Obstetrics_by_Ten_Teachers_19E_-_Kenny_Louise

256Obstetric emergencies

principle of all the manoeuvres is to reduce the anterior–posterior diameter of the shoulders and gain the maximum space in the maternal pelvis:

•Call for help.

•Ensure personnel are available to ‘scribe’. Document the time the head delivered, which

shoulder is anterior (this is the arm most vulnerable to injury) and the times at which each manoeuvre is employed.

•Drop the level of the delivery bed as low as it will go, and flatten the back of the bed so the woman

is completely flat. Remove the foot of the bed to allow access.

•Assess for and perform an episotomy, if needed.

•Using one assistant on each of the mother’s legs, flex and abduct the legs at the hip

(thighs to abdomen, known as MacRoberts manoeuvre). This flattens the lumbosacral spine and will facilitate delivery is around 90 per cent of cases.

•If this fails, suprapubic pressure should be applied by another assistant. This should be

applied over the posterior aspect of the anterior fetal shoulder and will act to push the shoulders together. It can be used in a constant and then rocking motion.

•If both these fail, then internal manoeuvres are necessary. The order of these will depend on the

skill and experience of the person conducting the delivery and the individual case. These manoeuvres have been named after famous obstetricians, but it is the process rather than the name that is important:

•An attempt can be made to rotate the baby, so that the shoulders enter the diagonal

to allow delivery. The first procedure is usually to insert a hand behind the anterior shoulder, and push it towards the chest (Rubin II). This will adduct the shoulders then push them into the diagonal. This

can be combined with pressure on the anterior aspect of the posterior shoulder to aid rotation (Woods’ screw). If this fails, an attempt can be made to rotate the baby in the opposite direction (reverse Woods’

screw). Delivery of the posterior arm can be attempted passing a hand into the vagina, in front of the posterior shoulder and deliver the posterior arm by swinging it in front of the fetal chest.

If these all fail, the patient can be moved on to all fours as this increases the anterior–posterior diameter of the inlet. In this position, the posterior arm can be delivered.

After this, manoeuvres of last resort include a symphysiotomy, in which the maternal symphysis is divided, Zavanelli’s, in which the head is reduced back into the vagina and a Caesarean section performed and intentional fracture of the fetal clavicle.

After delivery of the baby, the risks of maternal morbidity should be remembered: prevent the PPH and check for vaginal trauma.

Women will require debriefing after the delivery, and most obstetricians would suggest a Caesarean section in the next pregnancy.

Summary

Obstetric emergencies occur not uncommonly. The approach to them should be structured and regularly practised in training drills. In many cases, risk factors exist to enable prediction of emergencies and preventative steps to be taken. Documentation is crucial and lessons can be learnt from many emergency situations. For these reasons, most hospitals utilize an incident reporting system to allow reviews of these cases. Debriefing of the patient and their family after the event is vital.

Key points

•Use a structured approach to all emergencies.

•Call for help.

•Use the A (airway), B (breathing), C (circulation) approach to all maternal emergencies.

•Use drill-type training sessions.

•Documentation is vital.

•Debrief the patient and the family afterwards.

Additional reading

Grady K, Howell C, Cox C (eds). Managing obstetric emergencies and trauma. The MOET Course Manual, 2nd edn. London: RCOG Press, 2007.

Lewis G (ed.). The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers Lives: reviewing maternal deaths to make motherhood safer, 2003–2006. The Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH, 2007.

Magpie Trial Collaborative Group. Do women with preeclampsia, and their babies, benefit from magnesium

sulphate? The Magpie Trial: A randomised placebocontrolled trial. Lancet 2002; 359: 1877–90.

Royal College of Obstetricians and Gynaecologists. Placenta praevia and placenta praevia accreta: Diagnosis and management. Green-top Guidelines No. 27. London: RCOG, 2005.

Royal College of Obstetricians and Gynaecologists.

Shoulder dystocia. Green-top Guidelines No. 42.

London: RCOG, 2005.

Royal College of Obstetricians and Gynaecologists. Postpartum haemorrhage. Prevention and management. Green-top Guidelines No. 52. London: RCOG, 2009.

