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.

Placental mesenchymal dysplasia complicated with sudden fetal demise and amniotic fluid embolism: a case report.

BACKGROUND: Placenta mesenchymal dysplasia (PMD) is a rare placental anomaly associated with various fetal and maternal complications. Whether close ultrasound surveillance can prevent intrauterine fetal demise (IUFD) in patients with PMD is still under investigation. Amniotic fluid embolism (AFE) is a rare, lethal, and unpredictable maternal complication that has never been described in association with PMD. Here, we report a case of PMD, in which the fetus eventually demised in utero despite weekly color Doppler monitoring, and the mother subsequently encountered AFE during delivery. CASE PRESENTATION: A 43-year-old woman who had received three frozen embryo transfer, was found to have a singleton pregnancy with an enlarged multi-cystic placenta at 8 weeks' gestation. Fetal growth restriction (FGR) was noted since the 21stweek. The fetus eventually demised in-utero at 25 weeks despite weekly color Doppler surveillance. Cesarean section was performed under general anesthesia due to placenta previa totalis and antepartum hemorrhage. During surgery, the patient experienced a sudden blood pressure drop and desaturation followed by profound coagulopathy. AFE was suspected. After administration of inotropic agents and massive blood transfusion, the patient eventually survived AFE. PMD was confirmed after pathological examination of the placenta. CONCLUSIONS: While FGR can be monitored by color Doppler, our case echoed previous reports that IUFD may be unpreventable even under intensive surveillance in PMD cases. Although AFE is usually considered unpredictable, PMD can result in cumulative risk factors contributing to AFE. Whether a specific link exists between the pathophysiology of PMD and AFE requires further investigation.

, , ACUTE PULMONARY EMBOLISM BY AMNIOTIC FLUID - A RARE COMPLICATION OF PERINATAL PERIOD THAT SHOULD NOT BE FORGOTTEN.

OBJECTIVE: Amniotic fluid embolism (AFE) is a diagnostically challenging type of pulmonary embolism that occurs when amniotic fluid enters maternal circulation during delivery or postpartum. This obstetric complication is very rare but characterized by high mortality rate. The main symptoms are dyspnea, cardiovascular collapse, disseminated intravascular coagulation (DIC) and even sudden cardiac death. The aim of the article is to draw attention to AFE as a rare but possible and catastrophic complication of perinatal period. The authors present a 28-year-old woman who was admitted to obstetric ward during the first stage of labour. The patient developed sudden deterioration of her medical state with acute respiratory distress symptoms. An emergency cesarean section was performed, complicated by excessive bleeding. After a detailed assessment of the patient's condition and evaluation of the results of additional tests, we diagnosed AFE as the cause of the patient's deterioration. CONCLUSION: Conclusions: The case study shows how unpredictable, unpreventable and dangerous is AFE. It is still one of the main causes of maternal deaths in developed countries. Four diagnostic criteria proposed by the Society for Maternal-Fetal Medicine (SMFM) may accelerate diagnosis. AFE as a medical emergency, requires immediate multidisciplinary response and aggressive treatment. The initial medical care may be facilitated by the application of the general guidelines recommended by SMFM. The case report also emphasizes the need for further research on this disease, in particular on early detection and prevention.

Case report of amniotic fluid embolism coagulopathy following abortion; use of viscoelastic point-of-care analysis.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare, life threatening obstetric complication, often associated with severe coagulopathy. Induced abortions are extremely safe procedures however complications including AFE can occur. CASE PRESENTATION: A 29-year-old previously healthy woman, gravida 1 para 0, presented for a scheduled second trimester induced abortion via dilation and evacuation at 22-weeks gestation. The case was complicated by a suspected AFE with associated profound coagulopathy. Viscoelastic point-of-care coagulation analysis was used to successfully and swiftly guide management of her coagulopathy. CONCLUSION: AFE can occur in the setting of induced abortion. This case report suggests viscoelastic point-of-care coagulation analyzers may aid in the management of pregnancy-related coagulopathy by providing faster coagulation assessment than laboratory testing, and facilitating timely, targeted management of coagulopathy.

Risk factors, management, and outcomes of amniotic fluid embolism: A multicountry, population-based cohort and nested case-control study.

