胎粪吸入综合征的诊断和治疗

胎粪吸入综合征[1] (MAS)是新生儿期特有的呼吸道疾病 ,主要发生在足月儿及过期产儿 ,偶可发生在早产儿 ,发生率约为活产新生儿的 1.2 %～ 2 .2 %。其病因主要是由于胎儿发生宫内窘迫或产时窒息排出胎粪 ,吸入后发生肺部病变引起。临床上以低氧血症、高碳酸血症和酸中毒为特征 ,MAS是引起新生儿呼吸衰竭的主要原因之一。　　一、MAS的诊断1.病史 :( 1)大多数患儿有明确的宫内窘迫或出生窒息等缺氧史 ,Apgar评分常 <6分。 ( 2 )一般均有胎粪污染羊水史。羊水被胎粪污染后呈黄绿色或墨绿色 ,有时夹有胎粪颗粒或粪块 ,可自咽部或气管内吸出…     

胎粪吸入综合征新生儿脑组织氧饱和度的研究

目的：探讨胎粪吸入综合征(MAS)不同时相对新生儿局部脑组织氧饱和度(regionaloxygensatu-ration,rSO2)的影响因素及合并缺氧缺血性脑病时脑组织氧饱和度变化的意义。方法：根据MAS的临床表现分为无症状型、普通型、重型。应用TSNIR-3无创组织氧监测仪,测定其出生后1,3,5,7d时的脑组织氧饱和度变化,并与正常足月新生儿进行比较。结果：MAS无症状型与正常对照组的rSO2在出生后第1天(58.37±4.12vs60.43±2.85)、第3天(57.76±2.33vs60.17±3.46)比较差异有显著性(P<0.05);MAS普通型、重型生后的第1,3,5天时脑组织rSO2明显降低,MAS重型、普通型与无症状型、正常对照组的rSO2在出生后第1,3,5天比较差异有显著性(P<0.05)。MAS合并轻度HIE组与中~重度HIE组比较,rSO2在发病的第1天差异无显著性意义(P>0.05),第2,3,5天比较(57.60±3.60vs53.36±4.48;55.60±2.35vs51.36±3.20;56.80±2.78vs53.22±5.10)差异均有显著性意义(P<0.05)。结论：MAS患儿在生后的不同时相脑组织rSO2受到不同程度的影响,缺氧的加重和持续时间增加可使脑氧合功能进一步损害。     

无活力新生儿气管插管吸引胎粪的回顾性队列研究

目的 探讨胎粪污染羊水(meconium stained amniotic fluid,MSAF)无活力新生儿生后立即进行气管插管吸引胎粪的可行性.方法 采用队列研究方法,回顾性收集柘城县人民医院入住新生儿科MSAF无活力病例,2017年7月1日至2018年6月30日无吸引胎粪条件病例为对照组,2018年7月1日至20...     

新生儿胎粪吸入综合征血液淋巴细胞L-selectin水平变化

目的　了解新生儿胎粪吸入综合征 (MAS)患儿血液淋巴细胞L selectin水平变化 ,探讨其在MAS中意义。方法　采用流式细胞仪检测 2 1例MAS患儿生后d1及 2 5例足月健康新生儿脐血淋巴细胞表面L se lectin水平。结果　MAS患儿生后d1L selectin水平 [(82 .85± 8.71) % ]明显高于对照组。MAS患儿L selectin与生后 1h血 pH的相关系数为 0 .114。 结论　MAS患儿生后d1淋巴细胞L selectin明显增高 ,与血 pH无关。     

