[Maternal mortality due to Amniotic Fluid Embolism in France 2016-2018]. / Mortalité maternelle par embolie amniotique en France 2016­2018.

Amniotic embolism remains the 3rd leading cause of maternal death in France, with 21 maternal deaths over the 2016-2018 triennium. The women who died were more likely to be obese (25%), to benefit from induction of labor (71%) and be cared in a maternity hospital <1500 deliveries/year (45%), compared with the reference population (ENP 2016). The symptom occurred mainly during labor (95%) and the course was rapid, with a symptom-to-fatality interval of 4hours 45minutes (min: 25minutes - max: 8 days). Preventability was proposed for 35% of the deaths assessed, with areas for improvement identified in terms of technical skills (haemostasis procedures, management of polytransfusion), non-technical skills (communication) and health care organization (human resources, vital emergency plan, wide access to PSL). An autopsy was performed in 38% of deaths.

Current concepts in the use of cell salvage in obstetrics.

PURPOSE OF REVIEW: The worldwide leading cause of maternal death is severe maternal hemorrhage. Maternal hemorrhage can be profound leading to an entire loss of blood volume. In the past two decades, Patient Blood Management has evolved to improve patient's care and safety. In surgeries with increased blood loss exceeding 500 ml, the use of cell salvage is strongly recommended in order to preserve the patient's own blood volume and to minimize the need for allogeneic red blood cell (RBC) transfusion. In this review, recent evidence and controversies of the use of cell salvage in obstetrics are discussed. RECENT FINDINGS: Numerous medical societies as well as national and international guidelines recommend the use of cell salvage during maternal hemorrhage. SUMMARY: Intraoperative cell salvage is a strategy to maintain the patient's own blood volume and decrease the need for allogeneic RBC transfusion. Historically, cell salvage has been avoided in the obstetric population due to concerns of iatrogenic amniotic fluid embolism (AFE) or induction of maternal alloimmunization. However, no definite case of AFE has been reported so far. Cell salvage is strongly recommended and cost-effective in patients with predictably high rates of blood loss and RBC transfusion, such as women with placenta accreta spectrum disorder. However, in order to ensure sufficient practical experience in a multiprofessional obstetric setting, liberal use of cell salvage appears advisable.

Comparative analysis of hyperfibrinolysis with activated coagulation between amniotic fluid embolism and severe placental abruption.

Amniotic fluid embolism (AFE) and placental abruption (PA) are typical obstetric diseases associated with disseminated intravascular coagulation (DIC). AFE is more likely to be complicated with enhanced fibrinolysis than PA. AFE may have an additional mechanism activating fibrinolytic cascade. We aimed to compare the coagulation/fibrinolysis factors among AFE, PA, and peripartum controls. We assessed AFE cases registered in the Japanese AFE Registry, and PA cases complicated with DIC (severe PA) and peripartum controls recruited at our hospital. The following factors in plasma were compared: prothrombin fragment 1 + 2 (PF1 + 2), plasmin α2-plasmin inhibitor complex (PIC), tissue factor (TF), tissue plasminogen activator (tPA), annexin A2 (AnnA2), total thrombin activatable fibrinolysis inhibitor (TAFI) including its activated form (TAFIa), and plasminogen activator inhibitor-type 1 (PAI-1). PF1 + 2 and PIC were markedly increased in both AFE (n = 27) and severe PA (n = 12) compared to controls (n = 23), without significant difference between those disease groups; however, PIC in AFE showed a tendency to elevate relative to PF1 + 2, compared with severe PA. AFE had significantly increased tPA and decreased total TAFI levels compared with severe PA and controls, which might be associated with further plasmin production in AFE and underlie its specific fibrinolytic activation pathway.

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.

Amniotic fluid embolism: a reappraisal.

