Chapter 7 Normal labour and delivery
During pregnancy the uterus is usually in a quiescent state. In the third trimester women experience low amplitude, poorly synchronised Braxton Hicks or practice contractions. Substances which contribute to the inhibition of myometrial activity include progesterone from placental syncytiotrophoblast and chorion; myometrial parathyroid hormone-related peptide; and nitric oxide and relaxin from the myometrium, decidua, chorion and amnion in addition to prostacyclins. The process of myometrial contraction requires activation of calmodulin, a calcium-binding protein with calcium ions which then in turn activates the enzyme myosin light chain kinase to produce adenosine triphosphate to power actin and myosin filaments to slide over each other to produce shortening. Inhibitors of myometrial activity act by increasing intracellular levels of cyclic nucleotides to prevent release of calcium ions from intracellular stores or by reducing myosin light chain kinase activity.
Towards term a number of processes occur which predispose to activation or preparation of the myometrium for onset of labour. Formation of gap junctions by increases in contraction-associated proteins such as connexin-43 enhance cell to cell coupling. Receptors for oxytocin and stimulatory prostaglandins are also increased. These changes are associated with myometrial stretch when the uterus enlarges and with the higher levels of oestrogens derived partly from placental conversion of fetal dehydroepiandrosterone (DHEAS) where they also exert a local oestrogen effect. In addition to increased DHEAS production, activation of the fetal hypothalamic–pituitary–adrenal axis in late pregnancy results in more fetal cortisol biosynthesis. Fetal cortisol competes to reduce the local progesterone effect and stimulate synthesis of corticotrophin-releasing hormone from placenta and fetal membranes for production of prostaglandins by the latter structures.
Initiation of labour remains unclear, but prostaglandins have been implicated in myometrial contraction. Isoforms of phospholipase A2 or C, activated by varying requirements for calcium ions, liberate arachidonic acids from membrane phospholipids. Prostaglandin synthase in amnion and chorion convert arachidonic acids to primary prostaglandins. For prostaglandin E2 (PGE2) there are four main receptor subtypes labelled from EP-1 to EP-4. These receptors are distributed in the myometrium in varying concentrations. Stimulation of EP-1 and EP-3 results in contractions whereas stimulation of the other two receptors leads to relaxation. These together with corticotrophin-releasing hormone-related cyclic AMP in the lower uterine segment contribute to fundal dominance.
Onset of labour is associated with a substantial increased myometrial sensitivity to oxytocin stimulation and a three- to five-fold increase in oxytocin production by chorio-decidual tissue. Oxytocin raises concentrations of free calcium in the myocytes to promote myometrial contraction.
Fetal membranes covering the internal cervical os exhibit a decreased production of the 15-hydroxyprostaglandin dehydrogenase enzyme which metabolises prostaglandins. More local prostaglandin production is available for cervical effacement and dilatation. This effect is supplemented by release of collagenase through increased cytokine activity.
Onset of labour is most likely between midnight and 0500 hours when maternal secretion of oxytocin peaks and the myometrium is most sensitive to oxytocin and prostaglandin. These changes in steroid and protein concentrations return to non-pregnant levels 48–72 hours post partum.
Myometrial contraction exerts a pull in circular and longitudinal directions (Figure 7.1)
The term fundal dominance is used to describe travel of myometrial contractions from the fundus of the uterus towards the cervix. The starting point or pacemaker for myometrial activity is situated near the point of insertion of the fallopian tubes into the uterus. The spread of myoelectrical activity through the uterus requires 1 minute. Approximately another minute is needed for adequate relaxation. Blood vessels must traverse the myometrium to reach the placenta. Contractions occurring more than once every 2 minutes contribute to poor myometrial relaxation and reduce blood and hence oxygen supply to the fetus. When two contractions are noted every 10 minutes for an hour consider possible onset of labour. In established labour the rate of contractions ranges between 3 and 5 per 10 minutes.
In early labour the uterus is not working at maximum capacity. This may be because the number of myometrial cells contracting is limited or contraction is poorly synchronised or of short duration. As labour progresses contractions becomes more efficient and uterine work increases. Capacity for work cannot, however, increase indefinitely. A stable phase for ability to work results once maximal work output is achieved for the individual mother. When the stable phase is achieved (Figure 7.2a) additional stimulation by oxytocics is of little value and can be harmful. Uterine work has been expressed as:
Figure 7.2 (a) Graph of uterine activity with stable phase (plateau) for individual woman. (b) Montevideo unit = intensity (amplitude of recorded contraction) × contractions per 10 minutes. The Alexandra unit, a refinement, takes into consideration duration of the contraction.
The viscoelastic myometrium always exerts pressure on the amniotic fluid. The resting pressure or tone is usually 6–12 mmHg. Amniotic fluid is not compressible.
Figure 7.3 Intrauterine pressure measured by a catheter-tipped pressure transducer placed above presenting part is less affected by movement.
Intensity of uterine contractions increases throughout pregnancy. Towards term pressures up to 30 mmHg may be recorded. During labour intrauterine pressure increases to levels of 60–80 mmHg. Contractions of this intensity are still detectable for 48 hours post partum but the frequency diminishes after 12 hours.