BACKGROUND: Amniotic fluid embolism (AFE) remains one of the principal reported causes of direct maternal mortality in high-income countries. However, obtaining robust information about the condition is challenging because of its rarity and its difficulty to diagnose. This study aimed to pool data from multiple countries in order to describe risk factors, management, and outcomes of AFE and to explore the impact on the findings of considering United Kingdom, international, and United States AFE case definitions. METHODS AND FINDINGS: A population-based cohort and nested case-control study was conducted using the International Network of Obstetric Survey Systems (INOSS). Secondary data on women with AFE (n = 99-218, depending on case definition) collected prospectively in population-based studies conducted in Australia, France, the Netherlands, Slovakia, and the UK were pooled along with secondary data on a sample of control women (n = 4,938) collected in Australia and the UK. Risk factors for AFE were investigated by comparing the women with AFE in Australia and the UK with the control women identified in these countries using logistic regression. Factors associated with poor maternal outcomes (fatality and composite of fatality or permanent neurological injury) amongst women with AFE from each of the countries were investigated using logistic regression or Wilcoxon rank-sum test. The estimated incidence of AFE ranged from 0.8-1.8 per 100,000 maternities, and the proportion of women with AFE who died or had permanent neurological injury ranged from 30%-41%, depending on the case definition. However, applying different case definitions did not materially alter findings regarding risk factors for AFE and factors associated with poor maternal outcomes amongst women with AFE. Using the most liberal case definition (UK) and adjusting for the severity of presentation when appropriate, women who died were more likely than those who survived to present with cardiac arrest (89% versus 40%, adjusted odds ratio [aOR] 10.58, 95% confidence interval [CI] 3.93-28.48, p < 0.001) and less likely to have a source of concentrated fibrinogen (40% versus 56%, aOR 0.44, 95% CI 0.21-0.92, p = 0.029) or platelets given (24% versus 49%, aOR 0.23, 95% CI 0.10-0.52, p < 0.001). They also had a lower dose of tranexamic acid (median dose 0.7 g versus 2 g, p = 0.035) and were less likely to have had an obstetrician and/or anaesthetist present at the time of the AFE (61% versus 75%, aOR 0.38, 95% CI 0.16-0.90, p = 0.027). Limitations of the study include limited statistical power to examine factors associated with poor maternal outcome and the potential for residual confounding or confounding by indication. CONCLUSIONS: The findings of our study suggest that when an AFE is suspected, initial supportive obstetric care is important, but having an obstetrician and/or anaesthetist present at the time of the AFE event and use of interventions to correct coagulopathy, including the administration of an adequate dose of tranexamic acid, may be important to improve maternal outcome. Future research should focus on early detection of the coagulation deficiencies seen in AFE alongside the role of tranexamic acid and other coagulopathy management strategies.

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.

Incidence, risk factors, management and outcomes of amniotic-fluid embolism: a population-based cohort and nested case-control study.

OBJECTIVE: To describe the incidence, risk factors, management and outcomes of amniotic-fluid embolism (AFE) over time. DESIGN: A population-based cohort and nested case-control study using the UK Obstetric Surveillance System (UKOSS). SETTING: All UK hospitals with obstetrician-led maternity units. POPULATION: All women diagnosed with AFE in the UK between February 2005 and January 2014 (n = 120) and 3839 control women. METHODS: Prospective case and control identification through UKOSS monthly mailing. MAIN OUTCOME MEASURES: Amniotic-fluid embolism, maternal death or permanent neurological injury. RESULTS: The total and fatal incidence of AFE, estimated as 1.7 and 0.3 per 100 000, respectively, showed no significant temporal trend over the study period and there was no notable temporal change in risk factors for AFE. Twenty-three women died (case fatality 19%) and seven (7%) of the surviving women had permanent neurological injury. Women who died or had permanent neurological injury were more likely to present with cardiac arrest (83% versus 33%, P < 0.001), be from ethnic-minority groups (adjusted odds ratio [OR] 2.85, 95% confidence interval [95% CI] 1.02-8.00), have had a hysterectomy (unadjusted OR 2.49, 95% CI 1.02-6.06), had a shorter time interval between the AFE event and when the hysterectomy was performed (median interval 77 minutes versus 248 minutes, P = 0.0315), and were less likely to receive cryoprecipitate (unadjusted OR 0.30, 95% CI 0.11-0.80). CONCLUSION: There is no evidence of a temporal change in the incidence of or risk factors for AFE. Further investigation is needed to establish whether earlier treatments can reverse the cascade of deterioration leading to severe outcomes.

From appearance to essence: 10 years review of atypical amniotic fluid embolism.

