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Suspected amniotic fluid embolism following amniotomy: a case report.
Mato J
Journal: AANA Journal 76(1):53-59, 2008. 36 References
Reprint: Miami Beach Anesthesiology Associates, Mount Sinai Medical Center, Miami Beach, Florida (J Mato, CRNA, MSN) RO.01 JU0821/171 ©2008
Faculty Disclosure: Abstracted by R. Ouellette, who has nothing to disclose.

Amniotic fluid embolism (AFE), also referred to as anaphylactoid syndrome of pregnancy, is a rare obstetric emergency that may manifest itself at any time during pregnancy. AFE is believed to occur when the constituents of amniotic fluid enter the maternal circulation, leading to varying degrees of multi-organ compromise. There is no singular clinical presentation for AFE. Most likely, many subfulminant cases occur yearly. Half of the patients present with dyspnea, tachypnea, and cyanosis, while 25% present with shock that seems inconsistent with estimated blood loss. Pulmonary edema develops in 25% of cases, and 25% of patients die within the first hour after embolization. A small subset of patients, 10%, present with seizure activity, as described in the case report. The hallmark signs of AFE are respiratory failure, neurological symptoms, hypotension, and disseminated intravascular coagulation (DIC).

Care is supportive and directed at treating the suspected underlying cause and ensuing symptoms. The mainstays of treatment include hydration, cardiopulmonary resuscitation, administration of blood products, and use of vasopressors. Surgical and pharmacologic measures are instituted as needed.

AFE has been linked to several predisposing conditions, including advanced maternal age, tumultuous labor, intrauterine fetal demise, high parity, fetal macrosomia, placenta accreta, uterine rupture, and cesarean delivery. Prerequisites for embolization of amniotic fluid include ruptured amniotic membranes, ruptured cervical or uterine blood vessels, and the presence of a pressure gradient between the uterus and its vasculature, such as that created by rupture of amniotic membranes, intrauterine saline infusion, and the use of uterine stimulants.

A 40-year-old woman at 41 weeks gestation was admitted for post-term induction of labor, which was carried out with IV oxytocin for initiation and augmentation of uterine contractions and cervical misoprostol to induce cervical ripening. An atraumatic combined spinal-continuous epidural was administered with reported relief of labor pain. Approximately 3 hours after initiation of labor analgesia the anesthesia service team was called emergently to the patient's room with the patient unresponsive to verbal or tactile stimuli. The obstetrician said that approximately 5-10 minutes after amniotomy for augmentation of labor the patient became rigid and unresponsive, and her left hand twitched rapidly. Before the amniotomy the patient was calm, pleasant, communicative, and reported excellent analgesia. The patient's airway was secured with endotracheal intubation and transferred to the OR for emergency cesarean delivery due to decreased fetal heart tone. She developed DIC and ligation of the uterine vasculature was achieved. She was transferred to the SICU after surgery.

The patient was tracheally extubated on the 2nd postoperative day, awake, alert, and oriented. She was discharged home on the 7th postoperative day.