Physiological changes

Uterine involution

Involution is the process by which the postpartum uterus, weighing about 1 kg, returns to its prepregnancy state of less than 100 g. Immediately after delivery, the uterine fundus lies about 4 cm below the umbilicus or, more accurately, 12 cm above the symphysis pubis. However, within 2 weeks, the uterus can no longer be palpable above the symphysis. Involution occurs by a process of autolysis, whereby muscle cells diminish in size as a result of enzymatic digestion of cytoplasm. This has virtually no effect on the number of muscle cells, and the excess protein produced from autolysis is absorbed into the bloodstream and excreted in the urine. Involution

appears to be accelerated by the release of oxytocin in women who are breastfeeding, as the uterus is smaller than in those who are bottle-feeding. The height of the uterine fundus is measured daily to ascertain the trend in involution.

Signs: causes of delayed involution

•Full bladder

•Loaded rectum

•Uterine infection

•Retained products of conception

•Fibroids

•Broad ligament haematoma

A delay in involution in the absence of any other signs or symptoms, e.g. bleeding, is of no clinical significance.

Genital tract changes

Following delivery of the placenta, the lower segment of the uterus and the cervix appear flabby and there may be small cervical lacerations. In the first few days, the cervix can readily admit two fingers, but by the end of the first week it should become increasingly difficult to pass more than one finger, and certainly by the end of the second week the internal os should be closed. However, the external os can remain open permanently, giving a characteristic appearance to the parous cervix.

Lochia

Lochia is the blood-stained uterine discharge that is comprised of blood and necrotic decidua. Only the superficial layer of decidua becomes necrotic and is sloughed off. The basal layer adjacent to the myometrium is involved in the regeneration of new endometrium and this regeneration is complete by the third week. During the first few days after delivery, the lochia is red; this gradually changes to pink as the endometrium is formed, and then ultimately becomes serous by the second week. Persistent red lochia suggests delayed involution that is usually associated with infection or a retained piece of placental tissue. Offensive lochia, which may be accompanied by pyrexia and a tender uterus, suggests infection and should be treated with a broad-spectrum antibiotic. Retained placental tissue is associated with increased red blood cell loss and clots, and this may be suspected if the placenta and membranes were incomplete at delivery (see Chapter 14, Labour and Chapter 16, Obstetric emergencies). Management includes the use of antibiotics and evacuation of retained products under regional or general anaesthesia.

Puerperal disorders

Daily maternal observations include temperature, pulse, blood pressure, urinary function, bowel function, breast examination and feeding, assessment of uterine involution, appearance of lochia, perineal inspection, examination of legs and pelvic floor exercises. These observations should be made more frequently

in high-risk women or if an abnormality has been detected, for example the presence of maternal pyrexia. In the UK, it is traditional to check haemoglobin levels on day 3 unless otherwise indicated, and most women who are particularly symptomatic should be transfused if their haemoglobin level at this time is8 g/dL.

Perineal complications

Perineal discomfort is the single major problem for mothers, and about 80 per cent complain of pain in the first 3 days after delivery, with a quarter continuing to suffer discomfort at day 10. Discomfort is greatest in women who sustain spontaneous tears or have an episiotomy, but especially following instrumental delivery. A number of non-pharmacological and pharmacological therapies have been used empirically with varying degrees of success. However, local cooling (with crushed ice, witch hazel or tap water) and topical anaesthetics, such as 5 per cent lignocaine gel, provide short-term symptomatic relief. Effective analgesia following perineal trauma can be achieved with regular paracetamol. If necessary, diclofenac given rectally or orally may also be added. Codeine derivatives are not preferable, as they have a tendency to cause constipation.

Infections of the perineum are generally uncommon considering the risk of bacterial contamination during delivery; therefore, when signs of infection (redness, pain, swelling and heat) occur, especially when associated with a raised temperature, these must be taken seriously. Swabs for microbiological culture must be taken from the infected perineum, and broad-spectrum antibiotics (see below) should be commenced. If there is a collection of pus, drainage should be encouraged by removal of any skin sutures; otherwise infection would spread, with increasing morbidity and a poor anatomical result.

Spontaneous opening of repaired perineal tears and episiotomies is usually the result of secondary infection. Surgical repair should never be attempted in the presence of infection. The wound should be irrigated twice daily and healing should be allowed to occur by secondary intention. If there is a large, gaping wound, secondary repair should only be performed when the infection has cleared, there is no cellulitis or exudate present and healthy granulation tissue can be seen.

