肠道病毒71型重症手足口病致神经源性肺水肿的发病机制及治疗进展

重症手足口病是一种由肠道病毒引起的急性传染病,多发生于学龄前期儿童,肠道病毒71型是其主要病原.少数重症手足口病可累及神经系统和呼吸循环系统,引起脑干脑炎、神经源性肺水肿、肺出血、心肌炎等严重并发症.神经源性肺水肿是肠道病毒71型累及中枢神经系统后出现的急性肺水肿,临床上以进行性呼吸困难和持续低氧血症为特点,早期可仅有心率增快、血压升高等非特异性表现,诊断十分困难.当出现明显气促、大量泡沫痰、双肺湿啰音时,病死率极高.尽管重症手足口病的治疗手段不断进步,但神经源性肺水肿的病因及调控网络较复杂,导致临床疗效欠佳.因此,密切观察、早期诊断、合理治疗对改善预后有重要意义.该文就肠道病毒71型重症手足口病致神经源性肺水肿的发病机制及治疗进展进行阐述.     

重症手足口病并发神经源性肺水肿相关因素分析

目的 探讨重症手足口病并发神经源性肺水肿的临床相关因素和激素及丙球药物治疗对神经源性肺水肿发生的影响.方法 将2008年4月 - 2010年9月住院治疗的重症手足口病168例,其中神经源性肺水肿68例,以是否并发肺水肿分组,对神经源性肺水肿发生前的临床特征进行单因素χ2检验和多因素Logistic回归分析;又根据重症手足口病168例的用药情况分成冲击量甲泼尼龙组、非冲击量甲泼尼龙组和无甲泼尼龙组3组,对冲击量甲泼尼龙是否加丙球组的临床资料进行χ2检验.结果 不典型皮疹、面部红斑、易激动、呕吐、心率增快、血压增高、腹痛、白细胞升高、血糖升高、脑脊液白细胞及蛋白升高、咽/肛拭子EV71-RNA阳性与手足口病并发神经源性肺水肿的发生有关(P均＜ 0.05).多因素Logistic回归分析共筛选出4项发生神经源性肺水肿影响因素,分别是不典型皮疹、呕吐、EV71(+)、血糖高.另外冲击量甲泼尼龙组、非冲击量甲泼尼龙组、无甲泼尼龙组三组的神经源性肺水肿的发生率差异无统计学意义.将62例冲击量甲泼尼龙组以是否加用丙球冲击治疗分为2组,其神经源性肺水肿的发生差异具有统计学意义(χ2 ＝ 6.738,P ＜ 0.01).结论 手足口病并发神经源性肺水肿的相关因素有不典型皮疹、呕吐、EV71(+)、血糖升高.大剂量甲泼尼龙冲击治疗对阻断神经源性肺水肿的疗效不明显,丙球冲击治疗对阻断神经源性肺水肿有一定作用.     

重症手足口病并发神经源性肺水肿的机制

重症手足口病可并发神经源性肺水肿,严重者导致死亡.肺水肿的发生可能与中枢神经系统损伤后神经因素、体液因素、生物活性因子等多方面改变有关.研究重症手足口病并发神经源性肺水肿的发病机制从而采取积极有效的措施及时阻断并发症的发生具有重要意义.     

重症手足口病致神经源性肺水肿

神经源性肺水肿常由重症手足口病(肠道病毒EV71感染)引起,以突发呼吸困难、呼吸窘迫、咳粉红色泡沫痰、咯血及循环衰竭等为特点.同时伴意识障碍和神经系统异常表现.病情凶险,临床表现与心源性肺水肿有相似之处,需认真鉴别.对重症手足口病早发现,早诊断,早救治,可提高抢救成功率,降低病死率.实用儿科临床杂志,2009,24(10):732-733     

并发神经源性肺水肿的手足口病死亡患儿的临床特点研究

目的 研究并发神经源性肺水肿的手足口病生存患儿与死亡患儿的临床特点.方法 回顾性分析2009年至2013年我院收治的25例并发神经源性肺水肿的手足口病患儿的临床资料,对死亡和生存患儿的临床特点进行分析.结果 并发神经源性肺水肿的患儿病死率高达64％,年龄在4岁以内.死亡组患儿血乳酸水平明显高于生存组患儿（P＜0.05）,死亡组患儿pH值明显低于生存组患儿（P＜0.05）,死亡组患儿出现应激性溃疡、脑膜刺激征、肌力下降的例数明显高于生存组患儿（P＜0.05）.行血液净化治疗患儿的病死率低于未进行血液净化治疗的患儿（P＜0.05）.生存组患儿从出现神经源性肺水肿到进行呼吸机辅助通气的时间间隔要短于死亡组患儿（P＜0.05）.结论 合并神经源性肺水肿出现应激性溃疡、脑膜刺激征、肌力下降的患儿及血乳酸明显升高、pH明显下降的患儿病死率较高.患儿出现神经源性肺水肿后尽早进行呼吸机辅助通气可以在一定程度上提高生存率.血液净化治疗可能会提高合并神经源性肺水肿的危重症手足口病患儿的生存率.     

