颇具新意 ,因此受到医学界普遍关注。其实 ,现今在发展中国家 ,感染性疾病在小儿疾病中仍占首位 ,败…     

胎儿炎症反应综合征

胎儿炎症反应综合征是胎儿体内先天免疫系统被激活的一种状态,为生后72 h的新生儿炎症,其定义为以下几项中＞2项:(1)呼吸过快(＞60次/min),伴有呼吸困难或氧饱和度下降;(2)体温不稳(＞37.9℃或＜36℃);(3)毛细血管充盈时间＞3 s;(4)白细胞计数＞34×109/L或＜4×109/L;(5) CRP＞10mg/L;(6) IL-6或IL-8 ＞70 g/ml;(7) 16S rRNA基因PCR检测阳性.胎儿炎症反应综合征可由感染和非感染因素诱发,显著的特点就是针对外来的侵害胎儿免疫系统过度激活,导致炎症介质、细胞因子的失控性释放,多种炎症介质、细胞因子直接或间接激活凝血系统及干扰机体的抗凝系统,致凝血机制失常,多个系统参与的炎症反应贯穿这一过程.胎儿炎症反应综合征能导致早产、围生儿死亡、脑白质损伤、坏死性小肠结肠炎、影响胎肺的成熟及多器官的损害,为减少胎儿的损伤,对胎儿炎症反应综合征的恰当处理和预测是必要的.     

Medico-legal implications of the fetal inflammatory response syndrome

Babies who sustain long term neurologic injury and disability are frequent subjects in medical malpractice litigation. In the United States, the tort system enables adjudication of claims through a proscribed system. This paper will review salient elements of the tort system-duty, breach, causation, and damages- and how they apply to encephalopathic infants whose injuries are believed to be the result of fetal inflammatory response syndrome (FIRS) and/or hypoxic-ischemic damage. FIRS may confound the diagnosis of neonatal encephalopathy but may be a credible explanation for it as well. The ways in which FIRS may impact malpractice lawsuits are presented.     

糖皮质激素在全身炎症反应综合征中的应用

糖皮质激素因其抗炎机制在全身炎症反应综合征的治疗上已有较长时问的应用.研究显示,小剂量糖皮质激素(尤其以氢化可的松为主)的应用可以降低感染性休克患儿多器官功能障碍的机会、住院时间和病死率,并逐渐替代应用大剂量糖皮质激素的做法,但仍存在争议.推荐在儿科感染性休克的治疗中应用小剂量糖皮质激素,但仍需进一步研究探讨.     

新生儿全身炎症反应综合征

大量实验研究和临床资料表明 ,感染、创伤、休克等的转归 ,不但与原发损伤因素的强度有关 ,同时还与机体自身对损伤的反应强度有关。不同致病因素从对机体的损害到器官功能衰竭存在一条共同通路 ,即机体过度失控的炎症反应。基于以上认识 ,1991年美国胸科医师学会 (ACCP)和危重     

Neuroimaging findings associated with the fetal inflammatory response syndrome

The fetal inflammatory response syndrome (FIRS) is a condition whereby the fetus mounts an inflammatory response to intrauterine infection/inflammation. Clinical consequences include preterm premature rupture of membranes (PPROM), spontaneous preterm delivery, neonatal sepsis, bronchopulmonary dysplasia, and brain and other organ injury. Mechanisms leading to brain injury in FIRS have been investigated in animal and human studies. We review the neuroimaging findings of brain injury in FIRS, which overlap those of hypoxic-ischemic injury, and clinical correlation is necessary for a correct diagnosis. FIRS should be considered the primary diagnosis when neuroimaging findings such as periventricular leukomalacia are identified in preterm children born as a consequence of PPROM and spontaneous preterm labor. Additionally, FIRS should be considered in term infants who do not have the most common features of HIE (e.g. a sentinel event). Systematic histopathologic examination of the placenta and umbilical cord and/or detection of characteristic inflammatory markers in such cases are needed to establish the correct diagnosis.     

全身炎症反应综合征专题讨论会纪要

2006年3月25至26日,中华儿科杂志组织有关专家于广州市召开了全身炎症反应综合征（systemic inflammatory response syndrome,SIRS）专题讨论会。与会专家有新生儿、ICU专业：孙眉月、樊寻梅、曾其毅、陈贤楠、胡浩夫、封志纯;免疫专业：杨锡强、何晓琥、王宏伟、李永柏、李彩凤、胡坚、赵晓东、刘宇隆（香港）;肾脏专业：易著文、魏珉;成人ICU专家：刘大为、马朋林共18人。曾其毅、刘大为、陈贤楠和马朋林先后作了重点发言,董永绥教授发来书面发言稿,会议回顾和学习了SIRS提出和认识深化的过程。     

亚低温防治全身炎症反应综合征

目的 探讨亚低温能否抑制全身炎症反应综合征（ＳＩＲＳ）,从而阻止多器官功能障碍综合征（ＭＯＤＳ）的发生。方法 将９６只小鼠随机分成内毒素组、亚低温组、保温组及对照组。采用放射免疫法,分别于注射内毒素（ＬＰＳ）后１、２、４ｈ测定血清肿瘤坏死因子ａ（ＴＮＦ－α）,并用免疫组化法测定４组动物（４ｈ）肝、肺血管内皮细胞细胞间粘附分子１（ＩＣＡＭ－１）的表达情况。结果 亚低温组１、２、４ｈ的ＴＮＦ－α含量〖     