260 The puerperium

Bladder function

Voiding difficulty and over-distension of the bladder are not uncommon after childbirth, especially if regional anaesthesia (epidural/spinal) has been used. It is now known that after epidural anaesthesia the bladder may take up to 8 hours to regain normal sensation. During this time, about 1 L of urine may be produced and therefore if urinary retention occurs, considerable damage may be inflicted on the detrusor muscle. Over-stretching of the detrusor muscle can dampen bladder sensation and make the bladder hypocontractile, particularly with fibrous replacement of smooth muscle. In this situation, overflow incontinence of small amounts of urine may erroneously be assumed to be normal voiding. Fluid overloading prior to epidural analgesia, the antidiuretic effect of high concentrations of oxytocin during labour, increased postpartum diuresis (particularly in the presence of oedema) and increased fluid intake by breastfeeding mothers all contribute to the increased urine production in the puerperium. Therefore, an intake/output chart alone may not detect incomplete emptying of the bladder.

Women who have undergone a traumatic delivery, such as a difficult instrumental delivery, or who have suffered multiple/extended lacerations or

avulvovaginal haematoma, may find it difficult to void because of pain or periurethral oedema. Other causes of pain, such as prolapsed haemorrhoids, anal fissures, abdominal wound haematoma or even stool impaction of the rectum, may interfere with voiding. The midwife needs to be particularly vigilant after an epidural or spinal anaesthetic to avoid bladder distension. The distended bladder should either be palpable as a suprapubic cystic mass or it may displace the uterus laterally or upwards, thereby increasing the height of the uterine fundus.

In order to minimize the risk of over-distension of the bladder in women undergoing a Caesarean section under regional anaesthesia, a urinary catheter may be left in the bladder for the first 12–24 hours. The benefit of leaving a catheter in situ for about 12 hours after epidural insertion should be evaluated against

avigorously enforced postpartum voiding protocol and the small risk of urinary tract infection. However, any woman who has not passed urine within 4 hours of delivery should be encouraged to do so before resorting to catheterization. In general, a clean-catch specimen of urine should be sent for microscopy,

culture and sensitivity, and if the residual urine in the bladder is 300 mL, a catheter should be left in to allow free drainage for 48 hours.

Although vaginal delivery is strongly implicated in the development of urinary stress incontinence, it rarely poses a problem in the early puerperium. Therefore, any incontinence should be investigated to exclude a vesicovaginal, urethrovaginal or, rarely, ureterovaginal fistula. Obstetric fistulae are rare in the UK, but are a source of considerable morbidity in developing countries. Pressure necrosis of the bladder or urethra may occur following prolonged obstructed labour, and incontinence usually occurs in the second week when the slough separates. Small fistulae may close spontaneously after a few weeks of free bladder drainage; large fistulae will require surgical repair by a specialist.

Bowel function

Constipation is a common problem in the puerperium. This may be due to an interruption in the normal diet and possible dehydration during labour. Advice on adequate fluid intake and increase in fibre intake may be all that is necessary. However, constipation may also be the result of fear of evacuation due to pain from a sutured perineum, prolapsed haemorrhoids or anal fissures. Avoidance of constipation and straining is of utmost importance in women who have sustained a third-degree or fourth-degree tear. A large, hard bolus of stool in this situation would disrupt the repaired anal sphincter and cause anal incontinence. It is important to ensure that these women are prescribed lactulose and ispaghula husk (Fybogel, Regulan) or methylcellulose immediately after the repair, for a period of 2 weeks.

The high prevalence of anal incontinence and faecal urgency following childbirth has only recently been recognized. One prospective study using anal endosonography has identified evidence of occult anal sphincter trauma in one-third of primiparous women, although only 13 per cent admitted to defaecatory symptoms by 6 weeks postpartum. Larger, retrospective, short-term studies of parous women indicate a prevalence of between 6 and 10 per cent. Long-term anal incontinence following primary repair of a third-degree or fourth-degree tear occurs in 5 per cent of women, and anovaginal/rectovaginal fistulae occur in 2–4 per cent of these women (Figure 17.1). It is therefore important to consider a fistula as a cause of anal incontinence in the postpartum period,

particularly if the woman complains of passing wind or stool per vagina. Approximately 50 per cent of small anovaginal fistulae will close spontaneously over a period of 6 months, but larger fistulae will require formal repair.