重症手足口病并发神经源性肺水肿的危险因素分析

目的 探讨重症手足口病并发神经源性肺水肿的危险因素.方法 根据有无并发神经源性肺水肿将79例重症于足口病患儿分为两组,分析两组在临床症状、体征、实验窒检查及脑电图检查结果之间的差异,Logistic回归分析并发神经源性肺水肿的危险因素.结果 两组患儿在肠道病毒71型的感染率,高体温、肌阵挛、肢体麻痹、眼球调节障碍、心动...     

肠道病毒71型感染致重症脑干脑炎的临床特征和治疗

目的：分析肠道病毒71型（EV71）感染所致重症脑干脑炎的临床特征及治疗方法。方法：回顾性分析2008年5月至2008年12月32例EV71感染所致重症脑干脑炎的住院患儿病例资料。结果：32例中3岁以下的婴幼儿28例（88%）,主要表现为持续发热（>38.5℃）,频繁呕吐,四肢抖动。8例在病程3~4 d病情迅速恶化,突发心动过速、呼吸喘促、四肢末端凉等交感神经亢进征象,直至口鼻腔涌出血性泡沫痰,发生神经源性肺水肿或肺出血。给予积极降颅压,静脉点滴丙种球蛋白和甲基强的松龙抑制炎症反应,使用血管活性药物,保护心功能,限制液体入量,早期气管插管正压通气等治疗,痊愈23例,好转4例,放弃治疗2例,死亡3例。结论：EV71感染所致脑干脑炎多有突出的植物神经功能损害的临床特征,早期识别并正确处理神经源性肺水肿是救治成功的关键。［中国当代儿科杂志,2009,11（12）：967-969］     

肠道病毒71型感染与神经源性肺水肿

肠道病毒71型(E V71)感染是导致婴幼儿神经源性肺水肿的重要病原.肠道病毒71型感染损伤脑干,干扰免疫与内分泌系统,可能是其导致肺水肿的关键机制.根据其临床特征及病原学检查进行早期诊断,采取以早期呼吸支持为主要措施的综合治疗是抢救成功的关键.     

九例小儿神经源性肺水肿临床分析

目的探讨小儿神经源性肺水肿的病因及临床特征。方法回顾分析9例小儿神经源性肺水肿的临床表现、诊治经过及转归等临床资料。结果5例由重症手足口病引起;2例由急性播散性脑脊髓膜炎引起;1例由单纯急性脊髓炎引起;1例由颅脑外伤、出血引起。9例临床均表现为进行性呼吸困难和低氧血症,心率、呼吸增快,血压下降,肺部出现湿哕音,后期出现粉红色泡沫痰,X线胸片检查提示云雾状、片状阴影,其血生化检查白细胞总数、血糖、脑利钠肽升高,予积极治疗原发病,同时予机械通气、降低颅内压、血管活性药物（如米力农、酚妥拉明、多巴酚丁胺）使用、静脉滴注大剂量激素及静脉用丙种球蛋白,除1例由手足口病引起患儿死亡外,其余均救治成功。结论引起小儿神经源性肺水肿的病因主要为肠道病毒71型病毒感染导致手足口病和其他病毒感染引起的重症脑炎、脊髓炎、颅脑外伤等,临床上应提高对该病的认识,积极治疗原发病、应用降低颅内压药物、机械通气及使用血管活性药物、激素等措施是治疗神经源性肺水肿的重要手段。     

EV71感染并发神经源性肺水肿的研究现状

肠道病毒71型(EV71)感染并发神经源性肺水肿(NPE)是手足口病患儿的重要并发症和主要死因,确切的发病机制尚未完全明了.外周交感神经系统过度兴奋已得到公认,但其确切的中枢定位及机制尚无定论.近年来强调由脑干损伤和(或)全身炎症反应导致的细胞因子的释放增加了肺血管渗透性,在NPE的形成中也起着非常重要的作用.干预措施目前主要以神经系统受累和呼吸、循环衰竭的对症治疗为主,疫苗的探索处于动物实验阶段,应用于临床尚有一定的距离.     