OBJECTIVES: Using cases from our own experience and from the published literature on amniotic fluid embolism (AFE), we seek to improve on existing criteria for diagnosis and discern associated risk factors. Additionally, we propose a novel theory of pathophysiology. METHODS: This retrospective case review includes eight cases of AFE from two hospital systems and 21 from the published literature. All cases were evaluated using the modified criteria for research reporting of AFE by Clark et al. in Am J Obstet Gynecol, 2016;215:408-12 as well as our proposed criteria for diagnosis. Additional clinical and demographic characteristics potentially correlated with a risk of AFE were included and analyzed using descriptive analysis. RESULTS: The incidence of AFE was 2.9 per 100,000 births, with five maternal deaths in 29 cases (17.2 %) in our series. None of the cases met Clark's criteria while all met our criteria. 62.1 % of patients were over the age of 32 years and two out of 29 women (6.9 %) conceived through in-vitro fertilization. 6.5 % of cases were complicated by fetal death. Placenta previa occurred in 13.8 %. 86.2 % of women had cesarean sections of which 52.0 % had no acute maternal indication. CONCLUSIONS: Our criteria identify more patients with AFE than others with a low likelihood of false positives. Clinical and demographic associations in our review are consistent with those previously reported. A possible relationship between cesarean birth and risk of AFE was identified using our criteria. Additionally, we propose a new hypothesis of pathophysiology.

Extracorporeal Cardiopulmonary Resuscitation for Amniotic Fluid Embolism: Review and Case Report.

ABSTRACT: Amniotic fluid embolism (AFE) is a rare, sudden, and catastrophic complication of pregnancy that can result in cardiopulmonary arrest, potentially leading to death. The pathophysiology of an AFE includes an inflammatory and coagulopathic response due to fetal materials entering maternal circulation with the hallmark triad of symptoms: acute respiratory distress, cardiovascular collapse, and coagulopathy. Management of AFE should include high-quality cardiopulmonary resuscitation, immediate delivery of the fetus if applicable, early intubation to provide adequate oxygenation and ventilation, fluid volume resuscitation, and ongoing evaluation of coagulopathy. Priorities include thromoboelastography interpretation if available, control of hemorrhage and coagulopathy with blood component therapy, and cardiovascular support through inotropes and vasopressor administration. More recent approaches include implementing the A-OK (atropine, ondansetron, and ketorolac) protocol for suspected AFE protocol, extracorporeal cardiopulmonary resuscitation (ECPR), and extracorporeal membrane oxygenation (ECMO) therapies to increase survival and decrease complications. Venoarterial ECMO is the highest form of life support that provides support in patients with pulmonary and cardiac failure. ECPR is the application of Venoarterial ECMO during cardiopulmonary resuscitation in cases where the cause of arrest is believed to be reversible. Early implementation of ECPR during the acute phase of AFE can provide support for end-organ perfusion in place of the weakened and recovering heart while optimizing oxygenation, making venoarterial ECMO an ideal adjunctive therapy. Because of the rarity of AFE, many obstetrical teams may have limited prior experience in managing these catastrophic cases; however, with ongoing education and simulation, teams can be better prepared in the recognition and management of these life-threatening events.

Use of cell salvage at the time of cesarean delivery: a meta-analysis of randomized controlled trials.

OBJECTIVE: Excess blood loss from obstetrical hemorrhage requires transfusion of donor blood, a finite resource. Intraoperative cell salvage collects a patient's own blood that has been lost during cesarean delivery and returns it to their own circulation. We performed a meta-analysis to examine the perioperative outcomes in patients receiving cell salvage at the time of cesarean delivery. DATA SOURCES: Scopus, PubMed, Cochrane Central Register of Controlled Trials, Ovid Medline, and clinicaltrials.gov were searched from database inception through October 2023. STUDY ELIGIBILITY CRITERIA: Eligible studies included randomized controlled trials comparing the use of cell salvage to standard-of-care during cesarean delivery. METHODS: Two authors independently extracted data. Preferred Reporting Items of Systematic Reviews and Meta-Analysis guidelines were used for data extraction and quality assessment. The primary outcomes were the rate of donor blood transfusion and change in hemoglobin level. The secondary outcomes included transfusion reaction, amniotic fluid embolism, and length of hospital stay. Results were summarized as weighted mean difference or risk ratio with associated 95% confidence intervals. Heterogeneity was measured using Higgins I2. RESULTS: A total of 5 randomized controlled trials (n=3361) comparing cell salvage to standard care during cesarean delivery met the inclusion criteria. Primary analysis showed a significant decrease in receiving allogeneic blood transfusion with intraoperative cell salvage use vs standard care (odds ratio, 0.32; 95% confidence interval, 0.23-0.46), with no change in hemoglobin drop (mean difference, -0.77; 95% confidence interval, -1.67 to -0.14). The secondary outcomes showed no difference in transfusion reaction (odds ratio, 0.56; 95% confidence interval, 0.06-5.59), and length of hospital stay (mean difference, -1.90; 95% confidence interval, -4.85 to 1.06). No cases of amniotic fluid embolism were reported among the 1685 patients who received cell salvage. CONCLUSION: Use of cell salvage during cesarean delivery reduced the overall need for allogeneic blood transfusion without increasing the risk of complications, including no cases of amniotic fluid embolism.

