新生儿急性呼吸窘迫综合征的发病机制及诊断治疗进展

急性呼吸窘迫综合征是各种致病因素引起的急性、进行性、炎性肺损伤过程.新生儿急性呼吸窘迫综合征的病死率高达30％ ～ 60％.近年来随着对该病发病机制的深入研究,人们在其诊断、治疗方面也提出了很多新的观点.该文着重就新生儿急性呼吸窘迫综合征的发病机制、诊断及治疗的进展作一综述.     

脓毒症与急性呼吸窘迫综合征

重症脓毒症常并急性呼吸窘迫综合征，是导致死亡的重要原因，目前认为炎性反应在急性肺损伤或急性呼吸窘迫综合征的发病机制中起主要作用，保护性肺通气策略可应用于儿童急性呼吸窘迫综合征的治疗。     

急性呼吸窘迫综合征患儿肺力学特点

急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)的病因不一,发病机制各有所异,病情进展过程中肺力学的改变存在个体差异。顺应性、压力、容量等的变化与病因、病情轻重、年龄等密切相关。正确采用肺保护性通气策略、合理调节呼吸机参数、减少呼吸机相关性肺损伤是提高ARDS救治成功率的关键。因此,在ARDS机械通气治疗中必须高度注意患儿肺力学的特点和变化。     

血管内皮生长因子在急性肺损伤中的促炎作用

急性肺损伤(ALI)是由于各种肺内和肺外原因所致的原发性或继发性肺损伤,其病理改变主要为肺水肿(包括肺泡和肺间质水肿)、炎性细胞浸润和肺组织破坏。临床表现为严重呼吸功能障碍,氧合指数明显下降,其严重形式即为急性呼吸窘迫综合征(ARDS)。ALI发病机制复杂,迄今为止,确切的机     

急性弥散性肺部疾病与急性肺损伤

近年来,急性起病,表现为呼吸困难、发绀,影像学显示肺部弥散性病变的病例逐渐增多。此类疾病有免疫机制参与,起病急,常有呛咳,呼吸急促、困难,伴中度发热,肺存在广泛细湿音和其他干湿音,胸部X线和CT显示广泛肺间质、实质或气道异常病变。这些病例的原发病诊断困难,缺乏客观的金标准,有些病因不明,教科书和文献对疾病归类也存在分歧。按其临床表现也符合急性肺损伤(acutelunginjury ,ALI)或急性呼吸窘迫综合征(acuterespiratorydistresssyndrome,ARDS)诊断标准,但未存在严重感染和ARDS发病高危因素。此类病例是否诊断为ALI/ARDS…     

他汀类药物的研究进展及在急性呼吸窘迫综合征中的作用

急性呼吸窘迫综合征是儿童常见重症,威胁儿童的生命健康.其病理机制为肺部组织广泛的炎症反应.他汀类药物已广泛应用于心脑血管疾病的防治,目前研究发现他汀类药物具有抗炎及调节免疫的作用.本文将对他汀类药物的作用机制、在急性肺损伤及急性呼吸窘迫综合征中的作用机制和应用,以及他汀类药物的有效性和安全性进行综述.     

新生儿急性肺损伤/急性呼吸窘迫综合征

新生儿急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)是由多种原因引起的肺部弥散性损害,以顽固性低氧血症、呼吸窘迫、肺顺应性下降和弥散性渗出为主要特征,ARDS是ALI的严重形式。由于其病死率高,救治此类患儿仍是新生儿科医师面临的严峻挑战。本文对新生儿ALI/ARDS高危因素、发病机制、诊断标准及治疗进展作一介绍。     

紫草素对急性肺损伤保护作用的研究进展

急性肺损伤是由心源性因素以外的各种肺内外致病因素导致的急性、进行性缺氧性呼吸衰竭,其发展的严重阶段即是急性呼吸窘迫综合征.紫草素作为从中药紫草中提取的一种有效成分,具有多种药理作用.该文在介绍急性肺损伤和紫草素的基础上,重点就紫草素对急性肺损伤的相关保护作用进行综述.     

