五例羊水栓塞病例报告及文献复习

目的通过5例典型羊水栓塞病例及文献复习,分析探讨减少羊水栓塞病例不良结局的诊治要点。方法回顾性分析5例羊水栓塞病例的诊治、结局及相关文献复习。结果 1 16年间羊水栓塞的发生率约1/9 000;2高龄孕妇3例;应用前列腺素制剂改善宫颈条件和依沙吖啶引产各1例;其余3例未使用外源性宫缩剂;3发生于产后即刻2例、剖宫产术中1例、胎膜早破有规律宫缩但尚未临产1例、依沙吖啶引产产程中1例;4临床表现:两种类型,突发的急性肺动脉高压为首发症状者3例(3/5),产后出血凝血功能障碍首发症状者2例(2/5);均出现低血压、低氧血症;5结局:孕产妇死亡1例(1/5),永久性神经系统并发症2例(2/5),子宫切除3例(3/5)。未切除子宫远期预后良好2例(2/5)。围产儿死亡1例(1/5)。结论羊水栓塞罕见、凶险、难以预防,快速诊断和处理,特别是有经验的麻醉医生及时到场生命支持,是改善孕产妇结局的关键。     

胎儿娩出前羊水栓塞5例临床分析

目的:分析胎儿娩出前羊水栓塞(AFE)的临床表现和处理,总结早期诊断和治疗的重要性。方法:对成都市妇女儿童中心医院收治的5例胎儿娩出前发生AFE孕产妇的临床表现、诊断、治疗和母儿预后的临床资料进行回顾性分析。结果:1例猝死患者因突发呼吸心跳骤停,早期诊断困难,未及时行AFE相关治疗,母儿均死亡。4例存活患者,在出现相关早期症状时立即怀疑AFE并迅速开始抗过敏、解除肺动脉高压和剖宫产术,其中2例行心肺复苏,2例行输血等抗休克及纠正凝血功能障碍治疗,3例行子宫切除术,除1例因在家中发生AFE延误病情,围生儿死亡外,其余母儿结局良好。结论:AFE抢救成功的关键为早期诊断,并及时抗过敏和解除肺动脉高压,有效心肺复苏、纠正凝血功能障碍,及早行剖宫产术,必要时行子宫切除术。     

羊水栓塞的快速诊断

文献上最早报告羊水栓塞是在1926年,一直认为本症是引起母体死亡的重要原因。主要临床表现是在分娩期或产后早期出现呼吸困难、心动过速、低氧血症和凝血异常。羊水可能经子宫或宫颈内小静脉裂伤进入母体循环。羊水栓塞引起心肺功能变化的病因尚未完全阐明,由于羊膜粒状物质和/或血管活性介质释放而导致急性肺动脉高压可能是起作用的因素。本文报导作者根据Masson等的细胞学方法(1979)略加修改,用来快速诊断羊水栓塞,并附病案报告一例。细胞学诊断:用肝素化注射器抽取15ml肺动脉血,2,000转/分离心10分钟,弃去上清液。沉渣用     

羊水栓塞致急性肾功能衰竭的诊断及处理

羊水栓塞 (amnioticfluidembolism ,AFE)是一种少见且病势凶险的妊娠并发症 ,其临床表现以迅速出现、发展极快的心、肺功能衰竭和肺水肿 ,继之以凝血功能障碍而发生大出血以及急性肾功能衰竭为特征[1 ] 。羊水栓塞的典型临床经过可分为三个阶段。 (1 )休克 :由肺动脉高压引起的     

羊水栓塞致孕产妇死亡29例分析

对１９８９－１９９３年间北京地区因羊水栓塞所致的２９例孕产妇死亡病例进行了回顾性分析。结果发现：北京地区羊水栓塞的平均死亡率为５．９／１０万，占全部孕产妇死亡的１５．５％。其临床经过有１３例以产后出血、血不凝为主要表面；有１２例产程中使用过催产素；有半数以上的病发病后没有得到及时诊断。提示：发生羊水栓塞及死亡者多以凝血功能障碍为主要临床表现，产前催产素使用不当可能与羊水栓塞的发生有关。     

羊水栓塞的发病机制及诊治进展

目前认为羊水栓塞是白三烯、前列腺素、血栓素等物质进入母血循环引起的"妊娠过敏样综合征”.因而,促使肺支气管痉挛、血小板聚集、血管内凝血,主要表现为左心功能障碍导致的肺动脉压轻到中度增高.除临床症状、体征外,早期诊断依靠中心静脉及肺动脉插管吸出物中找到胎儿鳞状上皮细胞或碎屑及右心导管插入术获得血流动力学资料,免疫组化测定肺循环中的ET-1浓度及母亲血清中的sialy1Tn抗原的水平.羊水栓塞的确切诊断,主要是尸检发现肺血管内有胎儿细胞成分.羊水栓塞的治疗,主要是改善低氧血症,防止ARDS发生,保护心肌,抢救休克,保持心输出量及纠正血管内凝血.     

