Updated: February 2022
The birth of the placenta is my least favourite part of the birth process. 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 the concept of stages of labour is rubbish.
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. I cover the physiology of childbirth in-depth in my book Reclaiming Childbirth and my online course Childbirth Physiology.
Before 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. 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.
After baby is born
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, their feet stimulating the uterus to contract. Baby may attach to the breast and feed, however this is not essential for oxytocin release. Regardless, the baby remains attached to the placenta and on their mother.
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 a small gush of blood may be seen as the placenta separates and the umbilical cord lengthens as the placenta moves downwards.
After separation 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.
Here is an overview of how the placenta is born from my YouTube Channel:
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 – in fact it is more likely after c-section than vaginal birth.
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 or concerns about the woman, 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 maternal blood-brain barrier and influence instinctive bonding 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 (Kearney, Reed, Kynn et al. 2019) 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. 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. In fact, the research suggests that giving the oxytocic before or after the birth of the placenta makes no difference to the risk of PPH (Soltani et al. 2010 – Cochrane Review).
- Timing of clamping and cutting the cord: The risks of premature cord clamping are now well known, and a Cochrane review recommends delaying cord clamping. Most midwives I know (regardless of where they work) wait until the cord has stopped pulsing before clamping. Some are concerned about syntocinon crossing the placenta into the baby. However, syntocinon does not cross the placenta as previously thought. There is also a theory that the strong contraction caused by syntocinon will shunt excess blood from the placenta to baby. Again there is no evidence that this happens and during physiological birth all of the blood transfers to the baby – there is no ‘excess’ blood to shunt. There is also no evidence that waiting to clamp the cord increases the risk of jaundice (Rana et al. 2019)
- 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 easier 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.
- Whether or not controlled cord traction (CCT) 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). And another study found that CCT made no difference to the PPH rate and concluded (Deneux-Tharaux et al. 2013). So, women should 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. 2019; Salati et al. 2019). In summary, the reviews note that there is a ‘lack of high quality evidence’ but conclude that active management reduces the risk of haemorrhage in a ‘mixed risk’ population birthing in hospital. 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 regard to the last side effect – anecdotally, midwives report greater blood loss on the postnatal ward after the syntocinon or syntometrine has worn off but this is not measured in studies.
Both Cochrane reviews state that active management is not effective at reducing significant PPH for low risk women. When interpreting the review findings it is important to remember that all of the studies included were conducted in a hospital setting. The experimental group were those having ‘expectant’ management, and 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. Care providers in hospital settings can be inexperienced at supporting physiological placental birth (Reed, Kearney & Gabriel 2019; Kearney, Reed, Kynn et al. 2019).
Women with care providers experienced in supporting physiology have very different outcomes. A study by (Fahy, et al. 2010) compared active vs holistic physiological care. The midwives in the study were experienced with physiological placental births. 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.
As previously described, the baby plays an important role in assisting with the birth of the placenta. Therefore, undisturbed interactions between mother and baby are important in avoiding a PPH. A recent study looked at the impact of removing babies from their mother after birth and found that: “women who did not have skin to skin and breast feeding were almost twice as likely to have a PPH compared to women…” who did have this contact with their baby (Saxton et al. 2015). The authors conclude: “…this study suggests that skin to skin contact and breastfeeding immediately after birth may be effective in reducing PPH rates for women at any level of risk of PPH.”
Back to my initial title statement
A safe and effective physiological placental birth requires effective endogenous oxytocin release. This is 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 fundus (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.
The most important factor in ensuring a safe physiological birth of the placenta is a physiological birth of the baby.
However, in Australia (AIHW 2021) less than a quarter 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.
An interesting study by Nove et al. (2012) compared PPH rates between planned hospital birth vs planned homebirth. They adjusted for co-founders such as risk factors associated with PPH. The study found lower rates of PPH for women planning homebirth, even if transferred to hospital during labour or afterwards. The authors conclude: “Women and their partners should be advised that the risk of PPH is higher among births planned to take place in hospital compared to births planned to take place at home, but that further research is needed to understand (a) whether the same pattern applies to the more life-threatening categories of PPH, and (b) why hospital birth is associated with increased odds of PPH. If it is due to the way in which labour is managed in hospital, changes should be made to practices which compromise the safety of labouring women.”
Active management of the placenta will reduce 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.
- Birthing the placenta: women’s decisions and experiences
- Placentas and cord blood – The Midwives’ Cauldron Podcast
- Can I have a natural placental birth after induction? – Sara Wickham
- 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
- Placental birth: a history – PhD thesis Stojanovic 2012
- 30 Minute Third Stage – Gloria Lemay
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