危重呼吸道疾病和急性肺损伤

呼吸系统疾病是全球发病率最高的系统疾病群,而危重呼吸道疾病是急性肺损伤(ALI)发病诱因中的主要因素. 三种代表不同病理生理特征的发病机制,对危重呼吸道疾病发展到ALI起重要作用,即全身炎性反应、肺的双重打击学说及肺氧化还原不平衡学说.对发展到ALI的危重呼吸道疾病的治疗除经典应用抗感染、呼吸支持及血管活性药物等治疗以外,一些针对ALI发病的分子生物学机制的新的治疗策略如基因治疗或干细胞治疗也将会发挥更重要的作用.     

急性肺损伤与肺表面活性物质

急性肺损伤（ALI）是由多种病因（如感染、脓毒血症、外伤、休克、中毒等）引起的,以弥漫性肺毛细血管内皮细胞和肺泡上皮细胞损伤所致的渗透性肺水肿、肺萎陷、难治性低氧血症为主要特征的临床综合征。急性呼吸窘迫综合征     

TOLL样受体与重症感染后急性肺损伤

Toll样受体(TLR) 是一类先天性跨膜受体,是病原体相关分子模式的重要识别受体.TLR通过识别病原微生物体,在炎症反应初期经由两条信号传导通路,激活免疫细胞内核因子-κB等转录因子,释放炎性介质,增强宿主防御能力,TLR过度表达导致失控性炎症反应,造成组织损伤.在急性肺损伤(ALI)及急性呼吸窘迫综合征(ARDS)的发病机制中,TLR对炎症反应的启动及介导免疫调控方面有不可忽视的作用,其中尤以TLR2和TLR4最为重要.与TLR相关的免疫调控,有望成为临床治疗ALI/ARDS的重要靶点.     

儿童急性呼吸窘迫综合征肺复张策略的研究进展

近年来肺复张策略因可打开肺泡,减少肺泡萎陷所致的肺损伤,改善肺顺应性,提高动脉氧分压与氧合指数,减少肺内分流而成为急性呼吸窘迫综合征机械通气治疗手段之一.本文就肺复张在儿童急性呼吸窘迫综合征的应用做一综述.     

急性肺损伤时损伤标志物的研究进展

急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）是指心源性以外的各种肺内外致病因素导致的急性的、进行性的呼吸衰竭。ALI阶段若未给予有效的治疗干预则可能进展为ARDS,由于ARDS发病机制复杂,治疗效果不佳,其病死率仍然居高不下。目前ALI仍然缺乏有效的治疗方法,因而针对ALI发病机制及早期诊断方法的研究显得尤为重要。本文将就ALI时损伤标志物的相关研究进行综述,为ALI的早期诊断及以后的相关研究打下基础。     

INACTIVATION OF PULMONARY SURFACTANT AND THE TREATMENT OF ACUTE LUNG INJURIES

Inactivation of pulmonary surfactant may be important in acute lung injury and acute respiratory distress syndrome. Treatment of surfactant dysfunction by instilling exogenous surfactants may improve gas exchange and pulmonary mechanics. Surfactants used for treatment vary in their attributes and effects, so when various surfactants are considered for therapy, resistance to inactivation is an important consideration. Animal models of acute lung injury exist in which the relative merits of surfactants can be compared. We hypothesize that the surfactants most resistant to inactivation in vitro will be the ones that are most effective in treatment of animal models of acute lung injury. Surfactants with higher concentrations of surfactant proteins (specifically A, B, and C) are more resistant to inactivation. Nonionic polymers mimic surfactant proteins in preventing surfactant inactivation under some conditions. Adding nonionic polymers to surfactant containing minimal amounts of SP-B and SP-C markedly improves lung function of animals with lung injury. Making surfactants more "inactivation-proof" may improve surfactant therapy of acute lung injuries.     