PURPOSE: Amniotic fluid embolism (AFE) is an unpredictable and unpreventable complication of maternity. The presentation may range from relatively subtle clinical events to sudden maternal cardiac arrest. However, the neglected diagnosis of non-classical form of AFE (atypical AFE) is very common. The aim of this study was to examine population-based regional data from Suzhou, China. Based on the analysis of all available case reports, we put forward an outline of atypical AFE and investigate whether any variation identified could be ascribed to methodology. METHODS: Retrospective study from January 2004 to December 2013, 53 cases was identified from the database of Center for Disease Control (CDC) in the city of Suzhou. We investigated the presentations of atypical AFE and maternal characteristics with potential factors underlying AFE. Multiple-regression analysis was used to calculate adjusted odds ratios (ORs) and 95 % confidence intervals (CIs). RESULTS: The incidence of AFE was 6.91 per 100,000 deliveries (53/766,895). Seventeen deaths occurred, a mortality rate of 32 %. Atypical AFE may as the earlier stage or mild form of AFE, there was no death case in the study with timely remedy. The atypical AFE appear is obstetric hemorrhage and/or pulmonary and renal dysfunction postpartum. Hyperfibrinolysis and coagulopathy may the early laboratory findings of atypical AFE. Atypical and classical AFE shared the same risks, such as advanced maternal age, placental abnormalities, operative deliveries, eclampsia, cervical lacerations, and induction of labor. CONCLUSION: Staying alert to premonitory symptoms of AFE is critical to turn it to a remediable disease. Patient complaints such as breathlessness, chest pain, feeling cold, distress, panic, a feeling of nausea, and vomiting should elicit close attention. The management of a suspected episode of amniotic fluid embolism is generally considered to be supportive. Hysterectomy must be performed if there is further progression of symptoms. Due to advances in acute care, mortality has decreased in recent years, highlighting the importance of early detection and treatment.

Amniotic fluid embolism: update and review.

PURPOSE OF REVIEW: This article reviews our current understanding of amniotic fluid embolism (AFE), specifically the pathogenesis, treatment strategies, potential diagnostic tests and future therapeutic interventions for AFE. RECENT FINDINGS: The incidence and case mortality of AFE varies widely because of heterogeneous diagnostic criteria and varying reporting mechanisms across the world. Amniotic fluid embolism is thought to be caused by abnormal activation of immunologic mechanisms following entry of fetal antigens into maternal circulation. Mast cell degranulation and complement activation may play a role in this anaphylactoid or systemic inflammatory response syndrome. Development of serum biomarkers and immune-histochemical staining techniques to aid diagnosis and develop treatments are under development and evaluation. Treatment of AFE is supportive and directed at treating cardiovascular, pulmonary, and coagulation derangements. Treatment for coagulopathy (fresh frozen plasma, cryoprecipitate/fibrinogen concentrate, and antifibrinolytics) should be initiated promptly. Recombinant factor VIIa may lead to increased mortality and should not routinely be used. C1 esterase inhibitors may be a potential therapeutic option. SUMMARY: AFE is a devastating obstetric complication that requires early and aggressive intervention with optimal cardiopulmonary resuscitation, as well as hemorrhage and coagulopathy management. Biomarkers offer promise to aid the diagnosis of AFE, and immunomodulation may provide future therapeutic interventions to treat this lethal condition.

Koagulopatia ze zuzycia jako wiodacy objaw zatoru plynem owodniowym -opis przypadku.

Amniotic fluid embolism is a rare and diagnostically challenging obstetric disease of high mortality rate. We present a case of a 33-year old parturient after vaginal birth, who presented with severe hemorrhagic shock with low platelet count and coagulopathy resistant to treatment with plasma, platelets and coagulation factors and despite of surgical management of bleeding. Laboratory findings revealed consumptive coagulopathy. Other symptoms included dyspnea and atelectatic changes on chest x-ray, together with augmentation of the heart with no proof of ventricular insufficiency in echocardiographic examination. The suspected reason of these alterations was amniotic fluid embolism. The patient survived and came back to her usual activity after 22 days of treatment.

Cell Salvage in Obstetrics.

Intraoperative cell salvage is a strategy to decrease the need for allogeneic blood transfusion. Traditionally, cell salvage has been avoided in the obstetric population because of the perceived risk of amniotic fluid embolism or induction of maternal alloimmunization. With advances in cell salvage technology, the risks of cell salvage in the obstetric population parallel those in the general population. Levels of fetal squamous cells in salvaged blood are comparable to those in maternal venous blood at the time of placental separation. No definite cases of amniotic fluid embolism have been reported and appear unlikely with modern equipment. Cell salvage is cost-effective in patients with predictably high rates of transfusion, such as parturients with abnormal placentation.

[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 fluid embolism: pathophysiology and new strategies for management.

