RCOG Green-top guidelines reviewed

No. 1(B) Tocolytic drugs for women in preterm labour

No. 5
Management of ovarian hyperstimulation syndrome:
No. 7
Antenatal corticosteroids to prevent respiratory distress syndrome
No. 8
Amniocentesis and Chorionic Villus Sampling
No. 10a The management of severe pre-eclampsia / eclampsia
No. 12
Breast cancer in Pregnancy
No. 13
Chicken pox in pregnancy
No. 17
The investigation and treatment of couples w/ recurrent miscarriage
No. 19
Hormone replacement therapy and venous thromboembolism
No. 20a EXTERNAL CEPHALIC VERSION AND REDUCING THE INCIDENCE OF BREECH PRESENTATION
No. 20b The management of Breech Presentation
No. 21
THE MANAGEMENT OF TUBAL PREGNANCY
No. 22
Rh Prophylaxis, Anti-D Immunoglobulin
No. 23
Acute pelvic inflammatory disease
No. 24
Endometriosis, investigation and treatment
No. 25
Early Pregnancy Loss, Management
No. 26
Operative vaginal delivery
No. 27
Placenta Praevia and Placenta Praevia Accreta: Diagnosis and Management)
No. 28
Thromboembolic disease in pregnancy and the puerperium.
No. 29
THE MANAGEMENT OF THIRD- AND FOURTH-DEGREE PERINEAL TEARS
No. 30
Genital Herpes in Pregnancy, Management
No. 31
Small-for-Gestational-Age Fetus, Investigation and Management
No. 33
Polycystic Ovary Syndrome, Long-Term Consequences
No. 34
Ovarian Cysts in Postmenopausal Women
No. 35
Urodynamic Stress Incontinence, Surgical Treatment
No. 36
Prevention of early onset neonatal Group B streptococcal Disease:
No. 38. THE MANAGEMENT OF GESTATIONAL TROPHOBLASTIC DISEASE
No. 39
Management HIV in pregnancy
No. 40
Venous thromboembolism and hormonal contraception
No. 41
Chronic pelvic pain, initial management
No. 42
Shoulder dystocia
No. 43
Obstetric Cholestasis
No. 44
Preterm Prelabour Rupture of Membranes
No. 45
Birth after Previous Caesarean birth
No. 46
Vaginal Vault Prolapse
No. 47
Blood transfusion in Obstetrics
No. 48
Premenstrual syndrome
No. 49
Laparoscopic Injuries
No. 50
Umbilical Cord Prolapse
No. 51
Monochorionic Twin Pregnancy, Management
No. 52
Postpartum Haemorrhage, Prevention and Management
No. 53
Female Genital Mutilation Management
No. 54a The prevention of malaria in pregnancy
No. 54b The diagnosis and treatment of malaria in pregnancy
CMACE/RCOG Joint Guideline: Management of Women with Obesity in Pregnancy
RCOG Statement No. 5 Alcohol consumption & the outcomes of pregnancy

No 1. (B) Tocolytic drugs for women in preterm labour

Preterm birth is the single most important single determinant of adverse infant outcome. The most mortality and morbidity is
babies born before 34 weeks.

Tocolytics suppress uterine contractions: beta-blockers, calcium channel blockers, prostaglandin synthetase inhibitors,
nitric oxide donors and Oxytocin receptor antagonists. Ritodrine (beta-agonist) remains the most widely used.

Magnesium sulphate is used in the US

Tocolysis has also been advocated for the management of intrapartum fetal distress, impaired fetal growth and facilitate
external cephalic version at term.

RCG guideline reasonable not to use tocolytics. But they may be used to gain a few extra days for a completion of a
course of corticosteroids or in utero transfer

Tocolysis has not been associated with any clear effects on perinatal death

Ritodrine no longer seams to be the best choice. Atosiban or nifedipine appears preferable as they have fewer side
effects and seam to be comparable in effectiveness

Beta-agonist side effects include: palpitations, tremor, nausea, headache and chest pain. Pulmonary oedema well
recognised complication.

Nifedipine was associated with a better chance of delaying delivery for over 48 hours and a lower risk of RDS or
admission to a special care unit and fewer maternal adverse effects than beta-agonists, largely Ritodrine

Calcium channel blockers did seam to reduce of neonatal RDS and neonatal jaundice.

Atosiban is licensed in the UK. The initial bolus dose is 6.75mg over 1 minute, followed by an infusion of 18 mg/hour for 3
hours and then 6 mg/hour for to 45 hours.

Nifedipine has had advantage of oral use and its cheap. 10mg sublingually every 15 minutes for the first, contraction
stopped. Then 60-160 mg/day of slow release nifedipine.

No 5. Management of ovarian hyperstimulation syndrome:

Definition: OHSS is a systemic disease from vasoactive products released by hyperstimulated ovaries. There is increased
capillary permeability, leading to leakage of fluid from the vascular compartment, with third space fluid accumulation and
intravascular dehydration. Severe manifestations include thrombosis, renal and liver dysfunction and ARDS causing serious
morbidity. Mild forms of OHSS are common, affecting 33% of IVF cycles and 3-8% of IVF cycles are complicated by moderate
or severe OHSS. Majority of case happen after IVF, but may occur after clomifene and gonadotrophin ovulation induction.
Tests: body weight and abdominal girth measurement, pelvic US (ovarian size and ascites). Lab tests include haemoglobin,
haematocrit, serum creatinine and electrolyte and liver function tests. Chest x-ray in women with respiratory symptoms and
signs of hydrothorax, pulmonary infection and pulmonary embolism and also an ABG. ECG if a PE or pericardial effusion is
suspected.
Complications: ovarian torsion and haemorrhage with large cysts, pelvic infection, intra-abdominal haemorrhage, ectopic
pregnancy and appendicitis.
Mild OHSS
Moderate OHSS
Severe OHSS
Critical OHSS

Abdominal bloating, mild abdo pain, ovarian size < 8cm

Moderate abdominal pain, N&V, ascites on ultrasound, ovaries > 8cm
Clinical ascites (occasionally hydrothorax), oligouria, haemoconcentration >45%
haematocrit, hypoproteinaemia, ovary >12 cm
Tense ascites or large hydrothorax, haematocrit >55%, WCC > 25,000, anuria, oligouria,
thromboembolism, ARDS

Normal presents about 9 days after the ovulatory dose of HCG administered for follicular maturation.
High Risk: PCOS, women < 30, use of GnRH agonists, development of multiple follicles during treatment, exposure to
LH/hCG, and previous episodes of OHSS.
Treatment: mild OHSS and moderate can be treated as an outpatient. Analgesia using paracetamol or codeine, but NSAID
should be avoided. Women should be encouraged to drink to thirst, rather than to excess. Strenuous exercise and sexual
intercourse should be avoided for fear of injury or torsion of hyperstimulated ovary. Women should continue progesterone luteal
support but hCG luteal support is inappropriate. Always look out for worsening abdominal distension, shortness of breath,
decreased urinary output. Antiemetic such as prochlorperazine, metoclopramide and cyclizine. Hyponatraemia may be
dilutional as a result of antiduretic hormone hypersecretion. Diuretic should be avoided as they deplete intravascule volume.
Avoid the risk of hypervolaemia and worsening ascites.
Paracentesis (ultrasound guidance) should be considered in women who are distressed due to abdominal distension or in
whom oligouria persists despite adequate volume replacement. Repeated paracentese may be avoided by the use of a pigtail
or Suprapubic catheter that can be left in place. All women should receive support stockings and prophylactic heparin therapy.
The risk of thrombosis persists into the first trimester and heparin may be needed

No. 7 Antenatal corticosteroids to prevent respiratory distress syndrome

Respiratory delivery rate vary 6% to 15% of all deliveries. RDS is known to affect 40-50% of babies born before 32 weeks.

A Cochrane meta-analysis indicated that antenatal corticosteroids therapy reduces the incidence of RDS, neonatal death
and intraventricular haemorrhage

There is a clear benefit after PROM in reducing RDS

RDS reduction in babies born after 34 weeks did not reach statistical significance, although the trend was towards
benefit. Before 31 weeks, one case of RDS is prevented for every 5 women treated.

The optimal treatment-delivery interval for administration of antenatal corticosteroids is more than 24 hours but fewer than
7 days after the start of treatment

The use of antenatal steroids in multiple pregnancies is recommended, but a significant reduction in rates of RDS has not
been shown.

In preterm labour it is reasonable not to use tocolytic drugs, as there is no clear evidence that they improve outcome.
However short term use may be used to complete a course of corticosteroids.

Corticosteroids do not seam to increase the risk of infection. The use of corticosteroids in pregnancy complicated by
maternal diabetes is recommended, but a significant reduction in rates of RDS has not been demonstrated. Maternal
diabetes is a recognised risk factor for neonatal RDS.

In view of the adverse effects of maternal hypoglycaemia on fetal lung maturity it is possible that any benefit of
corticosteroids could be offset by corticosteroid-induced hyperglycaemia.

Every effort should be made to initiate corticosteroids in women between 24-34 weeks with threatened preterm labour,
antepartum haemorrhage, preterm rupture of membranes, any condition requiring preterm delivery

Between 35-36 weeks steroids can be considered

Corticosteroid are contraindicated in a woman suffering form systemic infection including TB. Caution in chorioamnitis.

Betametasone is the steroid of choice

No. 8 Amniocentesis and Chorionic Villus Sampling

Amniocentesis is the most common invasive prenatal diagnostic procedure undertaken in the UK. Most amniocenteses are
performed to obtain amniotic fluid for karyotyping from 15 weeks (15+0 ) onwards.
Chorionic villus sampling (CVS) is usually performed between 11 (11+0 ) and 13 (13+6 ) weeks of gestation and involves
aspiration or biopsy of placental villi. CVS can be performed using either a transabdominal or a transcervical approach.

Women should be informed that the additional risk of miscarriage following amniocentesis is around 1%. Women should
be informed that the additional risk of miscarriage following CVS may be slightly higher than that of amniocentesis carried
out after 15 weeks gestation.

Amniocentesis should be performed after 15 (15+0) weeks of gestation. Amniocentesis before 14 (14+0) weeks of
gestation (early amniocentesis) has a higher fetal loss rate and increased incidence of fetal talipes and respiratory
morbidity compared with other procedures.

CVS should not be performed before 10 (10+0) completed weeks of gestation.

Needle insertion during amniocentesis and transabdominal CVS should be carried out under

simultaneous ultrasound visualisation by the practitioner performing the ultrasound guidance.

Transplacental passage of the amniocentesis needle should be avoided unless it provides the only safe access to an
adequate pool of liquor. Maximum outer needle gauge size of 0.9 mm (20-gauge) should be used to perform
amniocentesis. Clinicians should use the CVS technique with which they are competent, using local anaesthesia for
transabdominal CVS.

Operators carrying out unsupervised amniocentesis and CVS should be trained to the competencies

expected of subspecialty training in maternal and fetal medicine, the RCOG Fetal Medicine Advanced

Training Skills Module (ATSM) or other international equivalent.

Clinical skills models, assessment of interaction with patients and supervised procedures should be an integral part of
training. Competency should be maintained by carrying out at least 30 ultrasound guided invasive procedures per annum.
Units and operators should carry out continuous audit of frequencies of multiple insertions, failures, bloody taps and post
procedure losses. Very experienced operators (more than 100 per annum) may have a higher success rate and a lower
procedure-related loss rate. Occasional operators who perform a low number of procedures per annum may have
increased rates of procedure-related loss. Further opinion should be sought from a more experienced operator if
difficulties are anticipated or encountered.

Women should be informed that third-trimester amniocentesis does not appear to be associated with a significant risk of
emergency delivery. Women should be informed that, compared with mid-trimester procedures, complications including
multiple attempts and bloodstained fluid are more common in third-trimester procedures.

No. 10a THE MANAGEMENT OF SEVERE PRE ECLAMPSIA/ECLAMPSIA

Severe pre-eclampsia and eclampsia are relatively rare but serious complications of pregnancy, with around 5/1000 maternities
in the UK suffering severe pre-eclampsia and 5/10 000 maternities suffering eclampsia. In eclampsia, the case fatality rate has
been reported as 1.8% and a further 35% of women experience a major complication.

Eclampsia is defined as the occurrence of one or more convulsions superimposed on pre-eclampsia. Preeclampsia is
pregnancy-induced hypertension in association with proteinuria (> 0.3 g in 24 hours) oedema and virtually any organ
system may be affected.5 Severe pre-eclampsia is variously defined. There is consensus that severe hypertension is
confirmed with a diastolic blood pressure 110 mmHg on two occasions or systolic blood pressure 170 mmHg on two
occasions and that, together with significant proteinuria (at least 1 g/litre), this constitutes severe pre-eclampsia. There is
less agreement about the degree of moderate hypertension, which together with other symptoms or signs constitutes
severe pre-eclampsia.

A diastolic blood pressure 100 mmHg on two occasions and significant proteinuria with at least two signs or symptoms
of imminent eclampsia will include many women with severe pre-eclampsia, although it is to be remembered that some
women who present with eclampsia have no prodromal signs. An important variant of severe pre-eclampsia is the HELLP
syndrome (haemolysis, elevated liver enzymes and low platelet count). Ultimately, as many clinical criteria are subjective,
women should be managed according to a careful clinical assessment rather than relying on overly precise criteria. Each
unit or region may wish to produce a locally adapted approach to implementation of the guideline addressing blood
pressure monitoring, including the use of mean arterial pressure, thresholds for the use of magnesium sulphate and
preferred first- and second-line anti-hypertensive agents. Clinical features of severe pre-eclampsia (in addition to
hypertension and proteinuria) are:
o symptoms of severe headache
o liver tenderness
o visual disturbance
o platelet count falling to below 100 x 106/l
o epigastric pain and/or vomiting
o abnormal liver enzymes (ALT or AST rising to above 70 iu/l)
o signs of clonus
o HELLP syndrome.
o Papilloedema
Some women will present with convulsions, abdominal pain or general malaise. In these cases, preeclampsia should always
be considered and the blood pressure taken and the urine analysed. Clinical symptoms are important components of
worsening disease, particularly headache and abdominal pain. However increasing oedema is not in itself a sign that should
determine management. Maternal tendon reflexes, although useful to assess magnesium toxicity, are not of value in assessing
the risk of convulsion, although the presence of clonus may be. Continuous oxygen saturation monitoring with a pulse oximeter
is valuable, as it will often give early signs of pulmonary oedema.
When taking blood pressure, the woman should be rested and sitting at a 45-degree angle. The blood pressure cuff should be
of the appropriate size and should be placed at the level of the heart. Multiple readings should be used to confirm the
diagnosis. Korotkoff phase 5 is the appropriate measurement of diastolic blood pressure. The method used should be
consistent and documented. Automated methods need to be used with caution, as they may give inaccurate blood pressure
readings in pre-eclampsia.
The usual screening test is visual dipstick assessment. A two plus dipstick measurement can be taken as evidence of
proteinuria but ideally a more accurate test (either a spot protein creatinine ratio or ideally a 24-hour urine collection) is
required to confirm this.
While it has to be acknowledged that there is poor predictive value from urine dipstick testing, approximate equivalence is 1+ =
0.3 g/l, 2+ = 1 g/l and 3+ = 3 g/l. Newer techniques such as protein/creatinine ratios have not been fully evaluated but may be a
valid alternative. A level of 0.03 g/mmol appears to be equivalent to 0.3 g/24 hours.
The blood pressure should be checked each 15 minutes until the woman is stabilised and then every 30 minutes in the initial
phase of assessment. The blood pressure should be checked 4-hourly if a conservative management plan is in place and the
woman is stable and asymptomatic. Assessment of the woman requires a full blood count, liver function and renal function
tests. These should be repeated at least daily when the results are normal but more often if the clinical condition changes or if
there are abnormalities. Clotting studies are not required if the platelet count is over 100 x 106/l. Close fluid balance with
charting of input and output is essential. A catheter with an hourly urometer is advisable in the acute situation, especially in the
immediate postpartum period.
In the acute setting, an initial assessment with cardiotocography should be undertaken. This gives information about fetal
wellbeing at that time but does not give any predictive information. Women in labour with severe pre-eclampsia should have
continuous electronic fetal monitoring. If conservative management is planned then further assessment of the fetus with
ultrasound measurements of fetal size, umbilical artery Doppler and liquor volume should be undertaken. Serial assessment
will allow timing of delivery to be optimised. The value of Doppler in other fetal vessels has yet to be clarified. The main
pathology affecting the fetus, apart from prematurity, is placental insufficiency leading to intrauterine growth restriction (IUGR).
IUGR occurs in around 30% of pre-eclamptic pregnancies. Ultrasound assessment of fetal size, at the time of the initial
presentation with hypertension, is a valuable one-off measurement to assess fetal growth. Growth restriction is usually
asymmetrical so measurement of the abdominal circumference is the best method of assessment. Reduced liquor volume is

also associated with placental insufficiency and fetal growth restriction. Serial estimations of liquor volume can detect fetal
compromise.
Antihypertensive treatment should be started in women with a systolic blood pressure over 160 mmHg or a diastolic blood
pressure over 110 mmHg. In women with other markers of potentially severe disease, treatment can be considered at lower
degrees of hypertension. Labetalol, given orally or intravenously, nifedipine given orally or intravenous hydralazine can be used
for the acute management of severe hypertension. In moderate hypertension, treatment may assist prolongation of the
pregnancy. Clinicians should use agents with which they are familiar. Atenolol, angiotensin converting enzyme (ACE) inhibitors,
angiotensin receptor-blocking drugs (ARB) and diuretics should be avoided. Nifedipine should be given orally not sublingually.
Labetalol should be avoided in women with known asthma. There has been a general consensus that blood pressure greater
than 170/110 mmHg requires treatment in the maternal interest. Desire to prevent the known risk of vascular damage due to
uncontrolled hypertension..
Methyldopa and labetalol were the most commonly used therapies in the UK. Methyldopa has been proven safe in long term
follow-up of the delivered babies, while some studies have suggested some benefits of labetalol. Doctors should use the drug
with which they are familiar. Atenolol is associated with an increase in fetal growth restriction. ACE inhibitors and ARBs would
appear to be contraindicated because of unacceptable fetal adverse effects. Diuretics are relatively contraindicated for
hypertension and should be reserved for pulmonary oedema. Magnesium sulphate should be considered for women with preeclampsia for whom there is concern about the risk of eclampsia. This is usually in the context of severe pre-eclampsia once a
delivery decision has been made and in the immediate postpartum period. If magnesium sulphate is given, it should be
continued for 24 hours following delivery or 24 hours after the last seizure, whichever is the later, unless there is a clinical
reason to continue. When magnesium sulphate is given, regular assessment of the urine output, maternal reflexes, respiratory
rate and oxygen saturation is important.
The principles of management should follow the basic principles of airway, breathing and circulation. Magnesium sulphate is
the therapy of choice to control seizures. A loading dose of 4 g should be given by infusion pump over 510 minutes, followed
by a further infusion of 1 g/hour maintained for 24 hours after the last seizure. Recurrent seizures should be treated with either
a further bolus of 2 g magnesium sulphate or an increase in the infusion rate to 1.5 g or 2.0 g/hour. Place the woman in the left
lateral position and administer oxygen. Assess the airway and breathing and check pulse and blood pressure. Pulse oximetry is
helpful. Once stabilised, plans should be made to deliver the woman but there is no particular hurry and a delay of several
hours to make sure the correct care is in hand is acceptable, assuming that there is no acute fetal concern such as a fetal
bradycardia. The womans condition will always take priority over the fetal condition. Magnesium sulphate is the therapy of
choice and diazepam and phenytoin should no longer be used as first-line drugs.
Urine output should be closely observed and if it becomes reduced below 20 ml/hour the magnesium infusion should be halted.
Magnesium toxicity can be assessed by clinical assessment as it causes a loss of deep tendon reflexes and respiratory
depression. If there is loss of deep tendon reflexes, the magnesium sulphate infusion should be halted. Calcium gluconate 1 g
(10 ml) over 10 minutes can be given if there is concern over respiratory depression.
Fluid restriction is advisable to reduce the risk of fluid overload in the intrapartum and postpartum periods. In usual
circumstances, total fluids should be limited to 80 ml/hour or 1 ml/kg/hour.
The regime of fluid restriction should be maintained until there is a postpartum diuresis, as oliguria is common with severe preeclampsia. If there is associated maternal haemorrhage, fluid balance is more difficult and fluid restriction is inappropriate. The
decision to deliver should be made once the woman is stable and with appropriate senior personnel present.
If the fetus is less than 34 weeks of gestation and delivery can be deferred, corticosteroids should be given, although after 24
hours the benefits of conservative management should be reassessed. Conservative management at very early gestations
may improve the perinatal outcome but must be carefully balanced with maternal wellbeing. The mode of delivery should be
determined after considering the presentation of the fetus and the fetal condition, together with the likelihood of success of
induction of labour after assessment of the cervix. The third stage should be managed with 5 units intramuscular Syntocinon
(Alliance) or 5 units intravenous Syntocinon given slowly. Ergometrine or Syntometrine (Alliance) should not be given for
prevention of haemorrhage, as this can further increase the blood pressure.
Clinicians should be aware of the risk of late seizures and ensure that women have a careful review
before discharge from hospital. Anti-hypertensive medication should be continued after delivery as dictated by the blood
pressure. It may be necessary to maintain treatment for up to 3 months, although most women can have treatment stopped
before this. Women with persisting hypertension and proteinuria at 6 weeks may have renal disease and should be considered
for further investigation. Clinicians should be aware that up to 44% of eclampsia occurs postpartum, especially at term, so
women with signs or symptoms compatible with pre-eclampsia should be carefully assessed.
Anti-hypertensive therapy should be continued after delivery. Although, initially, blood pressure may fall, it usually rises again at
around 24 hours postpartum. A reduction in anti-hypertensive therapy should be made in a stepwise fashion. There is no
reason why the woman cannot go home on treatment, to be weaned off therapy as an outpatient. After pre-eclampsia, blood
pressure can take up to 3 months to return to normal. However, it is good practice to avoid the use of alpha methyldopa in the
postnatal period because of risk of depression.
Corticosteroids have been used in HELLP syndrome. The current evidence suggests they lead to a more rapid resolution of the
biochemical and haematological abnormalities but there is no evidence that they reduce morbidity.
An assessment of blood pressure and proteinuria by the general practitioner at the 6 weeks postnatal check is recommended.
If hypertension or proteinuria persists then further investigation is recommended.
Women whose pregnancies have been complicated by severe pre-eclampsia or eclampsia should be offered a formal postnatal
review to discuss the events of the pregnancy. Preconceptional counselling should be offered where the events that occurred,
any risk factors and any preventative therapies can be discussed.

No. 12 Breast cancer in Pregnancy

Breast cancer remains the most common cancer in women, with a lifetime risk of almost 11% (one in nine) in the UK. There
has been an overall increase in the incidence of breast cancer but in the UK mortality has fallen by over 30% in the last
decade. It is likely that this is due to the widespread introduction of tamoxifen in treatment regimens and the introduction of
breast screening

Risk factors: Nulliparity is associated with an increased risk and parity reduces the risk, although there is evidence that
the risk of breast cancer is transiently increased after pregnancy. Early menarche and late age at first pregnancy are
associated with increased risk.5 A pregnancy that ends with preterm delivery has less transient increased risk and less
long-term protection. Pregnancy also increases the risk of breast cancer developing in carriers of BRCA1 and BRCA2
mutations. Carriers of these mutations who have children are significantly more likely to develop breast cancer by the age
of 40 years than carriers who are nulliparous, and each pregnancy is associated with an increased risk of cancer. Having
a baby at a young age does not appear to protect BRCA1/BRCA2 carriers against subsequent development of breast
cancer.

Women should be advised to breastfeed if possible, as this is likely to reduce their risk of breast cancer in addition to any
other benefit.

There is no evidence that termination of pregnancy after diagnosis of breast cancer is necessary to improve prognosis.

Women planning a pregnancy after treatment for breast cancer should consult their obstetrician, breast surgeon and
clinical oncologist.

Long-term survival after breast cancer does not appear to be affected by pregnancy.

It is recommended that pregnancy should be deferred for at least two years after treatment.

Breast-conserving surgery may not inhibit lactation but radiotherapy causes fibrosis and lactation is unlikely in an
irradiated breast. During treatment for breast cancer with chemotherapy or radiotherapy, women should not breastfeed.

No. 13 Chicken pox in pregnancy

Varicella, the primary infection with varicella zoster virus, in pregnancy may cause maternal mortality or serious morbidity. It
may also cause fetal varicella syndrome.

VZV is a DNA virus of the herpes family that is highly contagious and transmitted by respiratory droplets and by direct
contact with vesicle fluid. The primary infection is characterised by fever, malaise and a puritic rash that develops
maculopapules which become vesicular and crust over before healing.

The incubation period is 1-3 weeks. The disease is infectious 48 hours before the rash appears and continues to be
infectious until the vesicles crust over (5 days).

90% of population seropositive (IgG antibodies).

The virus can remain dormant in sensory nerve root ganglia but can be reactivated to cause a vesicular erythematous
skin rash in a dermatomal distribution (shingles).

Live attended virus of the oka strain of VZV is licensed. If a woman of reproductive age is vaccinated she should be
advised not to get pregnant for 3/12 and to avoid contact with other pregnant women should a post vaccination rash
occur. Transmission of the vaccine virus is rare in the absence of the rash. There has been no recorded cases of fetal
varicella syndrome from inadvertent exposure to the vaccine in pregnancy.

Women with seronegative for VZV IgG must be advised to avoid contact with chickenpox and shingles during pregnancy.

If there has been a contact, verify the contact and the susceptibility of the contact. Blood test to lab to confirm
seropositivity or not.

If pregnant woman is not immune to VZG and has had significant exposure, she should be given VZIG asap. VZIG is
effective when given for up to 10 days after contact. The administration of VZIG can be given after blood tests results

If a woman is given VZIG she should be managed as potentially infectious from 8-28 days after VZIG. A second dose
may need to be given in further exposure is reported after 3 weeks.

If there is a definite past history of chicken pox, it is reasonable to assume she is immune to varicella infection.

Rare anaphylactoid reaction have been reported. No blood borne infections have been recorded.

Excess morbidity attached to varicella infection in adults, pneumonia (10%), hepatitis and encephalitis, mortality

If pregnant woman develops the rash, they should contact GP, avoid hospital, good hygiene to prevent secondary
infection with bacteria. Aciclovir caution before 20 weeks. VZIG has no role when rash develops. If within 24 hours
acyclovir 800mg 5 times a day reduces duration of symptoms. There is no proven teratogenicity with acyclovir

Women with greater risk of pneumonitis are those who smoke, have chronic lung disease , are immunocompromised,
those who have a serious haemorrhagic rash or who are in the later half of pregnancy.

The maternal risks are bleeding, thrombocytopenia, DIC and hepatitis. GA may exacerbate symptoms. Epidural may be
safer that spinal, because the dura is not penetrated.

No increase in spontaneous miscarriage in the first trimester.

There is a small chance of developing fetal varicella syndrome if occur in first 28 weeks of pregnancy.

No. 17 The investigation & treatment of couples with recurrent miscarriage

Recurrent miscarriage is defined as the loss of three or more pregnancies. Recurrent miscarriage is a distressing problem that
affects 1% of all women. This incidence is greater than that expected by chance alone, since 1015% of all clinically
recognised pregnancies end in a miscarriage and the theoretical risk of three consecutive pregnancy losses is 0.34%. Maternal
age and previous number of miscarriages are two independent risk factors for a further miscarriage.