In the weeks before labour that portion of the uterus between the internal os and the reflection of the uterovesical fold of the peritoneum is attenuated by stretch and Braxton Hicks contractions to form the lower segment. This allows the presenting part of the fetus, particularly in primiparous women, to settle or engage into the pelvis.
Labour is traditionally divided into two stages:
Effacement precedes cervical dilatation. Initially uterine activity is expanded to achieve effacement. This period, the latent phase of labour, takes on average 9 ± 6 hours in the primiparas and 5 ± 4 hours in multiparas. The cervix is usually up to 2 cm dilated when labour begins. At the end of the latent phase cervical dilatation is usually between 3 cm and 4 cm. Once effaced further uterine activity produces rapid cervical dilatation of at least 1 cm per hour in both parous and nulliparous women. This, the active phase of labour takes on average 6 hours to reach full cervical dilatation (Figure 7.4). Multiparous women approach labour with more cervical effacement hence a shorter latent phase and thus a shorter labour.
Figure 7.4 Partogram. Primipara and multipara showing latent phase and steep active phase to full cervical dilatation.
It is common practice to plot the rate of cervical dilatation to indicate the progress of labour. This is usually charted on a single sheet of paper designed for recording labour events over a 24-hour period. Provision is also made for registering fetal heart rate (every 30 minutes), uterine contractions (every 30 minutes), rate of head descent and medication. Cervical dilatation detected by vaginal examination is recorded every 2–4 hours. This graphic representation of parturition (partogram) summarises and depicts, visually, the events in labour (Figure 7.5). Cervical dilatation lagging 2–3 hours behind that expected from the normal graph (Figure 7.6), should suggest to medical attendants the need for reassessment.
Uterine contractions cause further flexion and entry of the fetal head into the pelvis, usually in the occipito-transverse (Figure 7.7).
Descent occurs to the level of the ischial spines when levator ani muscles assist internal rotation to align the sagittal sutures for delivery through the widest anteroposterior diameter of the outlet.
Distension of the lower part of the vagina evokes reflexes which stimulate the urge to push. Pushing is achieved by the Valsalva response and contraction of diaphragmatic and abdominal muscles. The head stretches the vagina and vulva as it delivers. Extension occurs once the head passes beneath the symphysis pubis. Fetal membranes usually rupture before this stage (shown in sequence in Figure 7.8).
The head rotates to occipitolateral or restitutes to align naturally perpendicular to the shoulders. The shoulders, having entered the pelvis in the oblique diameter, rotate so the bisacromial diameter of the shoulder delivers in the anteroposterior diameter of the pelvic outlet. Further rotation of the head laterally accompanies rotation of the shoulders (Figure 7.9).
The shoulders deliver assisted by lateral flexion of the body. Once this is achieved the rest of the fetus delivers readily as the uterus contracts down (Figure 7.10).
Figure 7.7 The widest part of the inlet (a) (transverse diameter) and outlet (b) (anteroposterior diameter) is represented geometrically. The fetal head enters in the occipito-transverse then rotates to address anteroposterior diameter of outlet.
The squatting posture is well suited to delivery. A woman adopting the lithotomy position propped up with pillows and her legs drawn back essentially achieves this posture but has the added advantage of allowing attendant access to assist delivery.
Gloves and gown are mandatory for the attendant conducting the delivery. Women should be draped and the vulval area cleansed. Deliver onto sterile towels.
The medical attendant is usually stationed on the woman’s right. Place the left hand on the fetal head as it ‘crowns’ (passage of the biparietal eminences through the vulva) to maintain flexion and prevent expulsive delivery.
The right hand is used to guard the perineum and cover the anus with a sanitary pad. If necessary assist extension of the fetal head by lifting the chin. Consider if an episiotomy is needed.
Instruct the woman to pant once the head is crowned. This prevents forceful pushing, and repeated gentle increase in intra-abdominal pressure created by panting nudges the head out. Aspirate the mouth and then the nose of the baby at the first opportunity. Give 0.5–1 ml of Syntometrine (a combination of the synthetic oxytocic Syntocinon 5 units/ml and ergometrine maleate, 0.5 mg/ml) intramuscularly to the mother. The oxytocic effect is evident in 2.5 minutes (Syntocinon) to 7 minutes (ergometrine). It assists uterine contraction and placental separation and thereby controls blood loss. For mothers at risk of haemorrhage, give ergometrine intravenously (oxytocic effect in 1 minute).
Once external rotation is completed, direct the head gently downwards to assist delivery of the shoulders. When the anterior shoulder appears beneath the symphysis insert a finger into the anterior axilla and lift the body upwards watching the perineum at the same time to avoid extension of the episiotomy or tearing of the perineum.
Cut the cord within 1 minute of birth. This interval allows additional transfusion of more than a third of the fetal blood volume. Do not wait for cessation of pulsation as the placenta may be separated and fetal exsanguination can result. Free any loose cord around the neck over the head or shoulders and proceed with the delivery. If the cord is tight around the neck or fetal resuscitation is anticipated clamp, cut the cord at once and deliver the baby.
The third stage is the internal between delivery of the fetus and delivery of the placenta. Placental separation is shown by:
The placenta usually separates within 3 minutes and is delivered within 5 minutes after birth.
Box 7.3 Administration of entonox
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