The “Amniotic Fluid Embolism” Syndrome is a rare occurrence in obstetrics. Although it is rare, 80% of cases lead to mortality. Dr. Nguyen Cong Nghia, currently a PhD candidate in Reproductive Epidemiology at the University of North Carolina – Chapel Hill, USA, has written a special article for VietNamNet about this syndrome.
Amniotic Fluid Embolism is a very rare obstetric emergency. This syndrome occurs when amniotic fluid, fetal cells, air bubbles, pathogens, hair, or other fragments of fetal tissue enter the mother’s circulatory system, causing acute respiratory and circulatory failure.
This syndrome was first described by Meyer in 1926; however, clinical symptoms only drew the attention of obstetricians as late as 1941.
A thorough retrospective review of these cases was first conducted by Morgan in 1979. Since then, a national registry for this condition has been established in the United States.
The “Amniotic Fluid Embolism” syndrome occurs when amniotic fluid, fetal cells, air bubbles,
pathogens, hair, or other fragments of fetal tissue enter the mother’s circulatory system,
causing acute respiratory and circulatory failure. (Image: netterimages, VNN)
Rare, Difficult to Diagnose but Dangerous
The condition occurs at a very low frequency, about 1 case in 8,000 to 30,000 pregnancies. Only 3-4 cases are reported annually in the UK. However, the mortality rate for this condition is extremely high, approximately 80% of cases.
Due to the low number of cases, there is currently no clear evidence regarding risk factors. Nonetheless, previous views suggested that older mothers, those with multiple births, unusually rapid labor, large fetuses, or the use of uterotonics are associated with an increased risk for this condition.
Generally, amniotic fluid embolism occurs during labor, elective cesarean sections, but can also occur during abortion, infusion of amniotic fluid into the uterus, abdominal trauma, or even postpartum.
Experts consider this syndrome to be a form of “anaphylactic shock,” rather than merely a “vascular obstruction.” This is because it is believed that amniotic fluid and fetal cells entering the circulatory system trigger the mother’s anaphylactic response to antigens from the fetus.
However, there is a common misconception that the presence of fetal cells, such as epithelial or trophoblastic cells in the mother’s blood circulation (from the pulmonary artery), is a definitive diagnostic indicator. Data shows that these cells are often found in the blood circulation of those without this condition.
The presence of these cells is a question in suspected cases, but must be combined with the clinical picture of hemodynamic and respiratory disturbances to confirm the diagnosis.
Currently, experts are focusing on the breakdown of giant cells to release histamine and tryptase, while also activating a complex chain of other adverse reactions.
Intensive Care for Emergency Situations…
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| Examination of expectant mothers before childbirth. (Image: VNN) |
While awaiting further research results from experts, let us monitor the progression of this syndrome…
The pathological process typically occurs in two stages.
Stage 1 involves constriction of the pulmonary artery, elevated pulmonary arterial pressure, and acute right ventricular failure leading to hypoxemia. Hypoxemia causes destruction of myocardial and pulmonary capillaries, leading to left heart failure and acute respiratory syndrome.
Approximately 50% of cases that survive Stage 1 (lasting about 1 hour) will enter Stage 2, which is characterized by synchronous bleeding and disseminated intravascular coagulation.
The clinical picture appears rapidly with signs of acute shortness of breath, sometimes coughing, rapidly and suddenly dropping blood pressure, especially diastolic pressure, cyanosis around the mouth and extremities, potential cardiac arrest, or signs of acute pulmonary edema. In obstetric monitoring, fetal heart rate deceleration and late uterine bleeding may occur.
Differential diagnosis is necessary with many other syndromes such as thromboembolic obstruction, air embolism, septic shock, acute myocardial infarction, allergic shock due to other causes, placental abruption, or local anesthetic reactions.
Treatment is supportive rather than curative.
For this syndrome, the role of resuscitation staff and techniques is more crucial than that of obstetricians. In management, resuscitation specialists typically apply four main principles of treatment, including enhancing ventilation, improving oxygenation, supporting circulation, and correcting coagulopathy.
From an obstetric perspective, many authors recommend immediate cesarean delivery when possible, primarily to save the fetus, and subsequently to facilitate hemodynamic stabilization. During the cesarean section, it may be necessary to ligate both uterine arteries to control bleeding.
The treatment outcomes are low despite all these efforts. However, aggressive treatment can still offer hope for patient survival. For example, doctors at KK Women and Children Hospital reported two cases of patients surviving after intensive treatment in 2002. Detailed descriptions of their treatment can be found at http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijgo/vol1n2/amniotic.xml.
Current studies on this condition allow us to conclude that amniotic fluid embolism is a dangerous obstetric complication with a high mortality rate, unpredictable and unpreventable.
However, obstetricians must remain vigilant and provide aggressive treatment when it occurs to increase the chances of survival for both the mother and the fetus.
Dr. Nguyen Cong Nghia (PhD Candidate in Reproductive Epidemiology at the University of North Carolina – Chapel Hill)
