Updated: October 2014
The birth of the placenta is my least favourite part of the birth process. I know I have ‘issues’ and I’m working on them. Hopefully writing this blog post will be therapeutic as well as informative. I am going to refrain from referring to the birth of the placenta as the ‘third stage’ of labour because I don’t believe in the concept of stages of labour.
What’s the big deal?
Postpartum haemorrhage is historically and globally the leading cause of maternal death (World Health Organization). The most dangerous time for a woman during the birth process is after her baby is born, around the time the placenta is birthed. Whilst the mother and baby meet face to face, and the family greet their new member, there is a lot of important work going on behind the scenes (ie. inside the woman).
The physiology of placental birth
This is an overview of what happens to ensure the placenta is born and the blood vessels feeding the placenta stop bleeding. If you want references, the information is available in any half decent anatomy and physiology text book (eg. Coad & Dunstall 2011; Rankin & Stables 2010)
Before the baby is born
Birth does not happen in distinct stages and the birth of the placenta is part of a complex process that begins before the baby is born. Oxytocin makes the uterus contract. Oxytocin is released by the posterior pituitary gland (in the brain) during labour to regulate contractions. It is one of the key birthing/bonding hormones. I really don’t have the space here to get into any depth about birth hormones, so check out the work of Sarah Buckley to find out more. As the birth of the baby becomes imminent, high levels of oxytocin are circulating in the mother’s blood stream. This creates strong uterine contractions which move the baby through the vagina, and prepare the mother and baby for post-birth bonding behaviours.
Separation of the placenta
After the birth of the baby the contraction pattern is interrupted. The placenta transfers it’s blood volume to the baby ‘handing over’ the job of oxygenation to the lungs – the placenta is now emptier and less bulky. Instinctive mother-baby interactions stimulate further oxytocin release and the uterus responds by contracting. These interactions involve smell, touch (skin-to-skin), taste, sound… the baby ‘crawls’ on the mothers abdomen, his feet stimulating her uterus to contract. He may attach to the breast and feed, however this is not essential for oxytocin release. The placenta is compressed and the blood in the intervillious spaces (the interface between mother’s blood system and the placenta/baby’s blood system) is forced back into the spongy layer of the decidua (uterine lining). Retraction of the uterine muscle fibres constrict the blood vessels supplying the placenta, preventing blood from draining back through the maternal vascular tree (mother’s blood vessels feeding the placenta). This congestion results in the veins rupturing and the villi shearing off the uterine wall. A clot forms behind the placenta. The non-elastic placenta is unable to remain attached and peels away – usually starting from the middle.
At this point you may notice a small gush of blood as the placenta separates and the umbilical cord lengthen as the placenta moves downwards.
The placenta leaves the upper segment of the uterus and further strong contractions bring the walls of the uterus into opposition – compressing the blood vessels. At the same time the contracted uterine muscle fibres act as ‘living ligatures’ to the blood vessels running through them preventing further blood flow. An increase in the activity of the coagulation system means that clot formation in the torn blood vessels is maximised and the placental site is rapidly covered by a fibrin mesh.
As the placenta leaves the uterus the mother may feel the urge to push again and birth her placenta. Or, she may be far too busy with her new baby and the placenta will sit in her vagina until she moves.
This process is usually complete within an hour of the baby’s birth. However, sometimes it takes longer ie. hours… and hours. If you waited a long time to birth your placenta please post your story in the comments.
Pathology – when it doesn’t work
The bottom line is that the birth of the placenta and haemostatsis (prevention of excessive bleeding) relies on effective uterine contraction. Ineffective uterine contraction is the main cause of post partum haemorrhage (PPH). The other causes are perineal/cervical damage, or even more rarely clotting disorders.
There are 2 main causes of ineffective uterine contraction after birth:
- Hormonal – Inadequate circulating oxytocin or inadequate uterine response to oxytocin. Inadequate response is often because the oxytocin receptors in the uterus have become saturated eg. by large doses of syntocinon over a long period of time during an induction (Belghiti et al. 2011; Phaneuf et al. 2000).
- Mechanical – something is in the way and the uterus cannot contract. Most often this is a full bladder taking up space in the pelvis and stopping the uterus from contracting down. It can also be a large clot in the uterus or a partially detached placenta.
Most PPHs occur after the placenta is out. PPH can and does occur after a c-section too.