All couples with a history of recurrent miscarriage should have peripheral blood karyotyping performed. The finding of an
abnormal parental karyotype should prompt referral to a clinical geneticist. In approximately 35% of couples with
recurrent miscarriage, one of the partners carries a balanced structural chromosomal anomaly. The most common types
of parental chromosomal abnormality are balanced reciprocal or Robertsonian translocations.

In all couples with a history of recurrent miscarriage cytogenetic analysis of the products of conception should be
performed if the next pregnancy fails.

All women with recurrent miscarriage should have a pelvic ultrasound to assess uterine anatomy and
morphology. It is difficult to assess the exact contribution that congenital uterine anomalies make to recurrent pregnancy
loss. The diagnostic value of three-dimensional ultrasound has been explored and appears promising. Since threedimensional ultrasound offer both diagnosis and classification of uterine malformation its use may obviate the need for
diagnostic hysteroscopy and laparoscopy.

Cervical cerclage is associated with potential hazards related to the surgery and the risk of stimulating uterine
contractions and hence should only be considered in women who are likely to benefit. Cervical weakness is often overdiagnosed as a cause of mid-trimester miscarriage. The MRC/RCOG trial of elective cervical cerclage reported a small
decrease in preterm birth and delivery of very-lowbirthweight babies, but the benefit was most marked in women with
three or more second-trimester miscarriages or preterm births. However, there was no significant improvement in
perinatal survival.

Transabdominal cerclage has been advocated as a treatment for second-trimester miscarriage and the prevention of
early preterm labour in selected women with previous failed transvaginal cerclage and/or a very short and scarred cervix

Routine screening for occult diabetes and thyroid disease with oral glucose tolerance and thyroid function tests in
asymptomatic women presenting with recurrent miscarriage is uninformative. Systemic maternal endocrine disorders
such as diabetes mellitus and thyroid disease have been associated with miscarriage. Women with diabetes who have
high haemoglobin A1c levels in the first trimester are at risk of miscarriage and fetal malformation. The prevalence of
diabetes mellitus and thyroid dysfunction in women who suffer recurrent miscarriage is similar to that expected in the
general population.

There is insufficient evidence to evaluate the effect of progesterone supplementation in pregnancy to prevent a
miscarriage. There is insufficient evidence to evaluate the effect of human chorionic gonadotrophin (hCG) in pregnancy to
prevent miscarriage. Prepregnancy suppression of high luteinising hormone (LH) concentration among ovulatory women
with recurrent miscarriage and polycystic ovaries who hypersecrete LH does not improve the live birth rate.

Polycystic ovary morphology itself does not predict an increased risk of future pregnancy loss among ovulatory women
with a history of recurrent miscarriage who conceive spontaneously.

There is insufficient evidence to assess the effect of hyperprolactinaemia as a risk factor for recurrent miscarriage.
Routine screening for thyroid antibodies in women with recurrent miscarriage is not recommended. Immunotherapy,
including paternal cell immunisation, third-party donor leucocytes, trophoblast membranes and intravenous
immunoglobulin (IVIG), in women with previous unexplained recurrent miscarriage does not improve the live birth rate.

TORCH (toxoplasmosis, other [congenital syphilis and viruses], rubella, cytomegalovirus and herpes simplex virus)
screening is unhelpful in the investigation of recurrent miscarriage.

Screening for and treatment of bacterial vaginosis in early pregnancy among high risk women with a previous history of
second-trimester miscarriage or spontaneous preterm labour may reduce the risk of recurrent late loss and preterm birth.

Inherited thrombophilic defects, including activated protein C resistance (most commonly due to factor V Leiden gene
mutation), deficiencies of protein C/S and antithrombin III, hyperhomocysteinaemia and prothrombin gene mutation, are
established causes of systemic thrombosis.

These women can be reassured that the prognosis for a successful future pregnancy with supportive care alone is in the
region of 75%.
Primary antiphospholipid syndrome (APS) refers to the association between antiphospholipid antibodies (aPL) and adverse
pregnancy outcome or vascular thrombosis. Adverse pregnancy outcomes include (a) three or more consecutive miscarriages
before ten weeks of gestation, (b) one or more morphologically normal fetal deaths after the tenth week of gestation and (c)
one or more preterm births before the 34th week of gestation due to severe pre-eclampsia, eclampsia or placental insufficiency.
Where APS exists in chronic inflammatory disorders, such as systemic lupus erythematosus, it is referred as secondary APS.
The mechanisms by which aPL causes pregnancy morbidity include inhibition of trophoblastic function and differentiation and,
in later pregnancy, thrombosis of the uteroplacental vasculature. To diagnose APS it is mandatory that the patient should have
two positive tests at least six weeks apart for either lupus anticoagulant or anticardiolipin (aCL) antibodies of IgG and/or IgM

class present in medium or high titre. In detection of lupus anticoagulant, the dilute Russells viper venom time (dRVVT) test is
more sensitive and specific than either the activated partial thromboplastin time (aPTT) or the kaolin clotting time (KCL) tests.
Anticardiolipin antibodies are detected using a standardised enzymelinked immunosorbent assay (ELISA). The detection of
aPL is subject to considerable interlaboratory variation. This is due to temporal fluctuation of aPL titres in individual patients,
transient positivity secondary to infections, suboptimal sample collection and preparation and
lack of standardisation of laboratory tests for their detection. Antiphospholipid antibodies are present in 15% of women with
recurrent miscarriage. By comparison, the prevalence of aPL in women with a low risk obstetric history is less than 2%. In
women with recurrent miscarriage associated with aPL, the live birth rate in pregnancies with no pharmacological intervention
may be as low as 10%. Currently there is no reliable evidence to show that steroids improve the live birth rate of women with
recurrent miscarriage associated with aPL when compared with other treatment modalities; their use may provoke significant
maternal and fetal morbidity. Two small randomised controlled trials have reported that treating women who suffer recurrent
miscarriage associated with aPL with steroid therapy during pregnancy does not improve the live birth rate when compared
with aspirin or aspirin plus heparin. Steroid therapy is associated with significant maternal and fetal morbidity. In women with a
history of recurrent miscarriage and aPL, future live birth rate is significantly improved when a combination therapy of aspirin
plus heparin is prescribed. A randomised controlled trial showed that the live birth rate of women with recurrent miscarriage
associated with aPL treated with low-dose aspirin only is 40% and this is significantly improved to 70% when they are treated
with low-dose aspirin in combination with low-dose heparin. Pregnancies associated with aPL treated with aspirin and heparin
remain at high risk of complications during all three trimesters.

No. 19 Hormone replacement therapy and venous thromboembolism

Exogenous oestrogen used in OCP has long been known to cause VTE. HRT either sequential or continuous, also exposes
women to exogenous oestrogen. HRT however contains a physiological dose of oestrogen while OCP has a higher
pharmacological dose.
The haemostatic system is altered by the menopause, with increases in certain coagulation factors. HRT produces a reduction
in fibrinogen and factor VII activation, such as Willebrands factor and antithrombin and also enhances fibrinolysis. It is also
associated with increased resistance to activated protein C. With many opposing factors, the net effects are increase in
thrombin generation. The risk of VTE is double post menopausally.

In women using HRT, the risk of VTE was significantly associated with increased resistance to activated protein C, low
antithrombin and high factor IX.

Other risk factors include: age, obesity, varicose veins, previous VTE, deep venous insufficiency, immobility, disease and
cancer, surgery and trauma.

Universal screening for thrombophilic defects prior to or continuing the prescription of HRT is inappropriate. But a
personal and family history assessing the presence of VTE in 1 st and 2nd degree relative should be sought. Testing should
be done on those with previous VTE or strong family history of positive thrombophilia screen.

It is recommended that any women developing a VTE on HRT should be discontinued. If this cannot be achieved that
long-term anticoagulation should be considered.

Selective oestrogen receptor modulators (SERMs) should be considered to carry the same risk of thrombosis as
oestrogen-containing HRT.

HRT does not routinely stopped prior to surgery provided that appropriate thrombo-prophylaxis is considered.

The ultrasound probe should be enclosed in a sterile bag during any invasive prenatal procedure unless suitably audited
processes for probe decontamination and gel microbiological surveillance are in place. Separate sterile gel should be
used. Invasive prenatal procedures should not be carried out without reviewing available bloodborne virus screening
tests. Where women decline screening for bloodborne viruses and are being counselled for prenatal diagnostic
procedures, inform and document the potential risk of vertical transmission of infection to the fetus.

Review viral load and treatment regimens prior to invasive prenatal testing in women with HIV and consider delaying the
procedure until there is no detectable viral load if the woman is already on treatment. Consider antiretroviral therapy prior
to prenatal invasive procedures in women not yet on treatment for HIV. Invasive prenatal testing in the first or second
trimester can be carried out in women who carry hepatitis B or C.

Maternal RhD status should be available or obtained in every case. Prophylaxis with anti-D immunoglobulin must be
offered following each procedure

No. 20a External cephalic version & reducing incidence of Breech

External cephalic version (ECV) is the manipulation of the fetus, through the maternal abdomen, to a cephalic presentation.
Breech presentation complicates 34% of all term deliveries and a higher proportion of preterm deliveries. It is more common
where there has been a previous breech presentation. Women with a breech baby should be informed that attempting ECV
lowers their chances of having a caesarean section. Labour with a cephalic presentation following ECV is associated with a
higher rate of obstetric intervention than when ECV has not been required. The highest success rates are seen with
multiparous, non-white women with a relaxed uterus, where the breech is not engaged and the head is easily palpable.

Success rates are also higher with increasing liquor volume but, in practice, very high liquor volume may be associated with
spontaneous reversion.
Maternal weight, placental position, gestation, fetal size and position of the legs make less difference and are probably not
independent of other factors. An overall success rate of 40% for nulliparous, and 60% for multiparous women can usually be
achieved. Women should be counselled that, with a trained operator, about 50% of ECV attempts will be successful but this
rate can be individualised for them. The use of tocolysis with beta-sympathomimetics may be offered to women undergoing
ECV as it has been shown to increase the success rate. The use of tocolysis should be considered where an initial attempt at
ECV without tocolysis has failed. The success rate of ECV is increased by the use of tocolysis. This has been proven with
ritodrine, salbutamol and terbutaline but not with glyceryl trinitrate (GTN) as a patch or sublingually, or with nifedipine.
Intravenous and subcutaneous routes can be used.
Where ECV fails the possibility of a further attempt should be discussed. ECV should be offered from 36 weeks in nulliparous
women and from 37 weeks in multiparous women. Women should be counselled that ECV has a very low complication rate.
Women should be alerted to potential complications of ECV. ECV should be performed where facilities for monitoring and
immediate delivery are available. ECV should be performed where ultrasound to enable fetal heart rate visualisation,
cardiotocography and theatre facilities are available. Cardiotocography should be performed after the procedure. Kleihauer
testing is unnecessary but anti-D immunoglobulin is normally offered to rhesus-negative women.
The standard preoperative preparations for caesarean section are not necessary for women undergoing ECV. Women should
be advised that ECV can be painful and the procedure will be stopped if they wish. Absolute contraindications for ECV that are
likely to be associated with increased mortality or morbidity: where caesarean delivery is required; antepartum haemorrhage
within the last 7 days; abnormal cardiotocography; major uterine anomaly; ruptured membranes; multiple pregnancy (except
delivery of second twin). Relative contraindications where ECV might be more complicated: small-for-gestational-age fetus with
abnormal Doppler parameters; proteinuric pre-eclampsia; oligohydramnios; major fetal anomalies; scarred uterus; unstable lie.
There is insufficient evidence to support the use of postural management as a method of promoting spontaneous version over
ECV. Moxibustion should not be recommended as a method of promoting spontaneous version over ECV. There is no evidence
to support the use of postural management in the management of the breech presentation. Moxibustion, burnt at the tip of the
fifth toe (acupuncture point BL67) has been used to promote spontaneous version of the breech, with some success, and
appears to be safe.
ECV is rarely associated with complications. Nevertheless, a few case reports exist of complications such as placental
abruption, uterine rupture and fetomaternal haemorrhage, suggest a 0.5% immediate emergency caesarean section rate and
no excess perinatal morbidity and perinatal mortality. ECV does not appear to promote labour7 but is associated with
alterations in fetal parameters. These include a fetal bradycardia and a nonreactive cardiotocograph that are almost invariably
transient, alterations in umbilical artery and middle cerebral artery waveforms and an increase in amniotic fluid volume. The
significance of these is unknown.

No.20b The management of Breech Presentation

The incidence of breech presentation decreases from about 20% at 28 weeks of gestation to 34% at term, as most babies
turn spontaneously to the cephalic presentation. Persistent breech presentation may be associated with abnormalities of the
baby, the amniotic fluid volume, the placental localisation or the uterus. It may be due to an otherwise insignificant factor such
as cornual placental position or it may apparently be due to chance. There is higher perinatal mortality and morbidity with
breech than cephalic presentation, due principally to prematurity, congenital malformations and birth asphyxia or trauma.
Caesarean section for breech presentation has been suggested as a way of reducing the associated perinatal problems.
Women should be informed of the benefits and risks, both for the current and for future pregnancies, of planned caesarean
section versus planned vaginal delivery for breech presentation at term. Women should be informed that planned caesarean
section carries a reduced perinatal mortality and early neonatal morbidity for babies with a breech presentation at term
compared with planned vaginal birth.
Women should be informed that there is no evidence that the long term health of babies with a breech presentation delivered
at term is influenced by how the baby is born. In a secondary analysis of the data from the Term Breech Trial (not according to
group allocation), adverse perinatal outcome was lowest with prelabour caesarean section and increased with
caesarean section in early labour (latent phase), in active labour and vaginal birth. For women experiencing labour, adverse
perinatal outcome was also associated with labour augmentation, birth weight less than 2.8 kg, longer time between pushing
and delivery and no experienced clinician at delivery. Women should be advised that planned caesarean section for breech
presentation carries a small increase in serious immediate complications for them compared with planned vaginal birth.
Women should be advised that planned caesarean section for breech presentation does not carry any additional risk to longterm health outside pregnancy. Women should be advised that the long-term effects of planned caesarean section for term
breech presentation on future pregnancy outcomes for them and their babies is uncertain.
Women should be assessed carefully before selection for vaginal breech birth. Women with unfavourable clinical features
should be specifically advised of the increased risk to them and their babies of attempting vaginal breech birth. Routine
radiological pelvimetry is not necessary. Diagnosis of breech presentation for the first time during labour should not be a
contraindication for vaginal breech birth.
Factors regarded as unfavourable for vaginal breech birth include the following: other contraindications to vaginal birth (e.g.
placenta praevia, compromised fetal condition); clinically inadequate pelvis; footling or kneeling breech presentation; large
baby (usually defined as larger than 3800 g); growth-restricted baby (usually defined as smaller than 2000 g); Hyperextended

fetal neck in labour (diagnosed with ultrasound or X-ray where ultrasound is not available); lack of presence of a clinician
trained in vaginal breech delivery; previous caesarean section.
The presentation should be either frank (hips flexed, knees extended) or complete (hips flexed, knees flexed but feet not below
the fetal buttocks). If the babys trunk and thighs pass easily through the pelvis simultaneously, cephalopelvic disproportion is
unlikely. Labour induction for breech presentation may be considered if individual circumstances are favourable. Labour
augmentation is not recommended. Epidural analgesia should not be routinely advised; women should have a choice of
analgesia during breech labour and birth.
Continous electronic fetal heart rate monitoring should be offered to women with a breech presentation in labour. Fetal blood
sampling from the buttocks during labour is not advised. In the Term Breech Trial, the most common reasons for emergency
caesarean section were failure to progress (50%) and fetal distress (29%). Caesarean section should be considered if there
is delay in the descent of the breech at any stage in the second stage of labour. Women should be advised that, as most
experience with vaginal breech birth is in the dorsal or lithotomy position, that this position is advised. Episiotomy should be
performed when indicated to facilitate delivery. The arms should be delivered by sweeping them across the babys face and
downwards or by the Lovset manoeuvre (rotation of the baby to facilitate delivery of the arms). Suprapubic pressure by an
assistant should be used to assist flexion of the head. The Mauriceau-Smellie-Veit manoeuvre should be considered, if
necessary, displacing the head upwards and rotating to the oblique diameter to facilitate engagement. The aftercoming head
may be delivered with forceps, the Mariceau-Smellie-Veit manoeuvre or the Burns-Marshall method. If conservative methods
fail, symphysiotomy or caesarean section should be performed. Routine caesarean section for the delivery of preterm breech
presentation should not be advised.
The mode of delivery of the preterm breech presentation should be discussed on an individual basis with a woman and her
partner. Where there is head entrapment during a preterm breech delivery, lateral incisions of the cervix should be considered.
Women should be informed of the benefits, including reduced perinatal mortality, and risks, both for the current and for future
pregnancies, of planned caesarean section for breech presentation.
Women should be advised that planned caesarean section for breech presentation carries a very small increase in serious
immediate complications for them compared with planned vaginal birth. Routine caesarean section for twin pregnancy with
breech presentation of the second twin should not be performed. A practitioner skilled in the conduct of labour with breech
presentation and vaginal breech birth should be present at all vaginal breech births. If a unit is unable to offer the choice of a
planned vaginal breech birth, women who wish to choose this option should be referred to a unit where this option is available.
Practitioners supervising labour with a breech presentation or carrying out vaginal breech birth should have appropriate
training, which may include simulated training.

No 21. THE MANAGEMENT OF TUBAL PREGNANCY

There were 13 maternal deaths resulting from ectopic pregnancy in the UK during the period 199799. The incidence of
ectopic pregnancy has remained static in recent years (11.1/1000 pregnancies) and nearly 32000 ectopic pregnancies are
diagnosed in the UK within a three year period. Tubal pregnancy can be managed by laparotomy, operative laparoscopy,
medically and occasionally by observation alone. Management must be tailored to the clinical condition and future fertility
requirements of the woman.

A laparoscopic approach to the surgical management of tubal pregnancy, in the haemodynamically stable patient, is
preferable to an open approach.
Management of tubal pregnancy in the presence of haemodynamic instability should be by the most expedient method. In
most cases this will be laparotomy.
In the presence of a healthy contralateral tube there is no clear evidence that salpingotomy should be used in preference
to salpingectomy. The intrauterine pregnancy rates were similar when comparing the two groups but there was a trend
towards higher subsequent ectopic pregnancy in the salpingotomy arm
Laparoscopic salpingotomy should be considered as the primary treatment when managing tubal pregnancy in the
presence of contralateral tubal disease and the desire for future fertility
Medical therapy should be offered to suitable women, and units should have treatment and follow-up protocols for the use
of methotrexate in the treatment of ectopic pregnancy.
The most widely used medical treatment at present is intramuscular methotrexate given as a single dose calculated from
patient body surface area (50 mg/m2). For most women this will be between 75 mg and 90 mg. Serum hCG levels are
checked on days four and seven and a further dose is given if hCG levels have failed to fall by more than 15% between
day four and day seven.
Large uncontrolled studies have reported that about 14% of women will require more than one dose of methotrexate and
less than 10% of women treated with this regimen will require surgical intervention. This has also been reported in
randomised trials comparing methotrexate with laparoscopic surgery
Women most suitable for methotrexate therapy are those with a serum hCG below 3000 iu/l, and minimal symptoms.
Expectant management is an option for clinically stable women with minimal symptoms and a pregnancy of unknown
location. Using an initial upper level of serum hCG of 10001500 iu/l to diagnose pregnancy of unknown location, women

10

with minimal or no symptoms at risk of ectopic pregnancy should be managed expectantly with 4872 hours of follow-up
and should be considered for active intervention if symptoms of ectopic pregnancy occur, serum hCG levels rise above
the discriminatory level (1000 iu/l) or levels start to plateau.
Expectant management is an option for clinically stable asymptomatic women with an ultrasound diagnosis of ectopic
pregnancy and a decreasing serum hCG, initially less than serum 1000 iu/l.
When salpingotomy is used for the management of tubal pregnancy, protocols should be in place for the identification and
treatment of women with persistent trophoblast. Nonsensitised women who are rhesus negative with a confirmed or
suspected ectopic pregnancy should receive anti-D immunoglobulin. Women should be carefully advised, whenever
possible, of the advantages and disadvantages associated with each approach used for the treatment of ectopic
pregnancy. They should participate fully in the selection of the most appropriate treatment.

No. 22 Rh Prophylaxis, Anti-D Immunoglobulin

The development of anti-D antibodies generally results from fetomaternal haemorrhages (FMH) occurring in RhD negative
women who carry an RhD positive fetus. Post-delivery immunoprophylaxis using anti-D Immunoglobulin (anti-D Ig) began in
the UK in 1969. The programme has been an astounding success; deaths attributed to RhD alloimmunisation fell from
46/100,000 births before 1969 to 1.6/100,000 in 1990.
Studies have shown that 99% of women have a FMH less than 4ml at delivery. Up to 50% of larger FMHs occur after normal
deliveries. However, the following clinical circumstances are more likely to be associated with large FMH: traumatic deliveries
including caesarean section; manual removal of the placenta; stillbirths and intrauterine deaths; abdominal trauma during the
third trimester; twin pregnancies (at delivery); unexplained hydrops fetalis. 0.3% of women have a FMH greater than 15ml
which will not be covered by 1500iu of anti-D Ig. Hence, if the 1500iu dose is implemented without a test to quantitate FMH,
over 200 women each year in the UK will receive less protection than they do now. The recommended policy in the UK is to
obtain an anticoagulated blood sample as soon as possible (within two hours) after delivery and to undertake a Kleihauer
screening test to identify women with a large FMH who need additional anti-D Ig.
Intramuscular anti-D Ig is best given into the deltoid muscle as injections into the gluteal region often only reach the
subcutaneous tissues and absorption may be delayed.
For successful immunoprophylaxis, anti-D Ig should be given as soon as possible after the sensitising event but always within
72 hours. If it is not given before 72 hours, every effort should still be made to administer the anti-D Ig, as a dose given within
9-10 days may provide some protection. Women who are already sensitised should not be given anti-D Ig.
Ectopic pregnancy: Anti-D Ig should be given to all non-sensitised RhD negative women who have an ectopic pregnancy.
Spontaneous miscarriage: Anti-D Ig should be given to all non-sensitised RhD negative women who have a spontaneous
complete or incomplete abortion after 12 weeks of pregnancy. There is evidence that significant FMH only occurs after
curettage to remove products of conception but does not occur after complete spontaneous miscarriages. Anti-D Ig should
therefore be given when there has been an intervention to evacuate the uterus. On the other hand, the risk of immunisation by
spontaneous miscarriage before 12 weeks" gestation is negligible when there has been no instrumentation to evacuate the
products of conception and anti-D Ig is not required in these circumstances.
Threatened miscarriage: Anti-D Ig should be given to all non-sensitised RhD negative women with a threatened miscarriage
after 12 weeks of pregnancy. Where bleeding continues intermittently after 12 weeks" gestation, anti-D Ig should be given at 6weekly intervals. Evidence that women are sensitised after uterine bleeding in the first 12 weeks of pregnancy where the fetus
is viable and the pregnancy continues is scant though there are very rare examples. Against this background, routine
administration of anti-D Ig cannot be recommended. However it may be prudent to administer anti-D Ig where bleeding is
heavy or repeated or where there is associated abdominal pain particularly if these events occur as gestation approaches 12
weeks. The period of gestation should be confirmed by ultrasound.
Anti-D Ig should be given to all non-sensitised RhD negative women after the following potentially sensitising events during
pregnancy: invasive prenatal diagnosis (amniocentesis, chorion villus sampling, fetal blood sampling) other intrauterine
procedures (e.g. insertion of shunts, embryo reduction) antepartum haemorrhage, external cephalic version of the fetus, closed
abdominal injury, intrauterine death.
When more than 2 units of RhD positive blood have been transfused, consideration should be given to undertaking an
exchange transfusion to reduce the load of RhD positive red blood cells in the circulation and the dose of anti-D Ig required to
suppress immunisation. In this situation, the patient should be counselled regarding the implications of both non-intervention
(for future pregnancies) and of treatment, including any hazards from receiving donated blood, the exchange procedure itself
and of larger doses of anti-D Ig including IV anti-D

No. 23 Acute pelvic inflammatory disease

Pelvic inflammatory disease is usually the result of infection ascending from the endocervix causing endometritis, salpingitis,
parametritis, oophoritis, tubo-ovarian abscess and/or pelvic peritonitis. While sexually transmitted infections such as Chlamydia
trachomatis and Neisseria gonorrhoeae have been identified as causative agents, additional STIs including Mycoplasma
genitalium, anaerobes and other organisms may also be implicated. Delays of only a few days in receiving appropriate
treatment markedly increase the risk of sequelae, which include infertility, ectopic pregnancy and chronic pelvic pain.

11

A low threshold for empiric treatment of PID is recommended because of the lack of definitive clinical diagnostic criteria and
because the potential consequences of not treating of PID are significant. In clinically severe cases, referral to hospital for
treatment and further investigation is advisable.
The following clinical features are suggestive of a diagnosis of PID: bilateral lower abdominal tenderness (sometimes radiating
to the legs); abnormal vaginal or cervical discharge; fever (greater than 38C); abnormal vaginal bleeding (intermenstrual,
postcoital or breakthrough); deep dyspareunia; cervical motion tenderness on bimanual vaginal examination; adnexal
tenderness on bimanual vaginal examination (with or without a palpable mass).
The differential diagnosis of lower abdominal pain in a young woman includes: ectopic pregnancy; acute appendicitis;
endometriosis; irritable bowel syndrome (and, less commonly, other gastrointestinal disorders); complications of an ovarian
cyst, such as rupture or torsion; urinary tract infection; functional pain (pain of unknown physical origin).
Women with suspected PID should be tested for gonorrhoea and chlamydia. Testing for gonorrhoea should be with an
endocervical specimen and tested via culture (direct inoculation on to a culture plate or transport of swab to laboratory within
24 hours) or using a nucleic acid amplification test (NAAT). If gonorrhoea is detected using a NAAT, an additional endocervical
swab should be taken for gonococcal culture to allow the reporting of antibiotic sensitivities and revision of therapy if required
Testing for chlamydia should also be from the endocervix, preferably using a NAAT (such as polymerase chain reaction, strand
displacement amplification). Taking an additional sample from the urethra can increase the diagnostic yield for gonorrhoea and
chlamydia but is only recommended if the more sensitive NAAT is not available. A first catch urine or self-taken vulvovaginal
swab sample provides an alternative sample for some NAATs. The absence of endocervical or vaginal pus cells on a wetmount smear has a good negative predictive value (95%) for a diagnosis of PID but their presence is non-specific (poor
positive predictive value (17%). Interactions between antibiotic therapy and hormonal contraception and other patient
medications should be assessed and appropriate action taken. Outpatient antibiotic treatment should be commenced as soon
as the diagnosis is suspected. Outpatient antibiotic treatment should be based on one of the following regimens:

oral ofloxacin 400 mg twice daily plus oral metronidazole 400 mg twice daily for 14 days

intramuscular ceftriaxone 250 mg single dose,* followed by oral doxycycline 100 mg twice daily plus metronidazole
400 mg twice daily for 14 days.
When giving information to patients, the clinician should consider the following:
an explanation of what treatment is being given and its possible adverse effects
that following treatment fertility is usually maintained but there remains a risk of future infertility, chronic pelvic pain or ectopic
pregnancy
repeat episodes of PID are associated with an exponential increase in the risk of infertility
future use of barrier contraception will significantly reduce the risk of PID
the need to screen her sexual contacts for infection to prevent her becoming reinfected
clinically more severe disease is associated with a greater risk of sequelae
the earlier treatment is given the lower the risk of future fertility problems.
Inpatient antibiotic treatment should be based on intravenous therapy which should be continued until 24 hours after clinical
improvement and followed by oral therapy. Recommended regimens are:

ceftriaxone 2 g by intravenous infusion daily plus intravenous doxycycline 100 mg twice daily,* followed by oral
doxycycline 100 mg twice daily plus oral metronidazole 400 mg twice daily for a total of 14 days; * Oral doxycycline may
be used if tolerated.

intravenous clindamycin 900 mg three times daily plus intravenous gentamicin,* followed by either oral clindamycin 450
mg four times daily to complete 14 days
OR

oral doxycycline 100 mg twice daily plus oral metronidazole 400 mg twice daily to complete 14 days. * Gentamicin should
be given as a 2 mg/kg loading dose followed by 1.5 mg/kg three times daily [or a single daily dose of 7 mg/kg may be
substituted].

intravenous ofloxacin 400 mg twice daily plus intravenous metronidazole 500 mg three times daily for 14 days
In pregnancy, a combination of cefotaxime, azithromycin and metronidazole for 14 days may be used. Ofloxacin should be
avoided, where possible, in young women, when bone development is still occurring. Consideration should be given to
removing an intrauterine contraceptive device (IUD) in women presenting with PID, especially if symptoms have not resolved
within 72 hours. Surgical treatment should be considered in severe cases or where there is clear evidence of a pelvic abscess.
Consider drainage of an abscess and in noting its position, the possibility that the abscess may have arisen from the appendix
or colon.
When a sexually transmitted infection is either proven or likely to be the cause of PID, the current sexual partner(s) should be
contacted and offered health advice and screening for gonorrhoea and chlamydia. Referral of the index woman and her
partner to a genitourinary medicine/sexual health clinic is recommended to facilitate contact tracing and infection screening. In
the outpatient setting, review at 72 hours is recommended, particularly for those with a moderate or severe clinical
presentation. Women with PID who are also infected with HIV should be treated with the same antibiotic regimens as women
who are HIV negative. Women on hormonal contraception presenting with breakthrough bleeding should be screened for
genital tract infection, especially C. trachomatis. If a woman is likely to be at risk of future PID and requests an IUD for
contraception, the LNG-IUS would be the most appropriate choice.