Confusion in the monitoring of coagulation function in pregnant and neonate patients with severe disease: A case reports and brief literature review.

RATIONALE: Different populations have their own unique physiological and pathological characteristics. However, in specialized maternal and child hospitals, there is currently a lack of standardized methods for assessing coagulation dysfunction, both domestically and internationally. PATIENT CONCERNS: A 19-day-old neonate was transferred to neonatal intensive care unit with cyanosis, nasal bleeding for 6 hours, and a consciousness disorder for 5 hours. A 33-year-old woman presented with hydramnios and a 39 + 3week intrauterine pregnancy. All indicators before delivery were normal, but postpartum hemorrhage occurred after delivery. DIAGNOSES: We retrospectively analyzed 1 neonate with pulmonary hemorrhage accompanied by thrombocytopenia and 1 pregnant patient with amniotic fluid embolism. INTERVENTIONS: The new coagulation indicators, such as thrombin-antithrombin complex, plasmin-alpha 2 antiplasmin complex, thrombomodulin, and tissue plasminogen activator-plasminogen activator inhibitor-1 complex, have been indicated to be valuable. In neonates, it is necessary to continuously monitor special items combined with specific therapeutic agents, such as tranexamic acid. In cases where postpartum hemorrhage occurs with low fibrinogen levels, it is essential to effectively identify patients with severe amniotic fluid embolism from a high incidence of specimen clotting. OUTCOMES: The neonate's oxygen saturation stabilized, and after 5 days of treatment with low molecular weight heparin, thrombin-antithrombin complex and plasmin-alpha 2 antiplasmin complex returned to normal levels. The pregnant began to remove the remaining thrombus, the patient's condition recovered, and she had a good prognosis. LESSONS: For pregnant and neonatal critical illnesses, it is necessary to develop personalized coagulation monitoring programs that provide realistic and reasonable treatment recommendations. Such programs should consider the unique physiological and pathological characteristics of different populations to ensure effective management of critically ill patients.

Amniotic fluid embolism: A case report of good outcome with timely intensive multidisciplinary team involvement.

OBJECTIVE: Amniotic fluid embolism is one of the most serious pregnancy complications. It can cause sudden maternal collapse with high mortality and morbidity. We present a case report regarding the important of prompt decision making and multidisciplinary team work for management of amniotic fluid embolism to yield favorable maternal and neonatal outcome. CASE REPORT: This is a 35-year-old, gravida 2, para 1, woman underwent labor induction at gestational age of 37 + 6 weeks due to elective induction. She had sudden facial cyanosis and shortness of breath right after artificial rupture of membrane. Prompt decision of urgent cesarean section, aggressive and timely massive blood transfusion and multidisciplinary team work had spared patient from extracorporeal membrane oxygenation placement and prolonged hospitalization. A male infant was born with Apgar score 3' -> 5' with estimate body weight of 2958 gm; he was hospitalized for 10 days and no other complications was found at follow up pediatric outpatient clinic. CONCLUSION: One of the most dreadful, but rare pregnancy complications is amniotic fluid embolism (AFE). It can cause serious maternal and neonatal morbidity and mortality. Rapid recognition and multidisciplinary team management are essential to maternal and neonatal prognosis.

Massive platelet-rich thrombus formation in small pulmonary vessels in amniotic fluid embolism: An autopsy study.

