Amniotic fluid embolism - implementation of international diagnosis criteria and subsequent pregnancy recurrence risk.

OBJECTIVES: An international diagnostic criterion for amniotic fluid embolism (AFE) diagnosis has recently been published. Data regarding subsequent pregnancies is scarce. We sought to implement recent diagnostic criteria and detail subsequent pregnancies in survivors. METHODS: A case series of all suspected AFE cases at a tertiary medical center between 2003 and 2018 is presented. Cases meeting the diagnostic criteria for AFE were included. Clinical presentation, treatment, and outcomes described. Pregnancy outcomes in subsequent pregnancies in AFE survivors detailed. RESULTS: Between 2003 and 2018 14 women were clinically suspected with AFE and 12 of them (85.71%) met the diagnostic criteria for AFE. Three cases occurred during midtrimester dilation and evacuation procedures, and the remaining occurred in the antepartum period. Of the antepartum cases, mode of delivery was cesarean delivery or vacuum extraction for expedited delivery due to presentation of AFE in 8/9 cases (88.88%). Clinical presentation included cardiovascular collapse, respiratory distress and disseminated intravascular coagulopathy (DIC). Heart failure of varying severity was diagnosed in 75% (9/12) cases. Composite maternal morbidity was 5/12 (41.66%), without cases of maternal mortality. 11 subsequent pregnancies occurred in four AFE survivors. Pregnant women were followed by a high-risk pregnancy specialist and multidisciplinary team if pregnancy continued beyond the early second trimester. Six pregnancies resulted in a term delivery. No recurrences of AFE were documented. CONCLUSIONS: Use of a diagnostic criterion for diagnosis of AFE results in a more precise diagnosis of AFE. Nevertheless, the accuracy of clinical diagnosis is still high. Subsequent pregnancies were not associated with AFE recurrence.

Excessive fibrinolysis detected with thromboelastography in a case of amniotic fluid embolism: fibrinolysis may precede coagulopathy.

Amniotic fluid embolism (AFE) is a catastrophic condition in the peripartum period and still remains as a leading cause of maternal death. Although over 80% of cases of AFE cases are accompanied by coagulopathy, the pathology of disseminated intravascular coagulation is not well understood not only because of its rarity but also because of the limited availability of laboratory testing in emergent clinical settings. We describe a case of AFE whose characteristic data for coagulation and fibrinolysis were timely depicted with sequential thromboelastography. We believe that the point-of-care, which provides information for both coagulopathy and fibrinolysis, may provide crucial data not only for the treatment of postpartum hemorrhage in daily clinical practice but also for the elucidation of AFE pathophysiology.

Evaluation of the 4 diagnosis criteria proposed by the SMFM and the AFE foundation for amniotic fluid embolism in a monocentric population.

OBJECTIVE: The Society of Maternal Fetal Medicine (SMFM) and the Amniotic Fluid Embolism Foundation have recently proposed four diagnostic criteria for amniotic fluid embolism (AFE): presence of (1) sudden cardiac arrest or both respiratory and hemodynamic collapse, and (2) biological disseminated intravascular coagulopathy (DIC), and (3) absence of fever, and (4) clinical onset during labor or within 30 min of delivery. The objectives of our study were to describe the clinical presentation of women with a strong suspicion of AFE and to assess the validity of the four criteria proposed for AFE definition. MATERIAL AND METHODS: We performed a retrospective study including all patients with a strong suspicion of AFE who delivered between 2006 and 2018 at the Port Royal maternity unit, Paris. Strong suspicion of AFE was defined by a clinical presentation in favor of AFE associated with a biological pattern and/or autopsy result supporting AFE. The mention of AFE in files was essential to include the patients in our study. We estimated the incidence and mortality rate of AFE. Then, the presence of each of the four diagnosis criteria of the SMFM score was described, as well as the clinical and biological patterns. RESULTS: Among the 54 140 women who delivered during the study period, 14 had a strong suspicion of AFE (0.03 %), accounting for 25.9/100 000 deliveries (95 %CI (12.3-39.5/100,000)). All women had biological tests or autopsy supporting the diagnosis of AFE. Six of 14 patients (43 %) presented with all the four diagnostic criteria of the SMFM definition. All 14 women presented a hemodynamic collapse, but respiratory symptoms were lacking in 8 patients (57 %); 71 % fulfilled the criterion of biological DIC, and all patients had a clinical coagulopathy and a massive postpartum hemorrhage. Absence of fever was lacking in three women. In addition, all patients presented premonitory symptoms such as neurological disorders or irreversible and inaugural fetal bradycardia. CONCLUSION: The four SMFM diagnostic criteria were present in less than half of the women with a strong suspicion of AFE. We propose an alternative clinical and pragmatic definition to diagnose AFE, which has to be validated in the future. Early diagnosis of AFE based solely on clinical criteria can help clinicians anticipate the severity of the situation and optimize care.