12

No. 24 Endometriosis, investigation and treatment

Endometriosis is defined as the presence of endometrial-like tissue outside the uterus, which induces a chronic, inflammatory
reaction. The condition is predominantly found in women of reproductive age, from all ethnic and social groups. Treatment must
be individualised, taking the clinical problem in its entirety into account, including the impact of the disease and the effect of its
treatment on quality of life. Pain symptoms may persist despite seemingly adequate medical and/or surgical treatment of the
disease.This may suggest another source of pain, such as the uterus (adenomyosis), bladder (interstitial cystitis) or
musculoskeletal causes (pelvic floor muscle spasm). The most commonly affected sites are the pelvic organs and peritoneum,
although other parts of the body such as the bowel or lungs are occasionally affected. The extent of the disease varies from a
few,small lesions on otherwise normal pelvic organs to large, ovarian endometriotic cysts (endometriomas). There can be
extensive fibrosis in structures such as the uterosacral ligaments and adhesion formation causing marked distortion of pelvic
anatomy. Endometriosis typically appears as superficial powder-burn or gunshot lesions on the ovaries, serosal surfaces and
peritoneum:black, dark-brown or bluish puckered lesions, nodules or small cysts containing old haemorrhage surrounded by a
variable extent of fibrosis.Atypical or subtle lesions are also common, including red implants (petechial, vesicular, polypoid,
hemorrhagic, red flame-like) and serous or clear vesicles. Other appearances include white plaques or scarring and yellowbrown peritoneal discoloration of the peritoneum.
Endometriomas usually contain thick fluid, like chocolate. Such cysts are often densely adherent to the peritoneum of the
ovarian fossa and the surrounding fibrosis may involve the tubes and bowel. Deeply infiltrating endometriotic nodules extend
more than 5 mm beneath the peritoneum and may involve the uterosacral ligaments, vagina, bowel, bladder or ureters. The
depth of infiltration is related to the type and severity of symptoms.
Based on clinical and patient experience, endometriosis can cause the following symptoms: severe dysmenorrhoea; deep
dyspareunia; chronic pelvic pain; ovulation pain; cyclical or perimenstrual symptoms, such as bowel or bladder, with
or without abnormal bleeding or pain; infertility; chronic fatigue; dyschezia (pain on defaecation). There is considerable
overlap with other conditions such as irritable bowel syndrome and pelvic inflammatory disease.
Deeply infiltrating nodules are most reliably detected when clinical examination is performed during menstruation. Finding
pelvic tenderness, a fixed, retroverted uterus, tender uterosacral ligaments or enlarged ovaries on examination is suggestive of
endometriosis. There may also be nodules felt. For a definitive diagnosis of endometriosis, visual inspection of the pelvis at
laparoscopy is the gold standard investigation, unless disease is visible in the posterior vaginal fornix or elsewhere. Good
surgical practice is to use an instrument such as a grasper, via a secondary port, to mobilise the pelvic organs and to palpate
lesions, which can help determine their nodularity. It is also important to document in detail the type, location and extent of all
lesions and adhesions in the operative notes.
Positive histology confirms the diagnosis of endometriosis; negative histology does not exclude it. Whether histology should be
obtained if peritoneal disease alone is present is controversial. Visual inspection is usually adequate but histological
confirmation of at least one lesion is ideal. In cases of ovarian endometrioma (greater than 3 cm in diameter) and in deeply
infiltrating disease, histology should be obtained to identify endometriosis and to exclude rare instances of malignancy.
Compared with laparoscopy, transvaginal ultrasound (TVS) has limited value in diagnosing peritoneal endometriosis but it is a
useful tool both to make and to exclude the diagnosis of an ovarian endometrioma. Serum CA125 levels may be elevated in
endometriosis. However, compared with laparoscopy, measuring serum CA125 levels has no value as a diagnostic tool.
If a woman wants pain symptoms suggestive of endometriosis to be treated without a definitive diagnosis, a therapeutic trial of
a hormonal drug to reduce menstrual flow is appropriate. Definitive diagnosis includes counselling, adequate analgesia,
progestogens or the combined oral contraceptive. It is unclear whether the combined oral contraceptives should be taken
conventionally, continuously or in a tricycle regimen. A gonadotrophin-releasing hormone (GnRH) agonist may be taken but this
class of drug is more expensive and associated with more adverse effects and concerns about bone density. There is
inconclusive evidence to show whether NSAIDs (specifically naproxen) are effective in managing pain caused by
endometriosis. Suppression of ovarian function for 6 months reduces endometriosis-associated pain. Symptom recurrence is
common following medical treatment of endometriosis.
There are pilot data suggesting that the aromatase inhibitor, letrozole, may be effective although it is associated with significant
bone density loss. The LNG-IUS appears to reduce endometriosis-associated pain. The use of a GnRH agonist with add-back
(oestrogen and progestogen) therapy protects against bone mineral density loss at the lumbar spine during treatment and for
up to 6 months after treatment.
If there is clinical evidence of deeply infiltrating endometriosis, ureteric, bladder and bowel involvement should be assessed.
Consideration should be given to performing MRI or ultrasound (transrectal and/or transvaginal and/or renal), with or without
IVP and barium enema studies, to map the extent of disease as it may be multifocal. A guideline for the management of
suspected ovarian malignancy should be followed in cases of ovarian endometrioma.
The management of severe/deeply infiltrating endometriosis is complex. Surgery is usually required and multiple organs are
sometimes involved. Therefore, if disease of such severity is suspected or diagnosed, referral to a centre with the necessary
expertise to offer all available treatments in a multidisciplinary context, including advanced laparoscopic surgery and
laparotomy, is strongly recommended. Ablation of endometriotic lesions reduces endometriosis-associated pain compared with
diagnostic laparoscopy. Laparoscopic uterine nerve ablation by itself does not reduce endometriosis-associated pain.
Endometriosis associated pain can be reduced by removing the entire lesions in severe and deeply infiltrating disease. The
ideal regimen for HRT after bilateral oophorectomy is unclear and should be discussed on an individual basis. Ablation of

13

endometriotic lesions plus adhesiolysis to improve fertility in minimalmild endometriosis is effective compared with diagnostic
laparoscopy alone. Laparoscopic cystectomy for ovarian endometriomas is better than drainage and coagulation.
Postoperative hormonal treatment has no beneficial effect on pregnancy rates after surgery. Tubal flushing appears to improve
pregnancy rates in women with endometriosis-associated infertility. Treatment with IUI improves fertility in minimal to mild
endometriosis. IVF is appropriate treatment, especially if tubal function is compromised, if there is also male factor infertility,
and/or other treatments have failed. Laparoscopic ovarian cystectomy is recommended for endometriomas 4 cm in diameter.
Treatment with a GnRH agonist for 36 months before IVF in women with endometriosis increases the rate of clinical
pregnancy.

No. 25 The management of early pregnancy loss

Early pregnancy loss, defined as a loss within the first 12 completed weeks of pregnancy. Miscarriage occurs in 1020% of
clinical pregnancies4 and accounts for 50 000 inpatient admissions to hospitals in the UK annually. Historically, the majority of
women who miscarried underwent routine surgical uterine evacuation; that is, evacuation of retained products of conception
(ERPC). The recommended medical term for pregnancy loss under 24 weeks is miscarriage.
Biochemical pregnancy loss
Empty sac
Fetal loss
activity
Early pregnancy loss
Delayed miscarriage
Late pregnancy loss
Pregnancy of unknown location

Pregnancy not located on scan

Sac with absent or minimal structures
Previous CRL measurement with subsequent loss of fetal heart
Confirmed empty sac or sac with fetus but no FHA 12 weeks
As early pregnancy loss
Loss of FHA 12 weeks
No identifiable pregnancy on scan with positive hCG

All units should provide a dedicated outpatient early pregnancy assessment service. There are clinical and economic benefits
associated with this type of service.
The EPAU service should be comprehensive and ideally sited in a dedicated area with appropriate staffing. There should be
direct access for GPs and selected patient groups. To be effective, an EPAU requires an efficient appointments system, an
appropriate setting, ultrasound equipment (including transvaginal probes) and easy access to laboratory facilities for rhesus
antibody testing and selective serum human chorionic gonadotrophin (hCG) and progesterone estimation. The service should
be available on a daily basis during the normal working week, although many units offer an additional limited service at
weekends. Standardised information leaflets, referral and discharge letters should be available and regularly reviewed. Certain
patient groups, such as women who have had a previous ectopic pregnancy and those with repeated or recurrent miscarriage,
can be offered future access to the service by direct self-referral via the appointments system. Transvaginal scanning will be
required in the majority of women referred to an EPAU. Ultrasound assessment is particularly reliable in confirming the
diagnosis of complete miscarriage (positive predictive value 98%).12The sonographer should be formally trained in the use of
both transabdominal (TAS) and transvaginal ultrasound (TVS). EPAUs should use and develop diagnostic and therapeutic
algorithms of care. In particular, these should be available for the management of suspected ectopic pregnancy, intrauterine
pregnancy of uncertain viability and for pregnancy of unknown location. The use of the term indeterminate is confusing and
more specific definitions should be used (specifically pregnancy of unknown location and pregnancy of uncertain viability).
Pregnancy of unknown location: No signs of either intra- or extrauterine pregnancy or retained products of conception in a
woman with a positive pregnancy test. Pregnancy of uncertain viability: Intrauterine sac (<20mm mean diameter) with) no
obvious yolk sac or fetus or Fetal echo <6mm crownrump length with no obvious fetal heart activity. In order to confirm or
refute viability, a repeat scan at a minimal interval of 1 week is necessary. Serial serum hCG assay is particularly useful in the
diagnosis of asymptomatic ectopic pregnancy. Modern monoclonal antibody based kits can detect hCG at 25 iu/l, a level
reached 9 days postconception (day 23 of a 28-day cycle).17 Unit-specific discriminatory zones for serum hCG should be
defined to help exclude possible ectopic pregnancy. At levels above 1500 iu/l, an ectopic pregnancy will usually be visualised
with TVS Serum hCG levels need caution in interpretation. In cases of twin pregnancy or heterotopic pregnancy, a suboptimal
rise may be misleading.
Serum progesterone can be a useful adjunct when ultrasound suggests pregnancy of unknown location. TVS, serial serum
hCG levels and progesterone may all be required in order to establish a definite diagnosis. In the presence of pregnancy of
unknown location, a serum progesterone less than 20 nmol/l predicts spontaneous pregnancy resolution with a sensitivity of
93% and specificity of 94%. Levels above 25nmol/l are likely to indicate and above 60 nmol/l are strongly associated with
pregnancies subsequently shown to be normal.
Non-sensitised rhesus (Rh) negative women should receive anti-D immunoglobulin in the following situations: ectopic
pregnancy, all miscarriages over 12 weeks of gestation (including threatened) and all miscarriages where the uterus is
evacuated (whether medically or surgically). Anti-D immunoglobulin should only be given for threatened miscarriage under 12
weeks gestation when bleeding is heavy or associated with pain. It is not required for cases of complete miscarriage under 12
weeks of gestation when there has been no formal intervention to evacuate the uterus.
Screening for infection, including Chlamydia trachomatis, should be considered in women undergoing
surgical uterine evacuation. Consider vaginal swabs to exclude bacterial vaginosis if clinically indicated. There is insufficient
evidence to recommend routine antibiotic prophylaxis prior to surgical uterine evacuation. Antibiotic prophylaxis should be
given based on individual clinical indications. Surgical uterine evacuation should be offered to women who prefer that option.
Clinical indications for offering surgical evacuation include: persistent excessive bleeding, haemodynamic instability, evidence

14

of infected retained tissue and suspected gestational trophoblastic disease. Surgical uterine evacuation for miscarriage should
be performed using suction curettage. Consideration should be given to offering surgical evacuation techniques under local
anaesthesia or sedation for those women who prefer that approach. Medical methods are an effective alternative in the
management of confirmed first-trimester miscarriage.
Protocols should be developed locally with selection criteria, therapeutic regimens and arrangements for follow-up. To avoid
unnecessary anxiety, women should be informed that bleeding may continue for up to 3 weeks after medical uterine
evacuation. Higher success rates (7096%) were associated with incomplete miscarriage, high-dose misoprostol (12001400
micrograms), prostaglandins administered vaginallyand clinical follow-up without routine ultrasound. In missed miscarriages
(closed cervix and intact sac), effective regimens involve a higher dose of prostaglandin with longer duration of use32 or,
alternatively, priming with antiprogesterone. Incomplete miscarriage is usually managed with prostaglandin alone. One
randomised trial showed no statistical difference in efficacy between surgical and medical evacuation for incomplete
miscarriage and for early fetal demise at gestations less than 71 days or sac diameter less than 24mm. Expectant
management is another effective method to use in selected cases of confirmed first-trimester miscarriage. Medical and
expectant management should only be offered in units where women can access 24-hour telephone advice and emergency
admission if required.
Tissue obtained at the time of miscarriage should be examined histologically to confirm pregnancy and to exclude ectopic
pregnancy or unsuspected gestational trophoblastic disease. In terms of therapeutic intervention, patient choice should be
encouraged, as it is associated with positive quality-of-life outcomes.

No 26 Operative vaginal delivery

Operative vaginal delivery rates have remained stable at between 10% and 15%. In addition, there has been a growing
awareness of the short- and long-term morbidity of pelvic floor injury following operative vaginal delivery. All women should be
encouraged to have continuous support during labour. Use of a partogram, use of upright or lateral positions and avoiding
epidural analgesia, will reduce the need for operative vaginal delivery. Oxytocin in primiparous women with epidurals will
decrease the need for operative vaginal delivery. Delayed pushing in primiparous women with an epidural will reduce the risk of
rotational and mid-cavity deliveries.

Indication: Presumed fetal compromise. Maternal Medical indications to avoid Valsalva (e.g. cardiac disease Class III or
IV,a hypertensive crises, cerebral vascular disease, particularly uncorrected cerebral vascular malformations, myasthenia
gravis, spinal cord injury). Inadequate progress Nulliparous women: lack of continuing progress for three hours (total of
active and passive second stage labour) with regional anaesthesia, or two hours without regional anaesthesia
Multiparous women: lack of continuing progress for two hours (total of active and passive second stage labour) with
regional anaesthesia, or one hour without regional anaesthesia. Maternal fatigue/exhaustion
Higher rates of failure are associated with: maternal body mass index greater than 30; estimated fetal weight greater than 4000
g or clinically big baby; occipito-posterior position; mid-cavity delivery or when 1/5 head palpable per abdomen. The options
available for rotational delivery include Kielland forceps, manual rotation followed by direct traction forceps or rotational
vacuum extraction. Rotational deliveries should be performed by experienced operators, the choice depending upon the
expertise of the individual operator.

Vacuum extractor compared with forceps is: more likely to fail at achieving vaginal delivery; more likely to be associated
with cephalhaematoma; more likely to be associated with retinal haemorrhage; more likely to be associated with maternal
worries about baby; less likely to be associated with significant maternal; perineal and vaginal trauma; no more likely to
be associated with delivery by caesarean section; no more likely to be associated with low 5-minute Apgar scores; no
more likely to be associated with the need for phototherapy. In view of the reduction of maternal pelvic floor injuries, the
vacuum extractor has been advocated as the instrument of first choice.

Operative vaginal delivery should be abandoned where there is no evidence of progressive descent with each pull or
where delivery is not imminent following three pulls of a correctly applied instrument by an experienced operator.

Adverse outcomes, including unsuccessful forceps or vacuum delivery, should trigger an incident report as part of
effective risk management processes. Paired cord blood samples should be processed and recorded following all
attempts at operative vaginal delivery.

The use of sequential instruments is associated with an increased risk of trauma to the infant. However, the operator must
balance the risks of a caesarean section following failed vacuum extraction with the risks of forceps delivery following
failed vacuum extraction.

Caesarean section in the second stage of labour is associated with an increased risk of major obstetric haemorrhage,
prolonged hospital stay and admission of the baby to SCBU compared to completed instrumental delivery

The role of routine episiotomy for operative vaginal delivery is poorly evaluated and warrants further research.

There is insufficient data to make recommendations regarding prophylactic antibiotics in operative vaginal delivery. Good
standards of hygiene and aseptic techniques are recommended.

Women should be reassessed after an operative delivery for risk factors for venous thromboembolism

Regular paracetamol and diclofenac should be considered after an operative vaginal delivery in the absence of
contraindications.

15

The timing and volume of the first void urine should be monitored. All women undergoing an operative vaginal delivery
should have monitoring, such as a fluid balance chart, for at least 24 hours, to detect postpartum urinary retention. A postvoid residual should be measured if retention is suspected.
Women who have had spinal anaesthesia or epidural anaesthesia that has been topped up for a trial of labour may be at
increased risk of retention and should be offered an indwelling catheter, to be kept in place for at least 12 hours following
delivery to prevent asymptomatic bladder overfilling. Women should be offered physiotherapy-directed strategies to
prevent urinary incontinence.

No. 27 Placenta Praevia and Accreta: Diagnosis and Management

Placenta praevia exists when the placenta is inserted wholly or in part into the lower segment of the uterus. If it lies over the
cervical os, it is considered a major praevia, if not, then minor praevia exists. This diagnosis has evolved from the original
clinical IIV grading system and is determined by ultrasonic imaging techniques relating the leading edge of the placenta to the
cervical os. Transvaginal ultrasound is safe in the presence of placenta praevia and is more accurate than
transabdominal ultrasound in locating the placenta. An MRI can be used in TVS is unsatisfactory. A reasonable antenatal
imaging policy is to perform a transvaginal ultrasound scan on all women in whom a low-lying placenta is suspected from their
transabdominal anomaly scan (at approximately 2024 weeks) to reduce the numbers of those for whom follow-up will be
needed. A further transvaginal scan is required for all women whose placenta reaches or overlaps the cervical os at their
anomaly scan as follows: Women who bleed should be managed individually according to their needs. In cases of
asymptomatic suspected minor praevia, follow-up imaging can be left until 36 weeks. In cases with asymptomatic suspected
major placenta praevia, a transvaginal ultrasound scan should be performed at 32 weeks, to clarify the diagnosis and allow
planning for third-trimester management and delivery.
Antenatal imaging by colour flow Doppler ultrasonography should be performed in women with placenta praevia who are at
increased risk of placenta accreta. Where this is not possible locally, such women should be managed as if they have placenta
accreta until proven otherwise. Women with placenta praevia are at increased risk of having a morbidly adherent placenta if
they have an anterior placenta praevia and have previously been delivered by caesarean section, especially when there has
been a short caesarean to conception interval. Of the nine who had had an MRI, only four were correctly diagnosed and of the
13 who had ultrasound only four were correctly diagnosed. Women with major placenta praevia who have previously bled
should be admitted and managed as inpatients from 34 weeks of gestation. Those with major placenta praevia who remain
asymptomatic, having never bled, require careful counselling before contemplating outpatient care. Any home-based care
requires close proximity with the hospital, the constant presence of a companion and full informed consent from the woman.
It should be made clear to any woman being managed at home that she should attend hospital immediately if she experiences
any bleeding, any contractions or any pain (including vague Suprapubic period-like aches). Prior to delivery, all women with
placenta praevia and their partners should have had antenatal discussions regarding delivery, haemorrhage, possible blood
transfusion and major surgical interventions, such as hysterectomy, and any objections or queries dealt with effectively.
Decisions regarding blood availability during inpatient antenatal care should be based on clinical factors relating to individual
cases, as well as local blood bank services. Women with atypical antibodies form a particular high-risk group and discussions
in these cases should involve the local haematologist and blood bank. The use of cervical cerclage to reduce bleeding and
prolong pregnancy is not backed up by sufficient evidence to recommend this practice outside of a clinical trial. Tocolysis for
treatment of bleeding due to placenta praevia can be useful in selected cases. Prolonged inpatient care can be associated with
an increased risk of thromboembolism. Thus, gentle mobility should be encouraged together with the use of prophylactic
thromboembolic stockings. Prophylactic anticoagulation should be reserved for those at high risk of thromboembolism and, in
these cases, unfractionated heparin is to be preferred over the longer-acting low-molecular-weight preparations. The mode of
delivery should be based on clinical judgement supplemented by sonographic information. A placental edge less than 2 cm
from the internal os is likely to need delivery by caesarean section, especially if it is posterior or thick. Blood should be readily
available for the peripartum period. Requirements for crossmatched blood and what amount will depend on the clinical features
of each individual case and the local blood bank services available. When women have atypical antibodies, direct
communication with the local blood bank should enable specific plans to be made to match the individual circumstance. There
is no evidence to support the use of autologous blood transfusion for placenta praevia. Cell salvage may be considered in
cases at high risk of massive haemorrhage. The choice of anaesthetic technique for caesarean section for placenta praevia
must be made by the anaesthetist, in consultation with the obstetrician and mother, but there is increasing evidence to support
the safety of regional blockade.
Any woman going to theatre with known placenta praevia should be delivered by the most experienced obstetrician and
anaesthetist on duty. As a minimum requirement during a planned procedure, a consultant obstetrician and anaesthetist should
be present within the delivery suite. A junior doctor should not be left unsupervised when caring for these women. When an
emergency arises, consultant staff should be alerted and should attend as soon as possible. The timing of emergency surgery
will be influenced by individual circumstances but, where possible, elective caesarean section should be deferred to 38 weeks
to minimise neonatal morbidity.
Women with placenta praevia who have had a previous caesarean section are at high risk of having a morbidly adherent
placenta and should have been imaged antenatally. When placenta accreta is thought to be likely, consultant anaesthetic and
obstetric input are vital in planning and conducting the delivery. Crossed matched blood should be available and colleagues
from other specialties/ subspecialties may be alerted to be on standby to attend as needed. In the case of placenta accreta,
increta and percreta, the risk of haemorrhage, transfusion and hysterectomy should be discussed with the patient as part of the
consent procedure. There have been numerous case reports of placenta praevia accreta and its management, which include a
number of series where the placenta has been left in place at the end of the caesarean section. Management in these cases

16

has varied, with some having prophylactic or therapeutic uterine artery embolisation, or internal iliac artery ligation at the same
time as initial surgery, and some being treated following delivery with methotrexate. Successful pregnancies have been
reported after this approach but there have been cases of delayed haemorrhage necessitating hysterectomy. In contrast, some
cases have had no additional treatment after leaving the placenta in place and still had successful outcomes. Uterine artery
embolisation, where the placentas were left alone and disappeared months after delivery have been shown in France. Every
unit should have a protocol for the management of massive obstetric haemorrhage which includes: liaison with haematology;
giving warm blood rapidly; criteria for invasive monitoring; management of women who refuse blood products. Emergency
clinical scenarios and fire drills surrounding issues of massive obstetric haemorrhage and obtaining blood products urgently
should be run locally. Uterotonic agents may help in reducing the blood loss associated with bleeding from the relatively atonic
lower uterine segment, while bimanual compression, hydrostatic balloon catheterisation or uterine packing, or even aortic
compression,can buy time while senior help arrives. Additional surgical manoeuvres which may be considered include the BLynch suture, uterine or internal iliac artery ligation or hysterectomy. Arterial embolisation has been reported and is useful in
selected cases as long as the iliac vessels have not been tied off.

No. 28 Thromboembolic disease in pregnancy and the puerperium.

VTE remains the main direct cause of maternal death in the UK1 and sequential reports of Confidential Enquiries into Maternal
Deaths have highlighted failures in obtaining objective diagnoses and employing adequate treatment. The subjective, clinical
assessment of deep venous thrombosis (DVT) and pulmonary thromboembolism (PTE) is particularly unreliable in pregnancy
and a minority of women with clinically suspected VTE have the diagnosis confirmed when objective testing is employed.
However, VTE is up to ten times more common in pregnant women than in nonpregnant women of the same age4 and can
occur at any stage of pregnancy but the puerperium is the time of highest risk. Acute VTE should be suspected during
pregnancy in women with symptoms and signs consistent with possible VTE, particularly if there are other risk factors for VTE.
The symptoms and signs of VTE include leg pain and swelling (usually unilateral), lower abdominal pain, low-grade pyrexia,
dyspnoea, chest pain, haemoptysis and collapse.

Any woman with signs and symptoms suggestive of VTE should have objective testing performed expeditiously and
treatment with low-molecular-weight heparin until the diagnosis is excluded by objective testing, unless treatment is
strongly contraindicated.

Compression duplex ultrasound should be undertaken where there is clinical suspicion of DVT. If ultrasound is negative
and there is a low level of clinical suspicion, anticoagulant treatment can be discontinued.

Where there is clinical suspicion of acute PTE a chest X-ray should be performed. Compression duplex Doppler should
be performed where this is normal. If both tests are negative with persistent clinical suspicion of acute PTE, a ventilation
perfusion (V/Q) lung scan or a computed tomography pulmonary angiogram (CTPA) should be performed. Alternative or
repeat testing should be carried out where V/Q scan or CTPA and duplex Doppler are normal but the clinical suspicion of
PTE is high. Anticoagulant treatment should be continued until PTE is definitively excluded.

Women with suspected PTE should be advised that V/Q scanning carries a slightly increased risk of childhood cancer
compared with CTPA (1/280,000 versus less than 1/1,000,000) but carries a lower risk of maternal breast cancer (lifetime
risk increased by up to 13.6% with CTPA, background risk of 1/200 for study population). Where feasible, women should
be involved in the decision to undergo CTPA or V/Q scanning. Ideally, informed consent should be obtained before these
tests are undertaken. D-dimer testing should not be performed to diagnose acute VTE in pregnancy. In pregnancy, Ddimer can be elevated because of the physiological changes in the coagulation system and levels become abnormal at
term and in the postnatal period in most healthy pregnant women.

