Amniotic fluid embolism rescued using venoarterial extracorporeal membrane oxygenation without initial anticoagulation: A case report and literature review.

RATIONALE: Amniotic fluid embolism (AFE) is a fatal obstetric condition that often rapidly leads to severe respiratory and circulatory failure. It is complicated by obstetric disseminated intravascular coagulation (DIC) with bleeding tendency; therefore, the introduction of venoarterial extracorporeal membrane oxygenation (VA-ECMO) is challenging. We report the case of a patient with AFE requiring massive blood transfusion, rescued using VA-ECMO without initial anticoagulation. PATIENTS CONCERNS: A 39-year-old pregnant patient was admitted with a complaint of abdominal pain. An emergency cesarean section was performed because a sudden decrease in fetal heart rate was detected in addition to DIC with hyperfibrinolysis. Intra- and post-operatively, the patient had a bleeding tendency and required massive blood transfusions. After surgery, the patient developed lethal respiratory and circulatory failure, and VA-ECMO was introduced. DIAGNOSIS: Based on the course of the illness and imaging findings, the patient was diagnosed with AFE. INTERVENTIONS: By controlling the bleeding tendency with a massive transfusion and tranexamic acid administration, using an antithrombotic ECMO circuit, and delaying the initiation of anticoagulation and anti-DIC medication until the bleeding tendency settled, the patient was managed safely on ECMO without complications. OUTCOMES: By day 5, both respiration and circulation were stable, and the patient was weaned off VA-ECMO. Mechanical ventilation was discontinued on day 6. Finally, she was discharged home without sequelae. LESSONS: VA-ECMO may be effective to save the lives of patients who have AFE with lethal circulatory and respiratory failure. For safe management without bleeding complications, it is important to start VA-ECMO without initial anticoagulants and to administer anticoagulants and anti-DIC drugs after the bleeding tendency has resolved.

Sudden respiratory and circulatory collapse after cesarean section: Amniotic fluid embolism or other reasons? - a case report.

BACKGROUND: For a healthy parturient, a cardiopulmonary collapse that suddenly occurs shortly after an uneventful caesarean section is a relatively rare event and presents a significant challenge for the anesthesia provider. CASE PRESENTATION: Amniotic fluid embolism (AFE) is characterized by acute and rapid collapse and is well known to the obstetric team. Our patient experienced sudden cardiovascular collapse, severe respiratory difficulty and hypoxia, in the absence of other explanations for these findings at the time, and thus AFE was immediately become the focus of the consideration. However, there is no quick, standard laboratory test for AFE, therefore the diagnosis is one of exclusion based on presenting symptoms and clinical course. After given symptomatic treatment, the patient made an uneventful initial recovery in a short period and developed a rash. We recognized that the postpartum shock was associated with delayed anaphylaxis of antibiotics. CONCLUSIONS: These observations have implications for understanding whenever administering drugs in surgery, which may affect the anesthesiologist's judgment regarding the complications of anesthesia. Even though serious complications of common perioperative drugs may rarely occur, anesthesia providers should be aware of the consideration. Early recognition and effective treatment are more important than prompt diagnosis.

Can cell salvage be used for resuscitation in a patient with amniotic fluid embolism and hepatic laceration? A case report.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare disease that can lead to profound coagulopathy and hemorrhage, especially when combined with the laceration and bleeding of other organs. Intraoperative cell salvage (ICS) has been widely used for treating obstetric hemorrhage, but it remains unclear whether ICS can be used in the treatment of AFE. CASE PRESENTATION: We report the case of a 27-year-old woman at 39 weeks' gestation who suddenly developed severe abdominal pain, convulsions, loss of consciousness, and decreased vital signs during labor. Despite an emergency cesarean section being performed, the parturient experienced sudden cardiac arrest. Fortunately, the heart rate spontaneously recovered after effective cardiopulmonary resuscitation (CPR). Further abdominal exploration revealed right hepatic laceration with active bleeding. ICS was performed and the salvaged blood was promptly transfused back to the patient. Subsequently, the patient was diagnosed with AFE based on hypotension, hypoxia, coagulopathy, and cardiac arrest. The patient was transfused with 2899 mL salvaged blood during surgery with no adverse effects. At 60- and 90-day follow-ups, no complaints of discomfort or abnormal laboratory test results were observed in the mother or the baby. CONCLUSION: ICS was used to rescue patient with AFE, and ICS did not worsen the condition of patients with AFE. For pregnant women who received CPR, clinicians should explore the presence of hepatic laceration which can be fatal to patients.