重度胎粪吸入综合征并发急性呼吸窘迫综合征临床特征及转归分析

目的 探讨新生儿重度胎粪吸入综合征（meconium aspiration syndrome,MAS）并发急性呼吸窘迫综合征（acute?respiratory?distress syndrome,ARDS）的临床特征及转归,为临床诊治提供参考。 方法 回顾性收集2017年1月至2019年12月收治的60例重度MAS新生儿的临床资料,根据是否并发ARDS分为ARDS组（45例）与非ARDS组（15例）,比较两组患儿的临床特征及转归。 结果 60例重度MAS患儿中,45例（75%）发生ARDS。ARDS组出生后1 h动脉血气分析显示中位氧合指数显著高于非ARDS组（4.7 vs 2.1,P<0.05）;两组间入院时白细胞计数、C-反应蛋白、白细胞介素-6水平及住院期间降钙素原、C-反应蛋白、白细胞介素-6的峰值水平比较差异无统计学意义（P>0.05）。ARDS组休克发生率高于非ARDS组（84% vs 47%,P<0.05）,两组间持续性肺动脉高压、气胸、肺出血、缺氧缺血性脑病、颅内出血和弥漫性血管内凝血的发生率比较差异无统计学意义（P>0.05）。ARDS组较非ARDS组中位机械通气时间更长（53 h vs 3 h,P<0.05）。ARDS组治愈出院43例（96%）,死亡2例（4%）;非ARDS组治愈出院15例（100%）。 结论 重度MAS并发ARDS患儿呼吸窘迫出现早,机械通气时间长,休克发生率更高;建议在管理重度MAS患儿过程中密切监测氧合指数,及时诊断及治疗ARDS,同时密切评估组织灌注,积极防治休克。 引用格式:     

幼兔胎粪吸入后肺表面活性蛋白B动态改变及与右心室压力关系的探讨

目的　探讨胎粪吸入综合征 (MAS)并发持续肺动脉高压 (PPHN)的发病机制。方法(1)通过气管内灌入胎粪 0 .6ml kg和 4ml kg建立轻、重度幼兔胎粪吸入模型 ;(2 )应用右心室穿刺法经压力传感器与日本光电公司生产的RM 6 0 0 0型多道生理记录仪相连 ,测定轻度胎粪吸入组 16、2 4、48、72h和重度胎粪吸入组右心室收缩压 ;(3)用RT PCR检测技术检测肺表面活性物质蛋白B(SP B)mRNA的水平。结果　 (1)轻度胎粪吸入组右心室收缩压从胎粪吸入后 16h开始升高 (19.3± 0 .8)mmHg(1mmHg=0 .133kPa) ,2 4h达高峰 (2 6 .8± 1.1)mmHg,72h恢复正常 (14.2± 0 .3)mmHg。重度胎粪吸入组右心室收缩压为 (32 .7± 1.1)mmHg ,明显高于轻度胎粪吸入组和对照组 (q值分别为17.5 6、5 5 .78,P均 <0 .0 1) ;(2 )轻度胎粪吸入组肺组织SP BmRNA吸光度 (A值 )较对照组降低 ,2 4～48h达最低水平 ,为 (0 .74± 0 .0 8) ,72h基本恢复正常 (1.84± 0 .10 ) ,重度胎粪吸入组SP BA值为(0 .2 0± 0 .0 5 ) ,较轻度胎粪吸入组降低更明显。SP BmRNA的A值与右心室压亦呈明显负相关 (r =- 0 .84,P <0 .0 1,n =30 )。结论　 (1)胎粪吸入后肺表面活性物质减少 ,并与胎粪吸入浓度有关 ,提示MAS时肺病理生理改变及其严重程度与其表面活性物质功能障碍有     

肌钙蛋白Ⅰ在新生儿胎粪吸入综合征并心肌损伤诊断中的意义

目的 探讨心肌肌钙蛋白Ⅰ(CTn-Ⅰ)在新生儿胎粪吸入综合征(MAS)并心肌损伤诊断中的意义。方法：用化学发光免疫法及酶法分别测定35例合并心肌损伤的MAS患儿、30例无心肌损伤的MAS患儿及15例正常对照组血清CTn-Ⅰ及CK-MB的水平。结果：心肌损伤组生后2～3 d CTn-Ⅰ浓度为(0.67±0.13) ng/ml,较MAS对照组［(0.07±0.05) ng/ml］和正常对照组［(0.07±0.03) ng/ml］明显升高,差异有显著性意义(P<0.05)。结论：CTn-Ⅰ是诊断新生儿MAS并心肌损伤的特异性指标之一。     