OBJECTIVE: To identify pulmonary/uterine thrombus formation in amniotic fluid embolism (AFE). DESIGN: Retrospective, observational. SETTING: Nationwide. POPULATION: Eleven autopsy cases of AFE and control cases. METHODS: We assessed pulmonary and uterine thrombus formation and thrombus area in AFE and pulmonary thromboembolism (PTE) as a control. The area of platelet glycoprotein IIb/IIIa, fibrin, neutrophil elastase, citrullinated histone H3 (a neutrophil extracellular trap marker) and mast cell chymase immunopositivity was measured in 90 pulmonary emboli, 15 uterine thrombi and 14 PTE. MAIN OUTCOME MEASURES: Pathological evidence of thrombus formation and its components in AFE. RESULTS: Amniotic fluid embolism lung showed massive thrombus formation, with or without amniotic emboli in small pulmonary arteries and capillaries. The median pulmonary thrombus size in AFE (median, 0.012 mm2 ; P < 0.0001) was significantly smaller than that of uterine thrombus in AFE (0.61 mm2 ) or PTE (29 mm2 ). The median area of glycoprotein IIb/IIIa immunopositivity in pulmonary thrombi in AFE (39%; P < 0.01) was significantly larger than that of uterine thrombi in AFE (23%) and PTE (15%). The median area of fibrin (0%; P < 0.001) and citrullinated histone H3 (0%; P < 0.01) immunopositivity in pulmonary thrombi in AFE was significantly smaller than in uterine thrombi (fibrin: 26%; citrullinated histone H3: 1.1%) and PTE (fibrin: 42%; citrullinated histone H3: 0.4%). No mast cells were identified in pulmonary thrombi. CONCLUSIONS: Amniotic fluid may induce distinct thrombus formation in the uterus and lung. Pulmonary and uterine thrombi formation may contribute to cardiorespiratory collapse and/or consumptive coagulopathy in AFE.

Amniotic fluid embolism: A comparison of two classification systems in a retrospective 8-year analysis from two tertiary hospitals.

OBJECTIVE: Amniotic fluid embolism (AFE) is a rare life-threatening complication in obstetrics, but the diagnosis lacks a consensual definition. The objective of this study was to compare two different AFE classification systems by analysing the AFE cases from two university hospitals. MATERIAL AND METHODS: In this retrospective study, all patients with a strong suspicion of AFE between 2014 and 2021 at two university hospitals, LMU Women's University Hospital Munich, and Women's University Hospital Basel, were included. Patient records were checked for the ICD-10 code O88.1 (AFE). Diagnoses were confirmed through clinical findings and/or autopsy. The presence of the diagnostic criteria of the Society of Maternal foetal Medicine (SMFM) and the AFE Foundation (AFEF) and of a new framework by Ponzio-Klijanienko et al. from Paris, France, were checked and compared using Chi-square-test. RESULTS: Within our study period, 38,934 women delivered in the two hospitals. Six patients had a strong suspicion of AFE (0.015%). Only three of six patients (50%) presented with all the four diagnostic criteria of the SMFM/AFEF framework. All six patients met the criteria of the modified "Paris AFE framework". CONCLUSION: Using the "Paris AFE framework" based exclusively on clinical criteria can help clinicians to diagnose AFE, anticipate the life-threatening condition of the patient and prepare immediately for best clinical care.

Acute obstetric coagulopathy during postpartum hemorrhage is caused by hyperfibrinolysis and dysfibrinogenemia: an observational cohort study.

BACKGROUND: Postpartum hemorrhage (PPH) may be exacerbated by hemostatic impairment. Information about PPH-associated coagulopathy is limited, often resulting in treatment strategies based on data derived from trauma studies. OBJECTIVES: To investigate hemostatic changes associated with PPH. PATIENTS/METHODS: From a population of 11 279 maternities, 518 (4.6%) women were recruited with PPH ≥ 1000 mL or placental abruption, amniotic fluid embolism, or concealed bleeding. Routine coagulation and viscoelastometric results were collated. Stored plasma samples were used to investigate women with bleeds > 2000 mL or those at increased risk of coagulopathy defined as placenta abruption, amniotic fluid embolism, or need for blood components. Procoagulant factors were assayed and global hemostasis was assessed using thrombin generation. Fibrinolysis was investigated with D-dimer and plasmin/antiplasmin complexes. Dysfibrinogenemia was assessed using the Clauss/antigen ratio. RESULTS: At 1000 mL blood loss, Clauss fibrinogen was ≤2 g/L in 2.4% of women and 6/27 (22.2%) cases of abruption. Women with very large bleeds (>3000 mL) had evidence of a dilutional coagulopathy, although hemostatic impairment was uncommon. A subgroup of 12 women (1.06/1000 maternities) had a distinct coagulopathy characterized by massive fibrinolysis (plasmin/antiplasmin > 40 000 ng/mL), increased D-dimer, hypofibrinogenemia, dysfibrinogenemia, reduced factor V and factor VIII, and increased activated protein C, termed acute obstetric coagulopathy. It was associated with fetal or neonatal death in 50% of cases and increased maternal morbidity. CONCLUSIONS: Clinically significant hemostatic impairment is uncommon during PPH, but a subgroup of women have a distinct and severe coagulopathy characterized by hyperfibrinolysis, low fibrinogen, and dysfibrinogenemia associated with poor fetal outcomes.

