Cord presentation means that a loop of umbilical cord lies below the presenting part of the fetus, with intact membranes. If the membranes rupture this is known as a cord prolapse. The prolapse can be occult, i.e. alongside the presenting part, or frank, where the cord escapes through the cervix and may even be visible outside the vagina.

Incidence and facts

• Cord prolapse is reported as 0.4% in vertex presentations, 0.5% in frank breeches, 4–6% in complete breeches and 15–18% in footling breeches (American Academy of Family Physicians (AAFP), 2004).

• 50% of cord prolapse cases occur following artificial rupture of membranes (ARM) (Prabulos & Philipson, 1998).

• Umbilical cord prolapse is associated with poor perinatal outcomes, even when emergency delivery facilities are available (Prabulos & Philipson, 1998).

• Squire (2002) suggests that mortality is predominantly associated with congenital abnormities and prematurity rather than birth asphyxia per se.

• Occult cord prolapse is associated with less perinatal morbidity than frank prolapse (Prabulos & Philipson, 1998).

• In only 41% of cases, electronic fetal monitoring aided the diagnosis of cord prolapse (Murphy & MacKenzie, 1995).

Associated risk factors

• Any situation where the presenting part may not engage well in the pelvis, e.g. high presenting part, high parity, multiple birth, polyhydramnios, small/preterm baby, malpresentation (e.g. breech) (McGeown, 2001), ARM with a high presenting part (AAFP, 2004).

• Long umbilical cord (AAFP, 2004).

Signs and symptoms of cord prolapse

• Visible cord may protrude from vagina.

• Cord felt (often pulsating) on vaginal examination.

• Fetal bradycardia/prolonged late decelerations following rupture of membranes, possibly with fresh meconium liquor.

Practice recommendations/manoeuvres

• Call for help. If at home/birthing centre, call paramedic ambulance even if delivery appears imminent; if in second stage, also call midwife ventouse/forceps practitioner (if available). Give accurate and concise information when communicating with the receiving obstetric unit.

• Maintain pressure on presenting part. Keep the fingers in the vagina firmly pushing on the presenting part, particularly during contractions, to relieve cord compression until urgent delivery is achieved (AAFP, 2004). If achievable maintain pressure during ambulance transfer or while the woman is wheeled to a birth room/theatre (AAFP, 2004). This can be uncomfortable and stressful for whoever is performing the pressure.

• Remain calm and briefly explain to the woman and her partner what is happening and what is required of them. The clinician conducting internal pressure cannot participate in other activities and is ideally situated to offer supportive reassurance and explanations to the woman and her partner during this frightening situation.

Amniotic fluid embolism (AFE) is a rare but catastrophic condition, which is usually fatal (AAFP, 2004). A woman may collapse rapidly with no clear diagnosis at the time. AFE is an anaphylactic type reaction to amniotic fluid that has entered the woman’s circulation (AAFP, 2004). This results in left ventricular failure and pulmonary vasospasm resulting in acute lung injury. Clotting factors are also activated with disseminated intravascular coagulation (DIC) commonly resulting (Davis, 1999; Fahy, 2001; AAFP, 2004). The rapidly deteriorating situation can be extremely stressful for staff and birth partners, particularly as death so often results.

Incidence and facts

• Incidence of AFE is reported as 1:20 000 deliveries (AAFP, 2004), with a 26.4–61% mortality rate (AAFP, 2004; Confidential Enquiry into Maternal and Child Health (CEMACH), 2004). The perinatal mortality rate is 40%.

• CEMACH (2004) reports 5 deaths from AFE, with 19 cases reported to the National AFE Register.

• Risk factors include multiparity, abruption, intrauterine fetal demise, tumultuous labour and oxytocic hyperstimulation (AAFP, 2004). AFE remains unpredictable, rapidly progressive and unpreventable (CEMACH, 2004).

• Diagnosis may be confirmed by the presence of fetal squames and lanugo hair in the pulmonary vasculature at post-mortem (CEMACH, 2004), or reliant on clinical observations if autopsy is unavailable (AAFP, 2004). Fahy (2001) suggests that the more knowledgeable clinicians become about AFE, the more frequently it is diagnosed.

Signs and symptoms of AFE

Uterine dehiscence is defined as disruption of the uterine muscle with intact serosa (Royal College of Paediatrics and Child Health (RCOG), 2007). The more serious condition of uterine rupture is defined as disruption of the uterine muscle extending to and involving the uterine serosa or disruption of the uterine muscle with extension to the bladder or broad ligament (RGOG, 2007). Occasionally these events occur antenatally, but more often during labour, birth or prior to delivery of the placenta (RCOG, 2007).