胎粪吸入综合征与婴幼儿喘息的关系及随访

目的 探讨胎粪吸入综合征(MAS)与婴幼儿喘息的关系.方法 对2003年1月至2007年1月在我院住院的64例MAS患儿随访1年,观察其喘息的发病情况、特应性体质的表现及生后家庭成员是否有吸烟者,同时进行食物过敏原、吸入过敏原筛查及肺炎支原体抗体(MP-IgM)检测,并与对照组比较,分析MAS与早期婴幼儿喘息的相关性.结果 MAS患儿婴幼儿喘息的发生率为25.0%,显著高于对照组7.5%(P＜0.01);重度MAS婴幼儿喘息的发生率显著高于轻度MAS(P＜0.05);两组中有特应性体质的比较差异无统计学意义(P＞0.05);生后家庭成员中有吸烟者比较差异无统计学意义(P＞0.05);两组发生喘息的患儿中食物过敏原、吸入性过敏原筛查阳性率及MP-IgM阳性率比较差异均无统计学意义(P＞0.05).结论 早期婴幼儿喘息的发病与MAS密切相关,并与其轻重程度有关;MAS疾病本身可能导致喘息,建议有针对性地进行早期干预.     

肌钙蛋白Ⅰ在新生儿胎粪吸入综合征并心肌损伤诊断中的意义

目的　探讨心肌肌钙蛋白Ⅰ (CTn Ⅰ )在新生儿胎粪吸入综合征 (MAS)并心肌损伤诊断中的意义。方法　用化学发光免疫法及酶法分别测定 35例合并心肌损伤的MAS患儿、30例无心肌损伤的MAS患儿及 15例正常对照组血清CTn Ⅰ及CK MB的水平。结果　心肌损伤组生后 2～ 3dCTn Ⅰ浓度为 (0 .6 7± 0 .13)ng/ml,较MAS对照组 [(0 .0 7± 0 .0 5 )ng/ml]和正常对照组 [(0 .0 7± 0 .0 3)ng/ml]明显升高 ,差异有显著性意义 (P <0 .0 5 )。结论　CTn Ⅰ是诊断新生儿MAS并心肌损伤的特异性指标之一。     

胎粪吸入综合征的研究进展

胎粪吸入综合征(MAS)是由于胎儿发生宫内窘迫或产时窒息胎粪吸入发生肺部病变所引起,为新生儿期特有的呼吸道疾病,是引起初生新生儿呼吸衰竭的主要原因之一。主要发生在过期产儿及足月儿,偶可发生在早产儿。MAS发病率为活产新生儿的1.2%~2.0%,病死率为7%~15%。现将近年来有关MA     

Meconium aspiration syndrome: do we know?