Fatal amniotic fluid embolism: incidence, risk factors and influence on perinatal outcome.

PURPOSE: This study aimed to estimate the incidence of fatal amniotic fluid embolism, describe its risk factors, and analyze perinatal outcomes. METHODS: Maternity cases and newborn records of amniotic fluid embolism were collected from the Zhejiang Maternal Surveillance System from October 2006 to October 2019. This study strictly limited the diagnostic criteria for AFE and excluded suspicious cases in order to minimize false-positive AFE cases. The risk factors of fatal amniotic fluid embolism and the relationship between perinatal prognosis and AFE were investigated using logistic regression analysis, estimating the adjusted odds ratios (aORs) and 95% confidence intervals (CIs). RESULTS: 149 cases of amniotic fluid embolism were registered, of which 80 cases were fatal. The estimated fatal AFE incidence was 0.99 per 100,000. The occurrence of fatal AFE was significantly correlated with spontaneous vaginal delivery (aOR 12.3, 95% CI 3.3-39.2) and cardiac arrest (aOR 64.8, 95% CI 14.6-287.8). The average diagnosis time of fatal AFE is 85.51 min, and the peak period of female death is 1-12 h after the onset of the disease, accounting for 60% (48/80) of cases. Fatal amniotic embolism is a cause of intrauterine fetal death and fetal death during delivery (aOR 11.957, 95% CI 1.457-96.919; aOR 13.152, 95% CI 1.636-105.723). Of the 149 confirmed AFE cases, 11 cases of stillbirth occurred, 12 cases were stillborn, and 7 cases of neonatal death were reported. The perinatal mortality rate was 202 per 1000. CONCLUSIONS: Early detection, diagnosis, and treatment of amniotic fluid embolism are essential to avoiding fatal AFE. Clinicians should fully evaluate the pros and cons of choosing the delivery method for pregnant women. When cardiac arrest occurs in women with amniotic fluid embolism, obstetricians should be particularly careful and provide timely and effective treatment to minimize the fatality rate. The outcome of AFE is not only related to maternal survival but also plays a decisive role in the prognosis of the infant over the perinatal period.

Echocardiography findings in amniotic fluid embolism: a systematic review of the literature.

PURPOSE: Amniotic fluid embolism (AFE) is a leading cause of obstetrical cardiac arrest and maternal morbidity. The pathogenesis of hemodynamic collapse is thought to be from right ventricular (RV) failure; however, there is a paucity of data documenting echocardiography findings in this population. We undertook a systematic review of the literature to evaluate the echocardiography findings in patients with AFE. SOURCES: We retrieved all case reports and case series reporting AFE in Embase and MEDLINE from inception to 20 November 2021. Studies reporting AFE diagnosed by fulfilling at least one of three different proposed AFE criteria and echocardiography findings during hospitalization were included. Patient and echocardiographic data were retrieved, and univariate logistic regression analysis was performed for outcomes of interest. Bias was assessed using the Joanna Briggs Institute clinical appraisal tool for case series. PRINCIPAL FINDINGS: Eighty publications reporting on 84 patients were included in the final review. Fifty-five out of 82 patients with data (67%) showed RV dysfunction, including 11/82 (13%) with biventricular dysfunction; 14/82 (17%) had normal systolic function. No data on RV or left ventricular function were reported for two patients. The presence of RV dysfunction on echocardiography was associated with cardiac arrest (odds ratio [OR], 3.66; 95% confidence interval [CI], 1.39 to 9.67; P = 0.009), and a composite risk of cardiac arrest, maternal death or use of extracorporeal membrane oxygenation (OR, 3.86; 95% CI, 1.43 to 10.4; P = 0.007). A low risk of bias was observed in 15/84 (18%) cases. CONCLUSIONS: Right ventricular dysfunction on echocardiography is a common finding in AFE and is associated with a high risk of cardiac arrest. The finding of RV dysfunction on echocardiography may help diagnose AFE and help triage the highest risk patients with AFE. STUDY REGISTRATION: PROSPERO (CRD42021271323); registered 1 September 2021.