Amniotic fluid embolism and spontaneous hepatic rupture during uncomplicated pregnancy: a case report and literature review.

Amniotic fluid embolism (AFE) and spontaneous hepatic rupture both are extremely rare complications of pregnancy that can be fatal to mother and/or child. AFE is characterized by a sudden collapse of the cardiovascular system, a change in mental status, and disseminated intravascular coagulation (DIC), occurring immediately during labor, delivery, or postpartum, caused by the inflow of amniotic components into the maternal circulation. Spontaneous hepatic rupture during pregnancy which is most often occurs alongside hypertensive disorders, eclampsia, or HELLP syndrome. We report on the case of a 28-year-old woman (G3P2) who is suffering from AFE and spontaneous hepatic rupture, without history of hypertensive disorders, preeclampsia/eclampsia, or HELLP syndrome, and she died suddenly after delivering of a severe asphyxial neonate within 1 h with postpartum of hepatic rupture and massive hemorrhage. The lack of typical clinical signs and symptoms resulted to the difficulty of early diagnosis. If AFE and hepatic rupture is highly suspected in a pregnant patient, a collaborative multidisciplinary approach is mandatory. Pregnancy women is simultaneously complicated in amniotic fluid embolism and spontaneous hepatic rupture, similar cases are infrequent in the literature, which is reviewed in this report, explore the pathophysiological changes, we hope that can be helpful for the prevention, diagnosis and treatment of similar cases.

Extracorporeal Therapies for Amniotic Fluid Embolism.

BACKGROUND: Amniotic fluid embolism (AFE) is a catastrophic disease with significant mortality. Because the cardiopulmonary dysfunction associated with AFE is self-limited, the disease could be well suited to the use of extracorporeal therapies. CASE: A woman progressed into cardiac arrest immediately after an elective cesarean delivery. Owing to severe hypoxemia and hypotension, AFE was suspected and peripheral venoarterial extracorporeal membrane oxygenation was quickly initiated. Subsequent evolution was complicated by intrabdominal bleeding, which required massive transfusion and multiple surgeries. The patient recovered well, with a healthy newborn. We have identified 19 similar cases in the literature and present their outcomes as a series. CONCLUSION: Extracorporeal therapies can support severely ill women affected by AFE and could be considered even in the presence of disseminated intravascular coagulation and bleeding.

Amniotic fluid embolism: Pathophysiology from the perspective of pathology.

Amniotic fluid embolism (AFE) is recognized as a type of syndrome characterized by the abrupt onset of hypoxia, hypotension, seizures, or disseminated intravascular coagulopathy (DIC), occurring during labor, delivery, or immediately postpartum, caused by the inflow of amniotic components into the maternal circulation. AFE is a rare condition but one of the most serious obstetrical complications, resulting in a high mortality rate among pregnant women. Despite earlier recognition and intensive critical management, we often encounter patients who unfortunately do not recover from the exacerbation of AFE-related conditions. A major concern is that there are no effective evidence-based therapies for AFE, because its pathophysiology is still not well understood. This article reviewed AFE, focusing on the pathology and currently proposed pathophysiology.

Amniotic Fluid Embolism: A Rare Complication of Second-Trimester Amniocentesis.

Amniotic fluid embolism occurring following diagnostic amniocentesis is extremely rare. Only 2 cases have been reported in the English literature over the past 55 years, the most recent one approximately 3 decades ago. We present a case of amniocentesis at 24 weeks' gestation that was performed as part of an evaluation of abnormal fetal ultrasound findings. Immediately following amniotic fluid aspiration, maternal hemodynamic collapse occurred, initially diagnosed and treated as anaphylactic shock. Shortly after initial therapy, coagulopathy was noted and amniotic fluid syndrome suspected. Rapid response restored maternal hemodynamic stability; however, the fetus had suffered fatal damage.

Amniotic Fluid Embolism.

