Intrapartum transcervical amnioinfusion is an accepted therapeutic measure in the presence of variable decelerations with or without meconium-stained amniotic fluid.1 Widely varying protocols are being used and have been thought to be safe.2 Amniotic fluid embolism and or pulmonary oedema in patients undergoing amnioinfusion have been described in six cases reports although no causal link has been established. We report two fatal cases of probable amniotic fluid embolism after saline amnioinfusion.
A 23-year-old nulliparous woman presented to our hospital at 41+2 weeks of gestation with vaginal leakage of clear fluid for 5 hours. She was previously well and her pregnancy had been uncomplicated. On examination she was not anaemic, there was no tachycardia or fever and her blood pressure was 110/70 mmHg. Examination of her abdomen revealed a single term fetus in a cephalic presentation with reduced amniotic fluid. The uterus was soft with the vertex was at the pelvic brim and there were normal fetal heartbeats on auscultation. A vaginal examination confirmed ruptured membranes and revealed a soft, partly effaced cervix with a closed os.
Prostaglandin E2 gel (0.5 mg) was administered intra-cervically for cervical ripening with a second dose of 0.5 mg given 6 hours later. Five hours after the second dose, the uterus was contracting regularly and intermittent auscultation of the fetal heartbeat revealed no abnormality. Vaginal examination revealed that the cervix was fully effaced and 3 cm dilated. The membranes were absent and thick meconium-stained amniotic fluid was draining. An amnioinfusion with normal saline infused under gravity was administered through a transcervical sterile rubber catheter and labour was augmented with an infusion of 2.5 mU/minute oxytocin. The infusion rate was not changed through labour. A total of 1000 mL of saline was infused into the amniotic cavity over 1 hour 40 minutes. Within 3 hours of starting the amnioinfusion, the patient was found to be in second stage and had a spontaneous vaginal delivery of a 2.7-kg fetus in good condition. No additional oxytocics were administered at delivery. Immediately after delivery of the placenta, the patient had acute dyspnoea, hypotension, tachycardia, cyanosis and frothing at the mouth, which quickly evolved into a full cardiac arrest. The patient was intubated and cardiopulmonary resuscitation initiated promptly but she could not be revived. There had been no postpartum haemorrhage or trauma to the genital tract. The relatives did not give permission for a postmortem examination.
A 23-year-old woman with two living children (G3P2) presented at 40 weeks of pregnancy with vaginal leakage of fluid and labour pains. She had been previously well and her pregnancy had been uneventful. On examination she was not anaemic or pyrexial, and her blood pressure was 100/60 mmHg. Abdominal examination revealed a single term fetus in a cephalic presentation, with reduced amniotic fluid and mild uterine contractions every 5 minutes. On auscultation the fetal heart rate had variable decelerations. On vaginal examination the cervix was 3 cm dilated and 75% effaced, and thick meconium-stained amniotic fluid was draining. An amnioinfusion was started with normal saline infused under gravity, and labour was augmented with an infusion of oxytocin at 2.5 mU/minute. The oxytocin infusion rate remained constant throughout labour. One hour and 15 minutes later (by which time 750 mL saline had been infused), the patient became breathless and unresponsive with tachypnoea and peripheral cyanosis. Her pulse rate was 112 beats/minute and her blood pressure 120/80 mmHg. Respiratory examination did not reveal any bronchospasm or crepitations and her pupils were of normal size and reacted normally to light. 100% oxygen was administered through a facemask and an infusion of 10% dextrose infusion was commenced. Her serum electrolytes and blood glucose were normal. With this resuscitation the woman made some improvement, regaining full consciousness and responding appropriately to questioning. One hour later she was in second stage. An elective vacuum extraction was performed and a 2.8-kg fetus was delivered in good condition. Ten units oxytocin in 500 mL normal saline was started as an intravenous infusion soon after the baby was delivered. Immediately after delivery of the placenta the woman collapsed with severe hypotension and tachycardia. She also developed an atonic postpartum haemorrhage that was controlled with intravenous methyl ergometrine, an oxytocin infusion (10 U in 500 mL normal saline) and two intramuscular injections of 250 μg prostaglandin F2α 15 minutes apart. Bladder catheterisation revealed frank haematuria.
The patient was initially resuscitated with crystalloids following which 2 U of blood were transfused. There was no genital tract trauma. Laboratory investigations confirmed a coagulopathy (clotting time >30 minutes, fibrin degradation products present and diminished platelet counts). Four units of fresh frozen plasma were transfused, a dopamine drip was started and 100% oxygen was administered by facemask. During this time the systolic blood pressure fluctuated between 70 and 100 mmHg and the urine output was poor. Her central venous pressure was maintained around 10 cm of water. Shortly afterwards the woman developed another bout of vaginal bleeding, which responded to uterine massage and a further intramuscular injection of 250 μg prostaglandin F2α. Two more units of blood were transfused. One hour later she developed hypoxia and respiratory arrest. She was quickly intubated and ventilated and transferred to the intensive care unit. Twenty minutes later, however, she sustained a cardiac arrest from which she could not be revived. Again in this case the relatives refused an autopsy.