Amniotic fluid embolism

Abstract

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%.

Sudden maternal hypoxemia during elective cesarean section in a woman with placenta previa

“…As trigger(s) of smooth muscle constriction were not specified in this patient, differential diagnoses included mild AFE and mild anaphylaxis against undetermined substance(s) given during cesarean section. However, mild AFE was the most likely diagnosis based on circumstantial evidence, including scheduled cesarean section for placenta previa under latex-free conditions (the usual procedure in our institution) and timing of the episode, that is, 45 min after childbirth; the former is a well-known risk factor for AFE [9][10][11][12][13], and the latter is a well-known danger period for the occurrence of AFE [2]. In addition, this patient coughed preceding the event, and coughing is listed as a clinical sign of AFE [12].…”

“…Risk factors for AFE include cesarean section with or without labor and placenta previa [9][10][11][12][13]; for example, women with cesarean section without labor and those with placenta previa were reported to have 8.1-fold and 10.5-fold higher risks of AFE, respectively, compared to those without the respective characteristics in New South Wales, Australia [13]. Here, we describe a woman that experienced dry cough with a subsequent gradual decrease in blood pressure prior to a sudden fall in PaO 2 45 min after childbirth with scheduled cesarean section for placenta previa at term.…”

Amniotic Fluid Embolism Treated with Veno-Arterial Extracorporeal Membrane Oxygenation

“…AFE requires an influx of fetal components (platelet activating factor, phospholipase A2, thromboplastin, endothelin and prostaglandins) which have vasoactive and pro-coagulant properties. e late phase of the disease process is mediated by tissue factor found in amniotic fluid, which binds to Factor VII to activate the extrinsic coagulation cascade leading to DIC and severe hemorrhage [8].…”

“…e most common presenting signs and symptoms include hypotension (100%), hypoxia, altered mental status/encephalopathy, tonic-clonic seizures (10-50%), uterine atony, and DIC (83%) [8]. Four criteria must be present for diagnosis of AFE: (1) acute hypotension or cardiac arrest, (2) acute hypoxia, (3) coagulopathy or severe hemorrhage in the absence of other explanations, (4) all of these occurring during labor, cesarean delivery, dilation and evacuation, or within 30 minutes postpartum with no other explanation of findings [8].…”

Effective Management Of Patients With Amniotic Fluid Embolism In The Intensive Care Unit: Two Case Reports

“…This method includes the blood centrifugation for 10 min at 2000 RPM, washing the precipitate with saline, coating and the use of specific stains. The findings are usually positive until the third day of the invasion of the syndrome [11]. We did not have the relevant experience of death and so the diagnosis was based on standard combination of clinical and laboratory findings.…”