Shoulder dystocia is one of the most serious birth emergencies. It is caused by the impaction of the anterior shoulder of the fetus against the maternal symphysis pubis, or less commonly the posterior fetal shoulder on the sacral promontory, after delivery of the head (RCOG, 2005), requiring additional obstetric manoeuvres to release the shoulders (RCOG, 2005). Unless the baby is born within a few minutes of its head emerging, it is likely to die. Shoulder dystocia cannot be predicted (WHO, 2003); all midwives must be able to recognise and manage this emergency promptly (Brown, 2002).

Incidence and facts

• Shoulder dystocia occurs in 0.3–1% of babies weighing 2.5–4 kg and 5–7% of babies weighing 4–4.5 kg (AAFP, 2004).

• Over 50% of shoulder dystocias occur in normal sized babies with no identifiable risk factors (AAFP, 2004).

• Preconception and prenatal risk factors have extremely poor predictive value and therefore in clinical practice do not facilitate accurate, reliable prediction of shoulder dystocia (Gherman, 2002).

• Morbidity for the baby includes obstetric brachial plexus palsy (OBPP) injuries in 7–20% following dystocia, with 1–2% of those sustaining permanent injury (AAFP, 2004). Hypoxia, fractures of the clavicle/humerus, bruising and soft tissue damage may occur, and in severe cases, fetal death may result.

• Litigation may result from OBPP: 40–60 births from 1993 to 1997 resulted in claims (NHSLA, 2003).

• Morbidity for the woman includes trauma, blood loss, bruising to the perineum/ genital tract and surrounding tissues, episiotomy/serious tears, psychological trauma, as well as, in severe cases, grief at the death of her baby.

• Simulated training sessions have been found to improve performance in shoulder dystocia management (Deering et al., 2004).

Associated risk factors

All shoulder dystocia-associated risk factors have poor predictive value in clinical practice (WHO, 2003).

Antenatal associated risks:

• Macrosomia (AAFP, 2004) and previous baby >4.0 kg (CEMACH, 2004).

• Maternal diabetes, short stature and abnormal pelvic anatomy (AAFP, 2004).

• Previous instrumental delivery (AAFP, 2004).

• Post-dates pregnancy (AAFP, 2004).

• Previous shoulder dystocia (AAFP, 2004).

Intrapartum-associated risks:

• Prolonged first or second stage of labour (RCOG, 2005).

• Birthing semi-recumbent on a bed can restrict the movement of the coccyx and sacrum contributing to ‘bed-birth dystocia’ (Mortimore & McNabb, 1998; McGeown, 2001).

• Oxytocin augmentation (RCOG, 2005).

• Instrumental delivery (AAFP, 2004).

Recognising shoulder dystocia

Shoulder dystocia is usually preceded by a slow ‘bobbing’ delivery of the baby’s head; the baby’s chin then retracts against the perineum and ‘turtlenecks’ (AAFP, 2004). With the next contraction the baby will not deliver as its anterior shoulder is impacted against the symphysis pubis bone, due to the shoulder (bisacromial) diameter exceeding the diameter of the pelvic inlet (AAFP, 2004).

Beware of overdiagnosing shoulder dystocia. Sometimes anxious clinicians start to worry after only 1 or 2 minutes. Think: ‘has there been a contraction yet?’ Two minutes can seem like a long time, but no baby will be compromised at this point: this is quite normal. Spontaneous restitution of the shoulders may take one or two contractions. Premature traction without a contraction may give the false impression that dystocia is occurring.

Practice recommendations

Upright birthing positions improve the alignment of the mobile pelvic bones and improve the shape and capacity of the pelvis, optimising the chances of a ‘good fit’ between baby and pelvis (Simpkin & Ancheta, 2005). Common sense suggests that any woman at risk of shoulder dystocia should be discouraged from birthing in the semi-recumbent position.

Changing the woman’s position in itself can be beneficial in preventing/shifting impacted shoulders.

Do not clamp and cut a nuchal cord. This will cut off the only oxygen supply the baby has, and hypoxia will rapidly follow.

Avoid excessive traction. Once shoulder dystocia is diagnosed, do not put any further traction on the head. A previously healthy fetus will withstand up to 10 minutes of complete anoxia before there is a significant risk of brain damage (Pasternak, 1993). Whilst a fetus who has experienced prior fetal distress may not endure more than 5 minutes of anoxia (Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI), 1998) and it may be justifiable to resume traction if other manoeuvres have repeatedly failed, any OBPP injury following a head-to-body delivery of, say, 2–3 minutes will probably be judged in court to have been due to excessive traction (Johnson, 2005). Performing the manoeuvres correctly will certainly take more than 2–3 minutes.

Avoid fundal pressure which could increase shoulder impaction and cause serious injuries, including uterine rupture, haemorrhage and even maternal death.

Use of systematic manoeuvres. Most shoulder dystocias will resolve with these manoeuvres. Prophylactic use of McRoberts or other manoeuvres prior to clinical diagnosis of shoulder dystocia requires further evaluation (Poggi, 2004). Many midwives might respond however that prevention happens all the time: optimal positioning in the second stage, e.g. squatting/all fours (which might be described as physiological