糖皮质激素治疗儿童急性肺损伤/急性呼吸窘迫综合征的研究进展

儿童急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)是许多肺内疾病和(或)肺外疾病所致的严重应激反应和(或)严重炎症反应而导致的肺组织内皮和上皮受损引起的急性呼吸衰竭,病死率很高.糖皮质激素是目前临床使用最为广泛的抗纤维化和抗炎症药物,但由于其疗效差异较大,故在治疗ALI/ARDS中一直存在争议.近年研究表明其作用与糖皮质激素受体数量及亲和力有密切关系.     

Interleukin-1 receptor antagonist intron 2 variable number of tandem repeats polymorphism and respiratory failure in children with community-acquired pneumonia

OBJECTIVE: To determine whether the variable nucleotide tandem repeat polymorphism in intron 2 of the interleukin-1 receptor antagonist gene is associated with lung injury in children with community-acquired pneumonia. DESIGN: A prospective cohort of children diagnosed with community-acquired pneumonia. SETTING: Two pediatric hospitals. PATIENTS: Eight hundred fifty pediatric patients with community-acquired pneumonia were enrolled. INTERVENTIONS: Genotyping of the variable nucleotide tandem repeat polymorphism in intron 2 of the interleukin-1 receptor antagonist gene was performed on DNA isolated from whole blood. MEASUREMENTS AND MAIN RESULTS: The requirement for positive pressure ventilation or the diagnosis of acute lung injury or acute respiratory distress syndrome were the main outcomes of the study. Children (14 days-19 yrs) with community-acquired pneumonia (850) were enrolled; analysis was limited to African American (515) and Caucasian (232) patients. Of the 82 patients requiring positive pressure ventilation, 44 were diagnosed with acute lung injury or acute respiratory distress syndrome. Multivariate logistic regression analyses indicated that children without a copy of the A1 allele of the variable nucleotide tandem repeat polymorphism in intron 2 of the interleukin-1 receptor antagonist gene were more likely to need positive pressure ventilation compared to those with one or two copies of this allele (odds ratio = 2.65, confidence interval, 1.02-6.90). In addition, the absence of the A1 allele also appeared to be associated with the development of community-acquired pneumonia-induced acute lung injury/acute respiratory distress syndrome (odds ratio = 3.1, confidence interval, 0.99-9.67). CONCLUSIONS: In children with community-acquired pneumonia, absence of the A1 allele at the interleukin-1 receptor antagonist intron 2 polymorphic site is associated with increased risk for more severe lung injury, as measured by the need for positive pressure ventilation or the development of acute lung injury or acute respiratory distress syndrome. Conversely, presence of the A1 allele is associated with decreased risk for more severe lung injury in this patient population.     

儿童腺病毒肺炎肺损伤机制的研究进展

人腺病毒是一种DNA病毒,是我国儿童呼吸道感染的一种常见病原体。腺病毒感染后可触发多种机制,引起肺组织细胞的溶解和坏死,最终导致肺损伤及肺部后遗症,包括急性呼吸窘迫综合征、肺实变等急性期损伤及感染后闭塞性毛细支气管炎、单侧透明肺、支气管扩张、肺间质纤维化等肺部后遗症。现针对腺病毒感染引起儿童肺损伤的发病机制进行综述。     

Lung epithelial cell apoptosis during acute lung injury in infancy.

CONTEXT: Apoptosis of lung epithelial cells is implicated in the pathogenesis of acute lung injury. Most research on this subject has focused on adults. Very little is known about a potential interaction of this process with lung development in children. OBJECTIVE: To summarize the current literature on lung epithelial cell apoptosis and common causes of acute lung injury in infants and young children and to identify new areas of research. DESIGN: A Medline-based literature search. RESULTS AND CONCLUSIONS: Few studies have focused on lung epithelial cell apoptosis during common causes of acute lung injury in children. Nevertheless, the limited literature suggests that this may be an important mechanism during respiratory distress syndrome of infants and viral respiratory tract infection. Apoptosis is an essential process during lung development and maturation. Insufficient attention has been paid to potential consequences of this for the short- and long-term outcomes of acute lung injury.