Routine measurement of peak anti-Xa activity for patients on LMWH for treatment of acute VTE in pregnancy or
postpartum is not recommended except in women at extremes of body weight (less than 50 kg and 90 kg or more) or with
other complicating factors (for example with renal impairment or recurrent VTE) putting them at high risk.

Routine platelet count monitoring should not be carried out (unless unfractionated heparin has been given).

Collapsed, shocked patients need to be assessed by a team of experienced clinicians, including the on call consultant
obstetrician, who should decide on an individual basis whether a woman receives intravenous unfractionated heparin,
thrombolytic therapy or thoracotomy and surgical embolectomy. Intravenous unfractionated heparin is the preferred
treatment in massive PTE with cardiovascular compromise.

The on-call medical team should be contacted immediately. An urgent portable echocardiogram or CTPA within 1 hour of
presentation should be arranged. If massive PTE is confirmed or, in extreme circumstances prior to confirmation,
immediate thrombolysis should be considered. Maternity units should develop guidelines for the administration of
intravenous unfractionated heparin. Management should involve a multidisciplinary resuscitation team including senior
physicians, obstetricians and radiologists.

Treatment with therapeutic doses of subcutaneous LMWH should be employed during the remainder of the pregnancy.
Arrangements should be made to allow safe disposal of needles and syringes. Outpatient follow-up should include clinical
assessment and advice with assessment of blood platelets and peak anti-Xa levels if appropriate. Women receiving
therapeutic-dose unfractionated heparin should have their platelet count monitored at least every other day until day 14 or
until the unfractionated heparin is stopped, whichever occurs first.

Pregnant women who develop heparin-induced thrombocytopenia or have heparin allergy and require continuing
anticoagulant therapy should be managed with the heparinoid, danaparoid sodium or fondaparinux, under specialist
advice. Because of their adverse effects on the fetus, oral anticoagulants should not be used for antenatal VTE treatment.

17

The woman taking LMWH for maintenance therapy should be advised that once she is established in labour or thinks that
she is in labour, she should not inject any further heparin. Where delivery is planned, LMWH maintenance therapy should
be discontinued 24 hours before planned delivery. Regional anaesthetic or analgesic techniques should not be
undertaken until at least 24 hours after the last dose of therapeutic LMWH.
A thromboprophylactic dose of LMWH should be given by 3 hours after a caesarean section (more than 4 hours after
removal of the epidural catheter, if appropriate). The epidural catheter should not be removed within 12 hours of the most
recent injection.
In women receiving therapeutic doses of LMWH, wound drains (abdominal and rectus sheath) should be considered at
caesarean section and the skin incision should be closed with staples or interrupted sutures to allow drainage of any
haematoma. Any woman who is considered to be at high-risk of haemorrhage and in whom continued heparin treatment
is considered essential should be managed with intravenous, unfractionated heparin until the risk factors for haemorrhage
have resolved.
Therapeutic anticoagulant therapy should be continued for the duration of the pregnancy and for at least 6 weeks
postnatally and until at least 3 months of treatment has been given in total. Women should be offered a choice of LMWH
or oral anticoagulant for postnatal therapy after discussion about the need for regular blood tests for monitoring of
warfarin, particularly during the first 10 days of treatment. Women should be advised that neither heparin (unfractionated
or LMWH) nor warfarin is contraindicated in breastfeeding. Postpartum warfarin should be avoided until at least the third
day and for longer in women at increased risk of postpartum haemorrhage.
Graduated elastic compression stockings should be worn on the affected leg for 2 years after the acute event, if swelling
persists, to reduce the risk of post-thrombotic syndrome.

No. 29 The management of third and fourth degree tears

The overall risk of obstetric anal sphincter injury is 1% of all vaginal deliveries.

A third-degree perineal tear is defined as a partial or complete disruption of the anal sphincter muscles, which may
involve either or both the external (EAS) and internal anal sphincter (IAS) muscles. A fourth-degree tear is defined as a
disruption of the anal sphincter muscles with a breach of the rectal mucosa.

Where episiotomy is indicated, the mediolateral technique is recommended, with careful attention to the angle cut away
from the midline.

Risks include: birth weight over 4 kg (up to 2%); persistent occipitoposterior position (up to 3%); nulliparity (up to 4%);
induction of labour (up to 2%); epidural analgesia (up to 2%); second stage longer than 1 hour (up to 4%); shoulder
dystocia (up to 4%); midline episiotomy (up to 3%); forceps delivery (up to 7%).

First degree: Injury to perineal skin only.

Second degree Injury to perineum involving perineal muscles but not involving the anal sphincter.

Third degree: Injury to perineum involving the anal sphincter complex: 3a: Less than 50% of EAS thickness torn. 3b: More
than 50% of EAS thickness torn. 3c: Both EAS and IAS torn.

Fourth degree: Injury to perineum involving the anal sphincter complex (EAS and IAS) and anal epithelium.

All women having a vaginal delivery with evidence of genital tract trauma should be examined systematically to assess
the severity of damage prior to suturing.

All women having an operative vaginal delivery or who have experienced perineal injury should be examined by an
experienced practitioner trained in the recognition and management of perineal tears.

For repair of the external anal sphincter, either an overlapping or end-to-end (approximation) method can be used, with
equivalent outcome. Where the IAS can be identified, it is advisable to repair separately with interrupted sutures.

Repair of third- and fourth-degree tears should be conducted in an operating theatre, under regional or general
anaesthesia. When repair of the EAS muscle is being performed, either monofilament sutures such as polydiaxanone

(PDS) or modern braided sutures such as polyglactin (Vicryl) can be used with equivalent outcome.

When repair of the IAS muscle is being performed, fine suture size such as 3-0 PDS and 2-0 Vicryl may cause less
irritation and discomfort. When obstetric anal sphincter repairs are being performed, burying of surgical knots beneath the
superficial perineal muscles is recommended to prevent knot migration to the skin. Women should be warned of the
possibility of knot migration to the perineal surface, with long-acting and non-absorbable suture materials. The use of
broad-spectrum antibiotics is recommended following obstetric anal sphincter repair to reduce the incidence of
postoperative infections and wound dehiscence. The use of postoperative laxatives is recommended to reduce the
incidence of postoperative wound dehiscence.

Local protocols should be implemented regarding the use of antibiotics, laxatives, examination and follow-up of women
with obstetric anal sphincter repair. All women should be offered physiotherapy and pelvic-floor exercises for 612 weeks
after obstetric anal sphincter repair.

All women who have had obstetric anal sphincter repair should be reviewed 612 weeks postpartum by a consultant
obstetrician and gynaecologist. If a woman is experiencing incontinence or pain at follow-up, referral to a specialist
gynaecologist or colorectal surgeon for endoanal ultrasonography and anorectal manometry should be considered. A
small number of women may require referral to a colorectal surgeon for consideration of secondary sphincter repair.

18

Women should be advised that the prognosis following EAS repair is good, with 6080% asymptomatic at 12 months.
Most women who remain symptomatic describe incontinence of flatus or faecal urgency.
All women who sustained an obstetric anal sphincter injury in a previous pregnancy should be counselled about the risk
of developing anal incontinence or worsening symptoms with subsequent vaginal delivery.
All women who sustained an obstetric anal sphincter injury in a previous pregnancy should be advised that there is no
evidence to support the role of prophylactic episiotomy in subsequent pregnancies.
All women who have sustained an obstetric anal sphincter injury in a previous pregnancy and who are symptomatic or
have abnormal endoanal ultrasonography and/or manometry should have the option of elective caesarean birth.
When third- and fourth-degree repairs are performed, it is essential to ensure that the anatomical structures involved,
method of repair and suture materials used are clearly documented and that instruments, sharps and swabs are
accounted for.
The woman should be fully informed about the nature of her injury and the benefits to her of follow-up. This should
include written information where possible.

No. 30 Genital Herpes in Pregnancy, Management

Neonatal herpes is a viral infection with a high morbidity and mortality which is most commonly acquired at or near the time of
delivery. It is classified into three subgroups: disease localised to skin, eye and/mouth, local central nervous system (CNS)
disease (encephalitis alone) and disseminated infection with multiple organ involvement. Infants who present with skin, eye,
and/mouth symptoms alone have the best prognosis: death is unusual and, with antiviral treatment, neurological and/or ocular
morbidity is less than 2%. Disseminated disease and local CNS disease can present with or without skin, eye and/mouth
infection. Disseminated disease carries the worst prognosis: with antiviral treatment, mortality is around 30% and 17% have
long-term neurological sequelae. Infants with local CNS disease often present late (generally between 10 days and 4 weeks
postnatally); with treatment, mortality is around 6% and neurological morbidity 70%. The poor outcomes of disseminated and
local CNS disease have been attributed to delays between symptom onset and treatment.
Neonatal herpes may be caused by herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2), as either viral
type can cause genital herpes. Almost all cases of neonatal herpes occur as a result of direct contact with infected maternal
secretions, although cases of postnatal transmission have been described. Factors influencing transmission include the type of
maternal infection (primary or recurrent), the presence of transplacental maternal neutralising antibodies, the duration of
rupture of membranes before delivery, the use of fetal scalp electrodes and mode of delivery. The risks are greatest when a
woman acquires a new infection (primary genital herpes) in the third trimester, particularly within 6 weeks of delivery, as viral
shedding may persist and the baby is likely to be born before the development of protective maternal antibodies. Very rarely,
congenital herpes may occur as a result of transplacental intrauterine infection. Case reports suggest that the skin, eyes and
central nervous system may be affected and there may be intrauterine growth restriction or fetal death. Disseminated herpes is
more common in preterm infants and occurs almost exclusively is a result of primary infection in the mother. Although recurrent
genital herpes is associated with a very low risk of neonatal herpes, recurrent herpes at the time of delivery which is commonly
asymptomatic or unrecognised, may cause the localised forms of neonatal herpes, both local CNS disease and skin, eye and
mouth infection. Transplacentally acquired HSV antibodies do not prevent neurogenic virus spreading to the brain of the
neonate. Disseminated herpes, which may present with encephalitis, hepatitis, disseminated skin lesions or a combination of
these conditions, is rare in adults but has been more commonly reported in pregnancy, particularly in the immunocompromised.
The maternal mortality associated with this condition is high.
Symptomatic genital herpes infections are confirmed by direct detection of HSV. Specimens from ulcerated lesions are
sampled by swabbing the base of the ulcer and vesicular lesions are de-roofed and the fluid sampled. A swab for viral detection
should be used. Subsequent analysis is by viral culture or polymerase chain reaction (PCR). Women should be referred to a
genitourinary physician and management of the woman should be in line with her clinical condition. Oral or intravenous
aciclovir in standard doses should be offered. Typespecific HSV antibody testing, which can help to differentiate between
primary and recurrent infections, should be undertaken if a woman presents with a first episode of genital herpes in the third
trimester. Women should be informed of the potential risk and benefits of treatment with aciclovir. Aciclovir should be used with
caution before 20 weeks of gestation.
Caesarean section should be recommended to all women presenting with primary episode genital herpes lesions at the time of
delivery, or within 6 weeks of the expected date of delivery. For women who develop primary genital herpes lesions within 6
weeks of delivery and who opt for a vaginal birth, rupture of membranes should be avoided and invasive procedures should not
be used. Intravenous aciclovir given intrapartum to the mother and subsequently to the neonate may be considered. The
neonatologist should be informed. There is insufficient evidence to recommend use of daily suppressive aciclovir from 36
weeks of gestation to reduce the likelihood of HSV lesions at term for women who experience a primary episode of genital
herpes earlier in the current pregnancy.
Antiviral treatment is rarely indicated for treatment of recurrent episodes of genital herpes during pregnancy. Cultures during
late gestation to predict viral shedding at term are not indicated. A recurrent episode of genital herpes occurring during the
antenatal period is not an indication for delivery by caesarean section. For women with a history of recurrent genital herpes,
who would opt for caesarean delivery if HSV lesions were detected at the onset of labour, daily suppressive aciclovir given
from 36 weeks of gestation until delivery may be given to reduce the likelihood of HSV lesions at term.
Women presenting with recurrent genital herpes lesions at the onset of labour should be advised that the risk to the baby of
neonatal herpes is very small. Caesarean section is not routinely recommended for women with recurrent genital herpes
lesions at the onset of labour. The mode of delivery should be discussed with the woman and individualised according to the
clinical circumstances and the womans preferences. Women with recurrent genital herpes lesions and confirmed rupture of
membranes at term should be advised to have delivery expedited by the appropriate means. Invasive procedures in labour

19

should be avoided for women with recurrent genital herpes lesions. The neonatologist should be informed of babies born to
mothers with recurrent genital herpes lesions at the time of labour. Healthcare workers and family members with active HSV
infection, such as orolabial herpes or herpetic whitlow, should take measures to avoid transmission of the virus to the neonate.

No. 31 Small-for-Gestational-Age Fetus, Investigation & Management

SGA fetuses are a heterogeneous group comprising fetuses that have failed to achieve their growth potential (fetal growth
restriction, FGR) and fetuses that are constitutionally small. Approximately 5070% of fetuses with a birthweight below tenth
centile for gestational age are constitutionally small, and the lower the centile for defining SGA, the higher the likelihood of
FGR. On the other hand, a fetus with growth restriction may not be SGA. SGA fetuses are at greater risk of stillbirth, birth
hypoxia, neonatal complications impaired neurodevelopment, and possibly type 2 (non-insulin-dependent) diabetes and
hypertension in adult life. Methods employed to detect SGA fetuses include abdominal palpation, measurement of symphyseal
fundal height, ultrasound biometry, ultrasound estimated fetal weight and ultrasound Doppler flow velocimetry. Biometric tests
are designed to predict size and, if performed longitudinally, growth, but not wellbeing. Biophysical tests, on the other hand, are
not designed to predict size but fetal wellbeing. The presence of fetal wellbeing implies the absence of fetal acidaemia. This
distinction implies that the diagnosis of SGA would rely on biometric tests while abnormal biophysical tests are more indicative
of FGR than SGA.
Abdominal palpation has limited diagnostic accuracy to predict an SGA fetus. Physical examination of the abdomen by
inspection and palpation detects as few as 30% SGA fetuses. Therefore, if SGA is suspected, it is necessary to supplement
abdominal palpation with ultrasound biometric tests. Symphyseal fundal height (SFH) measurement has limited diagnostic
accuracy to predict an SGA neonate. Abdominal circumference (AC) and estimated fetal weight (EFW) are the most accurate
diagnostic measurements to predict SGA.
FORMULAE FOR ESTIMATION OF FETAL WEIGHT
Shepards formula:
Log10EFW = 1.2508 + (0.166 x BPD) + (0.046 x AC) (0.002646 x AC x BPD)
Aokis formula:
EFW = (1.25647 x BPD3) + (3.50665 x FAA x FL) + 6.3
Hadlocks formula:
Log10EFW = 1.3596 0.00386(AC x FL) + 0.0064(HC) + 0.00061(BPD x AC) + 0.0425 (AC) + 0.174 (FL).
Serial measurements of AC and EFW (growth velocities) are superior to single estimates of AC or EFW in the prediction of
FGR (abnormal neonatal ponderal index and skinfold thickness) and predicting poor perinatal outcome. Uterine artery Doppler
has limited use in predicting FGR. Although various Doppler studies of fetal circulation such as aortic to middle cerebral artery
pulsatility index ratio are used to predict FGR fetuses.
When a small fetus is diagnosed, assess for risk of chromosomal defects. Up to 19% of fetuses with an AC and EFW less than
the fifth centile may have chromosomal defects. The risk is higher when growth restriction is associated with structural
abnormalities, a normal liquor volume or a normal uterine or umbilical artery Doppler. Therefore, all growth-restricted fetuses
need an ultrasound anatomical survey as a minimum. It may also be appropriate to offer karyotyping.
Use umbilical artery Doppler as the primary surveillance tool. Measure liquor volume using either AFI or pocket depth as both
tests have similar diagnostic accuracy. When end diastolic flow is present (PED), delay delivery until at least 37 weeks,
provided other surveillance findings are normal. When end diastolic flow is absent or reversed, admission, close surveillance
and administration of steroids are required. If other surveillance results (biophysical profile, venous Doppler) are abnormal,
delivery is indicated. If gestation is over 34 weeks, even if other results are normal, delivery may be considered. Administer
steroids if gestation is below 36 weeks. Deliver in a unit where optimal neonatal expertise and facilities are available.
Intrapartum monitoring with continuous CTG is recommended.

No. 33 Polycystic Ovary Syndrome, Long-Term Consequences

PCOS is a common disorder, often complicated by chronic anovulatory infertility and hyperandrogenism with the clinical
manifestation of oligomenorrhoea, hirsutism and acne. Many women with this condition are obese and have a higher
prevalence of impaired glucose tolerance, type 2 diabetes and sleep apnoea. Most clinical data suggests a prevalence of 6
7% of the population. Diagnosis of PCOS can only be made when other aetiologies have been excluded (thyroid dysfunction,
congenital adrenal hyperplasia, hyperprolactinaemia, androgen-secreting tumours and Cushing syndrome). A consensus
definition using precise diagnostic criteria should be used when diagnosing PCOS to facilitate effective patient care and robust
clinical research. This has suggested a broader definition for PCOS, with two of the three following criteria being diagnostic of
the condition:

polycystic ovaries (either 12 or more peripheral follicles or increased ovarian volume (greater than 10 cm3)

oligo- or anovulation

clinical and/or biochemical signs of hyperandrogenism.

A raised luteinising hormone/follicle-stimulating hormone ratio is no longer a diagnostic criteria for PCOS owing to its
inconsistency. It should be noted that the diagnosis of PCOS can only be made when other aetiologies have been excluded.

20

The recommended baseline screening tests are thyroid function tests, a serum prolactin and a free androgen index (total
testosterone divided by sex hormone binding globulin (SHBG) x 100 to give a calculated free testosterone level). In cases of
clinical evidence of hyperandrogenism and total testosterone greater than 5 nmol/l, DHEAS and androstenodione, 17hydroxyprogesterone should be sampled and androgen-secreting tumours excluded.
Women diagnosed with PCOS should be informed of the possible long-term risks to health that are associated with their
condition. They should be advised regarding weight control and exercise.

Women presenting with PCOS, particularly if they are obese (body mass index greater than 30), have a strong family
history of type 2 diabetes or are over the age of 40 years, are at increased risk of type 2 diabetes and should be offered a
glucose tolerance test. However, if the fasting blood glucose is 5.6 mmol/l or greater, body mass index is greater than 30
or a strong family history of diabetes, then an oral glucose tolerance test should be arranged.

Women diagnosed with PCOS (or their partners) should be asked about snoring and daytime fatigue/somnolence and
informed of the possible risk of sleep apnoea, and offered investigation and treatment when necessary.

Clinicians need to be aware that conventional cardiovascular risk calculators have not been validated in women with
PCOS. In clinical practice, hypertension should be treated but lipid-lowering treatment is not recommended routinely.
Assess measurement of blood pressure, cholesterol, triglycerides and high-density lipoprotein cholesterol. The elevation
of risk factors in young women with PCOS may therefore put them at increased risk of developing accelerated
atherosclerosis resulting in myocardial infarction

Women who have been diagnosed as having PCOS before pregnancy (such as those requiring ovulation induction for
conception) should be screened for gestational diabetes before 20 weeks of gestation, with referral to a specialist
obstetric diabetic service if abnormalities are detected. Metformin is currently not licensed for use in pregnancy in the UK
and is not recommended for use in pregnancy.

Oligo- or amenorrhoea in women with PCOS may predispose to endometrial hyperplasia and later carcinoma. It is good
practice to recommend treatment with progestogens to induce a withdrawal bleed at least every 34 months. There does
not appear to be an association with breast or ovarian cancer and no additional surveillance is required.

Women diagnosed with PCOS should be advised regarding weight loss through diet and exercise.

Insulin-sensitising agents have not been licensed in the UK for use in women who are not diabetic. Although a body of
evidence has accumulated demonstrating the safety of these drugs, there is currently no evidence of a long-term benefit
for the use of insulin-sensitising agents such as metformin and the thiazolidinediones (troglitazone, rosiglitazone and
pioglitazone) to reduce insulin resistance and thereby reduce risk of developing diabetes and other metabolic sequelae.

Use of weight-reduction drugs may be helpful in reducing insulin resistance through weight loss. Orlistat and sibutramine
have been shown to significantly reduce body weight and hyperandrogenism in women with PCOS.

Ovarian electrocautery should be reserved for selected anovulatory women with a normal BMI.

Women should be advised that there is insufficient evidence in favour of either metformin or the oral contraceptive pill in
treating hirsutism or acne.

No. 34 Ovarian Cysts in Postmenopausal Women

Ovarian cysts are common in postmenopausal women, although the prevalence is lower than in premenopausal women. The
greater use of ultrasound and other radiological investigations means that an increasing proportion of these cysts will come to
the attention of gynaecologists. It is recommended that ovarian cysts in postmenopausal women should be assessed using
CA125 and transvaginal grey scale sonography. There is no routine role yet for Doppler, MRI, CT or PET. It is recommended
that a risk of malignancy index should be used to select those women who require primary surgery in a cancer centre by a
gynaecological oncologist. Ultrasound often fails to differentiate between benign and malignant lesions, and serum CA125
levels, although raised in over 80% of ovarian cancers, is raised in only 50% of stage I cases. In addition, levels can be raised
in many other malignancies and in benign conditions, including benign cysts and endometriosis.
RMI = U x M x CA125
U = 0 (for ultrasound score of 0); U = 1 (for ultrasound score of 1); U = 3 (for ultrasound score of 25)
Ultrasound scans are scored one point for each of the following characteristics: multilocular cyst; evidence of solid areas;
evidence of metastases; presence of ascites; bilateral lesions. M = 3 for all postmenopausal women dealt with by this guideline
Less than 25 is low risk (<3%), 25-200 is moderate risk (20%), greater than 250 is high risk (>75%).
If an ovarian malignancy is present then the appropriate management in the postmenopausal woman is to perform a
laparotomy and a total abdominal hysterectomy, bilateral salpingo-oophorectomy and full staging procedure by a specialist
oncology team. If a malignancy is revealed during laparoscopy or subsequent histology, it is recommended that the woman is
referred to a cancer centre for further management. All ovarian cysts that are suspicious of malignancy in a postmenopausal
woman, as indicated by a high risk of malignancy index, clinical suspicion or findings at laparoscopy are likely to require a full
laparotomy and staging procedure, through an extended midline incision, and should include:
cytology: ascites or washings
laparotomy with clear documentation
biopsies from adhesions and suspicious areas
TAH, BSO and infra-colic omentectomy
The laparotomy and staging procedure may include bilateral selective pelvic and para-aortic lymphadenectomy.
Simple, unilateral, unilocular ovarian cysts and echo-free with no solid parts or papillary formations, less than 5 cm in diameter,
have a low risk of malignancy. It is recommended that, in the presence of a normal serum CA125 levels, they be managed

21

conservatively, as more than 50% of these cysts will resolve spontaneously within three months. Aspiration is not
recommended for the management of ovarian cysts in postmenopausal women. Cytological examination of ovarian cyst fluid is
poor at distinguishing between benign and malignant tumours, and has a negative impact on disease free survival. It is
recommended that laparoscopic management of ovarian cysts in postmenopausal women should involve oophorectomy
(usually bilateral) rather than cystectomy.
LOW RISK: Less than 3% risk of cancer
Management in a gynaecology unit.
Simple cysts less than 5 cm in diameter with a serum CA125 level of less than 30 may be managed conservatively.
Conservative management should entail repeat US scans and serum CA125 measurement every 4 months for one year.
If the cyst does not fit the above criteria or if the woman requests surgery then laparoscopic oophorectomy is acceptable.
MODERATE RISK: approximately 20% risk of cancer
Management in a cancer unit.
Laparoscopic oophorectomy is acceptable in selected cases.
If a malignancy is discovered then a full staging procedure should be undertaken in a cancer centre.
HIGH RISK: greater than 75% risk of cancer
Management in a cancer centre.
Full staging procedure as described above

No. 35 Urodynamic Stress Incontinence, Surgical Treatment

Stress incontinence is a symptom or sign indicating that the woman has involuntary urine loss associated with exertion.
Urodynamic stress incontinence (previously known as genuine stress incontinence) is a solely urodynamic diagnosis which
occurs when an incompetent urethra allows leakage of urine in the absence of a detrusor contraction.
Anterior repair (anterior colporrhaphy) is less successful as an operation for continence than retropubic procedures and has
been superseded by sling procedures. Anterior repair still has a role in the treatment of prolapse without incontinence. The
serious complication rate is in the region of 1% and the incidence of de novo detrusor overactivity is less than 6%.Compared
with colposuspension there may be a shorter hospital stay and a 50% decrease in blood loss.
Burch colposuspension is the most effective surgical procedure for stress incontinence, with a continence rate of 8590% at
one year. The continence rate falls to 70% at five years; this shows better longevity than other methods of treatment. Voiding
difficulty has been reported in a mean of 10.3% of women after colposuspension (range 227%). De novo detrusor overactivity
has been described in a mean of 17% women (range 827%). Genitourinary prolapse (enterocele, rectocele) has been
reported in colposuspension follow up at five years in an average of 13.6% women (range 2.526.7%). Ureteric damage has
been reported. There was no reported mortality as a direct consequence of the procedure. The continence rate after Burch
colposuspension falls if previous continence surgery has been performed. In one study the continence rate fell from 84% for a
primary procedure to 63% for secondary surgery. Burch colposuspension is more effective than needle suspension and
provides a similar subjective continence rate to laparoscopic colposuspension. Similarly, when compared with suburethral sling
procedures, short-term comparisons only are available for sling procedures, which indicate a similar continence rate to
colposuspension.
The role of other suprapubic operations such as MarshallMarchettiKrantz, paravaginal repair and laparoscopic
colposuspension, is unclear. A characteristic complication of MMK was osteitis pubis, which occurs in 2.5% of patients who
undergo a MMK procedure. The operation was less successful than Burch colposuspension at correcting a cystocele.
Needle suspension procedures should not be performed: initial success rates are not maintained with time and the risk of
failure is higher than for retropubic suspension procedures.
Sling procedures, using autologous or synthetic materials, produce a continence rate of approximately 80% and an
improvement rate of 90%, with little reduction in continence over time. Only one synthetic sling procedure (tension-free vaginal
tape) has been subjected to randomised study to date. Numerous materials are available for use in a suburethral sling. As a
generalisation, autologous material is associated with a greater continence rate and fewer complications than either cadaveric
material or synthetic materials. Autologous rectus fascia and fascia lata are probably the most common materials in use.
Allogenic grafts harvested from a cadaveric donor and porcine dermal implants (Pelvicol, CR Bard) are also widely used.
Synthetic material tends to be associated with a risk of erosion and sinus formation. When compared with colposuspension
procedures, the suburethral sling carries a similar success rate. The American Urological Association considered that
Retropubic suspensions and slings are the most efficacious procedures for long-term success based upon cure/dry rate.
However, in the panels opinion, retropubic suspensions and sling procedures are associated with slightly higher complication
rates, including postoperative voiding difficulty and longer convalescence. In patients who are willing to accept a slightly higher
complication rate for the sake of long-term cure, retropubic suspensions and slings are appropriate choices. Injectable agents
have a lower success rate than other procedures: a short-term continence rate of 48% and an improvement rate of 76%. Long
term, there is a continued decline in continence. However, the procedure has a low morbidity and may have a role after other
procedures have failed, e.g. when a diagnosis of intrinsic sphincter deficiency is made.
A number of bulking agents have been used for the treatment of stress incontinence in women. The bulking agents (collagen,
Teflon [Dupont], fat, silicone, Durasphere [Carbon Medical Technologies]) are injected in a retrograde (more common) or
antegrade fashion in the periurethral tissue around the bladder neck and proximal urethra. E.g. glutaraldedehyde cross-linked
collagen and silicone, but efficacy deteriorates with time.
Artificial sphincters can be successfully used after previous failed continence surgery but have a high morbidity and need for
further surgery (17%).