Another complication can be a retained placenta ie. the placenta remains attached. The definition of a retained placenta varies – and I’m not game to put a timeframe on it. However, once you have done something (such as given an oxytocic drug – see below) you need to finish the job and get the placenta out. If you have not, and there is no bleeding then… how long is a piece of string?
Active management of placental birth
In the 1950s syntocinon (pitocin) hit the birth scene. Syntocinon is an artificial version of oxytocin and is now used extensively for induction of labour, augmentation of labour and to ‘actively manage’ the birth of the placenta. It differs from endogenous oxytocin in the way it is released into the blood stream – ie. in a consistent dose rather than in pulse like waves. Syntocinon is also unable to cross the blood-brain barrier and influence instinctive bonding behaviour (check out Moberg’s book about how oxytocin influences behaviour).
When used to actively manage placental birth, syntocinon mimics the physiology described above by initiating uterine contractions. How active management is carried out varies considerably and this drives midwifery students mad. Different practitioners do their own thing, and the literature is also inconsistent. Essentially syntocinon (10iu) is given to the mother by injection after the birth of the baby (although sometimes syntometrine). The cord is clamped and cut, and the placenta is usually pulled out using controlled cord traction – see the horrible picture above. The order and timing of these interventions varies, although obviously pulling the placenta out comes last. The areas of debate/negotiation are:
- Timing of injecting syntocinon: Originally syntocinon was given with the birth of the baby’s anterior shoulder. Nowadays it seems to be given after the birth of the baby. There is no research determining the best time. Syntocinon takes around 3 mins to work when given IM (into muscle) – so in theory to mimic physiology it probably should be given soon after the baby arrives. However, there is no evidence to support early administration of syntocinon, and Jackson et al. (2001) found that administering it after the birth of the placenta was just as effective at preventing PPH.
- Timing of clamping and cutting the cord: The risks of premature cord clamping are now well know. Most midwives I know (regardless of where they work) wait until the cord has stopped pulsing before clamping. This may have implications if the cord is not clamped before the syntocinon works. There are concerns (no research) about the impact of this bolus of syntocinon passing through the placenta to the baby and interfering with the baby’s oxytocin system. There is also a theory that the strong contraction will shunt excess blood from the placenta to baby. Some midwives wait until after the cord has stopped pulsing before giving syntocinon to avoid this. Giving the oxytocic after the birth of the placenta would eliminate the chance of either of the above concerns occurring.
- Whether to ‘drain’ the placenta: If the cord has been prematurely clamped, some of the baby’s blood is trapped in the placenta – this makes the placenta bigger and more bulky, and in theory/experience more difficult to get out. There is no research to support this… but many midwives will leave the placenta end of the cord unclamped and drain the trapped blood prior to attempting to deliver the placenta. Personally, this is my preference as I notice it is much easer to get an empty placenta out. Something I learned while collecting cord blood. Of course it is even better if all that blood is in the baby to whom it belongs.
- Whether or not controlled cord traction is used and when: It is standard practice to pull the placenta out after syntocinon has been injected, and the umbilical cord has been cut. Some midwives wait until they have seen signs of placental separation before pulling (trickle of blood and lengthening of the cord). I think this part of active management causes the most problems. If you pull on a placenta that has not yet separated you can partially detach it = some blood vessels are ‘torn and open’ but the uterus cannot contract because the placenta is in the way. Or, you can detach it before the syntocinon is working i.e. no contractions to stop the bleeding. Or worse case, and very rare scenario you can pull the uterus out (inverted uterus)! You can also, more commonly snap the umbilical cord – which often freaks everyone out. But a snapped cord is not a big drama. It just means the mother will have to get up and push her placenta out… Which brings me around to the idea of not pulling at all. A study by Gülmezoglu et al. (2012) found that the ‘omission of controlled cord traction’ did not increase the risk of severe haemorrhage (they only looked at severe). So, women have the option of getting upright and pushing, or having someone pull their placenta out for them. Or even perhaps pulling their own placenta out?
Active management is usually (not always) quicker than physiological. This is probably another reason it is favoured in hospital settings. Less time waiting for a placenta = less time stressing out about a potential PPH, and you can get the woman to the next station (postnatal ward) quicker.