Meconium is a common finding in amniotic fluid and placental specimens, particularly in the term or post-term pregnancy. The most important consequence of meconium-stained amniotic fluid (MSAF) is meconium aspiration syndrome (MAS), and at least 5% of infants born through MSAF develop MAS. MAS continues to be a threat to many newborns throughout the world, with a case fatality rate of 5% (as much as 40%), in addition to short- and long-term pulmonary and neurodevelopmental sequelae. The exact pathophysiology of meconium passage into the amniotic fluid and consequences of meconium aspiration are unknown. There are three prevailing and possibly compatible theories for mechanisms of meconium release. Firstly, meconium passage is probably related with the maturation of the gastrointestinal tract, because meconium passage in the preterm third trimester fetus has been reported to be a rare event, as typically it occurs near or post-term. Secondly, an alternate hypothesis for in utero meconium passage is that pathologic processes, such as stress via hypoxia or infection, can trigger meconium passage. However, the predictive values of MSAF for fetal distress and acidosis at birth are poor and controversial. Thirdly, an alternative route for the presence of MSAF in the presence of fetal hypoxia is reduced clearance of defecated meconium due to impaired fetal swallowing or unidentified placental dysfunction in addition to or instead of an increase in its passage. The pathophysiology of MAS is multifactorial and extremely complex. Meconium causes mechanical obstruction and pulmonary air leak, induces surfactant inactivation, causes pulmonary inflammation, and induces apoptosis. Preventing prolonged pregnancy by labor induction might reduce the risk of MSAF. Labor induction with prostaglandins appears to be associated with the occurrence of MSAF. Amnioinfusion for suspected umbilical cord compression has no clear effect on the occurrence of MSAF. Intrapartum suctioning of the naso- and oropharynx before delivery of the shoulders as well as postnatal endotracheal suctioning of vigorous infants with MSAF are no longer recommended. Currently, endotracheal suction is recommended only in neonates born through MSAF who are not vigorous at birth. Indications for mechanical ventilation in infants with MAS are arbitrary. Surfactant administration may reduce the severity of MAS. Bronchoalveolar lavage with surfactant in infants with MAS is risky and it cannot be recommended for routine use. At present, there is insufficient evidence to propose routine steroid therapy in the management of MAS. Although prophylactic antibiotics in infants with MAS are not justified, most of these patients receive antibiotics during the first days of life, before the diagnosis of pneumonia can be completely ruled out. Children surviving severe MAS are in fact reported to have higher prevalence of asthmatic symptoms and bronchiolar hyperreactivity than children in the general population. It remains undetermined how often and at what intensity systemic inflammation occurs in association with MAS and what its significance is for the outcome of infants with severe MAS.     

羊水胎粪污染新生儿复苏的前世今生：过去60年中美两国的演变史

出生于羊水胎粪污染的新生儿可发生新生儿胎粪吸入综合征、持续性肺动脉高压等并发症，甚至死亡。在过去的几十年里，羊水胎粪污染新生儿复苏已发生了几次重要的变革。最初，对于羊水胎粪污染新生儿，通常在其出生后立即采用喉镜直视下吸引声门下胎粪。自2015年起，美国儿科学会新生儿复苏指南不再推荐对羊水胎粪污染无活力新生儿“常规”给予气管插管吸引胎粪，但建议立即给予气囊面罩正压通气复苏。然而，最新版2021年中国新生儿复苏指南仍保留对无活力新生儿进行胎粪吸引的建议。该文旨在探讨过去60年中美两国新生儿复苏指南在羊水胎粪污染新生儿复苏方法中的差异及其原因。     

Meconium-stained amniotic fluid and meconium aspiration syndrome: a prospective study

BACKGROUND: The incidence of meconium aspiration syndrome (MAS), associated perinatal factors, morbidity and deaths varies widely. This study aimed to assess the perinatal attributes and morbidity associated with MAS. METHODS: Over a 2-year period, all neonates born through meconium-stained amniotic fluid (MSAF) were observed for respiratory distress (RD). Birth details, chest radiograph (CXR) and clinical course were documented. Neonates with consistent CXR findings whose RD could not otherwise be explained were defined as MAS. RESULTS: Of 409 neonates born through MSAF, meconium was thick in 196 (47.9%). Fifty-five (13.4%) had RD and 45 (11.3%) were consistent with MAS. Six (1.5%) neonates died. Mean (SD) birthweight and gestation of MAS infants were 2721.9 (510.2) g and 38.67 (1.09) weeks, respectively. About one-third were of low birthweight and 28 were born by caesarean section. On univariate analysis, caesarean delivery, meconium in the trachea and thick meconium were the significant perinatal factors for the development of MAS. On multiple regression analysis, thick meconium was the only independent factor for MAS (OR 7.08, 95% CI 3.08-16.27, p<0.001). An Apgar score of 相似文献   

The pros and cons of suctioning at the perineum (intrapartum) and post-delivery with and without meconium

Routine oronasopharyngeal suctioning (ONPS) of the infant at delivery is a common practice in the delivery room. ONPS is performed to remove lung fluid, meconium, or other secretions from the airway, thereby improving oxygenation and/or preventing aspiration. However, there are controversies regarding this practice, as it seems to be associated with complications. In the presence of clear amniotic fluid, routine ONPS in infants born vaginally and by cesarean section is associated with bradycardia, apnea, and delays in achieving normal oxygen saturations, with no benefit. Intrapartum ONPS and post-natal endotracheal suctioning of vigorous infants born through meconium-stained amniotic fluid (MSAF) does not prevent meconium aspiration syndrome (MAS). Although depressed infants born through MSAF are at risk of developing MAS, there is no evidence that endotracheal suctioning of these infants reduces MAS.     

