Precipitate labour and slow labour

Published on 09/03/2015 by admin

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Last modified 09/03/2015

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Precipitate labour and slow labour

Introduction

Abnormal uterine activity has no clear definition, partly because the range of normal uterine activity itself has no clear definition. It is tempting to refer to uterine ‘overactivity’ as that which results in labour progressing too quickly, and ‘inadequate’ uterine activity as that which is insufficient to provide adequate progress, but the rate of progress has no precise definition either and is dependent on parity. In practice, overactivity presents as rapid painful contractions often associated with fetal distress, and inadequate uterine activity as absent or slow cervical dilatation.

Precipitate labour has been defined as expulsion of the fetus within less than 3 h of the onset of contractions and results from uterine overactivity. Slow labour may result from inadequate uterine activity, cephalopelvic disproportion, or more commonly, a combination of the two.

Cephalopelvic disproportion refers to how well the fetal head fits through the pelvis and may occur if the fetal head is too big or the pelvis too small. It is subdivided into ‘true’ cephalopelvic disproportion if the head is in the correct position and ‘relative’ cephalopelvic disproportion if the obstruction is caused by the head presenting in a position other than occipitoanterior.

Precipitate labour

Spontaneous hypercontractility is rare, perhaps occurring in only 1:3000 pregnancies. The contractions may be excessively long in duration or be excessively frequent and there is a risk of fetal hypoxia due to interference with the placental blood supply. Spontaneous uterine hypercontractility may be associated with placental abruption (see p. 278).

Uterine hyperstimulation occurs much more commonly, however, and by definition is caused by the use of oxytocics. Both syntocinon (synthetic oxytocin that is administered by injection or infusion) and prostaglandins may be implicated. The choice of dosage regimens for each represents a compromise between efficacy and the risk of hyperstimulation. The appropriate dose of syntocinon remains controversial, but there is good evidence for starting at a low dose, around 0.5–4 mU/min, and increasing over 4 or 5 h to 12 mU/min. While the licensed maximum dose is currently 20 mU/min, some clinicians support the use of regimens up to 40 mU/min.

With prostaglandins, hyperstimulation is also a significant risk but is less likely if their administration is intravaginal, rather than oral, intracervical or directly extra-amniotic.

Precipitate labour resulting from either spontaneous hypercontractility or uterine hyperstimulation may lead to fetal distress. Placental blood supply is via intramyometrial blood vessels which are constricted during the contraction, and excessively long or frequent contractions reduce the chance of recovery in the short times when blood flow is returned (Fig. 44.1). Precipitate labour may also predispose to uterine rupture in parous women, particularly if there is a pre-existing caesarean section scar.

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Fig. 44.1Cardiotocograph trace in precipitate labour.

There is hyperstimulation secondary to syntocinon administration. When the syntocinon is stopped, the contractions become less frequent and the CTG improves.

Management of precipitate labour is largely dependent on the fetal condition. If a syntocinon infusion is running, it should be stopped and the mother given a tocolytic, e.g. a bolus of subcutaneous terbutaline or intravenous ritodrine. If severe fetal distress is apparent, it may be necessary to deliver the baby either instrumentally or by caesarean section, depending on the dilatation of the cervix. If a caesarean section is arranged, it is worth carrying out a vaginal examination prior to starting the operation, as the cervix may dilate rapidly during the time taken in the transfer to theatre, especially in a parous woman.

Precipitate labour is associated with complications for the mother including: cervical and perineal tears, retained placenta, postpartum haemorrhage and the need for a blood transfusion.

As mentioned above, it is important to remember that frequent uterine contractions are also a feature of placental abruption. Contractions with a frequency of more than one every 2 min are highly suggestive of this problem and these frequent contractions may increase the distress of a fetus already compromised by partial placental separation. The diagnosis of placental abruption is even more likely if there is associated lower abdominal pain, backache or vaginal bleeding. As a general rule, tocolytic drugs should not be used to manage the uterine hypercontractility associated with placental abruption, as uterine relaxation may exacerbate the bleeding and precipitate further placental separation.

Slow labour

Slow progress in labour is usually diagnosed by assessing the rate of cervical dilatation. As discussed on page 328 and 351, progress can be monitored on a partogram and alert lines can be used to identify women who are progressing slowly. Early identification and correction of abnormal labour makes it more likely that the mother will achieve a vaginal delivery. Unfortunately the definition of slow labour is controversial; traditional obstetric practice suggested that any nulliparous woman with a rate of cervical dilatation less than 1 cm/h required treatment for slow progress. More recently, a rate of cervical dilatation of < 0.5 cm/h has been adopted as the threshold.

Slow labour is associated with:

icon01.gif eventual fetal ‘distress’ and risk of fetal hypoxic injury

icon01.gif an increased risk of intrauterine infection leading to fetal and maternal morbidity

icon01.gif maternal anxiety and longer-term ‘psychological’ scarring

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