Occasionally syntometrine is used for active management. This is a mix of syntocinon and ergometrine. It is not generally used nowadays because the ergometrine acts on smooth muscle – all smooth muscle. Therefore the side effects are vomiting, raised blood pressure and potentially a retained placenta due to the cervix shutting… although I’m not convinced about the cervix closing firmly enough to trap a squishy placenta.
What the research tells us – and doesn’t tell us
The physiological vs active management of the ‘third stage’ has been going on since I was a student midwife (I did a literature review on it as an assessment). Today I am doing it the easy way and relying Cochrane to review the studies for me (Begley, et al. 2011; Westhoff, Cotter & Tolosa 2013). In summary, the reviews note that there is a ‘lack of high quality evidence’ but conclude that active management reduces the risk of haemorrhage. They also raise concerns about side effects – increased blood pressure, afterpains and vomiting (probably due to the use of syntometrine in some studies); reduced birthweight for baby (probably due to reduced blood volume following premature clamping); more women returning to hospital with bleeding (?). In regards to the last side effect – anecdotally midwives report greater blood loss on the post natal ward after the syntocinon or syntometrine has worn off but this is not measured in studies.
The important thing to remember when interpreting these findings is that all of the studies included were conducted in a hospital setting. The experimental group were those having ‘physiological’ management. The practitioners attending the ‘physiological’ placental births were most likely doing something that was not their usual practice, and they may have been unprepared for, or uncomfortable with this approach. A study that compared active vs holistic physiological care had very different findings (Fahy, et al. 2010). In this study the midwives attending the physiological placental births were familiar and comfortable with this approach. In contrast to previous studies, active management was associated with a seven to eight fold increase in PPH rates compared to a holistic physiological approach. Another retrospective study (Davis et al. 2012) found a twofold increase in large PPHs (1000mls+) for low risk women having an actively managed placental birth in New Zealand compared to those having a physiological placental birth. In summary – for women having undisturbed physiological births active management of the placenta increases their chance of having a PPH.
Back to my initial title statement
A safe and effective physiological placental birth requires effective endogenous oxytocin release. This is generally facilitated by:
- A physiological birth of the baby: No interventions during the birth process eg. induction, augmentation, epidural, medication, instructions or complications.
- An environment that supports oxytocin release: Privacy, low lighting, warmth and comfort. No strangers entering the birth space eg. paed or extra midwife.
- Undisturbed skin-to-skin contact between mother and baby: others must not handle the baby or engage the mother in conversation. These mother-baby interactions may result in breastfeeding, but this should not be ‘pushed’ as not all babies want to breastfeed immediately.
- No fiddling: No feeling the funds (uterus). No clamping, cutting or pulling on the umbilical cord. No clinical observations or ‘busying’ around the room.
- No stress and fear: Those in the room must be relaxed. The midwife needs to be comfortable with waiting and have patience. The mother must not be stressed as adrenaline inhibits oxytocin release. This is why a PPH often occurs after a complicated birth (eg. shoulder dystocia) and when the baby needs resuscitating.
- No prescribed timeframes: Many hospital policies require intervention within half an hour if the placenta has not birthed. This is not helpful and generates anxiety which is counter productive.
Of course this is a general list and some women are perfectly capable of birthing their placentas amongst the chaos of siblings and noise etc. Probably because it is their own, familiar chaos and they are relaxed in the midst of it. Others want the cord cut after it has stopped pulsing eg. if it is short. I think the most important factor in ensuring a safe physiological birth of the placenta is a physiological birth of the baby.
However, in Australia (AIHW 2011) only 21% of women go into spontaneous labour and continue to labour without augmentation. Out of that % how many labour without an epidural or other medication? Out of that % how many are birthing in the conditions described above? I pose the questions because these stats are not presented. I don’t need to ask the question because I am familiar with hospital practice… and most women are birthing in hospital.
Active management of the placenta will reduced the chance of a PPH in a setting that does not support physiology and in which routine intervention is the norm. There are further options within active management that can be negotiated (see above). Physiological placental birth is an option and possible if you manage to avoid induction, augmentation, an epidural or complications – but be aware of how difficult it may be, and don’t beat yourself up if it doesn’t happen.
Hastie C, Fahy KM. Optimising psychophysiology in third stage of labour: Theory applied to practice, Women Birth (2009), doi: 10.1016/j.wombi.2009.02.004
On Birth and Bleeding – Science & Sensibility