Fibrinogen may aid in the early differentiation between amniotic fluid embolism and postpartum haemorrhage: a retrospective chart review.

This study aimed to determine whether blood loss and fibrinogen can differentiate amniotic fluid embolism (AFE) from postpartum haemorrhage (PPH). This retrospective case-control study included nine patients with clinical AFE ("AFE group") and 78 patients with PPH managed at our tertiary care perinatal centre between January 2014 and March 2016. Patients meeting the Japanese diagnostic criteria for AFE were stratified into cardiopulmonary collapse-type AFE and disseminated intravascular coagulation (DIC)-type AFE groups. The relationship between blood loss and fibrinogen at onset was examined to compare DIC severity. Vital signs at onset were not significantly different. The AFE group had significantly less blood loss at onset (1506 mL vs 1843 mL, P = 0.0163), significantly more blood loss 2 h post-onset (3304 mL vs 1996 mL, P < 0.0001) and more severe coagulopathy and fibrinolysis. The blood loss/fibrinogen (B/F) ratio at onset was significantly higher in the DIC-type AFE group (23.15 ± 8.07 vs 6.28 ± 3.35 mL dL/mg, P < 0.0001). AFE was complicated by catastrophic DIC irrespective of blood loss at onset. Fibrinogen exhibited the strongest correlation among test findings at onset. The B/F ratio may help differentiate PPH from DIC-type AFE and diagnose clinical AFE, facilitating optimal replacement of coagulation factors during the early stages.

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 complicating medical termination of pregnancy.

BACKGROUND: Amniotic fluid embolism is always a severe complication and generally occurs during labour or immediately after childbirth. CLINICAL FEATURES: We report the case of a patient falling victim to amniotic fluid embolism after the medical termination of her pregnancy at 24 weeks of amenorrhea following the discovery of a teratoma-carrying foetus. The amniotic fluid embolism diagnosis was strongly suspected in the face of the sudden onset of severe arterial hypotension, hypoxic respiratory distress, a coma state and disseminated intravascular coagulopathy immediately after the delivery. Additional tests were conducted to support the diagnosis: cytological testing of a peripheral venous sample and maternal broncho-alveolar lavage fluid, dosing of tryptase and alpha-fetoprotein levels as well as screening for insulin-like growth factor binding protein 1. CONCLUSION: Amniotic fluid embolism is a rare and difficult diagnosis, especially in unconventional settings, yet it can be facilitated by screening for amniotic markers and tryptase.

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.

Neurocritical care complications of pregnancy and puerperum.

Neurocritical care complications of pregnancy and puerperum such as preeclampsia/eclampsia, hemolysis, elevated liver enzymes, low platelets syndrome, thrombotic thrombocytopenic purpura, seizures, ischemic and hemorrhagic stroke, postpartum angiopathy, cerebral sinus thrombosis, amniotic fluid emboli, choriocarcinoma, and acute fatty liver of pregnancy are rare but can be devastating. These conditions can present a challenge to physicians because pregnancy is a unique physiologic state, most therapeutic options available in the intensive care unit were not studied in pregnant patients, and in many situations, physicians need to deliver care to both the mother and the fetus, simultaneously. Timely recognition and management of critical neurologic complications of pregnancy/puerperum can be life saving for both the mother and fetus.

Evaluation of specific marker CK13 and CK10/13 combined with APM staining for the diagnosis of amniotic fluid embolism and aspiration.