22

No. 36 Prevention of early onset neonatal Group B streptococcal Disease:

GBS (streptococcus agalactiae) is recognised as the most frequent early-onset (less than 7 days) infection in the newborn
infants. The incidence in the UK without screening is 0.5/1000 births, similar to that in the US with screening and treatment,
despite comparable vaginal carriage rates. The US guideline is that any women colonised with GBS at 35-37 weeks or
labouring before this time receives intrapartum antibiotics. Intrapartum antibiotics have been shown to significantly reduce the
rate of early-onset disease. The mortality rate from GBS in the UK is 6% at term and 18% in pre-term infants.
Risk factor based screening: previous baby affected by GBS, GBS bacteriuria detected during the current pregnancy, preterm
labour, prolonged rupture of membranes (>18 hours), fever in labour.

Routine screening for antenatal GBS carriage is not recommended. If GBS picked up antentally treatment is not
recommended. Intrapartum antibiotics prophylaxis should be considered if GBS is detected incidentally. No good
evidence to support the administration of intrapartum antibiotics prophylaxis to women in whom GBS carriage was
detected in a previous pregnancy.

Intrapartum antibiotics should be offered to women with a previous baby with neonatal GBS disease.

If choriomanitis is suspected, broad spectrum antibiotics therapy including an agent against GBS should be used.

If a woman has GBS in the urine, antibiotic prophylaxis should be offered.

Antibiotics for GBS is unnecessary in SROM unless they are in labour

IV penicillin 3gram stat, then 1.5 grams 4 hourly until delivery. Clindamycin 900mg IV 8 hourly for allergy to penicillin,
antibiotics should be given at least 2 hours prior to delivery.

The rate of detection of GBS colonisation can be increased from 22% to 27% by sampling the lower vagina and rectum
rather than only the lower vagina

If 30% of the UK pregnant population is treated with penicillin, this might result in two deaths a year as a consequence of
penicillin anaphylaxis. The fetal effects of severe anaphylaxis have not been well reported. The widespread use of
antibiotics is known to contribute to the development of resistant organisms. This is a particular risk when broad-spectrum
antibiotics such as ampicillin are used but should not be ignored as a possibility when using penicillin. There is also a
possibility that exposure to antibiotics in the neonatal perinatal period may affect neonatal faecal flora, with a subsequent
impact on immune development and later allergy.

No 38. The management of gestational trophoblastic disease

Gestational trophoblastic disease (GTD) forms a group of disorders spanning the conditions of complete and partial molar
pregnancies through to the malignant conditions of invasive mole, choriocarcinoma and the very rare placental site
trophoblastic tumour (PSTT).

Complete moles are diploid and androgenic in origin, with no evidence of fetal tissue. Complete moles usually (7580%)
arise as a consequence of duplication of a single sperm following fertilisation of an empty ovum. Some complete moles
(2025%) can arise after dispermic fertilisation of an empty ovum.
Partial moles are usually (90%) triploid in origin, with two sets of paternal haploid genes and one set of maternal haploid
genes. Partial moles occur, in almost all cases, following dispermic fertilisation of an ovum. Ten percent of partial moles
represent tetraploid or mosaic conceptions. In a partial mole, there is usually evidence of a fetus or fetal red blood cells.
GTD (hydatidiform mole, invasive mole, choriocarcinoma, placental-site trophoblastic tumour) is a rare event in the UK,
with a calculated incidence of 1/714 live births.1 There is evidence of ethnic variation in the incidence of GTD in the UK,
with women from Asia having a higher incidence compared with non-Asian women (1/387 versus 1/752 live births). GTN
may develop after a molar pregnancy, a non-molar pregnancy or a live birth. The incidence after a live birth is estimated
at 1/50 000.
The classic features of molar pregnancy are irregular vaginal bleeding, hyperemesis, excessive uterine enlargement and
early failed pregnancy. Rarer presentations include hyperthyroidism, early onset pre-eclampsia or abdominal distension
due to theca lutein cysts. Very rarely, women can present with acute respiratory failure or neurological symptoms such as
seizures; these are likely to be due to metastatic disease.
Ultrasound examination is helpful in making a pre-evacuation diagnosis but the definitive diagnosis is made by
histological examination of the products of conception.
The ultrasound diagnosis of a partial molar pregnancy is more complex; the finding of multiple soft markers, including
both cystic spaces in the placenta and a ratio of transverse to anterioposterior dimension of the gestation sac of greater
than 1.5, is required for the reliable diagnosis of a partial molar pregnancy. Estimation of hCG levels may be of value in
diagnosing molar pregnancies: Hcg levels greater than two multiples of the median may help.
Suction curettage is the method of choice of evacuation for complete molar pregnancies. Suction curettage is the method
of choice of evacuation for partial molar pregnancies except when the size of the fetal parts deters the use of suction
curettage and then medical evacuation can be used. A urinary pregnancy test should be performed 3 weeks after medical
management of failed pregnancy if products of conception are not sent for histological examination.

23

Anti-D prophylaxis is required following evacuation of a molar pregnancy. Because of poor vascularisation of the chorionic
villi and absence of the anti-D antigen in complete moles, anti-D prophylaxis is not required.
There is theoretical concern over the routine use of potent oxytocic agents because of the potential to embolise and
disseminate trophoblastic tissue through the venous system.
Excessive vaginal bleeding can be associated with molar pregnancy and a senior surgeon directly supervising surgical
evacuation is advised.
The use of oxytocic infusion prior to completion of the evacuation is not recommended. If the woman is experiencing
significant haemorrhage prior to evacuation, surgical evacuation should be expedited and the need for oxytocin infusion
weighed up against the risk of tumour embolisation.
The histological assessment of material obtained from the medical or surgical management of all failed pregnancies is
recommended to exclude trophoblastic neoplasia. Ploidy status and immunohistochemistry staining for P57 may help in
distinguishing partial from complete moles.
Any woman who develops persistent vaginal bleeding after a pregnancy event is at risk of having GTN. A urine pregnancy
test should be performed in all cases of persistent or irregular vaginal bleeding after a pregnancy event. Symptoms from
metastatic disease, such as dyspnoea or abnormal neurology, can occur very rarely.
When there is diagnostic doubt about the possibility of a combined molar pregnancy with a viable fetus, advice should be
sought from the regional fetal medicine unit and the relevant trophoblastic screening centre.
In the situation of a twin pregnancy where there is one viable fetus and the other pregnancy is molar, the woman should
be counselled about the increased risk of perinatal morbidity and outcome for GTN.
Prenatal invasive testing for fetal karyotype should be considered in cases where it is unclear if the pregnancy is a
complete mole with a coexisting normal twin or a partial mole. Prenatal invasive testing for fetal karyotype should also be
considered in cases of abnormal placenta, such as suspected mesenchymal hyperplasia of the placenta. The outcome
for a normal pregnancy with a coexisting complete mole is poor, with approximately a 25% chance of achieving a live
birth. There is an increased risk of early fetal loss (40%) and premature delivery (36%). The incidence of pre-eclampsia is
variable, with rates as high as 20% reported.
Follow up after GTD is increasingly individualised. If hCG has reverted to normal within 56 days of the pregnancy event
then follow up will be for 6 months from the date of uterine evacuation. If hCG has not reverted to normal within 56 days
of the pregnancy event then follow-up will be for 6 months from normalisation of the hCG level.
All women should notify the screening centre at the end of any future pregnancy, whatever the outcome of the pregnancy.
hCG levels are measured 6-8 weeks after the end of the pregnancy to exclude disease recurrence.
The need for chemotherapy following a complete mole is 15% and 0.5 % after a partial mole. The development of
postpartum GTN requiring chemotherapy occurs at a rate of 1/50 000 births Women are assessed before chemotherapy
using the FIGO 2000 scoring system. Women with scores 6 are at low risk and are treated with single-agent
intramuscular methotrexate alternating daily with folinic acid for 1 week followed by 6 rest days. Women with scores 7
are at high risk and are treated with intravenous multi-agent chemotherapy, which includes combinations of methotrexate,
dactinomycin, etoposide, cyclophosphamide and vincristine. Treatment is continued, in all cases, until the hCG level has
returned to normal and then for a further 6 consecutive weeks.
The cure rate for women with a score 6 is almost 100%; the rate for women with a score 7 is 95%

Table 1 FIGO Scoring system32

FIGO SCORING
0
Age (years)
<40
Antecedent pregnancy
Mole
Interval months from end of index pregnancy to treatment 4
Pretreatment serum hCG (iu/l)
10
3
Largest tumour size, including uterus (cm)
3
Site of metastases
Lung
Number of metastases

Previous failed chemotherapy

1
2
4
>40

Abortion
Term
4 <7
7 13

>13

103 10
4
104 10
5 10
5
3 <5
5

Spleen, kidney Gastro-intestinal Liver, brain

14
58
>
8

Single drug 2 or more drug

Women should be advised not to conceive until their follow-up is complete. Women who undergo chemotherapy are
advised not to conceive for 1 year after completion of treatment. Women who receive chemotherapy for GTN are likely to
have an earlier menopause.
Women with high-risk GTN who require multi-agent chemotherapy which includes etoposide should be advised that they
may be at increased risk of developing secondary cancers.
Women with GTD should be advised to use barrier methods of contraception until hCG levels revert to normal. Once hCG
level have normalised, the combined oral contraceptive pill may be used. There is no evidence as to whether single-agent
progestogens have any effect on GTN. If oral contraception has been started before the diagnosis of GTD was made, the
woman can be advised to remain on oral contraception but she should be advised that there is a potential but low
increased risk of developing GTN. Intrauterine contraceptive devices should not be used until hCG levels are normal to
reduce the risk of uterine perforation.
Hormone replacement therapy may be used safely once hCG levels have returned to normal.

24

No.39 Management HIV in pregnancy

All pregnant women are recommended screening for HIV infection, syphilis, hepatitis B and rubella in every pregnancy at their
booking antenatal visit. If a woman declines an HIV test, this should be documented in the maternity notes, her reasons should
be sensitively explored and screening offered again at around 28 weeks. If a woman tests HIV negative at booking but is
judged by her clinician as being at continued high risk of acquiring HIV, offering a repeat HIV test should be considered. Rapid
HIV tests use rapid-test devices to deliver results within 20 minutes of the sample being taken. These tests are recommended
for all women with unknown HIV status in labour and a reactive result should be acted on immediately.
Women who require HIV treatment for their own health should take highly active anti-retroviral therapy (HAART) and continue
treatment postpartum. They may also require prophylaxis against Pneumocystis carinii pneumonia (PCP), depending on their
CD4 lymphocyte count. Women already taking HAART and/or PCP prophylaxis before pregnancy should not discontinue their
medication.
Avoidance of breastfeeding, anti-retroviral therapy and appropriate management of delivery has reduced mother-to-child
transmission rates from 2530% to less than 1%. All women should be advised to take anti-retroviral therapy. For women who
require HIV treatment for their own health, their prescribed HAART regimen should be continued throughout pregnancy and
postpartum. For women who do not require HIV treatment for their own health, HAART should be initiated between 20 and 28
weeks and discontinued at delivery. For women who do not require HIV treatment for their own health, have a plasma viral load
of less than 10 000 copies/ml and are prepared to be delivered by elective caesarean section, an acceptable alternative is
zidovudine (ZDV) monotherapy initiated between 20 and 28 weeks, given orally, 250 mg twice daily, and intravenously at
delivery. A decision about mode of delivery should be made by 36 weeks of gestation. Delivery by elective caesarean section at
38 weeks to prevent labour and/or ruptured membranes is recommended for:
women taking HAART who have a plasma viral load greater than 50 copies/ml
women taking ZDV monotherapy as an alternative to HAART
women with HIV and hepatitis C virus coinfection.
A planned vaginal delivery can be offered to women taking HAART who have a plasma viral load of less than 50 copies/ml.
Delivery by elective caesarean section for obstetric indications or maternal request should be delayed until 39+ weeks in
women whose plasma viral load is less than 50 copies/ml, to reduce the risk of transient tachypnoea of the newborn.
Pregnant women who are HIV positive should have additional blood tests for hepatitis C, varicella zoster, measles and
toxoplasma. Women taking HAART at the time of booking should be screened for gestational diabetes. Hepatitis B and
pneumococcal vaccination is recommended for all individuals who are HIV positive and can be safely administered in
pregnancy. Influenza vaccination can also be safely administered in pregnancy and the decision to immunise depends on the
time of year. Varicella zoster and measles, mumps and rubella vaccines are contraindicated in pregnancy. Women should be
screened for genital infections at booking and again at 28 weeks. Any infection detected should be treated according to
national guidelines, even if asymptomatic. Screening for aneuploidy should be offered to all women in accordance with national
guidelines for the general population. Women who are HIV positive who are considering invasive diagnostic testing should be
counselled in a fetal medicine unit and the advice of the HIV physicians sought about reducing the risk of HIV transmission.
Dating and anomaly scans should be offered to all women in accordance with national guidelines for the general population.
Monitoring of plasma viral load and drug toxicities should be undertaken as directed by the HIV physicians. A plan of care for
anti-retroviral therapy and mode of delivery should be made at 36 weeks following detailed discussion with the mother. Only
women with plasma viral loads of less than 50 copies/ml should be offered a planned vaginal delivery. This plan should be
reviewed when the woman presents in labour, after confirming that any recently performed viral load results are less than 50
copies/ml. In the absence of a documented mode of delivery plan or, in the event of uncertainty about viral load results, urgent
advice should be sought from the HIV physicians.
All women with threatened or established preterm labour and those with preterm prelabour rupture of membranes (PPROM)
should have a genital infection screen preformed and any infections, even if asymptomatic should be treated. The usual
indications for steroids apply.
Women should be counselled about the increased risk of preterm delivery associated with HAART.
For women presenting with threatened preterm labour, multidisciplinary team advice (HIV physicians and
paediatricians) should be sought so that, if preterm labour supervenes, there is a detailed plan of care.
For women in preterm labour, urgent multidisciplinary team advice should be sought about the choice of anti-retroviral
therapy. Infants born below 32 weeks of gestation may be unable to tolerate oral medication, so administering anti-retroviral
therapy to the mother just before and during delivery will provide prophylaxis to the neonate.
Where PPROM occurs after 34 weeks of gestation, delivery should be expedited. Augmentation may be considered if the
viral load is less than 50 copies/ml and there are no obstetric contraindications. Consideration should be given to starting
broad-spectrum intravenous antibiotics.
Where PPROM occurs before 34 weeks of gestation, oral erythromycin should be started in accordance with national
guidelines for the general population. Consideration should be given to starting broad-spectrum intravenous antibiotics.
Evidence of chorioamnionitis and fetal distress are indications for prompt delivery. In other cases, the decision as to whether to
expedite delivery should be made after multidisciplinary team consultation. Expert advice from outside the host institution may
be helpful.

No. 40 Venous thromboembolism and hormonal contraception

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29% of women in the UK are on Hormonal contraception COCP 18%, progesterone only 5%, progesterogen only
injectable or implant (3%) or mirena (1%).
Increased risk of VTE associated with age and most deaths associated with VTE occur in older women not on hormones.
Risks include: factor V Leiden mutation, prothrombin 20210A, protein C or protein S deficiency, antithrombin III deficiency
and acquired factors like antiphospholipid syndrome, pregnancy, contraceptive use, surgery, trauma, immobilisation and
malignancy.
The relative risk of VTE with COCP is 3 fold, the absolute risk is increases from 5 to 15 per 10,000 woman years.
The relative risk of venous thromboembolism is increased with combined oral contraceptive use. Nevertheless, the rarity
of venous thromboembolism in women of reproductive age means that the absolute risk remains small.
The term combined oral contraception is used here to describe monophasic preparations containing a low dose (2035
micrograms) of ethinyl estradiol in combination with a progestogen. Progestogens include norethisterone and
levonorgestrel: second generation; desogestrel and gestodene: third generation; and the newest progestogen,
drospirenone: fourth generation.Combined OCP containing levonorgestrel or norethisterone are associated with a lower
risk of venous thromboembolism than those containing desogestrel or gestodene.
A levonorgestrel- or norethisterone-containing combined oral contraceptive should be advised as a pill of first choice.
However, after counselling, a woman may choose a desogestrel- or gestodene containing combined pill.
The relative risk of venous thromboembolism increases in the first 4 months after starting combined oral contraception.
This risk decreases with increasing duration of use, although it remains above that of non-users. After discontinuation,
VTE risk falls to that of non-users within 3 months.

Risk table for combined oral contraceptive (COC) users and risk of venous
thromboembolism
Relative risk
Not using COC
COC containing levonorgestrel or norethisterone
COC containing gestodene or desogestrel
Pregnancy

3-fold increase
5-fold increase
12-fold increase

Absolute risk per 100 000 woman-years

5 in 100 000
15 in 100 000
25 in 100 000
60 in 100 000

Dianette contains 35 micrograms ethinyl oestradiol with 2 mg cyproterone acetate (a progestogen with anti-androgenic
properties). Dianette (four-fold increase in the risk of VTE with Dianette compared with a COC containing levonorgestrel) is not
licensed as a contraceptive but for treatment of acne or hirsutism. Dianette is not indicated solely as a contraceptive; it is a
treatment option for women with severe acne, which has not responded to oral antibiotics, or for moderately severe hirsutism; it
should be withdrawn 3-4 months after the treated condition has resolved.
Progestogen-only pills, injectables and levonorgestrel implants do not increase the risk of venous thromboembolism. There is
little evidence available on the etonorgestrel implant or levonorgestrel-releasing intrauterine system and the risk of venous
thromboembolism. No evidence is available on the risk of venous thromboembolism, if any, associated with progestogenonly
emergency contraception. Women with current venous thromboembolism should not use hormonal contraception. Women with
a personal history of venous thromboembolism should not use combined oral contraception but may use progestogen-only
methods. A woman who is less than 21 days postpartum should not use combined oral contraception. Combined oral
contraception can be used after day 21 postpartum if a woman is not breastfeeding. The progestogen-only pill, implant or
injection can be used safely before day 21 postpartum, even if a woman is breastfeeding.
Combined oral contraception can be commenced immediately following first- or second-trimester abortion. Progestogen-only
contraception can be commenced immediately following first- or second-trimester abortion.
Smokers over the age of 35 years should not use combined oral contraception but progestogen-only methods can be used.
Women with a body mass index over 30 should first consider progestogen-only methods but combined oral contraception can
be used after counselling. Combined oral contraception should be discontinued at least 4 weeks before major surgery where
immobilisation is expected. Progestogen-only methods need not be discontinued prior to surgery even when immobilisation is
expected. Hormonal methods do not need to be discontinued before minor surgery without immobilisation.

Superficial venous thrombosis: recommends that the benefits of COC and POC outweigh the risks in women with
varicose veins and superficial thrombophlebitis
Sickle cell disease: This chronic, inherited, haematological condition can be complicated by vaso-occlusion by poorly
deformable erythrocytes. Fetal and maternal morbidity and mortality are associated with sickling crises. An observational
study comparing hormonal (COC and POC) and barrier contraception in women with sickle cell disease showed no
significant difference in haemostatic variables. A reduction in painful sickle cell crises with use of depot
medroxyprogesterone acetate). Advises that benefits of combined contraception and POC outweigh the risks. An
observational study identified pulmonary hypertension in 32% of patients with sickle cell disease should be advised
against the use of combined contraception.
Inflammatory bowel disease: does not address inflammatory bowel disease, suggests that women with inflammatory
bowel disease should be offered the same contraceptive choices as other women.

Routine thrombophilia screening prior to hormonal contraceptive use is not recommended. A thrombophilia screen may be
considered in a woman with a history of venous thromboembolism in a first-degree relative under the age of 45 years who,

26

after counselling, still wishes to use combined oral contraception. A thrombophilia screen should be interpreted in consultation
with a haematologist or other expert, in conjunction with a detailed family history.
Approximately one in 3000 people have reduced levels of a natural anticoagulant (antithrombin III, protein C or protein S) and a
predisposition to VTE. As many as 1 in 20 people have Factor V Leiden or prothrombin gene mutation and a lesser degree of
predisposition to VTE. Antiphospholipid syndrome is less common, but is identified more often in women with recurrent
miscarriage than in the general population.

No. 41 Chronic pelvic pain, initial management

Chronic pelvic pain can be defined as intermittent or constant pain in the lower abdomen or pelvis of at least 6 months
duration, not occurring exclusively with menstruation or intercourse and not associated with pregnancy. There is frequently
more than one component to chronic pelvic pain. Assessment should aim to identify contributory factors rather than assign
causality to a single pathology.
In chronic pain, additional factors come into play and pain may persist long after the original tissue injury or may exist in the
absence of any such injury. Nerve damage following surgery, trauma, inflammation or infection may play a part in this process.
Pelvic pain which varies considerably over the menstrual cycle may be due to a variety of hormonally driven conditions. The
cardinal symptoms of dysmenorrhoea, dyspareunia and chronic pelvic pain are said to be characteristic of endometriosis.
However, in a prospective study of 90 women undergoing laparoscopy or laparotomy, symptoms alone were a poor predictor of
finding endometriosis at surgery. The combination of clinical examination and transvaginal ultrasound accurately identified
ovarian endometriosis but not peritoneal disease. Pelvic venous congestion has also been proposed as a cause of pelvic pain
with menstrual exacerbation.
Although many symptom complexes, such as irritable bowel syndrome, and pain perception itself may vary a little with the
menstrual cycle (with 50% of women experiencing a worsening of their symptoms in association with their period), strikingly
cyclical pain is usually gynaecological in nature.
It is thought that adhesions may be a cause of pain, particularly on organ distension or stretching. Dense vascular adhesions
are likely to be a cause of chronic pelvic pain, as dividing them appears to relieve pain. However, adhesions may be
asymptomatic.
Symptoms suggestive of irritable bowel syndrome or interstitial cystitis are often present in women with chronic pelvic pain.
These conditions may be a primary cause or a component of chronic pelvic pain. Musculoskeletal pain may be a primary
source of pelvic pain or an additional component resulting from postural changes.
Nerve entrapment in scar tissue, fascia or a narrow foramen may result in pain and dysfunction in the distribution of that nerve.
The initial history should include questions about the pattern of the pain and its association with other problems, such as
psychological, bladder and bowel symptoms, and the effect of movement and posture on the pain.
The examination is most usefully undertaken when there is time to explore the womans fears and anxieties. The examiner
should be prepared for new information to be revealed at this point.
Suitable samples to screen for infection, particularly chlamydia and gonorrhoea, should be taken if there is any suspicion of
pelvic inflammatory disease (PID). Ideally, all sexually active women below the age of 25 years who are being examined should
be offered opportunistic screening for Chlamydia. If the history suggests to patient and doctor that there is a nongynaecological component to the pain, referral to the relevant healthcare professional such as gastroenterologist, urologist,
genitourinary medicine physician, physiotherapist, psychologist or psychosexual counsellor should be considered.
Diagnostic laparoscopy has been regarded in the past as the gold standard in the diagnosis of chronic pelvic pain. It may be
better seen as a second line of investigation if other therapeutic interventions fail. Diagnostic laparoscopy may have a role in
developing a womans beliefs about her pain. Transvaginal scanning is an appropriate investigation to screen for and assess
adnexal masses. Transvaginal scanning and magnetic resonance imaging (MRI) are useful tests to diagnose adenomyosis.
The role of MRI in diagnosing small deposits of endometriosis is uncertain. Women with cyclical pain should be offered a
therapeutic trial using the combined oral contraceptive pill or a gonadotrophin-releasing hormone (GNRH) agonist for a period
of 36 months before having a diagnostic laparoscopy. The levonorgestrel-releasing intrauterine system could also be
considered. Ovarian suppression can be an effective treatment for pain associated with endometriosis. Response to ovarian
suppression can therefore be a useful diagnostic tool. The effect can be achieved with the combined oral contraceptive,
progestogens, danazol or GnRH agonist, all of which are equally effective but have differing adverse effect profiles. Other
proposed causes of cyclical pain, such as pelvic venous congestion, also appear to be well-controlled by ovarian suppression.
Women with irritable bowel syndrome should be offered a trial of antispasmodics. Women with irritable bowel syndrome should
try amending their diet to control symptoms.
Women should be offered appropriate analgesia to control their pain, even if no other therapeutic manoeuvres are yet to be
initiated. If pain is not adequately controlled, consideration should be given to referral to a pain management team or a
specialist pelvic pain clinic. Chronic pelvic pain is common affecting perhaps one in six of the adult female population. Much
remains unclear about its aetiology but chronic pelvic pain should be seen as a symptom with a number of contributory factors
rather than as a diagnosis in itself. As with all chronic pain, it is important to consider psychological and social factors as well
as physical causes of pain. Many non-gynaecological conditions, such as nerve entrapment or irritable bowel syndrome, may
be relevant. Women often present because they seek an explanation for their pain. The assessment process should allow
enough time for the woman to be able to tell her story. This may be therapeutic in itself. A pain diary may be helpful in tracking
symptoms or activities associated with the pain. Where pain is strikingly cyclical and no abnormality is palpable at vaginal
examination, a therapeutic trial of a GnRH agonist may be more helpful than a diagnostic laparoscopy. Other conditions, such

27

as irritable bowel syndrome, require specific treatment. Even if no explanation for the pain can be found initially, attempts
should be made to treat the pain empirically and to develop a management plan in partnership with the woman.