Handling the meconium-stained infant

Clinicians who care for infants in the delivery room or afterward must frequently manage many born through meconium-stained amniotic fluid (MSAF). Approximately 5% of infants born through MSAF develop meconium aspiration syndrome (MAS). This disorder can be severe in nature, with half or more of the affected children needing mechanical ventilation. It is frequently associated with pulmonary air leaks and the presence of persistent pulmonary hypertension. MAS is the most common disorder for which babies may be treated with extracorporeal life support. Various possibilities for preventing MAS exist during labor, parturition, and the first minutes of life. Proposed antenatal therapies include amnioinfusion; intrapartum maneuvers include oropharyngeal suctioning prior to delivery of the babies shoulders; the postnatal intervention of intubation for intratracheal suctioning should be reserved for the non-vigorous meconium-stained infant.     

What (not) to do at and after delivery? Prevention and management of meconium aspiration syndrome

Meconium aspiration syndrome (MAS) is a life-threatening disorder in newborn infants. Universal intrapartum suction of infants with meconium stained amniotic fluid (MSAF) and postnatal suction of vigorous infants have been used in an attempt to decrease the incidence and severity of the disease by clearing the airway. Both procedures have been proven fruitless when challenged through randomised control trials (RCTs). Endotracheal intubation and suctioning are currently recommended only for non-vigorous infants. Respiratory failure in infants with MAS is frequently treated initially with conventional or synchronized mechanical ventilation. Surfactant administration and high-frequency ventilation (HFV) are commonly used as rescue therapy for severe cases. Nitric oxide (NO) is added when severe pulmonary hypertension is demonstrated. ECMO is an option when other treatments have failed. In the pathophysiology of severe MAS, asphyxia and pulmonary hypertension are considered to be more important than the obstruction of the airways and/or damage to the lung produced by meconium.     

Consequences of meconium stained amniotic fluid: What does the evidence tell us?

Background

Meconium stained amniotic fluid (MSAF) is common and associated with meconium aspiration syndrome (MAS). Other consequences of meconium passage before birth are less well understood.

Methods

We reviewed the literature for original papers reporting on outcomes associated with MSAF.

Findings

Among preterm infants MSAF is more prevalent than previously believed and is associated with higher neonatal morbidity. Intrauterine exposure to meconium is associated with inflammation of tissues of the lung, chorionic plate and umbilical vessels and through various mechanisms may contribute to neonatal morbidity, independent of MAS. No compelling evidence supported an association between MSAF and increased neurological impairment, including early seizure activity.     

Is gastric lavage needed in neonates with meconium-stained amniotic fluid?

We compared the incidence of complications from meconium-containing gastric fluid in a group of neonates born with meconium-stained amniotic fluid (MSAF) who did not routinely have gastric lavage prior to feeds, versus a group who had elective gastric lavage before the first feed. In the first group, 275 neonates born with MSAF were fed without prior gastric lavage. While 13 developed feeding problems, the other 262 infants (95%) who did not undergo routine gastric lavage remained free of later feeding difficulties or secondary meconium aspiration. In the second group, all 227 neonates with MSAF had elective gastric lavage performed after birth. All remained free of later feeding difficulties or secondary meconium aspiration. Conclusion Our data suggest that gastric lavage is not necessary in most neonates born with meconium-stained amniotic fluid, regardless of the thickness of the meconium-stained fluid, as no complications from meconium-containing gastric fluid were observed. Received: 17 March 1998 / Accepted in revised form: 8 July 1998