OBJECTIVE: To explore the value of CK13 (Rab) and CK10/13(Mab) as objective and specific biomarkers combined with Alcian-Phloxine-Martius yellow (APM) staining for the diagnosis of amniotic fluid embolism (AFE) and amniotic fluid aspiration (AFA). METHODS: A retrospective study of forensic autopsy cases of 148 neonatal deaths and 19 maternal deaths in the perinatal stage was conducted at the Institute of Pathology and Forensic Medicine, Zhejiang University. Medical records were reviewed and monoclonal antibody for CK13 (Rab) and CK10/13 (Mab) as immunostaining of amniotic fluid squamous cells, APM staining, and Hematoxylin and Eosin (HE) staining were used to diagnose the AFE and AFA. Descriptive statistics of the patient population were analyzed using SPSS 20.0 software. RESULTS: Immunoreactivity of CK13 and CK10/13 specifically identified squamous cells of all the AFE and AFA cases. The amniotic fluid squamous cells were stained positive in a deep brown color with the monoclonal antibody to CK 13 and CK10/13 whereas the endothelial cells and alveolar epithelial cells were negative. There was no CK13 or CK10/13 expression in the non-AFE and non-AFA cases. With APM staining keratinized squamous cells were pink and mucus was blue-green in marked contrast with the surrounding tissue, which improved the detection rates of both keratinized squamous cells and mucus. CONCLUSIONS: CK13 (Rab) and CK10/13 (Mab) are valuable and reliable biomarkers of amniotic fluid squamous cells. APM reveals enriched mucus and keratinized squamous cells of amniotic fluid. Immunohistochemical detection of CK13 and CK10/13 combined with APM staining can improve the accuracy and reduce the difficulty in the diagnosis of AFE and AFA.

Chest pain syndromes in pregnancy.

Chest pain syndromes in pregnancy include numerous catastrophic cardiovascular events. Acute myocardial infarction, aortic dissection, pulmonary embolism, and amniotic fluid embolism are the most important causes of nonobstetric mortality and morbidity in pregnancy. Each of these could result in poor maternal and fetal outcomes if not diagnosed and treated in a timely fashion. However, their diagnosis and management is limited by fetal risks of diagnostic procedures, dangers of pharmacotherapy and interventions that have neither been widely studied nor validated. This article reviews the current literature on epidemiology, risk factors, pathogenesis, diagnosis, and management of 4 potentially lethal chest pain syndromes in pregnancy.

Immunohistochemical detection of meconium in the fetal membrane, placenta and umbilical cord.

OBJECTIVE: To develop the immunohistochemistry specific for meconium in the placenta, fetal membrane and umbilical cord. STUDY DESIGN: We previously reported the specific presence of zinc coproporphyrin I (ZnCP-I) in human meconium and demonstrated the possible diagnostic use of an elevation in maternal plasma ZnCP-I levels in cases of amniotic fluid embolism. In this study, we developed a new specific monoclonal antibody for ZnCP-I and applied it to the immunostaining of meconium in the placenta, fetal membrane, and umbilical cord. RESULTS: Immunoreactivity of ZnCP-I clearly and specifically identified meconium in the placenta, fetal membrane, and umbilical cord. It was especially useful in cases of severe chorioamnionitis to detect meconium in the macrophages surrounded by numerous neutrophils. In more than half of the cases, meconium was detected in clear amniotic fluid at delivery, suggesting previous exposure. CONCLUSIONS: Immunohistochemical detection of ZnCP-I is a highly sensitive histological diagnosis of meconium.

Fatal factors of clinical manifestations and laboratory testing in patients with amniotic fluid embolism.

AIMS: To identify factors leading to fatality of patients with amniotic fluid embolism (AFE). METHODS: Patients who had fatal or nonfatal AFE were registered at the Hamamatsu University School of Medicine in the Department of Obstetrics and Gynecology from 1992 to 2006. Data collected included information about demographics and clinical characteristics. The fatal factors among these data were identified using chi(2) analysis and the Mann-Whitney test. RESULTS: One hundred and thirty-five patients met the criteria, which included fatal (n = 65) and nonfatal AFE (n = 70). Maternal full-term gestational weeks, multiparous and noncesarean sections were the risk factors for death found in this study (p < 0.01). Sialyl Tn levels (mean +/- SD) in the serum of patients with fatal AFE (69.7+/- 126.4 U/ml) were higher compared to those with nonfatal AFE (48.3+/- 161.8 U/ml; p = 0.003). Each of three items (cardiac arrest, dyspnea or loss of consciousness) was more common in fatal AFE (p < 0.01). Maternal pregnancy and labor complications were not associated with the distinction between fatal and nonfatal AFE. CONCLUSION: Factors associated with patients with fatal AFE were identified. These included multiparity, noncesarean section at full-term and the three symptoms mentioned above. Sialyl Tn levels could be a possible prognostic fatality factor.

Maternal death following cardiopulmonary collapse after delivery: amniotic fluid embolism or septic shock due to intrauterine infection?