Secondary postpartum haemorrhage

Secondary postpartum haemorrhage (PPH) is defined as fresh bleeding from the genital tract between 24 hours and 6 weeks after delivery (see Chapter 16, Obstetric emergencies, for primary PPH). The most common time for secondary PPH is between days 7 and 14, and the cause is most commonly attributed to retained placental tissue. Associated features include crampy abdominal pain, a uterus larger than appropriate, passage of bits of placental tissue or tissue within the cervix and symptoms and signs of infection. The management of heavy bleeding includes an intravenous infusion, cross-match of blood, Syntocinon, an examination under anaesthesia and evacuation of the uterus. Antibiotics should be given if placental tissue is found, even without evidence of overt infection. If blood loss is not excessive, the use of pelvic ultrasound to exclude retained products is contentious; distinction between retained products and blood clot can be extremely difficult. Other causes of secondary PPH include endometritis, hormonal contraception, bleeding disorders, e.g. von Willebrand’s disease, and rarely choriocarcinoma.

Obstetric palsy

Obstetric palsy, or traumatic neuritis, is a condition in which one or both lower limbs may develop signs of a motor and/or sensory neuropathy following delivery. Presenting features include sciatic pain, footdrop, parasthesia, hypoaesthesia and muscle wasting. The mechanism of injury is unknown and it was previously attributed to compression or stretching of the lumbosacral trunk as it crosses the sacroiliac joint during descent of the fetal head. It is now believed that herniation of lumbosacral discs (usually L4 or L5) can occur, particularly in the exaggerated lithotomy position and during instrumental delivery. An orthopaedic opinion should be sought and management includes bed rest with a firm board beneath the mattress, analgesia and physiotherapy. Peroneal nerve palsy can occur when the nerve is compressed between the head of the fibula and the lithotomy pole, resulting in unilateral foot-drop. The development of urinary and faecal incontinence is most likely due to structural damage to the anal sphincter muscle and supporting fascia.

Symphysis pubis diastasis

Separation of the symphysis pubis can occur spontaneously in at least 1 in 800 vaginal deliveries.

Deliberate surgical separation of the pubis in labour (symphysiotomy) is rarely performed in

262The puerperium

extreme cases of shoulder dystocia. Spontaneous separation is usually noticed after delivery and has been associated with forceps delivery, rapid second stage of labour or severe abduction of the thighs during delivery. Common signs and symptoms include symphyseal pain aggravated by weight-bearing and walking, a waddling gait, pubic tenderness and a palpable interpubic gap. Treatment includes bed rest, anti-inflammatory agents, physiotherapy and a pelvic corset to provide support and stability.

Thromboembolism

The risk of thromboembolic disease rises five-fold during pregnancy and the puerperium. The majority of deaths occur in the puerperium and are more common after Caesarean section. If deep vein thrombosis or pulmonary embolism is suspected, full anticoagulant therapy should be commenced and a lower limb compression ultrasound and/or lung scan should be carried out within 24–48 hours (see Chapter 8, Antenatal obstetric complications and Chapter 16, Obstetric emergencies).

Puerperal pyrexia

Significant puerperal pyrexia is defined as a temperature of 38ºC or higher on any two of the first 10 days postpartum, exclusive of the first 24 hours (measured orally by a standard technique). A mildly elevated temperature is not uncommon in the first 24 hours, but any pyrexia associated with tachycardia merits investigation. In about 80 per cent of women who develop a temperature in the first 24 hours following a vaginal delivery, no obvious evidence of infection can be identified. The reverse holds true for women delivering by Caesarean section, when a wound infection should be considered. Common sites associated with puerperal pyrexia include chest, throat, breasts, urinary tract, pelvic organs, Caesarean or perineal wounds and legs (Table 17.1).

