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PowerPoint Discussion of Amniotic Fluid Embolism
Amniotic fluid embolism (AFE) is a rare but unpredictable and rapidly developing obstetric emergency. The exact incidence of AFE is unknown; however, the reported incidence ranges from 1 per 10,000 to 1 per 20,000 singleton births. Although there are no known risk factors for AFE, the reported incidence increases in the presence of one or more associated factors listed in Table 5-1 . Despite its rarity, AFE is a major cause of maternal mortality in the Western countries accounting for 8% to 10% of all maternal deaths in the United States, Canada, and England. The majority of cases of AFE develop during the active phase of labor, mostly during delivery. However, AFE can also develop at the time of cesarean section and even in the immediate postpartum period.
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Case 1: Amniotic Fluid Embolism
A 34-year-old G4P3 who was admitted at 41 weeks’ gestation for induction of labor. Ultrasound evaluation revealed an estimated fetal weight of 3942 g with an amniotic fluid index of 7 cm. Fetal heart rate revealed reassuring tracing with good variability and presence of accelerations. Cervical examination revealed vertex presentation with a Bishop score of 5. Physical examination revealed normal findings with blood pressure of 100/62 mm Hg. Laboratory findings revealed normal hematocrit and platelet count.
Oxytocin induction was started and 4 hours later she had artificial rupture of membranes with evidence of meconium staining. Cervical examination revealed cervix 4 cm dilation and 90% effaced. Approximately 1 hour later, the fetal heart rate tracing was reassuring, but uterine contractions were increased ( Fig. 5-1A ). Approximately 10 minutes later, cervical examination revealed anterior lip, increased uterine activity, and reassuring fetal heart rate (see Fig. 5-1B ). After the examination, there were variable decelerations, and 10 minutes later the patient complained of sudden onset of shortness of breath, became cyanotic, and lost consciousness. At that time, fetal monitoring revealed bradycardia and marked increase in uterine activity and tone (see Fig. 5-1C ). She had immediate resuscitation with oxygen and bagging followed by intubation, and the fetal heart rate revealed bradycardia and absent variability (see Fig. 5-1D ). Six minutes after cardiac arrest she had cesarean delivery in the room with delivery of a live infant weight of 4020 g with Apgar scores of 1, 4, and 7 at 1, 5, and 10 minutes, respectively. Maternal resuscitation efforts were discontinued after 30 minutes. Autopsy findings found massive amniotic fluid embolism. The infant had metabolic acidosis, but no seizures and was discharged home 7 days later.
Discussion
The etiology and pathogenesis of AFE remains poorly understood. It usually results from amniotic fluid entering the maternal circulation producing acute cardiovascular, hemodynamic, and hematologic abnormalities similar to those seen with anaphylaxis. The portal of entry of the amniotic fluid after membranes rupture could be at the site of placental implantation or at site of tears in the cervix or lower uterine segment. The fetal cells and biochemical mediators in the amniotic fluid are responsible for the majority of signs and symptoms seen in this syndrome ( Fig. 5-2 ).
