CASE REPORT: Maternal death after intrapartum saline amnioinfusion—report of two cases

Authors

  • Gowri Dorairajan,

    1. Department of Obstetrics and Gynaecology, Jawaharlal Nehru Institute of Postgraduate Education and Medical Research, Pondicherry, India
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  • S. Soundararaghavan

    1. Department of Obstetrics and Gynaecology, Jawaharlal Nehru Institute of Postgraduate Education and Medical Research, Pondicherry, India
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Dr G. Dorairajn, Type V/4 JIPMER campus, Dhanvantari Nagar, Pondicherry-605006, India.

Case report

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.

Case 1

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.

Case 2

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.

Discussion

The acute onset of dyspnoea, cyanosis and collapse resulting in rapid death in the first case can be best explained by amniotic fluid embolism. The patient did not have any underlying medical problems and there was no evidence of haemorrhage, deep vein thrombosis or any risk factors for pulmonary embolism. The absence of bronchospasm and the fact that collapse occurred more than 12 hours after the last dose of prostaglandin makes it unlikely that this was an adverse reaction to prostaglandins.

In the second case, the patient had a minor episode of hypoxia 1 hour 15 minutes after the amnioinfusion was started, from which she recovered. There was a precipitous progress of labour. The occurrence of postpartum collapse and hypoxia evolving into coagulopathy in the absence of underlying medical disorder or pre-eclampsia strongly suggests an amniotic fluid embolism.

So far five cases of amniotic fluid embolism3–5 and one case of pulmonary oedema6 associated with amnioinfusion have been detailed in the literature. In both the cases reported by Maher et al.,3 amnioinfusion was performed, as in this case, for thick meconium-stained amniotic fluid, but infused using an infusion pump at 8–10 mL/minute. One of the cases received oxytocin, had features of chorioamnionitis and underwent caesarean section at 1.5 cm dilation of cervix. The other showed features of hypoxia 3 hours after starting amnioinfusion from which she recovered, as had happened in our second case. This woman also had a precipitate labour and collapsed immediately after delivery.

In the case reported by Dragaich et al.4 there was meconium staining of the amniotic fluid and the amnioinfusion was performed using a pump set at 999 mL/hour. She developed pulmonary oedema after 1500 mL of amnioinfusion by which time she had also undergone a precipitate labour ending in a spontaneous vaginal delivery.

The cases reported by Dibble and Elliot5 were also associated with oxytocin use and precipitate labour. The case reported by Wegnelius et al.6 had pre-eclampsia and the amnioinfusion was given through a pump at 10 mL/minute. Again there was a precipitate labour with respiratory failure close to delivery.

Overall epidural analgesia was used in four of the six cases while two of the six women received an oxytocin infusion. Five of the six cases reported in the literature and both of our cases had precipitate labour after amnioinfusion with the amniotic fluid embolism occurring close to delivery.

Posner et al.7 observed a significant increase in uterine tone during and after amnioinfusion. It is possible that the increased amniotic pressure could facilitate the transport of amniotic fluid into the systemic circulation. It could also encourage precipitate labour (seen in seven of the eight cases including our two cases), although there is no evidence for this in the Cochrane meta-analysis.8 Both factors could lead to amniotic fluid embolism.

Intrapartum transcervical amnioinfusion of normal saline solution is being used in a number of centres. In our unit it has been routinely used when there is thick meconium-stained amniotic fluid in labour over the last three years. Approximately 8–10 cases are performed each month giving approximately 300 procedures in total. These are the only two deaths of this nature that we are aware of.

Amnioinfusion appears to be an effective technique. Pierce et al.9 analysed 13 prospective studies of intrapartum amnioinfusion for meconium-stained amniotic fluid and found that the procedure significantly reduced the frequency of meconium aspiration syndrome. The CRAMP (Zimbabwe)10 study also found significant reduction in meconium aspiration in the amnioinfused group. Hofmeyr8 reviewed 12 randomised controlled trials comparing no amnioinfusion with amnioinfusion for meconium-stained amniotic fluid in labour in a Cochrane Review and concluded that the procedure significantly reduces meconium aspiration syndrome and neonatal hypoxic ischaemic encephalopathy. However, he also pointed out that the studies were too small to address any serious maternal complications. The multicentre randomised controlled trial by Fraser et al. may further clarify the efficacy and effectiveness of amnioinfusion and evaluate any serious maternal complication.11

We report these cases as maternal deaths were associated with a well accepted and widely performed procedure. Though it may not justify abandoning this procedure, a reappraisal of the use of amnioinfusion and its complications would be worthwhile.

Accepted 10 May 2005

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