The registry program of amniotic fluid embolism (AFE) in Japan started in 2003. More than 400 hundred clinical diagnosed amniotic fluid embolism has been accumulated. Those data showed that there were two etiologies of AFE: the fetal materials create physical obstructions in the maternal microvessels in various organs, such as the lung; and (ii) the liquids cause an anaphylactoid reaction that leads to pulmonary vasospasm and activation of platelets, white blood cells and/or complements. The clinical findings showed that AFE was characterized mainly by cardiopulmonary collapse, the other involves the presence of disseminated intravascular coagulation (DIC) and atonic bleeding. Zinc coproporphyrin-1, sialyl Tn antigen (STN), complement C3, C4 and interleukin-8 have been used as serum markers of AFE. The levels of zinc coproporphyrin-1 and STN were increased in cardiopulmonary collapse type AFE, and a marked reduction of C3 and C4 was observed in DIC type AFE. At the primary medical institution, initial treatments for shock airway management, vascular management, fluid replacement, administration of anti-DIC therapy such as antithrombin, and administration of fresh frozen plasma should be provided. C1 esterase inhibitor activity in AFE cases was significantly lower than those of normal pregnant women. C1 esterase inhibitor may be a promising candidate of treatment of AFE.

Amniotic fluid embolism: 20-year incidence and case-fatality trends in the United States.

OBJECTIVE: To estimate incidence and case-fatality rates of amniotic fluid embolism (AFE) and to examine their temporal trends. STUDY DESIGN: Population-based retrospective cohort study using the 2000-2019 Health Care Cost and Utilization Project, Nationwide Inpatient Sample (HCUP-NIS). Annual population rates were estimated using HCUP-NIS specific weighting. Descriptive analyses and logistic regression described trends within the cohort. RESULTS: Over the study period, AFE incidence rate remained stable (mean 4.9 cases/100,000 deliveries) and the case-fatality rate declined (mean 17.7 %,95 % CI 16.40-10.09). Highest AFE incidence rates and fatality rates were in women ≥ 35 years, African-Americans, and in urban-teaching hospitals. AFE mortality rates decreased among Hispanics. CONCLUSION: AFE rates remained stable and fatality rates declined over time. Highest rates of AFE occurrence and death were in women who typically have greater risk of experiencing adverse obstetrical outcomes. Continued research into early diagnostic methods and effective treatments are needed to further improve AFE incidence and mortality rates.

Incidence, risk factors, and consequences of amniotic fluid embolism.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare but serious cause of maternal mortality whose aetiology remains obscure. Previous population-based studies have reported associations with labour induction and caesarean delivery. METHODS: We updated a previous analysis based on the US Nationwide Inpatient Sample from 1999 to 2008. We adapted a diagnostic validation algorithm to minimise false-positive diagnoses, along with statistical methods that account for the stratified random sampling design. RESULTS: Of the 8 571 209 deliveries recorded in the database, 276 met our case definition of AFE, of which 62 (22.9% of the 274 with known vital status) were fatal. Significant associations with AFE were observed for medical induction {adjusted odds ratio [aOR] = 1.7 [95% confidence interval (CI) 1.2, 2.5]}, caesarean delivery [aOR = 15.0; 95% CI 9.4, 23.9], instrumental vaginal delivery [aOR = 6.6; 95% CI 4.0, 11.1], and cervical/uterine trauma [aOR = 7.4; 95% CI 3.6, 14.9]. AFE was associated with increases in risk of stillbirth, hysterectomy, maternal death, and prolonged maternal length of delivery hospital stay. CONCLUSIONS: AFE remains an extremely serious obstetric complication with high risks of maternal and fetal mortality. The increased risks of AFE associated with labour induction and caesarean delivery have implications for elective use of these interventions.

Acute hypotension associated with intraoperative cell salvage using a leukocyte depletion filter during management of obstetric hemorrhage due to amniotic fluid embolism.

Amniotic fluid embolism (AFE) is a rare but catastrophic obstetric complication that can lead to profound coagulopathy and hemorrhage. The role of cell salvage and recombinant human Factor VIIa (rFVIIa) administration in such cases remains unclear. We present a case of AFE and describe our experience with the use of cell salvage and rFVIIa administration during the resuscitation. Cell salvage and transfusion through a leukocyte depletion filter was attempted after the diagnosis of AFE was made, but the attempted transfusion was immediately followed by hypotension and a worsening of hemodynamics. rFVIIa, on the contrary, was used with clinical improvement in coagulopathy and without apparent adverse thrombotic effect.

Cardiac magnetic resonance imaging in a patient with amniotic fluid embolism associated with severe cardiopulmonary complications.

