Pathophysiology Of Amniotic Fluid Embolism Research Articles

Echocardiography Findings in Amniotic Fluid Embolism: A Systematic Review of the Literature

(Can J Anesth/J Can Anesth. 2023;70:151–160) Amniotic fluid embolism (AFE) is a rare obstetric complication with a mortality rate ranging 20% to 60%. The pathophysiology of AFE is not well-defined. This study aimed to define the echocardiography findings in patients who suffer from AFE.

Mechanism and clinical characteristics in diagnosis and treatment of amniotic fluid embolism

Amniotic fluid embolism(AFE) is a fatal intrapartum complication. Typical AFE is characterized by respiratory and circulatory failure, followed by disseminated intravascular coagulation(DIC), while atypical AFE, which had a higher survival possibility, presents with unexplained DIC only. Recent findings support an anaphylactoid inflammatory mechanism underlying the pathophysiology of AFE. Milrinone is currently the first choice for AFE due to its several functions, such as reducing pulmonary artery pressure, and improving right ventricular function through lowering heart rate and positive inotropic action. A multidisciplinary team is required in the rescue of AFE and medical staff who are skilled in critical medicine (such as anesthesiologists) often play a pivotal role. Key words: Embolism, amniotic fluid; Mastocytosis; Hypersensitivity

842: Role of inflammation in uterine isthmus leading to uterine atony: pathophysiology of Amniotic Fluid Embolism.

842: Role of inflammation in uterine isthmus leading to uterine atony: pathophysiology of Amniotic Fluid Embolism.

Amniotic fluid embolism

Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse. Etiology largely remains unknown, but may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, or during the second trimester of pregnancy. It may also occur up to 48 hours post-delivery. It can also occur during abortion, after abdominal trauma, and during amnio-infusion. The pathophysiology of AFE is not completely understood. Possible historical cause is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The presenting signs and symptoms of AFE involve many organ systems. Clinical signs and symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc. Besides basic investigations lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialyl Tn etc are helpful in establishing the diagnosis. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.

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/AimIt 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 methodsThe 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). ResultsAll ACS components were detected in AF; their levels were higher in AF than in the maternal plasma: FXII - 29.17ng/mg protein vs. 0.94ng/mg protein (medians); FXI - 27.28ng/mg protein vs. 0.92ng/mg protein (medians); PK - 88442.04ng/mg protein vs. 113.44ng/mg protein (medians); HMWK - 4253.82ng/mg protein vs. 2857.96ng/mg protein (medians). The concentration of TF in amniotic fluid was 39.46pg/mg protein (median) vs. 0.41pg/mg protein (median) in blood plasma. Conclusions1.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: antepartum, intrapartum and demographic factors

Objective: To describe the incidence, antepartum, intrapartum and postpartum risk factors, and mortality rate of amniotic fluid embolism (AFE).Methods: We used 2001–2007 California health discharge data to identify cases of AFE by ICD-9 codes.Results: Of 3 556 567 deliveries during the time period, we identified 182 cases of AFE, resulting in a population incidence of 5.1 in 100 000. Twenty-four of the cases resulted in death, giving a case fatality rate of 13.2%. Non-Hispanic blacks had a higher than 2-fold odds of developing AFE. AFE increased significantly with maternal age, most significantly after age 39. Cardiac disease had a nearly 70-fold higher association with AFE, cerebrovascular disorders had a 25-fold higher association, while conditions such as eclampsia, renal disease, placenta previa and polyhydramnios had nearly 7- to 13-fold higher associations. Classical cesarean delivery, abruption placentae, dilation and curettage, and amnioinfusion were all procedures highly associated with AFE.Conclusion: Several antepartum and peripartum conditions and procedures are associated with significantly higher risks of amniotic fluid embolism. This information may contribute to a better understanding of the pathophysiology of AFE and potentially help identify those at the highest risk of developing this morbid condition.

An Overview of Amniotic Fluid Embolism: Past, Present and Future Directions

Objective: A recent report has highlighted that amniotic fluid embolism (AFE) is the first among maternal mor- tality in Japan. The clinical presentation is not the same with respect to symptoms, timing and subsequent course. Methods: This article reviews the English language literature for pathophysiology on AFE based on the clinical and ani- mal studies. Results: First, AFE syndrome may be divided into three subgroups designated the classical subtype, the anaphylactoid subtype and the DIC subtype, each having a distinct pattern of clinical symptoms and disease severity. Second, AFE- associated reactions can be classified as an anaphylactoid reaction or complement activation to fetal antigens or an idio- syncratic reaction. Host idiosyncrasy may be a major cause of hypersensitivity reaction. Third, the AFE reaction may be caused by a combination of immunologic and vasospastic factors. Finally, the development of effective markers for diag- nosing entry of amniotic fluid into the maternal circulation would have an impact on early diagnosis and AFE-related mortality. Conclusion: This review summarizes new insights into the pathophysiology of AFE, with a focus on the potential direc- tion of future research. Keyword: Amniotic fluid embolism, Anaphylactoid, Hypersensitivity, Meconium, Vasospasm.

Intralipid for Amniotic Fluid Embolism (AFE)?