No. 42 Shoulder dystocia

Shoulder dystocia is defined as a delivery that requires additional obstetric manoeuvres to release the shoulders after gentle
downward traction has failed. Shoulder dystocia occurs when either the anterior or, less commonly, the posterior fetal shoulder
impacts on the maternal symphysis or sacral promontory. 0.6% incidence. There can be a high perinatal mortality and morbidity
associated with the condition, even when it is managed appropriately. Maternal morbidity is also increased, particularly
postpartum haemorrhage (11%) and fourth-degree perineal tears (3.8%). Brachial plexus injuries complicating 416% of such
deliveries. Most cases resolve without permanent disability, with fewer than 10% resulting in permanent brachial plexus
dysfunction. Brachial plexus injuries is 1/2300 live births. Neonatal brachial plexus injury is the single most common cause for
litigation related to shoulder dystocia. Where there is Erbs palsy, it is important to determine whether the affected shoulder
was anterior or posterior at the time of delivery, because damage to the plexus of the posterior shoulder is considered not due
to action by the accoucheur.
Factors associated with shoulder dystocia
Pre-labour
Intrapartum
Previous shoulder dystocia
Prolonged first stage of labour
Macrosomia
Secondary arrest
Maternal body mass index > 30 kg/m2
Oxytocin augmentation
Induction of labour
Assisted vaginal delivery
Diabetes mellitus
Prolonged second stage of labour
Clinicians should be aware of existing risks but must always be alert to the possibility of shoulder dystocia with any delivery
There is no evidence to support induction of labour in women without diabetes at term where the fetus is thought to be
macrosomic. Induction of labour in women with diabetes mellitus does not reduce the maternal or neonatal morbidity of
shoulder dystocia. Elective caesarean section should be considered to reduce the potential morbidity for pregnancies
complicated by suspected fetal macrosomia associated with maternal diabetes mellitus. Either caesarean section or vaginal
delivery is appropriate after a previous shoulder dystocia. The decision should be made by the woman and her carers. If
shoulder dystocia is anticipated then some pre-emptive preparation may help. Routine traction in an axial direction may be
employed to diagnose shoulder dystocia.
The attendant health-carer should routinely observe for: difficulty with delivery of the face and chin; the head remaining tightly
applied to the vulva or even retracting; failure of restitution of the fetal head; failure of the shoulders to descend. Immediately
after recognition of shoulder dystocia, extra help should be called. Fundal pressure should not be used for the treatment of
shoulder dystocia (increased risk of uterine rupture). Episiotomy is not necessary for all cases but should be used for access if
needed to do VE manipulations.
The McRoberts manoeuvre should be performed first (single most effective intervention) it is flexion and abduction of the
maternal hips, positioning the maternal thighs on her abdomen. It straightens the lumbo-sacral angle, rotates the maternal
pelvis cephalad and is associated with an increase in uterine pressure and amplitude of contractions. The McRoberts
manoeuvre is the single most effective intervention, with reported success rates as high as 90%. It has a low rate of
complication and therefore should be employed first. Suprapubic pressure can be employed together with McRoberts
manoeuvre to improve success rates. Suprapubic pressure reduces the bisacromial diameter and rotates the anterior shoulder
into the oblique pelvic diameter. The shoulder is then free to slip underneath the symphysis pubis with the aid of routine traction
External suprapubic pressure is applied in a downward and lateral direction to push the posterior aspect of the anterior
shoulder towards the fetal chest. It is advised that this is applied for 30 seconds. There is no clear difference in efficacy
between continuous pressure or rocking movement. Advanced manoeuvres should be used if the McRoberts manoeuvre and
suprapubic pressure fail. If these simple measures (the McRoberts manoeuvre and suprapubic pressure) fail, then there is a
choice to be made between the all-fours-position and internal manipulation. The individual circumstances should guide the
accoucheur. For a slim mobile woman without epidural anaesthesia and with a single midwifery attendant, the allfours- position
is probably the most appropriate. For a less mobile woman with epidural anaesthesia in place and a senior obstetrician in
attendance, internal manoeuvres are more appropriate.
Delivery of the fetal shoulders may be facilitated by rotation into an oblique diameter or by a full 180-degree rotation of the fetal
trunk. Delivery may also be facilitated by delivery of the posterior arm. The fetal trunk will either follow directly or the arm can
be used to rotate the fetal trunk to facilitate delivery. Delivery of the posterior arm has a high complication rate: 12% humeral
fractures in one series, but the neonatal trauma may be a reflection of the refractory nature of the case, rather than the
procedure itself. Third-line manoeuvres require careful consideration to avoid unnecessary maternal morbidity and mortality. It
is difficult to recommend a time limit for the management of shoulder dystocia, as there are no conclusive data available.
Several third-line methods have been described for those cases resistant to all simple measures. These include cleidotomy
(bending the clavicle with a finger or surgical division), symphysiotomy (dividing the symphyseal ligament) and the Zavanelli
manoeuvre. It is rare that these are required. After delivery, the birth attendants should be alert to the possibility of postpartum
haemorrhage and third- and fourth-degree perineal tears. Record the condition of the baby (Apgar score); umbilical cord blood
acid-base measurements.
The HELPERR mnemonic

28

H Call for help

E Evaluate for episiotomy
L Legs (the McRoberts manoeuvre)
P Suprapubic pressure
E Enter manoeuvres (internal rotation)
R Remove the posterior arm
R Roll the patient

No. 43 Obstetric Cholestasis

In England, obstetric cholestasis (previously referred to as intrahepatic cholestasis of pregnancy) affects 0.7% of pregnancies
in multi-ethnic populations and 1.21.5% of women of Indian-Asian or Pakistani- Asian origin. For example, in Chile, 2.4% of all
pregnancies are affected, with 5% prevalence in women of Araucanian-Indian origin. Obstetric cholestasis is a multifactorial
condition of pregnancy characterised by intense pruritus in the absence of a skin rash, with abnormal liver function tests
(LFTs), neither of which have an alternative cause and both of which remit following delivery. The clinical importance of
obstetric cholestasis lies in the potential fetal risks, which may include spontaneous prematurity, iatrogenic prematurity and
intrauterine death. There can also be significant maternal morbidity in association with the intense pruritus and consequent
sleep deprivation.
Pregnancy-specific reference ranges for LFTs should be used (the upper limit of normal throughout pregnancy is 20% lower
than the nonpregnant range). Other causes of itching and of liver dysfunction should be excluded. Postnatal resolution of
pruritus and LFTs should be confirmed. In obstetric cholestasis, the pruritus is typically worse at night, is often widespread and
may involve the palms of the hands or the soles of the feet. Other causes of pruritus must be excluded. The skin should be
inspected and care must be taken to differentiate dermatographia artefacta (skin trauma from intense scratching), which may
be seen in obstetric cholestasis, from other common skin conditions such as eczema and pruritic eruption of pregnancy. Other
evidence of cholestasis should be sought, including pale stool, dark urine and family history of obstetric cholestasis.
In clinical practice, abnormalities in transaminases, gamma glutamyl transferase, bilirubin and/or bile salts are considered
sufficient to support the diagnosis of obstetric cholestasis. Bilirubin is only raised infrequently and most women will have
increased levels of one or more of the remaining three LFTs.
A viral screen for hepatitis A, B, C, Epstein Barr and cytomegalovirus, a liver autoimmune screen for chronic active hepatitis
and primary biliary cirrhosis (for example, anti-smooth muscle and antimitochondrial antibodies) and liver ultrasound should be
carried out before the diagnosis is confirmed. Pre-eclampsia and acute fatty liver of pregnancy are pregnancy specific causes
of abnormal LFTs that might form part of the differential diagnosis in atypical or early cases. Once obstetric cholestasis is
diagnosed, it is reasonable to measure LFTs weekly. Postnatal LFTs should be deferred for at least 10 days. Obstetricians
should be aware (and should advise women) that the current stillbirth rate for obstetric cholestasis is comparable to that in the
general population. The risk of stillbirth in untreated obstetric cholestasis is unclear. Obstetricians should be aware (and
should advise women) that the incidence of premature birth is increased, both spontaneous and iatrogenic and that the
evidence for an increased risk of meconium-stained liquor, caesarean section or postpartum haemorrhage is inconclusive.
Delivery decisions should not be based on the degree of abnormality of biochemical tests, as current data are not robust
enough to demonstrate or exclude a correlation between maternal levels of liver enzymes or bile salts and intrauterine death.
No specific fetal monitoring modality for the prediction of fetal death can be recommended. Ultrasound is not a reliable method
for preventing fetal death in obstetric cholestasis.
Obstetricians should be aware that there are insufficient data to support or refute the popular practice of early (37 weeks of
gestation) induction of labour aimed at reducing late stillbirth. The timing and risks of delivery should be discussed on an
individual basis. Topical emollients are safe but their efficacy is unknown (Diprobase, Balneum Plus, calamine lotion and
aqueous cream with menthol).
Systemic treatments aimed at relieving pruritus, not subjected to randomised controlled trials (RCTs) include cholestyramine, a
poorly tolerated bile acid chelating agent, which may improve pruritus in some women but may also exacerbate vitamin K
deficiency (which has been associated with fetal intracranial haemorrhage). It is not in clinical use. Antihistamines such as
chlorpheniramine may provide some welcome sedation at night but do not make a significant impact on pruritus. Activated
charcoal and guar gum do not relieve pruritus. There is insufficient evidence to show whether S adenosyl methionine is
effective for either control of maternal symptoms or for improving fetal outcome.
There are insufficient data to support the widespread use of ursodeoxycholic acid (UDCA) (can displace more hydrophobic
endogenous bile salts from the bile acid pool and thereby protect the hepatocyte membrane from their damaging toxicity,
enhance bile acid clearance across the placenta from the fetus). Women should be aware of the lack of robust data concerning
improvement in pruritus, protection against stillbirth and safety to the fetus or neonate.
Dexamethasone should not be first-line therapy for obstetric cholestasis. It is reasonable to offer a daily supplement of watersoluble vitamin K to all women from diagnosis of obstetric cholestasis. If there is frank steatorrhoea or prolongation of the
prothrombin time, the clinical case for the use of vitamin K is stronger. Women should be offered follow-up to ensure that LFTs
have returned to normal and to provide appropriate counselling.

No. 44 Preterm Prelabour Rupture of Membranes

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PPROM complicates only 2% of pregnancies but is associated with 40% of preterm deliveries and can result in significant
neonatal morbidity and mortality. The three causes of neonatal death associated with PPROM are prematurity, sepsis and
pulmonary hypoplasia. Women with intrauterine infection deliver earlier than noninfected women and infants born with sepsis
have a mortality rate four times higher than those without sepsis.
The diagnosis of spontaneous rupture of the membranes is best achieved by maternal history followed by a sterile speculum
examination. Ultrasound examination is useful in some cases to help confirm the diagnosis. Digital examination should be
avoided where PPROM is suspected.
A series of tests have been used to confirm membrane rupture; the most widely used has been the Nitrazine test, which
detects pH change, which has a sensitivity of 90% and a false positive rate of 17%. More recently, other tests have been
evaluated in the diagnosis of ruptured membranes and fetal fibronectin and raised insulin-like growth factor binding protein-1 in
cervical/vaginal secretions have reported sensitivities of 94% and 75% and specificities of 97%, respectively. Women should be
observed for signs of clinical chorioamnionitis at least 12-hourly.
A weekly high vaginal swab and at least a weekly maternal full blood count should be considered. Fetal monitoring using
cardiotocography should be considered where regular fetal surveillance is required. Biophysical profile scoring or Doppler
velocimetry should not be considered as first-line surveillance or diagnostic tests for fetal infection. The criteria for the
diagnosis of clinical chorioamnionitis include maternal pyrexia, tachycardia, leucocytosis, uterine tenderness, offensive vaginal
discharge and fetal tachycardia. Maternal pyrexia (above 37.8C), offensive vaginal discharge and fetal tachycardia (rate above
160 beats/minute) indicate clinical chorioamnionitis. The laboratory tests of leucocytosis and raised C-reactive protein in the
prediction of chorioamnionitis are unknown. Although weekly culture of swabs from the vagina are often taken as part of the
clinical management of women with PPROM. HVS may indicate group B streptococcus, which provides the opportunity for
intrapartum antibiotic therapy. Abnormal biophysical profile scores and increased systolic/diastolic ratios in the umbilical artery
have been shown to be markers of intrauterine infection. Cardiotocography is useful because a fetal tachycardia, if present,
may represent a late sign of infection. Routine amniocentesis is not recommended for women with PPROM.
Intrauterine infection, as defined by positive amniotic fluid cultures, is found in 36% of women with PPROM. Most infections are
subclinical without obvious signs of chorioamnionitis. Positive amniotic fluid cultures increase the risks of preterm delivery,
neonatal sepsis, respiratory distress syndrome, chronic lung disease, periventricular leukomalacia, intraventricular
haemorrhage and cerebral palsy.
Erythromycin (250 mg orally 6 hourly) should be given for 10 days following the diagnosis of PPROM. Co-amoxiclav is not
recommended for women with PPROM because of concerns about necrotising enterocolitis. Antenatal corticosteroids should
be administered in women with PPROM. Prophylactic tocolysis in women with PPROM without uterine activity is not
recommended. Women with PPROM and uterine activity who require intrauterine transfer or antenatal corticosteroids should
be considered for tocolysis.
Transvaginal amnioinfusion in labour is not recommended for women with preterm rupture of membranes. Transabdominal
amnioinfusion is not recommended as a method of preventing pulmonary hypoplasia in very preterm PPROM. Fibrin sealants
are not recommended as routine treatment for second-trimester oligohydramnios caused by PPROM. Women should be
considered for outpatient monitoring of PPROM only after rigorous individual selection by a consultant obstetrician. Outpatient
monitoring should be considered only after a period of 4872 hours of inpatient observation. Women should be advised of the
signs and symptoms of chorioamnionitis and under what circumstances they should seek specialist advice. Women being
monitored at home for PPROM should take their temperature twice daily or should be advised of the symptoms associated with
infection. There should be clearly described local arrangements for the frequency of outpatient visits and what should be
carried out at these visits.
Delivery should be considered at 34 weeks of gestation. Where expectant management is considered beyond 34 weeks of
gestation, women should be counselled about the increased risk of chorioamnionitis and its consequences versus the
decreased risk of serious respiratory problems in the neonate, admission for neonatal intensive care and caesarean section.

No. 45 Birth after Previous Caesarean birth

Planned VBAC (vaginal birth after caesarean) refers to any woman who has experienced a prior caesarean birth who plans to
deliver vaginally rather than by ERCS (elective repeat caesarean section).

Maternal outcomes: Uterine rupture is defined as a 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: Uterine dehiscence is
defined as disruption of the uterine muscle with intact uterine serosa: Other outcomes: hysterectomy, thromboembolism,
haemorrhage, transfusion requirement, viscus injury (bowel, bladder, ureter), endometritis, maternal death.
Neonatal respiratory morbidity is defined as the combined rate of transient tachypnoea of the newborn (TTN) and respiratory
distress syndrome (RDS).
Hypoxic ischaemic encephalopathy (HIE) is defined as hypoxia resulting from a decrease in the blood supply to a bodily
organ, tissue, or part caused by constriction or obstruction of the blood vessels, which results in compromised neurological
function manifesting during the first few days after birth. HIE refers to a subset of the much broader category of neonatal
encephalopathy, in which the aetiology is felt to be intrapartum hypoxicischemic injury.
Women with a prior history of one uncomplicated lower-segment transverse caesarean section, in an otherwise uncomplicated
pregnancy at term, with no contraindication to vaginal birth, should be able to discuss the option of planned VBAC and the
alternative of a repeat caesarean section (ERCS). The antenatal counselling of women with a prior caesarean birth should be
documented in the notes. There should be provision of a patient information leaflet with the consultation. A final decision for
mode of birth should be agreed between the woman and her obstetrician before the expected/planned delivery date (ideally by

30

36 weeks of gestation). A plan for the event of labour starting prior to the scheduled date should be documented. Women
considering their options for birth after a single previous caesarean should be informed that, overall, the chances of successful
planned VBAC are 7276%.
There are numerous other factors associated with a decreased likelihood of planned VBAC success: VBAC at or after 41
weeks of gestation, birth weight greater than 4000 g; no epidural anaesthesia, previous preterm caesarean birth, cervical
dilatation at admission less than 4 cm, less than 2 years from previous caesarean birth, advanced maternal age, non-white
ethnicity, short stature and a male infant.
Women with a prior history of one classical caesarean section are recommended to give birth by ERCS. Women with a
previous uterine incision other than an uncomplicated low transverse caesarean section incision who wish to consider vaginal
birth should be assessed by a consultant with full access to the details of the previous surgery. Women with a prior history of
two uncomplicated low transverse caesarean sections, in an otherwise uncomplicated pregnancy at term, with no
contraindication for vaginal birth, who have been fully informed by a consultant obstetrician, may be considered suitable for
planned VBAC. Previous high vertical classical caesarean section (200900/10,000 risk of uterine rupture) where the uterine
incision has involved the whole length of the uterine corpus. These include: women with a prior inverted T or J incision
(190/10,000 rupture risk) and women with prior low vertical incision (200/10,000 rupture risk).
There is insufficient and conflicting information on whether the risk of uterine rupture is increased in women with previous
myomectomy or prior complex uterine surgery. Women considering the options for birth after a previous caesarean should be
informed that planned VBAC carries a risk of uterine rupture of 2274/10,000. There is virtually no risk of uterine rupture in
women undergoing ERCS. Uterine rupture in an unscarred uterus is extremely rare at 0.52.0/10,000 deliveries; this risk is
mainly confined to multiparous women in labour.
Women considering the options for birth after a previous caesarean should be informed that planned VBAC compared with
ERCS carries around 1% additional risk of either blood transfusion or endometritis. Maternal death from uterine rupture in
planned VBAC occurs in less than 1/100,000 cases in the developed world. Women considering planned VBAC should be
informed that this decision carries a 23/10,000 additional risk of birth-related perinatal death when compared with ERCS. The
absolute risk of such birth-related perinatal loss is comparable to the risk for women having their first birth.
Women considering the options for birth after a previous caesarean should beinformed that plannedVBAC carries an 8/10,000
risk of the infant developing hypoxic ischaemic encephalopathy. The effect on the long-term outcome of the infant upon
experiencing HIE is unknown.
Women considering the options for birth after a previous caesarean should be informed that attempting VBAC probably
reduces the risk that their baby will have respiratory problems after birth: rates are 23% with planned VBAC and 34% with
ERCS. Women considering the options for birth after a previous caesarean should be informed that ERCS may increase the
risk of serious complications in future pregnancies.
Women who are preterm and considering the options for birth after a previous caesarean should be informed that planned
preterm VBAC has similar success rates to planned term VBAC but with a lower risk of uterine rupture.
A cautious approach is advised when considering planned VBAC in women with twin gestation, fetal macrosomia and short
interdelivery interval, as there is uncertainty in the safety and efficacy of planned VBAC in such situations.
Women should be advised to have continuous electronic fetal monitoring following the onset of uterine
contractions for the duration of planned VBAC. An abnormal cardiotocograph (CTG) is the most consistent finding in uterine
rupture and is present in 5587% of these events.
Early diagnosis of uterine scar rupture followed by expeditious laparotomy and resuscitation is essential to reduce associated
morbidity and mortality in mother and infant. There is no single
pathognomic clinical feature that is indicative of uterine rupture but the presence of any of the following peripartum should raise
the concern of the possibility of this event: abnormal CTG: severe abdominal pain, especially if persisting between
contractions; chest pain or shoulder tip pain, sudden onset of shortness of breath; acute onset scar tenderness; abnormal
vaginal bleeding or haematuria; cessation of previously efficient uterine activity; maternal tachycardia, hypotension or shock;
loss of station of the presenting part.
The diagnosis is ultimately confirmed at emergency caesarean section or postpartum laparotomy. The routine use of
intrauterine pressure catheters in the early detection of uterine scar rupture is not recommended.
Women should be informed of the two- to three-fold increased risk of uterine rupture and around 1.5-fold increased risk of
caesarean section in induced and/or augmented labours compared with spontaneous labours. Women should be informed that
there is a higher risk of uterine rupture with induction of labour with prostaglandins. There should be careful serial cervical
assessments, preferably by the same person, for both augmented and non-augmented labours, to ensure that there is
adequate cervicometric progress, thereby allowing the planned VBAC to continue. The decision to induce, the method chosen,
the decision to augment with oxytocin, the time intervals for serial vaginal examination and the selected parameters of progress
that would necessitate and advise on discontinuing VBAC should be discussed with the woman by a consultant obstetrician.
In the NICHD study, the rates of caesarean section in women undergoing planned VBAC were 33%, 26% and 19% for induced,
augmented and spontaneous labour groups, respectively.
The additional risks in augmented VBAC mean that: although augmentation is not contraindicated it should only be preceded
by careful obstetric assessment, maternal counselling and by a consultant-led decision. Oxytocin augmentation should be
titrated such that it should not exceed the maximum rate of contractions of four in 10 minutes; the ideal contraction frequency
would be three to four in 10 minutes. Careful serial cervical assessments, preferably by the same person, are necessary to
show adequate cervicometric progress, thereby allowing augmentation to continue.

No. 46 Vaginal Vault Prolapse

31

The International Continence Society defines post-hysterectomy (apical) vaginal prolapse as descent of the vaginal cuff scar
below a point that is 2 cm less than the total vaginal length above the plane of the hymen.
McCall culdoplasty at the time of vaginal hysterectomy is a recommended measure to prevent enterocele formation. A small
randomised trial compared vaginal Moschowitz-type operation, McCalls culdoplasty and peritoneal closure of the cul-de-sac as
preventive measures against the development of enterocele. It included 100 women and showed that McCalls culdoplasty was
more effective than vaginal Moschowitz or simple closure of the peritoneum in preventing enterocele at 3 years follow-up. The
technique involves approximating the uterosacral ligaments using continuous sutures, so as to obliterate the peritoneum of the
posterior cul-de-sac as high as possible.
Suturing the cardinal and uterosacral ligaments to the vaginal cuff at the time of hysterectomy is a recommended measure to
avoid vault prolapse. Sacrospinous fixation at the time of vaginal hysterectomy is recommended when the vault descends to
the introitus during closure. Assessment of the woman should be comprehensive and objective, addressing quality of life,
looking for all pelvic floor defects and should be based on standard tools. The role of conservative measures for posthysterectomy vaginal vault prolapse is unclear.
Conservative measures include pelvic-floor exercises and different types of pessaries, of which ring and shelf are the most
commonly used. These measures have been assessed for prolapse in general, rather than posthysterectomy vaginal vault
prolapse. There is no evidence to suggest whether pelvic-floor exercises are helpful in vault prolapse. Pessaries, especially
shelf ones, preclude sexual intercourse and are therefore more suitable for women who are not sexually active. They also
require changing every 68 months to prevent ulceration of the vaginal vault. If left for a long period, there is a risk of calcium
deposition, as well as of erosion and fistula formation.
Anterior and posterior repair along with obliteration of the enterocele sac are inadequate for posthysterectomy vaginal vault
prolapse. Abdominal sacrocolpopexy and sacrospinous fixation should be considered in terms of their relative benefits and
risks. Abdominal sacrocolpopexy is an effective operation for post-hysterectomy vaginal vault prolapse. In comparison,
sacrospinous fixation may have a higher failure rate but has lower postoperative morbidity. Complications were rare but
included: sacrocolpopexy: blood transfusion , bladder injury , incisional hernia , mesh rejection , wound infection sacrospinous
fixation: blood transfusion, bladder injury, rectovaginal haematoma, vaginal pain. Abdominal sacrocolpopexy is more suitable
for sexually active women, as sacrospinous fixation is associated with exaggerated retroversion of the vagina, leading to a less
physiological axis than following sacrocolpopexy.
There is no evidence to recommend bilateral or unilateral sacrospinous fixation. Iliococcygeus fixation does not reduce the
incidence of anterior vaginal wall prolapse associated with vaginal sacrospinous fixation and should not be routinely
recommended. Caution is advised with vaginal uterosacral ligament suspension, although it is effective for posthysterectomy
vaginal vault prolapse, there is a risk of ureteric injury.
Clinicians should be aware that laparoscopic procedures involve a high level of expertise and longer operation times.
Laparoscopic sacrocolpopexy appears to be as effective as open sacrocolpopexy. The ureters are particularly at risk during
laparoscopic uterosacral ligament suspension. There is insufficient evidence to judge the value of other laparoscopic
techniques.
Colpocleisis is a safe and effective procedure that can be considered for those women who do not wish to retain sexual
function. Colpocleisis entails closure of the vagina, which is suitable for frail women who do not want to retain sexual function.
Different techniques have been described, including vaginectomy, pursestring closure of the vagina, colpocleisis after
performing standard anterior and posterior vaginal wall repair, purse-string closure of enterocele followed by approximation of
pervesical and rectovaginal fascia and high levator plication and LeFort colpocleisis, where a bridge of tissue is created
between the anterior and posterior vaginal wall, to stop vault prolapse from protruding.
Sling procedures should not be used without adequate patient counselling and special provisions for audit and research. There
is insufficient evidence to judge the safety and effectiveness of total mesh reconstruction. Vault suspension to the anterior
abdominal wall can be a simple measure. However, there are not enough studies assessing this technique to judge its value.

No. 47 Blood transfusion in Obstetrics

Reducing obstetrical need for transfusion: Anaemia should be treated. If the haemoglobin level is less than 10.5 g/dl in the
antenatal period, consider haematinic deficiency once haemoglobinopathies have been excluded. Oral iron should be the
preferred first-line treatment for iron deficiency. Parenteral iron is indicated when oral iron is not tolerated, absorbed or patient
compliance is in doubt. Parenteral therapy offers a shorter duration of treatment and a quicker response than oral therapy. It is,
however, more invasive and expensive to administer. Iron sucrose is given in multiple doses whereas iron dextran may be
given as a single total-dose infusion. Recombinant human erythropoietin (rHuEPO) is mostly used in the anaemia of end-stage
renal disease. rHuEPO has been used both antenatally and postpartum in women without end-stage renal disease without any
adverse maternal, fetal or neonatal effects. Use rHuEPO in clinical practice for non-end-stage renal anaemia is still to be
established and should only be used in the context of a controlled clinical trial. Anaemia not due to haematinic deficiency (for
example, haemoglobinopathies and bone marrow failure syndromes) should be managed by blood transfusion where
appropriate in close conjunction with a haematologist. Blood loss at delivery should be minimised. Active management of the
third stage of labour is recommended to minimise blood loss. Women at high risk of haemorrhage should be advised to deliver
in hospital. Optimal management of women on anticoagulants, such as low-molecular-weight heparin, will minimise blood loss.
All women should have their blood group and antibodies status checked at booking and at 28 weeks of gestation. Women
should have a group-and-save or crossmatch sample taken according to a locally agreed and regularly monitored maximum
surgical blood ordering schedule (MSBOS), depending on the obstetric diagnosis. If any blood component therapy is
contemplated, a sample for group-and-save must be sent to the blood transfusion laboratory.

32

Patient blood samples used for crossmatching red cells should be no more than 7 days old. Only Kell-negative blood should be
used for transfusion in women of childbearing age, owing to the high risk of alloimmunisation and subsequent haemolytic
disease of the newborn (unless a women is known to be Kell positive). Unlike anti-c, anti-K in pregnancy is more likely to have
been induced by previous transfusion; this can be prevented. Cytomegalovirus (CMV) seronegative red cells and platelets
should be used for CMV seronegative pregnant women. Where the CMV status is unknown, CMV seronegative products
should be used to avoid transmission of CMV to the fetus although the UK policy of universal leucocyte depletion substantially
reduces if not eliminates the risk of CMV transmission. Urgent transfusion should not be delayed if CMV seronegative
components are not immediately available. For women with known placenta praevia, some obstetric centres make 2 units of
crossmatched red cells available in the issue fridge. These units should be replaced every week by newly crossmatched units.
In pregnancy, pre-autologous deposit is not recommended. Cell salvage is recommended for women in whom an
intraoperative blood loss of more than 1500 ml is anticipated. Cell salvage should only be used by healthcare teams who use it
regularly and have the necessary expertise and experience. Consent should be obtained and its use in obstetric patients
should be subject to audit and monitoring. However, it will not remove fetal blood cells and therefore adequate anti-D
immunisation (as determined by Kleihauer test 1 hour after the procedure) will be required to prevent rhesus immunisation in
Rh D-negative women. Where there is no history of irregular antibodies and none are detected during screening, group-specific
compatible blood can be provided within 10 minutes plus transport time. If irregular antibodies are found, or are known to have
been present on a previous occasion, then blood must be crossmatched, as obtaining compatible blood may need several
units to be crossmatched. Antibodies may delay crossmatch greatly and this should be taken into account when planning care.
In an extreme situation and when the blood group is unknown, O Rh D negative red cells should be given (although these may
be incompatible for patients with irregular antibodies). There are no firm criteria for initiating red cell transfusion. The decision
to perform blood transfusion should be made on both clinical and haematological grounds. Transfusion is rarely indicated in the
stable patient when Hb is greater than 10 g/dl and is almost always indicated when less than 6 g/dl. In what circumstances
should fresh frozen plasma (FFP) and cryoprecipitate be used? It is essential that regular full blood counts (FBC) and
coagulation screens are performed during the bleeding episode. FFP, cryoprecipitate and platelets should not be given on
clinical suspicion alone unless there is delay in obtaining blood results. Infusion of FFP should be considered before 1 blood
volume is lost. In the bleeding woman with disseminated intravascular coagulation (DIC), a combination of FFP, platelets and
cryoprecipitate is indicated. The FFP and cryoprecipitate should ideally be of the same group as the recipient. If unavailable,
FFP of a different ABO group is acceptable, provided that it does not have a high titre anti-A or anti-B activity. No anti-D
prophylaxis is required if an Rh D negative woman receives Rh D positive FFP or cryoprecipitate. Fibrinogen levels should be
maintained above 1.0 g/l by the use of FFP as above or two pools of cryoprecipitate. There is insufficient evidence to suggest
that FFP is useful in major blood loss in the absence of DIC. Its use should be guided by the use of coagulation tests. The
platelet count should not be allowed to fall below 50 x 109/l in the acutely bleeding patient. A platelet transfusion trigger of 75 x
109/l is recommended to provide a margin of safety. Platelets may not be on-site in many units, so their need should be
anticipated and good communication with the transfusion laboratory maintained. Rh D-negative women should receive Rh Dnegative platelets. The platelets should ideally also be group compatible. Anti-Rh D immunoglobulin (at a dose of 250 iu) will
be needed if the platelets are Rh D positive and the recipient Rh D negative. This is not necessary if a caesarean hysterectomy
has been performed. The use of rFVIIa may be considered as a treatment for life-threatening postpartum haemorrhage but
should not be considered as a substitute for, nor should it delay the performance of, a life-saving procedure such as
embolisation or surgery, nor the transfer to a referral centre. There is no evidence to support the prophylactic use of rFVIIa to
reduce blood loss for caesarean sections. In the event of intractable obstetric haemorrhage, the administration of rFVIIa may
be an option to be discussed with the haematologists. The availability and use of rFVIIa may be limited, owing to its financial
cost and therefore it is advisable to consult with the local haematology department to determine its availability and prepare
advance local guidance on indications for its use in managing intractable haemorrhage. Consideration should be given to
keeping rFVIIa in the blood bank stock in case of any bleeding emergency. Alternatively, a protocol should be available for
procuring it urgently. If the Hb is less than 7 g/dl in labour or in the immediate postpartum period, the decision to transfuse
should be made according to the individuals medical history, age and symptoms.
If the Hb is less than 78 g/dl in postnatal period, where there is no continuing or threat of bleeding, the decision to transfuse
should be made on an informed individual basis. In fit, healthy, asymptomatic patients there little evidence of the benefit of
blood transfusion. If unexpected severe bleeding is encountered, investigations should be made postnatally into possible
bleeding diatheses. These investigations should be performed on a non-urgent basis at least 36 months after delivery. Hb
should be optimised before delivery to prevent avoidable anaemia. The pharmacological, mechanical and surgical procedures
to avert the use of banked blood and blood components should be considered at an early stage.