羊水栓塞临床表现及早期识别

羊水栓塞是一种产科特有的罕见且极为凶险的并发症。临床表现可以分为心肺功能衰竭型和出血凝血功能异常型。起病可以是凶猛型或者缓慢型。主要临床表现包括前驱症状、心肺功能衰竭、出凝血障碍、全身脏器损害和胎儿窘迫等。只有早期识别，才能进行早期干预，为治疗争取时间，降低羊水栓塞病死率。     

羊水栓塞病人心肺功能变化

羊水栓塞是由于羊水物质进入母体循环，而引起的严重的综合征，典型表现为突发性低血压，低血氧及凝血功能障碍，但临床表现有很大差异，可在短期内猝死，也有仅以凝血功能障碍为主要表现者。甚至有报道羊水中有形物质在肺内形成一囊性肿物，但患者在一死产分娩后无任何羊水栓塞的临床表现，只是3个月后因右侧胸痛而经CT发现肺部肿物，术后证实为羊水物质形成的肿块。     

羊水栓塞症的诊断与急救

羊水栓塞症是一种严重的产科并发症,起病急,病情险,死亡率高。据统计发病率为1/8000～1/80000妊娠,一旦发生有25～50％在1小时内死亡。总死亡率>86％。本病病例少,且病情经过急,往往不能充分检查出来而病人即已死亡。其主要的病理表现为(1)肺动脉高压及肺水肿,急性右心衰竭及循环衰竭。(2)过敏性休克。(3)全身低氧血症。(4)弥散性血管内凝血(DIC)。一、诊断 (一)临床表现大致可分为三个阶段:     

妊娠合并肺动脉高压临床研究进展

妊娠合并肺动脉高压是妊娠期严重危害母婴安全的一类合并症,尤其是妊娠合并重度肺动脉高压。目前将任何原因引起的肺动脉高压均列为妊娠禁忌类,严重的肺动脉高压、低氧血症、紫绀、血栓栓塞是孕产妇死亡的危险因素。对胎儿的影响包括流产、早产、胎儿生长受限、低出生体重儿、新生儿窒息和新生儿死亡等。了解妊娠合并肺动脉高压的妊娠风险及预后影响因素,规范妊娠期综合管理对改善母儿预后具有重要意义。     

Squamous and trophoblastic cells in the maternal pulmonary circulation identified by invasive hemodynamic monitoring during the peripartum period

The antemortem diagnosis of amniotic fluid embolism has traditionally relied on the identification of amniotic fluid debris in the maternal circulation by central venous or pulmonary arterial catheterization. Pulmonary artery blood specimens from 14 term pregnant women with severe pregnancy-induced hypertension suggest that squamous or trophoblastic cells may be normally present in the maternal pulmonary circulation during the peripartum period and that their presence is not pathognomonic of clinically significant amniotic fluid embolism.     

羊水栓塞DIC的处理及肝素使用问题

弥散性血管内凝血（disseminated intravascular coagulation，DIC）是羊水栓塞（amniotic fluid embolism，AFE）病理改变的重要原因之一。DIC造成大量凝血因子消耗和红细胞破坏，并加重肺动脉高压，也是AFE出血的主要原因。早期发现DIC，有助于AFE的诊断。减少促凝物质进入血液循环、抗凝治疗可阻断DIC的进一步发展。肝素应在DIC高凝期或低凝期早期使用，同时需补充凝血因子，监测凝血功能的变化。     

羊水栓塞的液体管理

羊水栓塞救治过程中，实施有效的液体复苏及管理，不仅为后续的救治措施争取时间，同时也可以为纠正失血及凝血功能障碍奠定基础，避免由于容量状态失常导致器官损伤。羊水栓塞液体管理包括右心衰竭阶段掌控容量负荷避免心衰肺水肿加重并维持血液动力学稳定、循环支持阶段的液体复苏和DIC阶段限制性液体复苏。     

Fruchtwasserembolie

Amniotic fluid embolism is a rare disorder with a high mortality rate. The amniotic fluid and corpuscular components can enter the maternal circulation via uterine veins (amnioninfusion). During the first stage of amniotic fluid embolism foreign substances are deposited in the pulmonary vascular bed leading to pulmonary hypertension, acute cor pulmonale, and cardiogenic shock. The second phase of the clinical picture is characterized by disseminated intravascular coagulation (DIC) with reactive hyperfibrinolysis. If dyspnea, cyanosis, anxiety, or loss of consciousness occur during or shortly after birth, amniotic fluid embolism must be considered immediately. Priority is given to medical intensive care of cardiopulmonary insufficiency and control of coagulopathy. After the mother’s condition has been adequately stabilized, vaginal delivery should be finished as quickly as possible. If this is not feasible, the only recourse to save the child is emergency cesarean section. Massive vaginal hemorrhage due to uterine atony and DIC can be expected postpartum. For that reason uterotonic medication (oxytocin, ergot alkaloids) must be administered, but prostaglandins are contraindicated.     