In 1998 it was first showed that intravenous Intralipid could prevent or improve resuscitation from cardiovascular collapse by severe bupivacaine overdose in rats. Since then published examples now include toxicities related to verapamil, diltiazem, amlodipine, quetiapine and sertraline, haldoperidol, lamotrigine, olanzapine, propranolol, atenolol, nevibolol, doxepin, dosulepin, imipramine, amitriptyline, glyosphate herbicide, flecainide, venlafaxine, moxidectin, and others. Amniotic fluid embolism (AFE) is a rare but potentially catastrophic obstetric emergency. Despite earlier recognition and aggressive treatment, morbidity and mortality rates remain high. An estimated 5% - 15% of all maternal deaths in Western countries are due to AFE. The pathophysiology of AFE is not completely understood. AFE most commonly occurs during labor, delivery, or the immediate postpartum period. However, it has been reported to occur up to 48 h postpartum. Pulmonary hypertension and right heart strain/failure may be the result of physical amniotic fluid debris in the pulmonary vasculature or, perhaps more likely, result from circulating pulmonary vasoconstrictive mediators. Therapy with Intralipid in male rats resulted in 100% survival and prevented Pulmonary arterial hypertension-induced right ventricular failure by preserving right ventricular pressure and right ventricular ejection fraction and preventing right ventricular hypertrophy and lung remodeling. In preexisting severe Pulmonary arterial hypertension, Intralipid attenu-ated most lung and right ventricular abnormalities. The beneficial effects of Intralipid in Pulmonary arterial hypertension seem to result from the interplay of various factors, among which preservation and/or stimulation of angiogenesis, suppression and/or reversal of inflammation, fibrosis and hypertrophy, in both lung and right ventricular, appear to be major contributors. In conclusion, Intralipid not only prevents the development of Pulmonary arterial hypertension and right ventricular failure but also rescues preexisting severe Pulmonary arterial hypertension. Intralipid treatment is a new treatment for AFE (amniotic fluid embolism) which was never suggested before. Animal studies should be done in order to evaluate this new treatment modality.

Paradoxical Embolization by Amniotic Fluid Seen on the Transesophageal Echocardiography

Paradoxical Embolization by Amniotic Fluid Seen on the Transesophageal Echocardiography

The syndrome of amniotic fluid embolism: A potential contribution of bradykinin

Amniotic fluid embolism is a potentially fatal complication of pregnancy; although several hypotheses have been formulated, the pathophysiology of this condition is not well known. An exaggerated release of bradykinin, which is activated by products of the amniotic fluid that enter the maternal circulation, could explain the symptoms that are present in amniotic fluid embolism. The objective of this study was to assess whether bradykinin is involved in amniotic fluid embolism. The plasma bradykinin-generating capacity was measured serially in a patient who experienced amniotic fluid embolism. The plasma bradykinin-generating capacity was found to be very low at the time of the initial clinical manifestations, which were characterized by severe hypotension, cardiorespiratory arrest, and coagulopathy. This study suggests a potential role for bradykinin release in the pathophysiology of amniotic fluid embolism.

Amniotic fluid embolism as cause of death in a car accident—a case report

Amniotic fluid embolism (AFE), a relatively rare complication in pregnancy, has a high mortality rate. We describe a case of a 38-week pregnant woman with such an embolism leading to almost immediate death after a blunt abdominal trauma inflicted in a motor vehicle accident and probably associated with improper positioning of a seat belt. It has been assumed that the pathophysiology of amniotic fluid embolism is related to an anaphylactoid reaction and that mast cell degranulation indicates this mechanism. Moreover, immunohistochemical antitryptase staining of pulmonary tissue samples in our case revealed mast cell degranulation.

Amniotic Fluid Embolism: Early Findings of Transesophageal Echocardiography

Amniotic Fluid Embolism: Early Findings of Transesophageal Echocardiography

AMNIOTIC FLUID EMBOLISM

Amniotic fluid embolism occurs rarely but is one of the leading causes of maternal mortality in the United States. The risk of death associated with this syndrome is 60% to 80% with half of survivors suffering long-term neurologic disability. The pathophysiology of amniotic fluid embolism is poorly understood. A review of the largest case series to date concluded that the physiologic and hematologic manifestations bear a greater resemblance to septic and anaphylactic shock than to any embolic phenomenon. Care of the patient who suffers amniotic fluid embolism is supportive. To date, no therapeutic interventions have been found to improve survival.

Delayed amniotic fluid embolism following Caesarean section under spinal anaesthesia

A case of amniotic fluid embolus is described with an acute onset occurring 90 min after surgical delivery in a mildly pre-eclamptic primigravida undergoing Caesarean section for a breech presentation. Severe disseminated intravascular coagulation and massive postpartum haemorrhage were corrected and she went on to make a full recovery. The pathophysiology of amniotic fluid embolism is discussed and new diagnostic tests are reviewed. It is suggested that in this patient an amniotic fluid collection in dilated uterine veins was mobilised as venous tone returned following the offset of spinal anaesthesia and sympathetic blockade.

Arachidonic Acid Metabolites and the Pathophysiology of Amniotic Fluid Embolism

Arachidonic Acid Metabolites and the Pathophysiology of Amniotic Fluid Embolism