Chest complications

Chest complications are most likely to appear in the first 24 hours after delivery, particularly after general anaesthesia. Atalectasis may be associated with fever and can be prevented by early and regular chest physiotherapy. Aspiration pneumonia (Mendleson’s

syndrome) must be suspected if there is wheezing, dyspnoea, a spiking temperature and evidence of hypoxia.

Genital tract infection

Genital tract infection following delivery is referred to as puerperal sepsis and is synonymous with older descriptions of puerperal fever, milk fever and childbed fever. It was not realized until the midnineteenth century that the high maternal mortality and morbidity were due to poor hygiene of the birth attendants; the establishment of lying-in hospitals and overcrowding perpetuated the condition to epidemic proportions. Until 1937, puerperal sepsis was the major cause of maternal mortality. The discovery of sulphonamides in 1935 and the simultaneous reduction in the virulence of the haemolytic streptococcus resulted in a dramatic fall in maternal mortality. The Confidential Enquiry into Maternal and Child Health (UK) reported that, in 2003–5, genital tract sepsis accounted for 14 per cent of direct causes of maternal death. Although some of these cases followed miscarriage or occurred antenatally after preterm prelabour rupture of membranes (PPROM), the majority of deaths occurred post-natally, indicating that puerperal fever was a significant factor in maternal death.

Aetiology of genital tract infections

A mixed flora normally colonizes the vagina with low virulence. Puerperal infection is usually polymicrobial and involves contaminants from the bowel that colonize the perineum and lower genital tract. The organisms most commonly associated with puerperal genital infection are listed in the box below. Following delivery, natural barriers to infection are temporarily removed and therefore organisms with a pathogenic potential can ascend from the lower genital tract into the uterine cavity. Placental separation exposes a large raw area equivalent to an open wound, and retained products of conception and blood clots within the uterus can provide an excellent culture medium for infection. Furthermore, vaginal delivery is almost invariably associated with lacerations of the genital tract (uterus, cervix and vagina). Although these lacerations may not need surgical repair, they can become a focus for infection similar to iatrogenic wounds, such as Caesarean section and episiotomy.

Aerobes

•Gram-positive

•Beta-haemolytic streptococcus, groups A, B, D

•Staphylococcus epidermidis and aureus

•Enterococci – Streptococcus faecalis

•Gram-negative

•Escherichia coli

•Haemophilus influenzae

•Klebsiella pneumoniae

•Pseudomonas aeruginosa

•Proteus mirabilis

•Gram-variable

• Gardenella vaginalis

Anaerobes

•Peptococcus sp.

•Peptostreptococcus sp.

•Bacteroides – B. fragilis, B. bivius, B. disiens

•Fusobacterium sp.

Miscellaneous

•Chlamydia trachomatis

•Mycoplasma hominis

•Ureaplasma urealyticum

264 The puerperium

v Signs of puerperal pelvic infection

•Pyrexia and tachycardia

•Uterus – boggy, tender and larger

•Infected wounds – Caesarean/perineal

•Peritonism

•Paralytic ileus

•Indurated adnexae (parametritis)

•Bogginess in pelvis (abscess)

Symptoms of puerperal pelvic infection

•Malaise, headache, fever, rigors

•Abdominal discomfort, vomiting and diarrhoea

•Offensive lochia

•Secondary PPH

Table 17.2 Investigations for puerperal genital infections

Chlamydia trachomatis puerperal parametritis may develop in one-third of women who had a preexisting infection, but presentation is usually delayed. Investigations for puerperal genital infections are shown in Table 17.2.

There are a number of factors that determine the clinical course and severity of the infection, namely the general health and resistance of the woman, the virulence of the offending organism, the presence of haematoma or retained products of conception and

the timing of antibiotic therapy and associated risk factors. The common methods of spread of puerperal infection are as follows:

•An ascending infection from the lower genital tract or primary infection of the placental site may

spread via the Fallopian tubes to the ovaries, giving rise to a salpingo-oophoritis and pelvic peritonitis. This could progress to a generalized peritonitis and the development of pelvic abscesses.

•Infection may also spread by contiguity directly into the myometrium and the parametrium,

giving rise to a metritis or parametritis, also referred to as pelvic cellulitis. Pelvic peritonitis and abscesses may also occur.