RéSUMé: OBJECTIF: L'embolie amniotique (EA) est l'une des principales causes d'arrêt cardiaque obstétrical et de morbidité maternelle. Il est présumé que la pathogenèse du choc hémodynamique provient d'une défaillance ventriculaire droite (VD). Cependant, il y a peu de données documentant les constatations de l'examen échocardiographique dans cette population. Nous avons effectué une revue systématique des données probantes visant à évaluer l'utilité de l'échocardiographie chez les patientes atteintes d'embolie amniotique. SOURCES: Nous avons évalué tous les rapports de cas et séries de cas rapportant une EA dans les bases de données Embase et MEDLINE de leur création jusqu'au 20 novembre 2021. Les études rapportant une EA diagnostiquée en remplissant au moins l'un des trois critères d'EA proposés et les résultats échocardiographiques pendant l'hospitalisation ont été incluses. Les données sur les patientes et échocardiographiques ont été colligées, et une analyse de régression logistique univariée a été effectuée pour les issues cliniques d'intérêt. Le risque de biais a été évalué à l'aide de l'outil d'évaluation clinique de l'Institut Joanna Briggs pour les séries de cas. CONSTATATIONS PRINCIPALES: Quatre-vingts publications incluant 84 patientes ont été incluses dans la revue finale. Cinquante-cinq des 82 patientes présentant des données (67 %) avaient une dysfonction du VD incluant 11/82 (13 %) avec une dysfonction biventriculaire. Quatorze patientes sur 82 (17 %) avaient une fonction systolique normale. Aucune donnée sur la fonction du ventricule droit ou gauche n'a été rapportée pour deux patientes. La présence d'une dysfonction du VD à l'échocardiographie était associée à un arrêt cardiaque (rapport de cotes [RC], 3,66; intervalle de confiance à 95 % [IC], 1,39 à 9,67; P = 0,009), et à un risque composite d'arrêt cardiaque, de décès maternel ou d'utilisation de l'oxygénation par membrane extracorporelle (ECMO) (RC, 3,86; IC 95 %, 1,43 à 10,4; P = 0,007). Un faible risque de biais a été observé dans 15/84 (18 %) des cas. CONCLUSION: La dysfonction ventriculaire droite à l'échocardiographie est une constatation courante dans l'embolie amniotique et est associée à un risque élevé d'arrêt cardiaque. La découverte d'une dysfonction du VD à l'échocardiographie peut aider à diagnostiquer l'embolie amniotique et à identifier les patientes atteintes d'embolie amniotique les plus à risque. ENREGISTREMENT DE L'éTUD: PROSPERO (CRD42021271323); enregistrée le 1er septembre 2021.

Amniotic fluid embolism-induced cardiopulmonary collapse successfully treated with combination VA-ECMO and Impella CP.

Amniotic fluid embolism (AFE) is a rare but potentially fatal complication of pregnancy. Prompt and aggressive resuscitative strategies are crucial in promoting survivability. We present a case of AFE resulting in cardiopulmonary collapse and subsequent cardiac arrest where we were able to safely deliver the baby and resuscitate the mother with veno-arterial extracorporeal membrane oxygenation and Impella CP-a novel combination known as ECPELLA. We discuss the implications of this approach as a more efficacious strategy in resuscitating AFE-induced cardiogenic shock and arrest.

Unexpected serum phosphorus lost in an amniotic fluid embolism patient.

BACKGROUND: Serum phosphorus concentration reflects body energy equilibrium and functions of the kidney and the coagulation system. It is regulated by serum calcium concentration and parathyroid hormone (PTH). CASE REPORT: We present a case of constant low concentrations of serum phosphorus in a 34-year-old female who was diagnosed with amniotic fluid embolism (AFE) and was continuously treated with extracorporeal membrane oxygenation (ECMO), continuous renal replacement therapy (CRRT) and blood component transfusion during an observational period of 11 days. CONCLUSION: This case highlights that the release of inorganic phosphorus from platelets and plasma into the blood prompts PTH secretion. The administration of active vitamin D supplement and PTH antagonism should be considered to neutralize the negative regulatory effect of PTH on serum phosphorus and to benefit patients' recovery in the intensive care unit.