全身炎症反应综合征发生机制及临床干预

全身炎症反应综合征（systemic Inflammatory Response Syndrome,简称SIRS）是机体遭遇伤害刺激（如感染、创伤、休克、烧伤等）时宿主防御反应不断扩大,超出机体正常代偿能力,导致广泛组织细胞损伤的病理生理学过程。被认为是各种原因引起多器官功能障碍综合征（MODS）的共同通路。自20世纪80年代认识SIRS,90年代初期正式提出SIRS概念和诊断标准,到今天对SIRS开展全球、不同层面的广泛研究,临床医学及医学生物学研究人员走过了漫长而艰辛的历程。然而遗憾的是,到目前为止,关于SIRS病理生理过程的认识仍处于初级阶段,其相应的临床干预对策缺乏有效性和特异性。因此,对该课题的探讨仍是当今危重病医学面临的巨大挑战。     

小儿全身炎症反应综合征早期敏感炎症因子的研究

目的研究筛选小儿全身炎症反应综合征(SIRS)早期敏感炎症因子指标,为今后的合理早期干预提供理论依据。方法用化学发光酶免疫分析法(CLEIA)测定SIRS患儿血白介素1β(IL-1β),白介素-6(IL-6),白介素-8(IL-8),肿瘤坏死因子-α(TNFα-),采用酶联免疫吸附比色法(ELISA)测定血白介素-10(IL-10),白介素-13(IL-13)。结果SIRS患儿与对照组比较血TNFα-明显升高,血IL-6阳性率明显升高,有显著性差异(P<0.05),其他指标则无统计学意义(P>0.05)。结论血清TNFα-和IL-6是SIRS早期检测敏感指标。     

地塞米松、静脉注射丙种球蛋白在全身炎症反应综合征中的应用

目的　 探讨治疗全身炎症反应综合征 (SIRS)的有效方法 ,阻断SIRS的发展放大 ,减少多器官功能不全综合征(MODS)的发生及预防多器官功能衰竭 (MOF)。 方法 　对 112例中、重度SIRS患儿随机分为对照组、治疗组 ,治疗组在对照组治疗的基础上 ,加用地塞米松、大剂量静脉注射丙种球蛋白。 结果 　两组在体温降至正常所需时间 ,白细胞恢复正常所需时间 ,治愈出院所需时间进行对比 ,治疗组均短于对照组 (P <0 0 5 ) ,MOF发生率明显低于对照组 (P <0 0 5 ) ,差异有显著性。 结论 　加用地塞米松、静脉注射丙种球蛋白治疗中、重度SIRS效果良好。     

Therapeutic interventions for fetal inflammatory response syndrome (FIRS)

Fetal inflammatory response syndrome (FIRS) is a condition defined by systemic inflammation in the fetus, a rapid increase of pro-inflammatory cytokines into the fetal circulation (including interleukin-1 and interleukin-6), as well as a cellular response (such as increased neutrophils, monocyte/macrophages, and T cells) and the presence of funisitis. FIRS can lead to death and multisystem organ damage in the fetus and newborn. Brain injuries and subsequent risk of cerebral palsy and cognitive impairments are the most threatening long-term complications. This paper reviews the definition of FIRS, summarizes its associated complications, briefly describes the available methods to study FIRS, and discusses in more detail the potential therapeutic candidates that have been so far studied to protect the fetus/newborn from FIRS and to alleviate its associated complications and sequelae.     

Procalcitonin does discriminate between sepsis and systemic inflammatory response syndrome

Aims

To evaluate whether procalcitonin (PCT) and C reactive protein (CRP) are able to discriminate between sepsis and systemic inflammatory response syndrome (SIRS) in critically ill children.

Methods

Prospective, observational study in a paediatric intensive care unit. Kinetics of PCT and CRP were studied in patients undergoing open heart surgery with cardiopulmonary bypass (CPB) (SIRS model; group I¹) and patients with confirmed bacterial sepsis (group II).

Results

In group I, PCT median concentration was 0.24 ng/ml (reference value <2.0 ng/ml). There was an increment of PCT concentrations which peaked immediately after CPB (median 0.58 ng/ml), then decreased to 0.47 ng/ml at 24 h; 0.33 ng/ml at 48 h, and 0.22 ng/ml at 72 h. CRP median concentrations remained high on POD1 (36.6 mg/l) and POD2 (13.0 mg/l). In group II, PCT concentrations were high at admission (median 9.15 ng/ml) and subsequently decreased in 11/14 patients who progressed favourably (median 0.31 ng/ml). CRP levels were high in only 11/14 patients at admission. CRP remained high in 13/14 patients at 24 h; in 12/14 at 48 h; and in 10/14 patients at 72 h. Median values were 95.0, 50.9, 86.0, and 20.3 mg/l, respectively. The area under the ROC curve was 0.99 for PCT and 0.54 for CRP. Cut off concentrations to differentiate SIRS from sepsis were >2 ng/ml for PCT and >79 mg/l for CRP.

Conclusion

PCT is able to differentiate between SIRS and sepsis while CRP is not. Moreover, unlike CRP, PCT concentrations varied with the evolution of sepsis.