•Infection may also spread to distant sites via lymphatics and blood vessels. Infection from the

uterus can be carried by uterine vessels into the inferior vena cava via the iliac vessels or, directly, via the ovarian vessels. This could give rise to a septic thrombophlebitis, pulmonary infections or a generalized septicaemia and endotoxic shock.

Common risk factors for puerperal infection

•Antenatal intrauterine infection

•Caesarean section

•Cervical cerclage for cervical incompetence

•Prolonged rupture of membranes

•Prolonged labour

•Multiple vaginal examinations

•Instrumental delivery

•Manual removal of the placenta

•Retained products of conception

•Non-obstetric, e.g. obesity, diabetes, human immunodeficiency virus (HIV)

In contrast to pelvic inflammatory disease unrelated to pregnancy, tubal involvement in puerperal sepsis is in the form of perisalpingitis, which, rarely, causes tubal occlusion and consequent infertility. Tubo-ovarian abscesses are also a rare complication of puerperal sepsis.

Mild to moderate infections can be treated with a broad-spectrum antibiotic, e.g. co-amoxiclav or a cephalosporin, such as cefalexin, plus metronidazole. Depending on the severity, the first few doses should be given intravenously.

With severe infections, there is a release of inflammatory and vasoactive mediators in response to the endotoxins produced during bacteriolysis. The resultant local vasodilatation causes circulatory embarrassment and hence poor tissue perfusion. This phenomenon is known as septicaemic/ septic/endotoxic shock, and delay in appropriate management could be fatal.

Necrotizing fasciitis is a rare but frequently fatal infection of skin, fascia and muscle. It can originate in perineal tears, episiotomies and Caesarean section wounds. Perineal infections can extend rapidly to involve the buttocks, thighs and lower abdominal wall. A variety of bacteria can be involved, but anaerobes predominate and Clostridium perfringens is usually identified. In addition to general signs of infection, there is extensive necrosis, crepitus and inflammation. As well as the measures usually taken to manage septic shock, wide debridement of necrotic tissue under general anaesthesia is absolutely essential to avoid mortality. Split-thickness skin grafts may be necessary at a later date.

Prevention of puerperal sepsis

Increased awareness of the principles of general hygiene, a good surgical approach and the use of aseptic techniques have contributed to the decline in severe puerperal sepsis. However, the risk of sepsis is higher following Caesarean section, particularly when performed after the onset of labour. There is now overwhelming evidence that prophylactic antibiotics during emergency Caesarean section reduce the risk of post-operative infection, namely wound infection, metritis, pelvic abscess, pelvic thrombophlebitis and septic shock. A single intraoperative dose of antibiotics (amoxiclav or cephalosporin plus metronidazole) should be given after clamping of the umbilical cord to avoid unnecessary exposure of the baby to antibiotics. The benefit of prophylaxis for elective Caesarean section is of greater significance in units where the background infectious morbidity is high.

The breasts

Anatomy

The breasts are largely made up of glandular, adipose and connective tissue (Figure 17.2). They lie superficial

Pectoralis major muscle

Lactiferous

sinus

Fat

Glandular

tissue

Figure 17.2 The breast during lactation

to the pectoralis major, external oblique and serratus anterior muscles, extending between the second and sixth rib from the sternum to the axilla. A pigmented area called the areola, which contains sebaceous glands, surrounds the nipple. During pregnancy, the areola becomes darker and the sebaceous glands become prominent (Montgomery’s tubercles). The breast is comprised of 15–25 functional units arranged radially from the nipple and each unit is made up of a lactiferous duct, a mammary gland lobule and alveoli. The lactiferous ducts dilate to form a lactiferous sinus before converging to open in the nipple. Contractile myoepithelial cells surround the ducts as well as the alveoli.

Physiology

The human species is unique in that most of the breast development occurs at puberty and is therefore primed to produce milk within 2 weeks of hormonal stimulation. It is hypothesized that, unlike animals, female breasts have an erotic role to attract the male to procreate. The control of mammary growth and development is not fully understood and many hormones may contribute to this process. In general, oestrogens stimulate proliferation of the lactiferous ducts (possibly with adrenal steroids and growth hormones), while progesterone is responsible for the development of the mammary lobules. During early pregnancy, lactiferous ducts and alveoli proliferate, while in later pregnancy the alveoli hypertrophy in