No. 48 Premenstrual syndrome

Approximately 5% of women experience severe premenstrual symptoms which include depression, anxiety, irritability and loss
of confidence, and physical symptoms including bloating and mastalgia. There is currently no consensus in the management of
PMS, with a wide range of treatment options available. PMS is a condition which manifests with distressing physical,
behavioural and psychological symptoms, in the absence of organic or underlying psychiatric disease, which regularly recurs
during the luteal phase of each menstrual (ovarian) cycle and which disappears or significantly regresses by the end of
menstruation

Mild Does not interfere with personal/social and professional life

33

Moderate Interferes with personal/social and professional life but still able to function and interact, although may be
suboptimally

Severe Unable to interact personally/socially/professionallywithdraws from social and professional activities (treatment
resistant)
The precise aetiology of PMS remains unknown but cyclical ovarian activity and the effect of estradiol and progesterone on the
neurotransmitters serotonin and gamma-aminobutyric acid (GABA) appear to be key factors. Absence of PMS before puberty,
in pregnancy and after the menopause supports the theory thatcyclical ovarian activity is important. The prevalence of severe
PMS is variable between 3% to 30%. PMS appears more prevalent in women who are obese, perform less exercise and are of
lower academic achievement. There is a lower incidence of PMS in women using hormonal contraception.
When assessing women with PMS, symptoms should be recorded prospectively, over two cycles using a symptom diary, as
retrospective recall of symptoms is unreliable. When treating women with PMS: general advice about exercise, diet and stress
reduction should be considered before starting treatment women with marked underlying psychopathology as well as PMS
should be referred to a psychiatrist symptom diaries (DRSP) should be used to assess the effect of treatment.
When treating women with PMS, referral to a gynaecologist should be considered when simple measures have been explored
and failed and when the severity of the PMS justifies gynaecological intervention. When treating women with PMS, an
integrated approach is beneficial. This may include complementary medicines which themselves may not be evidence based.
Physical and psychological symptoms of PMS improve with SSRIs. In view of their proven efficacy and safety in adults,
SSRIs/SNRIs should be considered one of the firstline pharmaceutical management options in severe PMS. Prescribing should
be restricted to those health professionals (gynaecologists, psychiatrists or GPs) who have a particular expertise in this area.
The Commission on Human Medicines (formerly the Committee on Safety of Medicines) endorses the view that SSRIs are
effective medicines in the treatment of depression and anxiety conditions and that the balance of risks and benefits in adults
remains positive in their licensed indications. When treating women with PMS, it is recommended that SSRI therapy should be
withdrawn gradually to avoid withdrawal symptoms, if given on a continuous basis. This is unnecessary if treatment is with lowdose luteal-phase. Women with PMS treated with SSRIs should be warned of possible adverse effects such as nausea,
insomnia and reduction in libido. SSRIs and SNRIs should be prescribed by psychiatrists and doctors with a special interest,
when treating women with PMS, as a few suicides in young people with depression have been reported. The use of newer
SSRIs, such as citalopram, may produce resolution of symptoms where other SSRIs have failed. Severe PMS also improves
significantly with either luteal-phase or symptom onset dosing of escitalopram with good tolerability.17Women with more severe
PMS may respond better to luteal-phase dosing than symptom-onset dosing. When treating women with PMS, newer
contraceptive pill types may represent effective treatment for PMS and should be considered as one of the first-line
pharmaceutical interventions. When treating women with PMS, emerging data suggest that consideration should be given to
use of the contraceptive pill continuously rather than cyclically. Percutaneous estradiol, either as an implant or as a patch,
combined with cyclical progestogen, has been shown to be effective for the management of physical and psychological
symptoms of severe PMS. When treating women with PMS, alternative barrier or intrauterine methods of contraception should
be used when estradiol (patches and implant) are used to suppress ovulation. When treating women with PMS, treatment with
the lowest possible dose of progestogen is recommended to minimise adverse effects. Women should be informed that low
systemic levels of levonorgestrel released by the levonorgestrel intrauterine system (LNG-IUS) can initially produce PMS-type
adverse effects (as well as bleeding). When treating women with PMS with estradiol, women should be informed that there are
insufficient data to advise on the long-term effects on breast and endometrial tissue. Women with PMS should be advised that,
although treatment with low-dose danazol (200 mg twice daily) is effective, its use should be considered in light of its potential
irreversible virilising effects. Women treated with danazol for PMS should be advised to use contraception during treatment.
Early resort to GnRH therapy is not recommended and prolonged use should be retained for women with the most severe
symptoms. GnRH analogue therapy results in profound cycle suppression and elimination of premenstrual symptoms. Lack of
efficacy suggests a questionable diagnosis rather than a limitation of therapy. When treating women with severe PMS with
GnRH analogues: therapy should be recommended as second- or even third-line treatment therapy should not be used as a
first-line treatment, except for women with the most severe PMS, due to its hypoestrogenic effects add-back hormone therapy
is recommended. One trial used low-dose GnRH to eliminate symptoms without ovulation suppression; however, it showed no
benefit over placebo. When treating women with PMS where add-back hormone therapy is required, continuous combined
HRT or tibolone should be recommended, as it reduces menopausal symptoms without reappearance of PMS-like
progestogenic effects. When treating women with PMS, with GnRHa therapy: Treatment should only be continued for 6 months
when used alone. Treatment should be combined with HRT to reduce trabecular bone density loss. Women on longterm
treatment should have annual measurement of bone mineral density (ideally by dual energy X-ray absorptiometry). Treatment
should be stopped if bone density declines significantly in scans performed 1 year apart. General advice about how exercise,
diet and smoking affect bone mineral density should be given. There is insufficient evidence to recommend the routine use of
progesterone or progestogens for women with PMS.
When treating women with severe PMS, hysterectomy and bilateral salpingo-oophorectomy has been shown to be of benefit.
When treating women with PMS, surgery should not be contemplated without preoperative use of GnRH analogues as a test of
cure and to ensure that HRT is tolerated. Such therapy should be reserved for extremely severe PMS sufferers in whom other
treatment has failed. When treating women with PMS, HRT should be considered in women undergoing surgical oophorectomy
before the age of 50 years.

No. 49 Laparoscopic Injuries

34

One of the difficulties of bowel damage associated with laparoscopic surgery is the likelihood that it may not be immediately
recognised and could present some time later, often after discharge from hospital. This potentially serious complication may
require major abdominal reparative surgery and sometimes a temporary colostomy. The rate of major complications was
1.4/1000 procedures comprising intestinal injuries (0.6/1000), urological injuries (0.3/1000) and vascular injuries 0.1/1000).
Women must be informed of the risks and potential complications associated with laparoscopy. This should include discussion
of the risks of the entry technique used: specifically, injury to the bowel, urinary tract and major blood vessels, and later
complications associated with the entry ports: specifically, hernia formation. Surgeons must be aware of the increased risks in
women who are obese or significantly underweight and in those with previous midline abdominal incisions, peritonitis or
inflammatory bowel disease. These factors should be included in patient counselling where appropriate. Surgeons intending to
perform laparoscopic surgery should have appropriate training, supervision and experience. Surgeons undertaking
laparoscopic surgery should be familiar with the equipment, instrumentation and energy sources they intend to use. Surgeons
undertaking laparoscopic surgery should ensure that nursing staff and surgical assistants are appropriately trained for the roles
they will undertake during the procedure.
The most effective way to reduce complications of laparoscopic entry is to optimise insertion of the primary trocar and cannula,
although there is controversy as to the safest technique for achieving this. Gynaecologists have tended to favour the closed or
Veress needle entry technique, whereby the abdominal cavity is insufflated with carbon dioxide gas before introduction of the
primary trocar and cannula. The Royal College of Surgeons of England recommends that the open (Hasson) approach be used
in all circumstances. This latter method uses a small incision to enter the peritoneal cavity under direct vision.
In most circumstances the primary incision for laparoscopy should be vertical from the base of the umbilicus (not in the skin
below the umbilicus). Care should be taken not to incise so deeply as to enter the peritoneal cavity. The Veress needle should
be sharp, with a good and tested spring action. A disposable needle is recommended, as it will fulfil these criteria. The
operating table should be horizontal (not in the Trendelenburg tilt) at the start of the procedure. The abdomen should be
palpated to check for any masses and for the position of the aorta before insertion of the Veress needle.
The lower abdominal wall should be stabilised in such a way that the Veress needle can be inserted at right angles to the skin
and should be pushed in just sufficiently to penetrate the fascia and the peritoneum. Two audible clicks are usually heard as
these layers are penetrated. Excessive lateral movement of the needle should be avoided, as this may convert a small
needlepoint injury in the wall of the bowel or vessel into a more complex tear. An intra-abdominal pressure of 2025 mmHg
should be used for gas insufflation before inserting the primary trocar. The distension pressure should be reduced to 1215
mmHg once the insertion of the trocars is complete. This gives adequate distension for operative laparoscopy and allows the
anaesthetist to ventilate the patient safely and effectively. It is necessary to achieve a pressure of 2025 mmHg before
inserting the trocar, as this results in increased splinting and allows the trocar to be more easily inserted through the layers of
the abdominal wall. When the same force is applied to an abdomen distended to 25 mmHg, the depth is 5.6 cm (range 48
cm). The mean volume of CO2 required to reach this pressure was 5.58 litres. No adverse effect on circulation or respiratory
function was observed as long as the patient is lying flat.
The primary trocar should be inserted in a controlled manner at 90 degrees to the skin, through the incision at the thinnest part
of the abdominal wall, in the base of the umbilicus. Insertion should be stopped immediately the trocar is inside the abdominal
cavity. Once the laparoscope has been introduced through the primary cannula, it should be rotated through 360 degrees to
check visually for any adherent bowel. If this is present, it should be closely inspected for any evidence of haemorrhage,
damage or retroperitoneal haematoma. If there is concern that the bowel may be adherent under the umbilicus, the primary
trocar site should be visualised from a secondary port site, preferably with a 5-mm laparoscope. On completion of the
procedure, the laparoscope should be used to check that there has not been a through-and-through injury of bowel adherent
under the umbilicus by visual control during removal.
When the Hasson open laparoscopic entry is employed, confirmation that the peritoneum has been opened should be made by
visualising bowel or omentum before inserting the blunt tipped cannula. Once the fascial edges are incised, they should be
held by a lateral stay suture on either side of the incision. Once the peritoneum is opened, the fascial sutures are then pulled
firmly into the suture holders on the cannula to produce an airtight seal with the cone of the cannula. Gas is insufflated directly
through the cannula to produce the pneumoperitoneum. The blunt trocar is withdrawn only after the abdomen is partially
distended. At the end of the procedure, the fascial defect should be closed using the stay sutures (and possibly additional
sutures) to minimise the risk of herniation. Direct trocar insertion is an acceptable alternative trocar insertion method.
Palmers point is the preferred alternative trocar insertion site, except in cases of previous surgery in this area or splenomegaly.
Secondary ports must be inserted under direct vision perpendicular to the skin, while maintaining the pneumoperitoneum at
2025 mmHg. During insertion of secondary ports, the inferior epigastric vessels should be visualised
laparoscopically to ensure the entry point is away from the vessels. During insertion of secondary ports, once the tip of the
trocar has pierced the peritoneum it should be angled towards the anterior pelvis under careful visual control until the sharp tip
has been removed. Secondary ports must be removed under direct vision to ensure that any haemorrhage can be observed
and treated, if present. The open (Hasson) technique or entry at Palmers point are recommended for the primary entry in
women with morbid obesity. If the Veress needle approach is used, particular care must be taken to ensure that the incision is
made right at the base of the umbilicus and the needle inserted vertically into the peritoneum. The Hasson technique or
insertion at Palmers point is recommended for the primary entry in women who are very thin.

No. 50 Umbilical Cord Prolapse

35

Cord prolapse has been defined as the descent of the umbilical cord through the cervix alongside (occult) or past the
presenting part (overt) in the presence of ruptured membranes. Cord presentation is the presence of the umbilical cord
between the fetal presenting part and the cervix, with or without membrane rupture. In the case of breech presentation, the
incidence is slightly higher than 1%. It has been reported that male fetuses appear to be predisposed to cord prolapse. The
incidence is influenced by population characteristics and is higher where there is a large percentage of multiple gestations.
Prematurity and congenital malformations account for the majority of adverse outcomes associated with cord prolapse in
hospital settings1 but birth asphyxia is also associated with cord prolapse. Asphyxia may also result in hypoxicischaemic
encephalopathy and cerebral palsy. The principal causes of asphyxia in this context are thought to be cord compression and
umbilical arterial vasospasm preventing venous and arterial blood flow to and from the fetus.
Risk factors for cord prolapse
General
Multiparity ; Low birth weight, less than 2.5 kg
Prematurity less than 37 weeks
Fetal congenital anomalies
Breech presentation; Transverse, oblique and unstable lie
(when the
longitudinal axis of the fetus is changing repeatedly); Second
twin; Polyhydramnios; Unengaged presenting part; Low-lying
placenta, other abnormal placentation

Procedure related
Artificial rupture of membranes
Vaginal manipulation of the fetus with ruptured membranes
External cephalic version (during procedure) Internal podalic
version
Stabilising induction of labour
Insertion of uterine pressure transducer

Some authorities have also speculated that cord abnormalities (such as true knots or low content of Whartons jelly) and fetal
hypoxiaacidosis may alter the turgidity of the cord and predispose to prolapse. Induction of labour with prostaglandins is not
associated with cord prolapse.
Routine ultrasound examination is not sufficiently sensitive or specific for identification of cord presentation antenatally and
should not be performed to predict increased probability of cord prolapse, unless in the context of a research setting.
With transverse, oblique or unstable lie, elective admission to hospital after 37+6 weeks of gestation should be discussed and
women should be advised to present quickly if there are signs of labour or suspicion of membrane rupture. Women with
noncephalic presentations and preterm prelabour rupture of the membranes should be offered admission. Artificial membrane
rupture should be avoided whenever possible if the presenting part is mobile. If it becomes necessary to rupture the
membranes, this should be performed with arrangements in place for immediate caesarean delivery. Vaginal examination and
obstetric intervention in the context of ruptured membranes and a high presenting part carry the risk of upward displacement
and cord prolapse. Upward pressure on the presenting part should be kept to a minimum in such women. Rupture of
membranes should be avoided if, on vaginal examination, the cord is felt below the presenting part. When cord presentation is
diagnosed in established labour, caesarean section is usually indicated.
Cord presentation and prolapse may occur without outward physical signs and with a normal fetal heart rate pattern. The cord
should be examined for at every vaginal examination in labour and after spontaneous rupture of membranes if risk factors are
present or if cardiotocographic abnormalities commence soon thereafter. With spontaneous rupture of membranes in the
presence of a normal fetal heart rate patterns and the absence of risk factors for cord prolapse, routine vaginal examination is
not indicated if the liquor is clear. Cord prolapse should be suspected where there is an abnormal fetal heart rate pattern
(bradycardia, variable decelerations etc), particularly if such changes commence soon after membrane rupture, spontaneously
or with amniotomy. Speculum and/or digital vaginal examination should be performed at preterm gestations when cord
prolapse is suspected. When cord prolapse is diagnosed before full dilatation, assistance should be immediately called and
preparations made for immediate delivery in theatre. There are insufficient data to evaluate manual replacement of the
prolapsed cord above the presenting part to allow continuation of labour. This practice is not recommended. To prevent
vasospasm, there should be minimal handling of loops of cord lying outside the vagina. To prevent cord compression, it is
recommended that the presenting part be elevated either manually or by filling the urinary bladder. Bladder filling can be
achieved quickly by inserting the end of a blood giving set into a Foleys catheter. The catheter should be clamped once 500
750 ml has been instilled. It is essential to empty the bladder again just before any delivery attempt, be it vaginal or caesarean
section. Cord compression can be further reduced by the mother adopting the kneechest position or head-down tilt (preferably
in left-lateral position).
Tocolysis can be considered while preparing for caesarean section if there are persistent fetal heart rate abnormalities after
attempts to prevent compression mechanically and when the delivery is likely to be delayed. The suggested tocolytic regimen
is terbutaline 0.25 mg subcutaneously. Although the measures described above are potentially useful during preparation for
delivery, they must not result in unnecessary delay.
A caesarean section is the recommended mode of delivery in cases of cord prolapse when vaginal delivery is not imminent, to
prevent hypoxiaacidosis. A category 1 caesarean section should be performed with the aim of delivering within 30 minutes or
less if there is cord prolapse associated with a suspicious or pathological fetal heart rate pattern but without unduly risking
maternal safety. Verbal consent is satisfactory. Category 2 caesarean section is appropriate for women in whom the fetal heart
rate pattern is normal. Regional anaesthesia may be considered in consultation with an experienced anaesthetist. The 30minute decision-to-delivery interval is the acknowledged target for category 1 caesarean section.
Vaginal birth, in most cases operative, can be attempted at full dilatation if it is anticipated that delivery would be accomplished
quickly and safely. Breech extraction can be performed under some circumstances, such as after internal podalic version for
the second twin. A practitioner competent in the resuscitation of the newborn should attend all deliveries with cord prolapse.
Paired cord blood samples should be taken for pH and base excess measurement. Women should be advised, over the
telephone if necessary, to assume the kneechest face-down position while waiting for hospital transfer. During emergency
ambulance transfer, the kneechest is potentially unsafe and the left-lateral position should be used. All women with cord

36

prolapse should be advised to be transferred to the nearest consultant-led unit for delivery, unless an immediate vaginal
examination by a competent professional reveals that a spontaneous vaginal delivery is imminent. Preparations for transfer
should still be made. The presenting part should be elevated during transfer by either manual or bladder filling methods. It is
recommended that community midwives carry a Foley catheter for this purpose and equipment for fluid infusion. To prevent
vasospasm, there should be minimal handling of loops of cord lying outside the vagina.
Expectant management should be discussed for cord prolapse complicating pregnancies with gestational age at the limits of
viability. Uterine cord replacement may be attempted. Postnatal debriefing should be offered to every woman with cord
prolapse.

No. 51 Monochorionic Twin Pregnancy, Management

Postnatal debriefing should be offered to every woman with cord prolapse. Monochorionic (MC) and dichorionic (DC) twin
pregnancies share increased risks of preterm birth, fetal growth restriction, pre-eclampsia, maternal pregnancy symptoms and
postpartum haemorrhage. The particular challenges of monochorionic pregnancies arise from the vascular placental
anastomoses that are almost universal and connect the umbilical circulations of both twins: twintwin transfusion syndrome
(TTTS), the consequences to the co-twin of fetal death and the management of discordant malformations. In addition,
monochorionic, monoamniotic pregnancies (1% of twin pregnancies) carry a very high risk of cord entanglement. TTTS
complicates 1015% of MC pregnancies; the placentas are more likely to have unidirectional arteryvein anastomoses and
less likely to have bidirectional arteryartery anastomoses. A number of features of TTTS still elude full understanding;
discordant activation of the reninangiotensin system may be important. TTTS is found in monochorionic, monoamniotic
(MCMA), as well as monochorionic, diamniotic (MCDA) pregnancies. TTTS is more common in MCDA pregnancies than
MCMA pregnancies, possibly reflecting that there are more protective arteryartery anastomoses in the latter.
Rarely (in approximately 5% of cases), the transfusion may reverse during pregnancy, with the donor fetus demonstrating
features of a recipient fetus and vice versa. The pathophysiological basis for this is unclear. Reverse transfusion can occur
following laser surgery to the placenta. Unequal placental sharing and peripheral, velamentous cord insertions are common in
TTTS. Significant intrauterine size discordance occurs in MC twins in the absence of TTTS in approximately 10% of
pregnancies. All women with a twin pregnancy should be offered an ultrasound examination at 1013 weeks of gestation to
assess viability, chorionicity, major congenital malformation and nuchal translucency.
A photographic record should be retained, in the case notes, of the ultrasound appearances of the membrane attachment to
the placenta. If there is uncertainty about the diagnosis of chorionicity, a photographic record of the ultrasound appearance of
the membrane attachment to the placenta should be retained in the case notes and a second opinion should be sought. If there
is doubt in the diagnosis of chorionicity, the woman should be referred to a specialist without delay, as chorionicity is best
determined before 14 weeks. Chorionicity is better assessed by ultrasound before 14 weeks than after 14 weeks. 3% of MC
placentas have two placental masses (bipartite), so these are not necessarily dichorionic.
The diagnosis of TTTS is based on ultrasound criteria:

the presence of a single placental mass

concordant gender

oligohydramnios with maximum vertical pocket [MVP] less than 2 cm in one sac and polyhydramnios in other sac (MVP
8 cm) (some would say 8 cm at 20 weeks and 10 cm over 20 weeks)12

discordant bladder appearances severe TTTS

haemodynamic and cardiac compromise severe TTTS.

Clinicians and women should be aware that MC twin pregnancies have higher fetal loss rates than DC twin pregnancies,
mainly due to second trimester loss and, overall, may have a propensity to excess neurodevelopmental morbidity. Nuchal
translucency measurements should be offered to women with MC pregnancies who wish to have fetal aneuploidy screening.
The place of nuchal translucency measurements in predicting TTTS is unclear, with different studies demonstrating varying
sensitivity and specificity. All monochorionic twins should have a detailed ultrasound scan which includes extended views of
the fetal heart. A fetal echocardiographic assessment should be considered in the assessment of severe TTTS. Fetal
ultrasound assessment should take place every 23 weeks in uncomplicated monochorionic pregnancies from 16 weeks.
Umbilical artery waveforms in MC twins may show cyclical absent or reversed end diastolic velocities. These are more
common in discordant growth restriction (45%) than uncomplicated (5%) or severe TTTS pregnancies (2%). Women with
monochorionic twin pregnancies should be asked to report sudden increases in abdominal size or breathlessness, as this may
be a manifestation of TTTS.
Table 1 The Quintero classification system
I
There is a discrepancy in amniotic fluid volume with oligohydramnios of a maximum vertical pocket (MVP) 2 cm in
one sac and polyhydramnios in other sac (MVP 8 cm). The bladder of the donor twin is visible and Doppler studies
are normal
II
The bladder of the donor twin is not visible (during length of examination, usually around 1 hour) but Doppler studies
are not critically abnormal
III
Doppler studies are critically abnormal in either twin and are characterised as abnormal or reversed end-diastolic
velocities in the umbilical artery, reverse flow in the Ductus venosus or pulsatile umbilical venous flow
IV
Ascites, pericardial or pleural effusion, scalp oedema or overt hydrops present
V
One or both babies are dead

37

Twintwin transfusion syndrome should be managed in conjunction with regional fetal medicine centres with recourse to
specialist expertise. Severe twintwin transfusion syndrome presenting before 26 weeks of gestation should be treated by laser
ablation rather than by amnioreduction or septostomy. Anastomoses may be missed at laser ablation and TTTS can recur later
in up to 14% of pregnancies treated by laser ablation. Laser ablation can be performed in mono- and dichorionic triplet
pregnancies. It is appropriate to aim for vaginal birth of monochorionic twins unless there are accepted, specific clinical
indications for caesarean section, such as twin one lying breech or previous caesarean section. Delivery should be planned for
3637 weeks of gestation, unless there is an indication to deliver earlier.
After the single fetal death in a monochorionic pregnancy, the risk to the surviving twin of death or neurological abnormality is
of the order of 12% and 18%, respectively. Clinicians should be aware that the risks are much higher than in dichorionic
pregnancies and that management of such pregnancies is complex. It should be recognised that the risks of fetal death and
disability in childhood are not restricted to monochorionic pregnancies with a prior diagnosis of twin-to-twin transfusion
syndrome. Single fetal death in a monochorionic pregnancy should be referred and assessed in a regional fetal medicine
centre. Fetal anaemia may be assessed in the surviving twin by measurement of the fetal middle cerebral artery peak systolic
velocity using Doppler sonography. Most monochorionic, monoamniotic twins have cord entanglement and are best delivered
at 32 weeks, by caesarean section, after corticosteroids. Clinicians and women should be aware that triplet pregnancies that
include a monochorionic pair have higher fetal loss rates than trichorionic triplet pregnancies. They may also be complicated by
twintwin transfusion syndrome. Therefore, increased ultrasound surveillance is warranted.
Monochorionic twins that are discordant for fetal anomaly must be referred at an early gestation for assessment and
counselling in a regional fetal medicine centre.