Amniotic fluid embolism (AFE) is a rare but serious and potentially deadly complication of pregnancy that is unpreventable and unpredictable. Most AFE events occur during labor; however, approximately one third happen during the immediate postpartum period. Presentation is abrupt and thought to be an abnormal response to fetal materials entering maternal circulation through the placental insertion site. Care providers must recognize the signs and symptoms of AFE and react quickly to treat potential complications. This can be challenging as there are no set diagnostic criteria or specific laboratory tests. Generally, the diagnosis is based on clinical status when the classic triad of hypoxia, hypotension, and subsequent coagulopathy are noted in a laboring woman or woman who just gave birth, and no other plausible explanation can be determined. Proper treatment of AFE requires a multidisciplinary approach to decrease maternal morbidity and mortality. Knowledge, simulation, and familiarization of a Massive Obstetric Transfusion protocol can help all members of the perinatal team recognize and respond to women with AFE in a timely and effective manner. A case study is presented of a woman with a seemingly normal obstetric course that became complicated rapidly following development of an AFE.

Amniotic Fluid Embolism.

Amniotic fluid embolism remains one of the most devastating conditions in obstetric practice with an incidence of approximately 1 in 40,000 deliveries and a reported mortality rate ranging from 20% to 60%. The pathophysiology involves an abnormal maternal response to fetal tissue exposure associated with breaches of the maternal-fetal physiologic barrier during parturition. This response and its subsequent injury involve activation of proinflammatory mediators similar to that seen with the classic systemic inflammatory response syndrome. Maternal treatment is primarily supportive, whereas prompt delivery in the mother who has sustained cardiopulmonary arrest is critical for improved newborn outcome.

An example of prompt and appropriate multidisciplinary management leading to an exceptionally good outcome: a case complicated by amniotic fluid embolism.

Amniotic fluid embolism (AFE) is a rare and serious phenomenon; we describe a rare case of AFE occurring after a second trimester surgical termination in a private clinic, which, with prompt transfer and appropriate multidisciplinary management, had an exceptionally good outcome. The patient developed hypotension, respiratory arrest and disseminated intravascular coagulopathy following the procedure but with aggressive management she made a full recovery without any neurological or long-term sequelae.

Amniotic fluid embolism: despite progress, challenges remain.

PURPOSE OF REVIEW: This article reviews the incidence, pathophysiology, risk factors, diagnosis, and management of amniotic fluid embolism (AFE). RECENT FINDINGS: AFE is a leading cause of maternal morbidity and mortality despite an incidence of approximately 7 to 8 per 100,000 births. Recent reevaluation of AFE suggests that the presence of fetal tissue in maternal circulation alone is not sufficient to cause the clinical syndrome, but rather an individual's response to this fetal tissue. The 'anaphylactoid reaction' associated with AFE shares many clinical and metabolic aspects of septic shock. Acute dyspnea followed by cardiovascular collapse, coagulopathy, and neurological symptoms, such as coma and seizures may all be associated with the clinical AFE syndrome. Specific biochemical markers have been described, but are of limited clinical value because of the rapid progression of the disease process. Treatment is based on an interdisciplinary approach that consists of a combination of prompt, aggressive hemodynamic resuscitation, provision of end-organ support, correction of hemostatic disorders, and delivery. SUMMARY: Although AFE cannot be prevented, early diagnosis and intervention may lead to better outcomes for both the mother and the fetus. Clinical suspicion, traditional laboratory data, or intravascular cellular debris (demonstrated only in 50% of patients) are insufficient to make a definitive diagnosis of AFE. An evolving array of novel biomarkers may help differentiate AFE from other conditions, but none of them currently provide sufficient 'early warning' ability to make real-time impact on diagnosis and/or treatment of AFE.

Embolismo de líquido amniótico: mitos y realidades etiopatogénicas de un síndrome potencialmente fatal / Amniotic fluid embolism: etiopathogenic realities and myths of a potentially fatal syndrome

Fundamento: el embolismo de líquido amniótico es un síndrome catastrófico que ocurre durante el trabajo de parto, el parto o inmediatamente. De incidencia variable, es la segunda causa de muerte materna en muchas partes del mundo y que reporta tasas de hasta un 60 por ciento en países desarrollados. En las últimas dos décadas un trabajo de investigación más riguroso ha mejorado enormemente la comprensión de esta condición.Objetivo: exponer los elementos más recientes que intentan explicar la etiología y la fisiopatología del embolismo de líquido amniótico.Método: se realizó una revisión en 32 bibliografías entre revistas y textos clásicos, a través de la biblioteca virtual cubana, Lilacs, PubMed y Medline.Desarrollo: la embolia de líquido amniótico es, desde un punto de vista fisiopatológico, parecida al síndrome de respuesta inflamatoria sistémica, común en condiciones tales como choque séptico, en el que una respuesta anormal del huésped es la principal responsable de las manifestaciones clínicas. La teoría bimodal es la regla: una fase temprana caracterizada por vasoespasmo e hipertensión pulmonar y fallo ventricular derecho; otra tardía donde prima el fallo ventricular izquierdo, el edema pulmonar, el shock y los trastornos de la coagulación.Conclusiones: la base fisiopatológica de toda esta secuencia de alteraciones hemodinámicas parece implicar una secuencia compleja de reacciones resultantes de la activación anormal de sistemas mediadores pro inflamatorios similares a los presentes en el síndrome de respuesta inflamatoria sistémica, que sigue al casi universal paso de antígenos fetales a la circulación materna durante el proceso de parto(AU)

