Brain damage caused by excessive syntocinon during labour

BACKGROUND TO THE CASE

Following an uneventful first pregnancy J was born at Withington Hospital, Manchester on May 21 1974.

His 18 year old mother had been admitted to hospital the previous day for induction of labour as she was one week overdue. All ultrasound scans had shown normal fetal development.

Induction of labour was carried out at 10.00 hours on May 21 by artificial rupture of the amniotic membrane (ARM). The cervix was approx. 2 cms dilated and clear amniotic fluid was released, suggesting that the baby was not in distress at this time.

Spontaneous contractions did not follow the ARM so at 11.45 hours a syntocinon infusion was commenced. This was gradually increased over the next 2 hours from an initial rate of 2-3 milliunits (mU) per minute to 20 mU/ min.

By 13.45 labour was established with strong contractions occurring every 2 or 3 minutes and lasting 40 seconds. The fetal heart rate was recorded every 15 minutes for the next hour and remained normal (in 1974 continuous fetal heart monitoring was not regarded as mandatory with an uncomplicated pregnancy).

At 15.10 a vaginal examination was performed to assess the progress of labour. The cervix had dilated rapidly and was very close to full dilatation. There is no record of a fetal heart rate after 14.45 but ‘FHHR' (fetal heart heard: regular) is recorded on the labour chart. It has been known for a long time that induction of labour with syntocinon increases the risk of fetal hypoxia secondary to over stimulation of the uterine muscle, and this is why frequent recording of the fetal heart rate is essential.

At 15.15 the syntocinon infusion was still at the rate of 20 mU/ min. and the contractions were recorded as 1-1:2; that is between 5 and 10 contractions every 10 minutes. This is a frequency that rarely occurs in spontaneous labour and is above the accepted limit for syntocinon induced labour. The correct response at this stage would have been to reduce the rate of the infusion, but in fact it was continued at this high rate for a further hour.

At 15.25 the cervix is noted as fully dilated but there is still no record of the fetal heart rate. At 16.15 a live male infant was delivered following an episiotomy and what was considered to be a normal delivery.

The baby was born in a very poor condition with an APGAR score of 1 at 1 minute, 2 at 5 minutes and only 4 at 10 minutes. He was clearly severely asphyxiated but there was no paediatrician present at the birth (or indeed on the premises if the labour notes are to be believed) and he was eventually intubated by a midwife after 10 minutes.

John went on to develop convulsions and all the signs of severe hypoxic ischaemic encephalopathy. He is now 34 years of age and suffers from spastic quadriplegia and multiple joint contractures. He has a scoliosis and epilepsy and is profoundly mentally impaired. He cannot speak and requires tube feeding and is completely dependent upon others for all aspects of his care.

THE CLAIMANT'S CASE

The claimant alleged that the dose of syntocinon given to his mother during her labour was excessive resulting in over stimulation of the uterine muscle. With powerful contractions as frequent as 1:1-2 the uterus had no time to relax adequately in between the contractions resulting in a reduced blood supply to the fetus leading to hypoxia, circulatory collapse and ultimately brain damage.

He also alleged that had the fetal heart rate been properly checked at 15 minute intervals during the first stage of labour and after every contraction during the second stage, as it should have been, it would have become clear soon after 14.45 (when the recordings ceased) that he was in distress. Steps would then have been taken to alleviate this, such as reducing or stopping the syntocinon and summoning medical assistance. It is likely that had this happened John would have been delivered shortly after 15.30, at the latest, and before he suffered serious injury.

It was also claimed (given the capacity of a fetus to withstand even a severe hypoxic insult without sustaining significant injury for up to 10 minutes) that if J had been delivered even as late as 16.02 and given prompt and effective resuscitation he would have escaped uninjured.

COURT PROCEEDINGS

The defendant initially indicated an intention to defend the claim on the basis that J's severe brain injury could have been caused by a stroke at, or shortly before, birth, rather than by intra partum hypoxia.

Proceedings were issued on December 20 2006 and a defence was served on March 30 2007. In July 2007 directions were given by a District Judge who ordered a split trial

Following exchange of medical evidence and the meeting of experts in February 2008 the defendant accepted liability for both breach of duty and causation.

The trial for assessment of damages is set down for February 2010.

An interim payment has been requested to enable the family to move to more appropriate premises and for a full care regime to be set up.

For the claimant

Olivia Scates
JMW Solicitors
1, Byrom Place
Manchester
M3 3HG

For the defendant

Sue Tyson
Hempsons Solicitors
Portland Tower
Portland Street
Manchester
M13LF

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