PROBLEM: The amniotic fluid embolism (AFE) syndrome is a catastrophic complication of pregnancy frequently associated with maternal death. The causes and mechanisms of disease responsible for this syndrome remain elusive. METHOD OF STUDY: We report two cases of maternal deaths attributed to AFE: (1) one woman presented with spontaneous labor at term, developed intrapartum fever, and after delivery had sudden cardiovascular collapse and disseminated intravascular coagulation (DIC), leading to death; (2) another woman presented with preterm labor and foul-smelling amniotic fluid, underwent a Cesarean section for fetal distress, and also had postpartum cardiovascular collapse and DIC, leading to death. RESULTS: Of major importance is that in both cases, the maternal plasma concentration of tumor necrosis factor-alpha at the time of admission to the hospital and when patients had no clinical evidence of infection was in the lethal range (a lethal range is considered to be above 0.1 ng/mL). CONCLUSION: We propose that subclinical intraamniotic infection may be a cause of postpartum cardiovascular collapse and DIC and resemble AFE. Thus, some patients with the clinical diagnosis of AFE may have infection/systemic inflammation as a mechanism of disease. These observations have implications for the understanding of the mechanisms of disease of patients who develop cardiovascular collapse and DIC, frequently attributed to AFE. It may be possible to identify a subset of patients who have biochemical and immunological evidence of systemic inflammation at the time of admission, and before a catastrophic event occurs.

Amniotic fluid embolism treated with emergency extracorporeal membrane oxygenation: a case report.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare disorder classically characterized by the abrupt onset of hypotension, hypoxia and consumptive coagulopathy during delivery or in the immediate postpartum period. It is postulated that amniotic fluid,fetal cells, hair or other debris enters the maternal circulation, causing cardiopulmonary collapse. The precise pathophysiologic mechanism remains elusive, treatment is supportive, and AFE carries a mortality of up to 80%. CASE: A 21-year-old woman, gravida 2, para 1, at 33+ weeks' gestation with an uncomplicated pregnancy, was admitted with preterm uterine contractions and underwent a low-transverse cesarean section for malpresentation after tocolysis failure. Surgery was without complications; however, 75 minutes postoperatively the patient experienced cardiopulmonary collapse with loss of vital signs. After 20 minutes of cardiopulmonary resuscitation, extracorporeal membrane oxygenation (ECMO) was begun. The patient's status improved rapidly, she was discharged 7 days postoperatively in good condition and remains without sequelae. CONCLUSION: Though there is no definitive treatment for AFE, ECMO provided oxygenation and allowed the patient to recover. ECMO may be useful in the treatment of severe cases of AFE.

Embolia de líquido amniótico: Criterio diagnóstico en dos casos fatales / Amniotic fluid embolism: Diagnostic criteria in two fatal cases

La embolia de líquido amniótico continúa siendo una causa importante de mortalidad materna. Presentamos la información obtenida por medio de la cateterización cardíaca derecha y la ecocardiografía, en dos pacientes que desarrollaron embolia de líquido amniótico y fallecieron por shock y coagulación intravascular diseminada a pesar del tratamiento intensivo. Aunque la fisiopatología continúa siendo discutida, la embolia por líquido amniótico se puede diagnosticar y manejar a partir de los valores hemodinámicos y el ecocardiograma.

Amniotic fluid embolism still remains an important cause of maternal mortality. We present information obtained by echocardiography and right cardiac catheterization of two patients who developed amniotic fluid embolism and died from shock and disseminated intravascular coagulation despite intensive medical treatment. Although the pathophysiology remains controversial, amniotic fluid embolism can be presumptively diagnosed and managed with hemodynamic values and echocardiography.

Embolia de liquido amniótico — relato de caso / Amniotic fluid embolism — a case report

A embolia de liquido amniótico continua sendo complicação da gravidez de elevada mortalidade, impossível de ser prevenida. O seu diagnóstico é essencialmente clínico e de exclusão, uma vez que os exames para o seu diagnóstico definitivo carecem de especificidade e sensibilidade. O seu manejo baseia-se em medidas suportivas. devendo ser feito, de preferência, em centros de tratamento intensivo, com monitorização invasiva adequada. Neste artigo, é relatado o caso de uma paciente de 31 anos com todos os elementos clínicos para o diagnóstico de embolia de liquido amniótico e cujo tratamento intensivo resultou em melhora.