Amniotic fluid embolism (AFE) is a rare but devastating complication of pregnancy. Acute circulatory failure and obstetric disseminated intravascular coagulopathy are often associated with AFE and lead to poor prognosis of this syndrome. Although many reports of AFE and its cardiopulmonary complications exist, their etiology remains unknown. Classically, it was believed that the fatal cardiopulmonary complication in AFE is due to acute and severe pulmonary hypertension caused by critical obstruction of the pulmonary vessels by embolized amniotic fluid. However, recent hypotheses are suggesting that anaphylactic reaction or a cytokine effect induced by amniotic fluid is the main pathophysiological mechanism. We report a case in which cardiac magnetic resonance imaging was performed at the chronic stage of AFE. Late gadolinium enhancement (LGE) was detected at the mid-wall of the left ventricle with no evidence of pulmonary hypertension. This finding suggests that the pathophysiological mechanism of severe cardiac complications in AFE may include direct left ventricular myocardial injury through an immune reaction or cytokine release, rather than pulmonary embolism.

Amniotic fluid embolism: incidence, risk factors, and impact on perinatal outcome.

OBJECTIVE: To extend our previous work on AFE in Canada by including stricter criteria for case identification and by examining risks for stillbirth, neonatal mortality and serious maternal and neonatal morbidity. DESIGN: Population-based cohort study. SETTING: Canada. POPULATION OR SAMPLE: In all, 4,508,462 hospital deliveries from fiscal year 1991/92 to 2008/09. METHODS: To reduce false-positive diagnoses, we restricted our analysis to AFE cases with cardiac arrest, shock or severe hypertension, respiratory distress, mechanical ventilation, coma, seizure, or coagulation disorder. Linkage of maternal and neonatal records, available since 2001/02, enabled us to examine the effects of AFE on neonatal outcomes. Detailed demographic and clinical data facilitated control for a broad array of potential confounding variables. MAIN OUTCOME MEASURES: Amniotic fluid embolism, in-hospital neonatal death, asphyxia, mechanical ventilation, bacterial sepsis, seizure, nonimmune haemolytic or traumatic jaundice and length of hospital stay. RESULTS: A total of 292 AFE cases were identified, of which only 120 (40%) were confirmed after applying our additional diagnostic criteria, yielding an AFE incidence of 2.5 per 100,000 deliveries. Of the 120 confirmed cases, 33 (27%) were fatal. Significant modifiable risk factors included medical induction, caesarean delivery, instrumental vaginal delivery, and uterine or cervical trauma. Amniotic fluid embolism was associated with significantly increased risks of stillbirth and neonatal asphyxia, mechanical ventilation, sepsis, seizures and prolonged length of hospital stay. CONCLUSIONS: Amniotic fluid embolism remains a rare but serious obstetric outcome, with several important modifiable risk factors and major implications for maternal, fetal and neonatal health.

Current concepts of immunology and diagnosis in amniotic fluid embolism.

Amniotic fluid embolism (AFE) is one of the leading causes of maternal mortality and morbidity in developed countries. Current thinking about pathophysiology has shifted away from embolism toward a maternal immune response to the fetus. Two immunologic mechanisms have been studied to date. Anaphylaxis appears to be doubtful while the available evidence supports a role for complement activation. With the mechanism remaining to be elucidated, AFE remains a clinical diagnosis. It is diagnosed based on one or more of four key signs/symptoms: cardiovascular collapse, respiratory distress, coagulopathy, and/or coma/seizures. The only laboratory test that reliably supports the diagnosis is the finding of fetal material in the maternal pulmonary circulation at autopsy. Perhaps the most compelling mystery surrounding AFE is not why one in 20,000 parturients are afflicted, but rather how the vast majority of women can tolerate the foreign antigenic presence of their fetus both within their uterus and circulation?

Severe maternal morbidity and mortality from amniotic fluid embolism in the Netherlands.

We have assessed the incidence, symptoms and risk factors of amniotic fluid embolism in the Netherlands. Data were retrieved from two nationwide registration systems. From 1983 to 2005 the maternal mortality ratio of amniotic fluid embolism increased from 0.11 to 0.63 (odds ratio (OR) 5.8, 95% confidence interval (CI) 1.3-25.3). The most common signs and symptoms of amniotic fluid embolism were dyspnea and massive obstetric hemorrhage. In the majority of women, onset of symptoms was intrapartum or immediately postpartum. Potential risk factors of developing amniotic fluid embolism were maternal age >30, multiparity (OR 3.3, 95% CI 1.02-10.5), cesarean section (OR 1.3, 95% CI 0.3-5.2) and induction of labor (OR 2.1, 95% CI 2.1-6.1). Perinatal mortality was increased to 38.1% compared with 0.98% in the general pregnant population (p < 0.001) High maternal age and multiparity are the most important risk factors for developing amniotic fluid embolism.