Background: amniotic fluid embolism is a catastrophic syndrome that takes place during the onset of labor or during the labor. This syndrome of variable incidence is the second cause of maternal death in many regions of the world. Rates up to 60 percent are reported in developed countries. A more rigid investigation has greatly increased the comprehension of this condition in the last two decades.Objective: to set out the most recent elements that try to explain the etiology and physiopathology of amniotic fluid embolism.Method: a review of 32 bibliographies, including journals and classic texts, was made through the Cuban virtual library, Lilacs, PubMed and Medline.Development: amniotic fluid embolism is, from the physiopathological point of view, similar to the systemic inflammatory response syndrome, and it is common in conditions like septic shock, in which the abnormal response of the host is the main responsible for the clinical manifestations. Bimodal theory is the rule: an early stage characterized by vasospasm and pulmonary hypertension and heart failure; and a late stage where left heart failure, pulmonary edema, shock and coagulation disorders predominate.Conclusions: the physiopathological basis of this sequence of hemodynamic changes seems to entail a complex sequence of reactions that result from the abnormal activation of proinflammatory mediator systems, similar to those present in the systemic inflammatory response syndrome that follows the almost universal flow of fetal antigens to the maternal circulation during labor(AU)

Amniotic Fluid Embolism: Anaphylactic Reactions With Idiosyncratic Adverse Response.

PROBLEM: Amniotic fluid embolism (AFE) is a rare but severe emergency in obstetrics. The aim of the present study was to investigate the pathophysiology of AFE. METHODS: A search was conducted between 1966 and 2014 through the English-language literature (online MEDLINE PubMed database) using the keyword amniotic fluid embolism combined with anaphylaxis, anaphylactoid, complement activation, mast cells, fetal antigens, and idiosyncratic. RESULTS: Amniotic fluid embolism is a rare clinical entity but a severe obstetric emergency that can be lethal even in previously healthy women in labor or in the early postpartum period. There appears to be at least 2 mechanisms. First, adverse reactions in AFE are usually unexpected and fetal antigen dose dependent. Given the disastrous entry of amniotic fluid into the maternal circulation, they experience a sudden cardiopulmonary collapse (mechanical obstruction subtype). Second, anaphylactic and anaphylactoid reactions of the remaining AFE are also relatively unexpected and fetal antigen dose independent and can occur at the first exposure to amniotic fluid components. They are associated with complement activation and subsequent postpartum hemorrhage. Cardiac mast cells constitute a central pathogenesis of anaphylactic (immunoglobulin E-dependent) and anaphylactoid (immunoglobulin E-independent) reactions. CONCLUSIONS: Recent immunologic studies provide a new approach to the study of the pathophysiology of AFE.

Unresponsive primipara after rupture of membranes.

Amniotic fluid embolism, also called anaphylactoid syndrome of pregnancy, is a rare but severe problem in obstetrics. It occurs in 8/100,000 births and the maternal mortality is up to 90%. We report the case of a patient with amniotic fluid embolism who was transferred to our hospital. The initial presentation was an unresponsive patient after spontaneous rupture of the membranes. The massive hypotension and coagulopathy as well as fetal bradycardia of 60 bpm led, after stabilisation of the mother, to an emergency caesarean section. The neonate expired hours later, despite neonatological intensive care. During the operation, we had to deal with massive bleeding due to the coagulopathy. Through interdisciplinary teamwork including Bakri postpartum balloon insertion through the obstetrics team, uterine artery embolism by the interventional radiologists and transfusion of blood products, the maternal life was saved and the patient was discharged 9 days after admission.

Amniotic fluid embolism pathophysiology suggests the new diagnostic armamentarium: ß-tryptase and complement fractions C3-C4 are the indispensable working tools.