The importance of extensive sampling and examination of cervix in suspected cases of amniotic fluid embolism

Amniotic fluid embolism is an important complication of pregnancy with high mortality. The diagnosis of amniotic fluid embolism is generally made postmortem and rests upon the histological demonstration of amniotic fluid debris, including foetal epithelial squames and hair, in the pulmonary vasculature. We have made the diagnosis of amniotic fluid embolism in two patients by detection of the amniotic fluid debris in the blood vessels of the cervix in their hysterectomy specimens. These two patients presented with profuse primary postpartum haemorrhage and evidence of disseminated intravascular coagulation after uneventful deliveries. Amniotic fluid debris were only demonstrated in the blood vessels of the cervix but not in the corpus. This observation emphasizes the importance of a thorough histological examination of the cervix in cases of suspected amniotic fluid embolism. Received: 28 January 1994 / Accepted: 6 April 1994     

Amniotic fluid embolism. Three case reports with a review of the literature

Amniotic fluid embolism is a catastrophic event of the intra- and early postpartum period which may also be seen with cesarean delivery and during abortions. Presenting symptomatology includes respiratory distress with cyanosis, shock, and possibly tonic-clonic seizures. DIC frequently occurs. The pathogenesis may include entry of amniotic fluid through lacerations or ruptures of the uterus or cervix, through endocervical veins and through abnormal uteroplacental sites, such as with placental abruption, placenta previa, or placenta accreta. Amniotic fluid probably causes cardiovascular-respiratory symptoms by pulmonary vascular obstruction and through a vasoactive substance causing pulmonary vascular constriction. The lethality of amniotic fluid may be enhanced by a high particulate content or meconium staining. The diagnosis of amniotic fluid embolism may be made ante mortem by demonstrating amniotic fluid debris in central blood samples or expectorated sputum. Postmortem diagnosis often requires meticulous examination of the pulmonary microvasculature with the utilization of special stains. Treatment is directed towards symptoms of shock, arterial hypoxemia, and DIC. Acute renal failure may complicate the picture after shock. If the patient survives the embolic and coagulative problems, recovery is usually complete without long-term sequelae.     

Amniotic fluid embolism

A critical review of animal and human data leads to a reassessment of traditional concepts of amniotic fluid embolism. Left ventricular failure, rather than pulmonary hypertension, is the major hemodynamic derangement consistently seen in humans. The detection of squamous cells in the pulmonary artery blood of pregnant women is not pathognomonic for amniotic fluid embolism.     

Non-haemorrhagic obstetric shock.

The causes of non-haemorrhagic obstetric shock (pulmonary thromboembolism, amniotic fluid embolism, acute uterine inversion and sepsis) are uncommon but responsible for the majority of maternal deaths in the developed world. Clinically suspected pulmonary thromboembolism should be treated initially with heparin and objective testing should be performed. If the diagnosis is confirmed, heparin is usually continued until delivery, following which anticoagulation in the puerperium is achieved with either warfarin or heparin. Amniotic fluid embolism is a rare complication of pregnancy, occurring most commonly during labour. The management of amniotic fluid embolism involves maternal oxygenation, the maintenance of cardiac output and blood pressure, and the management of any associated coagulopathy. Acute uterine inversion arises most commonly following mismanagement of the third stage of labour. The shock in uterine inversion is neurogenic in origin, although there may also be profound haemorrhage. The management of this condition includes maternal resuscitation and replacement of the uterus either manually, surgically or by hydrostatic pressure. Genital tract sepsis remains a significant cause of maternal death, the most common predisposing factor being prolonged rupture of the fetal membranes. The management of septic shock in pregnancy includes resuscitation, identification of the source of infection and alteration of the systemic inflammatory response.     

羊水栓塞与产科血栓栓塞性肺栓塞诊治的异同点

羊水栓塞及血栓栓塞性肺栓塞都是产科发生率低但致死率很高的急症,对于产时或产后突发的心肺衰竭要考虑羊水栓塞或血栓栓塞性肺栓塞的可能性,迅速的鉴别诊断及正确的治疗极为重要,文章对两者的鉴别诊断及治疗的异同点进行了总结。     

Amniotic fluid embolism: an overview and case report

This article gives an overview of amniotic fluid embolism, which still carries a fatality rate of approximately 86% and which accounts for 9% of all maternal deaths. A case report is presented which ended with a fatal outcome. Photomicrographs show fetal squames and lanugo hairs in the pulmonary capillaries as well as ones aspirated from the right atrium. The treatment is discussed in terms of acute primary and acute secondary care. Acute primary care centers around the prompt recognition and treatment of pulmonary edema. This is apparently due to the mechanical blockade of the pulmonary vasculature and particulate matter from the amniotic fluid and also to an anaphylactoid reaction adding to the pulmonary arteriolar spasm. The acute secondary treatment deals with combating the almost inevitable disseminated intravascular coagulation and uterine atony. Being always alert to the possible occurrence of this condition and being able to institute appropriate therapy rapidly are necessary for a successful outcome.