Supervisors info:
Νικόλαος Παπαντωνίου, Καθηγητής, Ιατρική, ΕΚΠΑ
Δημήτριος Κασσάνος, Καθηγητής, Ιατρική, ΕΚΠΑ
Χαράλαμπος Χρέλιας, Καθηγητής, Ιατρική, ΕΚΠΑ
Summary:
In normal situations, amniotic fluid is completely isolated from the maternal intravascular compartment. If an opening exists between the amniotic sac and uterine veins, amniotic fluid can be bolused into maternal circulation producing an embolism. Amniotic fluid emboli (AFE), may contain squamous cells, lanugo, vernix, mucin and meconium. Because of the anaphylaxis-like symptoms, some researchers believe AFE sould be more accurately termed “anaphylactoid syndrome of pregnancy”.
AFE only occurs when there is a breech in the barrier between amniotic fluid and maternal circulation. There are 3 routes where this may occur. They are through endocervical veins, uterine trauma sites and the placenta attachment site.
In the 70 years since AFE was first reported, it still remains a syndrome whose etiology is not clearly understood. The clinical manifestations of AFE have been described in numerous accounts. It was believed for years that when an amniotic fluid bolus was pumped into the maternal circulation, there was an intense showering of microscopic fetal debris particles that caused an acute occlusion of part of the mother’s pulmonary microvasculature. The sudden respiratory distress and cyanosis were thought to be related to right-sided heart failure or corpulmonale. However, the real evidence are indicative of left-sided heart failure.
It is postulated that the initial insult to the pulmonary system due to the exposure of the amniotic fluid debris may be because of a transient vasospasm, acute pulmonary hypertension, resulting in severe hypoxia.
Of the patients who survive the initial hemodynamic collapse, 70% develop noncardiogenic pulmonary edema that resembles acute respiratory distress syndrome, 45% develop a disseminated intravascular coagulation (DIC), within 30 minutes to 4 hours. In the absence of laboratory confirmation, spontaneous gingival bleeding, catheter site bleeding, and epitaxis strongly suggest DIC. There also may be the occurrence of neurological manifestations, such as seizures, confusion, or coma.
Amniotic fluid has procoagulant properties. Increased thromboplastic activity also occurs. Amniotic fluid lacks plasmin and plasmin activator, but it does contain plasmin proactivator. Plasmin is generated from an inactive precursor called plasminogen. It is speculated that thrombin generation in the pulmonary vasculature leads to plasmin and kinin production, which, in the absence of antiplasmin, perpetuates its own generation. If thrombin generation occurs in an environment with excess plasmin proactivator, a rapid coagulopathy develops. Fibrinogenolysis yields an increase in fibrin split products. The increase in fibrin split products is implicated in the development of severe uterine atony, which is found to stimulate the secretion of vascular endothelium, which in animal studies demonstrate myometrial and myocardial depression. This may contribute to the uterine atony and unstable hemodynamics seen in AFE syndrome.
The rarity of AFE or anaphylactoid syndrome of pregnancy, coupled with difficulty in diagnosing this syndrome, can result in fatal complications. The ability to recognize the signs and symptoms of AFE quickly and accurately and to begin treatment promptly remains a challenge for the anesthesia provider and the obstetrician. Even with aggressive resuscitation efforts and high-technology treatment, survival is rare. Reporting of suspected AFE cases to the National Registry for AFE, as well as the publication of case studies and potentially successful management protocols, help to further the understanding and treatment of this complex and life-threatening syndrome.