Amniotic fluid embolism (AFE) is an uncommon obstetric condition involving pregnant women during labor or in the initial stages after delivery. Its incidence is estimated to be around 5.5 cases per 100,000 deliveries. Therefore, this paper investigated the pathophysiological mechanism, which underlies AFE, in order to evaluate the role of immune response in the development of this still enigmatic clinical entity. The following databases (from 1956 to September 2014) Medline, Cochrane Central, Scopus, Web of Science and Science Direct were used, searching the following key words: AFE, pathophysiology, immune/inflammatory response, complement and anaphylaxis. The main key word "AFE" was searched singularly and associated individually to each of the other keywords. Of the 146 sources found, only 19 were considered appropriate for the purpose of this paper. The clinical course is characterized by a rapid onset of symptoms, which include: acute hypotension and/or cardiac arrest, acute hypoxia (with dyspnoea, cyanosis and/or respiratory arrest), coagulopathies (disseminated intravascular coagulation and/or severe hemorrhage), coma and seizures. The pathology still determines a significant morbidity and mortality and potential permanent neurological sequelae for surviving patients. At this moment, numerous aspects involving the pathophysiology and clinical development are still not understood and several hypotheses have been formulated, in particular the possible role of anaphylaxis and complement. Moreover, the detection of serum tryptase and complement components and the evaluation of fetal antigens can explain several aspects of immune response.

Activation contact system (ACS) and tissue factor (TF) in human amniotic fluid: measurements of ACS components and TF, and some implications on the pathophysiology of amniotic fluid embolism.

BACKGROUND/AIM: It is believed that the amniotic fluid-derived TF, in the case of amniotic fluid embolism (AFE), contributes to acute disseminated intravascular coagulation (DIC) and obstetric shock in the mother. However, the role of amniotic fluid-derived contact phase coagulation factors that irrupt into the bloodstream simultaneously with TF is still unknown. Our study objective was to identify and measure the concentrations of CAS components and TF in amniotic fluid. MATERIAL AND METHODS: The study group consisted of 30 healthy parturients with uneventful pregnancy and birth. Amniotic fluid (AF) and maternal blood were sampled at the end of the first stage of labor. The components of ACS, i.e. factors XII and XI (FXII, FXI), prekallikrein (PK), high molecular weight kininogen (HMWK), and tissue factor (TF) were measured by immunoenzymatic method (ELISA). RESULTS: All ACS components were detected in AF; their levels were higher in AF than in the maternal plasma: FXII--29.17 ng/mg protein vs. 0.94 ng/mg protein (medians); FXI--27.28 ng/mg protein vs. 0.92 ng/mg protein (medians); PK--88442.04 ng/mg protein vs. 113.44 ng/mg protein (medians); HMWK--4253.82 ng/mg protein vs. 2857.96 ng/mg protein (medians). The concentration of TF in amniotic fluid was 39.46 pg/mg protein (median) vs. 0.41 pg/mg protein (median) in blood plasma. CONCLUSIONS: 1.The ACS components, i.e. FXII, FXI, PK and HMWK, are the constituents of amniotic fluid. 2.The concentrations of the amniotic fluid-derived factors having a coagulation initiation potential, i.e. TF and contact phase coagulation factors, are higher in amniotic fluid than in mother's blood plasma.

[Amniotic fluid embolism as a cause of maternal death].

This article reports the case of death of a puerperal woman resulting from amniotic fluid embolism. The diagnosis was established based on the results of the pathohistological study that revealed the presence of mucoproteides and epithelial scales in pulmonary blood vessels and capillaries.

Amniotic components in the uterine vasculature and their role in amniotic fluid embolism.

AIM: To evaluate whether the presence of amniotic components in the maternal uterine vasculature could be a specific pathological indicator for amniotic fluid embolism (AFE). METHODS: Medical records of patients treated between January 2006 and March 2013 were retrospectively examined to identify patients who underwent post-partum hysterectomy or autopsy due to maternal death. Three subjects with AFE with disseminated intravascular coagulation (DIC)-type post-partum hemorrhage (PPH), and 13 non-AFE subjects were included in analysis. Histochemical staining using hematoxylin-eosin (HE) and alcian blue, and immunohistochemical staining for sialyl-Tn were conducted to detect amniotic components in the maternal uterine vasculature. RESULTS: Alcian blue was positive for amniotic components in the uterine vasculature of all subjects with AFE and of several subjects without AFE. Similarly, HE and sialyl-Tn were negative in some AFE subjects and positive in some non-AFE subjects. CONCLUSIONS: The presence of maternal intravascular fetal material is not a specific indicator for AFE with DIC-type PPH. Therefore, the presence of fetal components in the uterine vasculature is unlikely to be a definitive indicator for AFE.