Hemorrhagic pulmonary edema and cardiac failure following isolated head injury. Treatment with dobutamine and nitroglycerin (author's transl)

A 12 year boy with an isolated head injury and subdural hematoma developed neurogenic pulmonary edema and intraoperatively a low cardiac output syndrome. The postoperatively depressed cardiac function and hemorrhagic pulmonary edema were treated with Dobutamine and Nitroglycerin given intravenously. The beta-1-stimulating catecholamine was used because of its positive inotropic effect, to reduce pulmonary capillary pressure and to improve the afterload. Nitroglycerin applied in a low dosage with exclusive venodilator effect was added for treatment of pulmonary edema and left ventricular failure. About 2 1/2 h after the start of the treatment pulmonary edema had subsided and circulation was stabilized.     

Pulmonary edema associated with child abuse: case reports and review of the literature

Pulmonary edema has been an unreported finding in the evaluation of abused children. We describe 2 cases of pulmonary edema in abused infants, 1 after confessed suffocation and the other after inflicted head injury. A review of the literature regarding postobstructive and neurogenic pulmonary edema suggests useful inferences for the forensic evaluation of maltreated children who present with this finding.     

Neurogenic pulmonary edema in childhood.

Three patients presenting with pulmonary edema associated with head trauma and increased intracranial pressure are described. Pulmonary edema is a clearly recognized complication of head trauma; the pathogenic mechanisms appear to be regulated by increased intracerebral pressure, sympathetically induced vascular hypertension, and increased pulmonary capillary permeability. If there is evidence that neurogenic pulmonary edema is the underlying etiology, therapeutic modalities should be directed at reducing intracranial pressure and strict attention paid to the interaction between intrathoracic and intracranial pressures in order to avoid the high mortality rate associated with this condition.     

Sudden death in toddlers with viral meningitis, massive cerebral edema, and neurogenic pulmonary edema and hemorrhage: report of two cases.

Viral (lymphocytic) meningitis typically does not cause sudden death, especially in the absence of severe inflammation in the brain or other organs. We report 2 toddlers with clinical evidence of a viral infection who died unexpectedly and were found at autopsy to have lymphocytic meningitis associated with severe brain edema, transtentorial herniation, neurogenic pulmonary edema and hemorrhage, and cardiomegaly. Influenza A virus, demonstrated in tracheal epithelium by immunocytochemistry, is the presumed cause of the mild meningitis in 1 case; adenovirus was cultured from swabs of the brain and anus in the 2nd case. Current concepts of neurogenic pulmonary edema and acute cardiac dysfunction associated with intracranial disease are discussed in considering the mechanism of sudden death in these toddlers. These cases emphasize the possibility that mild intracranial viral infections may be a rare cause of sudden death via lethal cardiopulmonary complications. They also underscore the importance of a comprehensive autopsy, including detailed neuropathologic examination and viral testing, in determining of the cause of unexpected death in toddlers.     

Neurogenic pulmonary edema associated with pediatric status epilepticus

Neurogenic pulmonary edema (NPE) can result from various central nervous system disorders such as brain malignancies, traumatic brain injuries, infections, and seizures. Although the pathogenesis is not completely understood, NPE creates an increase in pulmonary interstitial and alveolar fluid. In adults, it has been reported with prolonged seizure activity. In pediatric patients, pulmonary edema has rarely been reported after status epilepticus, and respiratory compromise is most often due to anticonvulsant-related respiratory depression. Treatment for NPE is largely supportive. If unrecognized, it can lead to hypoxia and respiratory arrest. We report a case of status epilepticus-related pulmonary edema in a female toddler, the youngest patient to be reported in the literature.     

15例肠道病毒71型感染重症手足口病临床特征及病原基因型分析

目的 探讨肠道病毒71型(enterovirus 71,EV71)感染重症手足口病患儿的临床特征及病原的基因型.方法 采用荧光定量PCR方法对15例重症手足口病患儿的临床标本进行EV71检测,RT-PCR扩增VP1基因目的片段测序,确定基因型.回顾性分析15例患儿的临床资料.结果 15例重症病例EV71核酸阳性,测序系C4型.全部病例均有体温异常,早期有不同程度神经系统受累.起病至出现重症合并症平均时间为1.26d.11例发展为神经源性肺水肿.4例予经鼻持续气道正压通气,11例气管插管呼吸机辅助通气.3例死亡,1例放弃,11例治愈.结论 重症EV71感染起病初期就有不同程度神经系统受累,多数发展为神经源性肺水肿,EV71基因型为C4型.早期识别、及早呼吸支持可降低病死率.     

Extracorporeal membrane oxygenation as rescue therapy for methadone-induced pulmonary edema

Opioid-induced pulmonary edema has been previously reported, but its mechanism remains unclear. The use of extracorporeal membrane oxygenation as rescue therapy for methadone-induced pulmonary edema has not been reported in the literature. We describe 2 cases of methadone ingestion complicated by pulmonary edema, acute respiratory distress syndrome, and circulatory failure successfully managed with venoarterial extracorporeal membrane oxygenation.