No. 52 Postpartum Haemorrhage, Prevention and Management

Primary postpartum haemorrhage (PPH) is the most common form of major obstetric haemorrhage. The traditional definition of
primary PPH is the loss of 500 ml or more of blood from the genital tract within 24 hours of the birth of a baby. PPH can be
minor (5001000 ml) or major (more than 1000 ml). Major could be divided to moderate (10002000 ml) or severe (more than
2000 ml). The recommendations in this guideline apply to women experiencing primary PPH of 500 ml or more. Secondary
PPH is defined as abnormal or excessive bleeding from the birth canal between 24 hours and 12 weeks postnatally. Obstetric
haemorrhage remains one of the major causes of maternal death in both developed and developing countries. In the 2003
2005 report of the UK Confidential Enquiries into Maternal Deaths, haemorrhage was the third highest direct cause of maternal
death (6.6 deaths/million maternities) with a rate similar to the previous triennium.
Primary PPH involving an estimated blood loss of 5001000 ml (and in the absence of clinical signs of shock) should prompt
basic measures (close monitoring, intravenous access, full blood count, group and screen) to facilitate resuscitation should it
become necessary. If a woman with primary PPH is continuing to bleed after an estimated blood loss of 1000 ml (or has clinical
signs of shock or tachycardia associated with a smaller estimated loss), this should prompt a full protocol of measures to
achieve resuscitation and haemostasis.
Risk factors may present antenatally or intrapartum; care plans must be modified when risk factors present. Clinicians must be
aware of risk factors for PPH and should take these into account when counselling women about place of delivery essential for
the wellbeing and safety of both the mother and the baby. Most cases of PPH have no identifiable risk factors. Active
management of the third stage of labour lowers maternal blood loss and reduces the risk of PPH. Prophylactic oxytocics should
be offered routinely in the management of the third stage of labour in all women as they reduce the risk of PPH by about 60%.
For women without risk factors for PPH delivering vaginally, oxytocin (5 iu or 10 iu by intramuscular injection) is the agent of
choice for prophylaxis in the third stage of labour. For women delivering by caesarean section, oxytocin (5 iu by slow
intravenous injection) should be used to encourage contraction of the uterus and to decrease blood loss. A bolus dose of
oxytocin may possibly be inappropriate in some women, such as those with major cardiovascular disorders, suggesting that a
low-dose infusion might be a safer alternative. Syntometrine ( Alliance) may be used in the absence of hypertension (for
instance, antenatal low haemoglobin) as it reduces the risk of minor PPH (500-1000 ml) but increases vomiting. Misoprostol is
not as effective as oxytocin but it may be used when the latter is not available, such as the home-birth setting. All women who
have had a previous caesarean section must have their placental site determined by ultrasound. Where facilities exist,
magnetic resonance imaging (MRI) may be a useful tool and assist in determining whether the placenta is accreta or percreta.
Women with placenta accreta/percreta are at very high risk of major PPH. If placenta accreta or percreta is diagnosed
antenatally, there should be consultant-led multidisciplinary planning for delivery. Consultant obstetric and anaesthetic staff
should be present, prompt availability of blood, fresh frozen plasma and platelets be confirmed and the timing and location for
delivery chosen to facilitate consultant presence and access to intensive care. Available evidence on prophylactic occlusion or
embolisation of pelvic arteries in the management of women with placenta accreta is equivocal. The outcomes of prophylactic
arterial occlusion require further evaluation.
Presenting
antenatally
and
associated with a substantial
increase in the incidence of PPH;

Presenting
antenatally
and
associated with a significant
increase in the incidence of PPH;

Becoming apparent during labour and delivery;

Suspected or proven placental

abruption
Known placenta praevia
Multiple pregnancy
Pre-eclampsia/gestational

Previous PPH
Asian ethnicity
Obesity (BMI >35)
Anaemia (<9 g/dl)

Delivery by emergency caesarean section;

Delivery by elective caesarean section; Induction
of labour; Retained placenta; Mediolateral
episiotomy; Operative vaginal delivery; Prolonged
labour (> 12 hours); Big baby (> 4 kg); Pyrexia in

38

hypertension

labour; Age (> 40 years, not multiparous)

Basic measures for MINOR PPH (blood loss 5001000 ml, no clinical shock): Intravenous access (14-gauge cannula x 1);
Commence crystalloid infusion.
Full protocol for MAJOR PPH (blood loss > 1000 ml and continuing to bleed OR clinical shock): Assess airway. Assess
breathing. Evaluate circulation. Oxygen by mask at 1015 litres/minute. Intravenous access (14-gauge cannula x 2, orange
cannulae). Position flat. Keep the woman warm using appropriate available measures. Transfuse blood as soon as possible.
Until blood is available, infuse up to 3.5 litres of warmed crystalloid Hartmanns solution (2 litres) and/or colloid (12 litres) as
rapidly as required. The best equipment available should be used to achieve RAPID WARMED infusion of fluids. Special blood
filters should NOT be used, as they slow infusions. Recombinant factor VIIa therapy should be based on the results of
coagulation. Fluid therapy and blood product transfusion (please refer to sections 6.2.1 and 6.2.2): Crystalloid Up to 2 litres
Hartmanns solution; Colloid up to 12 litres colloid until blood arrives; Blood Crossmatched; If crossmatched blood is still
unavailable, give uncrossmatched group-specific blood OR give O RhD negative blood; Fresh frozen plasma 4 units for every
6 units of red cells or prothrombin time/activated; partial thromboplastin time > 1.5 x normal (1215 ml/kg or total 1 litres);
Platelets concentrates if PLT count < 50 x 109; Cryoprecipitate If fibrinogen < 1 g/l.
Causes for PPH may be considered to relate to one or more of the four Ts:
tone (abnormalities of uterine contraction)
tissue (retained products of conception)
trauma (of the genital tract)
thrombin (abnormalities of coagulation).
The most common cause of primary PPH is uterine atony. However, clinical examination must be undertaken to exclude other
or additional causes:
retained products (placenta, membranes, clots)
vaginal/cervical lacerations or haematoma
ruptured uterus
broad ligament haematoma
extragenital bleeding (for example, subcapsular liver rupture)
uterine inversion.
When uterine atony is perceived to be a cause of the bleeding, the following mechanical and pharmacological measures
should be instituted, in turn, until the bleeding stops:
Bimanual uterine compression (rubbing up the fundus) to stimulate contractions.
Ensure bladder is empty (Foley catheter, leave in place).
Syntocinon 5 units by slow intravenous injection (may have repeat dose).
Ergometrine 0.5 mg by slow intravenous or intramuscular injection (contraindicated in women with hypertension).
Syntocinon infusion (40 units in 500 ml Hartmanns solution at 125 ml/hour) unless fluid restriction is necessary.
Carboprost 0.25 mg by intramuscular injection repeated at intervals of not less than 15 minutes to a maximum of 8 doses
(contraindicated in women with asthma).
Direct intramyometrial injection of carboprost 0.5 mg (contraindicated in women with asthma), with responsibility of the
administering clinician as it is not recommended for intramyometrial use.
Misoprostol 1000 micrograms rectally.
If pharmacological measures fail to control the haemorrhage, initiate surgical haemostasis sooner rather than later. Intrauterine
balloon tamponade is an appropriate firstline surgical intervention for most women where uterine atony is the only or main
cause of haemorrhage. If this fails to stop the bleeding, the following conservative surgical interventions may be attempted,
depending on clinical circumstances and available expertise:
balloon tamponade
haemostatic brace suturing (such as using procedures described by B-Lynch or modified compression sutures)
bilateral ligation of uterine arteries
bilateral ligation of internal iliac (hypogastric) arteries
selective arterial embolisation.
It is recommended that a laminated diagram of the brace technique be kept in theatre. Resort to hysterectomy SOONER
RATHER THAN LATER (especially in cases of placenta accreta or uterine rupture). A second consultant clinician should be
involved in the decision for hysterectomy.
Secondary PPH is often associated with endometritis. When antibiotics are clinically indicated, a combination of ampicillin
(clindamycin if penicillin allergic) and metronidazole is appropriate. In cases of endomyometritis (tender uterus) or overt sepsis,
then the addition of gentamicin is recommended. Surgical measures should be undertaken if there is excessive or continuing
bleeding, irrespective of ultrasound findings. A senior obstetrician should be involved in decisions and performance of any
evacuation of retained products of conception as these women are carrying a high risk for uterine perforation.

No. 53 Female Genital Mutilation Management

Female genital mutilation is defined as all procedures involving partial or total removal of the external female genitalia or other
injury to the female genital organs, whether for cultural or other non-therapeutic reasons. The 1985 Act states that it is an
offence for any person: (a) to excise, infibulate or otherwise mutilate the whole or any part of the labia majora or clitoris of

39

another person; or (b) to aid, abet, counsel or procure the performance by another person of any of those acts on that other
persons own body.
I
II
III
IV

Partial or total removal of the clitoris and/or the prepuce (clitoridectomy)

Partial or total removal of the clitoris and the labia minora, with or without excision of the labia majora (excision)
Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or
the labia majora, with or without excision of the clitoris (infibulation)
All other harmful procedures to the female genitalia for non-medical purposes, e.g. pricking, piercing,a incising,
scraping and cauterising

Traditionally, female genital mutilation is practised mainly in Africa but it is also found, to a lesser extent, in India and Indonesia.
Urgent guidance should be sought from a child protection expert for children thought to be at risk of female genital mutilation.
Healthcare workers must not undertake or assist with female genital mutilation, even with the intention of lessening the medical
impact of the procedure. UK law Terminology used with individual women should be that which does not cause upset or a
sense of disapproval. Clinicians must be aware of the high complication rates related to female genital mutilation and these
should be taken into account when counselling about place of delivery and assessing the risk of the
pregnancy.
Females admitted acutely after female genital mutilation should be assessed quickly for signs of acute blood loss and sepsis,
offered analgesia and tetanus toxoid vaccination if this had not previously been administered. Consideration should be given to
antibiotic prophylaxis in the absence of overt sepsis. Consideration should be given to the need for urinary catherisation.
Healthcare workers should be familiar with the complications of female genital mutilation.
Acute complications of female genital mutilation include; death (including consequence of substandard anaesthesia); severe
pain; localised infection and abscess formation; septicaemia; tetanus; haemorrhage; acute retention of urine; hepatitis and HIV.
Gynaecologists and specialist nurses should be aware of the physical and psychological implications of female genital
mutilation. Healthcare workers should be aware the internal pelvic examination (including cervical cytology testing) might be
impossible without general anaesthesia.
Late gynaecological complications and consequences include: apareunia; superficial dyspareunia; sexual dysfunction with
anorgasmia; chronic pain; keloid scar formation; dysmenorrhoea (including haematocolpos); urinary outflow obstruction;
recurrent urinary tract infections; HIV and hepatitis infection; implantation dermoid cysts; vaginal lacerations during sexual
intercourse and rape; pelvic infection; post-traumatic stress disorder; difficulty passing urine and faeces (WHO 2008); labial
fusion (type II); repeated mutilation (type III) owing to unsuccessful healing; difficulty conceiving (failed intercourse, pelvic
infection and obstructed menstruation); difficulty in gynaecological examination; difficulty in cervical cytology screening;
difficulty of evacuation of the uterus following abortion. Fistulae are rare but can be the result of injury at the initial procedure,
following attempts at coitus, or defibulation and after vaginal birth. A casecontrol study suggests significantly higher
prevalence of post-traumatic stress disorder (30%) and other psychiatric syndromes (48%) than women who had not
undergone mutilation. Post-traumatic stress disorder was often accompanied by memory problems.
Potential maternal consequences of female genital mutilation include: fear of childbirth; increased likelihood of caesarean
section; increased likelihood of postpartum haemorrhage; increased likelihood of episiotomy; increased likelihood of severe
vaginal lacerations (including fistula formation); extended hospital stay; difficulty performing vaginal examinations in labour;
difficulty in applying fetal scalp electrodes; difficulty in performing fetal blood sampling; difficulty in catheterising of the bladder.
Hospitals with a high number of women with female genital mutilation should nominate a specialist midwife and an obstetrician.
They can also act as link persons for maternity units with fewer affected women. All maternity healthcare workers must be
familiar with the nature and higher rates of complications related to female genital mutilation and should take this into account
when offering advice about antenatal and delivery care, including recommendations about the place of birth.
Maternity units should adopt a process for questioning all women born in (or with recent ancestry of) those parts of the world
associated with female genital mutilation. This can be based on the family origin questioning (FOQ) used for
haemoglobinopathy screening. Discussions must take into account language difficulties, psychological vulnerability and cultural
differences. Healthcare workers should actively demonstrate knowledge and respect. The consultation should include a
psychological assessment and referral to a psychologist should be discussed with the woman. Physical examination by an
obstetrician or appropriately trained midwife or nurse should be strongly recommended to identify whether antenatal surgery
would be beneficial. Physical examination should also be recommended to reassess women who have had a previous
defibulation, as some may have undergone a further infibulation. A diagram or medical photography (with consent) can be used
to limit repetitive examinations, to aid explanations to the woman and to communicate with a hospital or clinic that has
developed expertise in the assessment and management of women with genital mutilation. A preformatted sheet, including a
predrawn diagram, should be considered for the identification of the type of genital mutilation, the need for antenatal
defibulation and for planning of intrapartum care.
Women should be recommended to undergo defibulation before conception, especially if difficult surgery is anticipated.
Gynaecology and maternity units with little experience of genital mutilation should consult with a centre that has developed
expertise in the assessment and management of affected women. It must be remembered that defibulation does not restore
physical or emotional normality. Urine should be screened for bacteriuria before surgery. Blood should be sent for group and
serum save because of the risk of haemorrhage. Defibulation may be carried out in any suitable outpatient room equipped for
minor procedures or in an operating theatre. Ideally, the surgeon or midwife should have personal experience of defibulation. In
emergency situations, senior obstetric help must be called. Before defibulation, identification of the urethra should be
attempted and a catheter passed. Incision should be made along the vulval excision scar. Cutting diathermy reduces the
amount of bleeding. The use of fine absorbable suture material such as polyglactin 910 (Vicryl Rapide, Ethicon) is
recommended. Prophylactic antibiotic therapy should be considered. Adequate pain relief is essential to limit the risk of further

40

psychological harm. The psychological needs of the woman should be taken into account when deciding the best form of pain
relief. Genital mutilation is not an absolute indication for caesarean birth unless the woman has such an extreme form of
mutilation with anatomical distortion that makes defibulation impossible. Decisions about delivery must take into account the
psychological needs of the woman. Episiotomy should be recommended if inelastic scar tissue appears to be preventing
progress but careful placement is essential to avoid severe trauma to surrounding tissues, including bowel. Women with
genital mutilation should usually be strongly recommended to deliver in a maternity unit with immediate access to facilities for
emergency obstetric care.
Women who have undergone successful defibulation and an uncomplicated vaginal birth (and no repeat procedure) can be
considered for birth in midwifery-led units. Intravenous access and group and save serum should be strongly recommended.
Epidural anaesthesia should be offered to women who find difficulty tolerating vaginal examination. Epidural anaesthesia
should be recommended if anterior episiotomy is needed in labour.

No. 54a The prevention of malaria in pregnancy

Malaria infection in pregnancy carries significant risks to mother and baby. Malaria infection in pregnancy may result in reduced
birth weight in the fetus and this may have health consequences in later life. Pregnant women should consider the risks of
travel to malaria endemic countries and consider postponing their trip, unless travel is unavoidable.
Inform women about bite prevention measures, including skin repellents, knock-down mosquito sprays, insecticide-treated bed
nets, clothing and room protection. Repellents the evidence favours skin repellents containing 50% DEET. Knock-down
mosquito sprays: permethrin and pyrethroids sprays kill resting and flying mosquitoes. Insecticide treated bed nets: long lasting
pyrethroid-impregnated bed nets offer significant protection. Clothing that covers the body and forms a barrier from biting
mosquitoes will reduce the risk of Malaria. Room protection: electrically heated mats will kill mosquitoes in the room. Inform
women (and their general practitioner) of the risks and benefits of chemoprophylaxis versus the risks of malaria. Remind
women that there is no malaria prophylaxis regimen that is 100% protective. Mefloquine (5mg/kg once a week) is the
recommended drug of choice for prophylaxis in the second and third trimesters for chloroquine-resistant areas. While
chloroquine and proguanil are safe, they are no longer efficacious in areas of chloroquine resistance and provide women with
suboptimal prophylaxis if recommended. With very few areas in the world free from chloroquine resistance, mefloquine is
essentially the only drug considered safe for prophylaxis in pregnant travellers. Recommendations for breastfeeding mothers
are the same as for pregnancy.

No.54b The diagnosis and treatment of malaria in pregnancy

Malaria is the most important parasitic infection in humans and is the tropical disease most commonly imported into the UK,
with approximately 1500 cases reported each year and rising, apart from 2008. Approximately 75% of cases are caused by
Plasmodium falciparum and there is an average of 515 deaths a year (mortality rate approximately 0.51.0%)
Malaria in pregnancy is detrimental to the woman and her fetus and collective data demonstrate that the risk of adverse effects
from untreated malaria in pregnancy outweigh those of treatment. The protozoan parasites P. falciparum, P. vivax, P. malariae
and P. ovale (extremely rarely P. knowlesi), are transmitted by the bite of a sporozoite-bearing female anopheline mosquito.
After a period of pre-erythrocytic development in the liver, the blood stage infection, which causes the disease, begins.
Parasitic invasion of the erythrocyte consumes haemoglobin and alters the red cell membrane. This allows P. falciparum
infected erythrocytes to cytoadhere (or stick) inside the small blood vessels of brain, kidneys and other affected organs.
Cytoadherence and rosetting (adherence of uninfected red blood cells) interfere with microcirculatory flow and metabolism of
vital organs. The hallmark of falciparum malaria in pregnancy is parasites sequestered in the placenta. Sequestered parasites
evade host defence mechanisms: splenic processing and filtration. Sequestration is not known to occur in the benign malarias
due to P. vivax, P. ovale and P. malariae. In pregnancy, the adverse effects of malaria infection result from:
the systemic infection, comparable to the effects of any severe febrile illness in pregnancy: maternal and fetal
mortality, miscarriage, stillbirth and premature birth
the parasitisation itself: fetal growth restriction and low birth weight, maternal and fetal anaemia, interaction with
HIV, susceptibility of the infant to malaria.
Pregnant women with 2% or more parasitised red blood cells are at higher risk of developing severe malaria and should be
treated with the severe malaria protocol. There are no specific symptoms or signs and malaria infection may present with a flulike illness. A history of travel to a malaria endemic area should be sought in a pregnant woman with pyrexia of
unknown origin.

Symptoms: Fever/chills/sweats, headache, muscle pain, nausea, vomiting, diarrhoea, cough, general malaise.

Signs: jaundiced, elevated temperature, perspiration, pallor, splenomegaly, respiratory distress

Microscopy and rapid diagnostic tests are the standard tools available. The diagnosis of malaria in pregnancy, as in nonpregnant patients, relies on microscopic examination (the current gold standard) of thick and thin blood films for parasites
(Appendix 2) or the use of rapid diagnostic tests which detect specific parasite antigen or enzyme. Rapid diagnostic tests are
less sensitive than malaria blood film. In a febrile patient, three negative malaria smears 1224 hours apart rules out the
diagnosis of malaria. Other important prognostic factors that should be reported on a peripheral blood smear result are: the

41

presence and count of mature trophozoites and schizonts of P. falciparum finding malaria pigment in more than 5% of the
polymorphonuclear leucocytes in the peripheral blood film. In severe malaria, particularly in pregnancy, fatality rates are high
(1520% in nonpregnant women compared with 50% in pregnancy).
Treat malaria in pregnancy as an emergency. Admit pregnant women with uncomplicated malaria to hospital and pregnant
women with severe and complicated malaria to an intensive care unit. Intravenous artesunate is the treatment of choice for
severe falciparum malaria. Use intravenous quinine if artesunate is not available. Use quinine and clindamycin to treat
uncomplicated P. falciparum (or mixed, such as P. falciparum and P. vivax). Use chloroquine to treat P. vivax, P. ovale or P.
malariae. Primaquine should not be used in pregnancy. Seek advice from infectious diseases specialists, especially for severe
and recurrent cases.
Do not persist with oral therapy if vomiting is persistent. Treat the fever with antipyretics. Screen women with malaria for
anaemia and treat appropriately. Write a management plan for follow-up, to ensure detection of relapse.
The 7-day course of quinine has significant adverse effects, principally cinchonism,19 which includes tinnitus, headache,
nausea, diarrhoea, altered auditory acuity and blurred vision. This can lead to non-compliance, which frequently leads to
failure.16,6366 For this reason, hospitalisation can be useful, as compliance with each dose of quinine and clindamycin can
be observed and this may lead to improved cure rates.
Malaria in pregnancy is unique and the ability of P. falciparum to sequester in the placenta challenges the normal way
antimalarial drug efficacy is assessed. Polymerase chain reaction (PCR)-confirmed prolonged submicroscopic carriage with
subsequent recurrence has been reported in pregnant women for months following drug treatment for uncomplicated P.
falciparum. Most recurrence is around day 2842 but latereported recurrence, so far unique to pregnancy, has been reported to
occur at 85 days with quinine, 98 days with artesunate, 63 days with artemether-lumefantrine and 121 days with mefloquine.
Weekly screening by blood film until delivery allows these women to be detected positive before becoming symptomatic.
Monitor for hypoglycaemia regularly, as it can be profound and persistent in malaria in pregnancy and can be exacerbated by
quinine. Prevent mortality from pulmonary oedema and acute respiratory distress syndrome by clinical assessment of jugular
venous or central venous pressure, aimed at keeping right arterial pressure less than 10 cm H2O.Women who are severely
anaemic should be transfused slowly, preferably with packed cells and intravenous frusemide 20 mg. Alternatively, exchange
transfusion may be considered in centres where this can be performed safely. Secondary bacterial infection should be
suspected if the patient becomes hypotensive.
Pulmonary oedema is a grave complication of severe malaria, with a high mortality of over 50%.In some women, acute
respiratory distress syndrome can occur in addition to the pulmonary oedema. Once this syndrome develops, the patient needs
fluid restriction. Severe anaemia is associated with maternal morbidity, an increased risk of postpartum haemorrhage and
perinatal mortality. Secondary bacterial infection, principally Gram-negative septicaemia, has been reported; the patient is
collapsed with a systolic blood pressure less than 80 mmHg in the supine position.
Preterm labour, fetal growth restriction and fetal heart rate abnormalities can occur in malaria in pregnancy. In severe malaria
complicated by fetal compromise, a multidisciplinary team approach (intensive care specialist, infectious disease specialist,
obstetrician, neonatologist) is required to plan optimal management of mother and baby. Stillbirth and premature delivery in
malaria in pregnancy are best prevented with prompt and effective antimalarial treatment. Uncomplicated malaria in pregnancy
is not a reason for induction of labour. Pharmacological thromboprophylaxis should be weighed up against the risk of
haemorrhage and should be withheld if the platelet count is falling or less than 100, indicating thrombocytopenia. Peripartum
malaria is an indication for placental histology and placenta, cord and baby blood films to detect congenital malaria at an early
stage. Inform women of the risk of vertical transmission and, in the presence of positive placental blood films, that fever in the
infant could indicate malaria; a blood film from the baby is required for confirmation.
Vertical transmission to the fetus can occur particularly when there is infection at the time of birth and the placenta and cord are
blood film positive for malaria (Appendix 2). All neonates whose mothers developed malaria in pregnancy should be screened
for malaria with standard microscopy of thick and thin blood films at birth and weekly blood films for 28 days.

CMACE/RCOG Joint Guideline: Management of Women with

Obesity in Pregnancy
Maternal obesity has become one of the most commonly occurring risk factors in obstetric practice. Obesity in pregnancy is
usually defined as a Body Mass Index (BMI) of 30 kg/m2 or more at the first antenatal consultation. There are three different
classes of obesity: BMI 30.034.9 (Class I); BMI 35.039.9 (Class 2); and BMI 40 and over (Class 3 or morbid obesity), which
recognise the continuous relationship between BMI and morbidity and mortality. The prevalence of obesity in pregnancy has
also been seen to increase, rising from 910% in the early 1990s to 1619% in the 2000s.
Obesity in pregnancy is associated with an increased risk of a number of serious adverse outcomes, including miscarriage,
fetal congenital anomaly, thromboembolism, gestational diabetes, pre-eclampsia, dysfunctional labour, postpartum
haemorrhage, wound infections, stillbirth and neonatal death. There is a higher caesarean section rate and lower
breastfeeding rate in this group of women compared to women with a healthy BMI. There is also evidence to suggest that
obesity may be a risk factor for maternal death: the Confidential Enquiry into Maternal and Child Healths report on maternal
deaths in the 20032005 triennium showed that 28% of mothers who died were obese, whereas the prevalence of obesity in
the general maternity population within the same time period was 16-19%.

42

Primary care services should ensure that all women of childbearing age have the opportunity to optimise their weight before
pregnancy. Advice on weight and lifestyle should be given during family planning consultations, and weight, body mass index
and waist circumference should be regularly monitored.
Women of childbearing age with a BMI 30 should receive information and advice about the risks of obesity during pregnancy
and childbirth, and be supported to lose weight before conception. Compared to women with a healthy pre-pregnancy weight,
pregnant women with obesity are at increased risk of miscarriage, gestational diabetes, pre-eclampsia, venous
thromboembolism, induced labour, caesarean section, anaesthetic complications and wound infections, and they are less likely
to initiate or maintain breastfeeding. Babies of obese mothers are at increased risk of stillbirth, congenital anomalies,
prematurity, macrosomia and neonatal death. Intrauterine exposure to maternal obesity is also associated with an increased
risk of developing obesity and metabolic disorders in childhood.
It is important that women are aware of the increased risk of maternal and fetal complications associated with obesity, and they
should be advised about the possible strategies to minimise them prior to conception. Interpregnancy weight reduction among
women with obesity has been shown to significantly reduce the risk of developing GDM.
Women with a BMI 30 wishing to become pregnant should be advised to take 5mg folic acid supplementation daily, starting at
least one month before conception and continuing during the first trimester of pregnancy.
Women with a raised BMI are at increased risk of NTD.
The findings from the studies above suggest that obese women should receive higher doses of folate supplementation in order
to minimise the increased risk of fetal NTDs. Health professionals should take particular care to check that women with a
booking BMI 30 are following advice to take 10micrograms Vitamin D supplementation daily during pregnancy and while
breastfeeding. The main source of vitamin D is synthesis on exposure of the skin to sunlight.
All pregnant women should have their weight and height measured using appropriate equipment, and their body mass index
calculated at the antenatal booking visit. Measurements should be recorded in the handheld notes and electronic patient
information system. All pregnant women with a booking BMI 30 should be provided with accurate and accessible information
about the risks associated with obesity in pregnancy and how they may be minimised. Women should be given the opportunity
to discuss this information.
Pregnant women with a booking BMI 40 should have an antenatal consultation with an obstetric anaesthetist, so that potential
difficulties with venous access, regional or general anaesthesia can be identified. An anaesthetic management plan for labour
and delivery should be discussed and documented in the medical records. Epidural re-site rates have been reported to
increase with increasing BMI,21 and the initial failure rate of epidural cannulation in parturients with morbid obesity has been
reported to be as high as 42% in one hospital. For these reasons, an early epidural may be advisable. It is recognised that
obesity may increase the risk of aspiration of gastric contents under general anaesthesia, difficult endotracheal intubation and
postoperative atelectasis. These women are also more likely to have co-morbidites such as hypertension and ischaemic heart
disease.
Women with a booking BMI 40 should have a documented assessment in the third trimester of pregnancy by an appropriately
qualified professional to determine manual handling requirements for childbirth and consider tissue viability issues.
Women with a booking BMI 30 should be assessed at their first antenatal visit and throughout pregnancy for the risk of
thromboembolism. Antenatal and post delivery thromboprophylaxis should be considered.
A woman with a BMI 30 who also has two or more additional risk factors for thromboembolism should be considered for
prophylactic low molecular weight heparin (LMWH) antenatally. This should begin as early in pregnancy as practical. All women
receiving LMWH antenatally should usually continue prophylactic doses of LMWH until six weeks postpartum, but a postnatal
risk assessment should be made. Women with a BMI 30 should be encouraged to mobilise as early as practicable following
childbirth to reduce the risk of thromboembolism.
All women with a BMI 40 should be offered postnatal thromboprophylaxis regardless of their mode of delivery.
Women with a BMI 30 who have one or more additional persisting risk factors for thromboembolism should also be considered
for LMWH for seven days after delivery. Women with a BMI 30 who have two or more additional persisting risk factors should
be given graduated compression stockings in addition to LMWH.
An appropriate size of arm cuff should be used for blood pressure measurements taken at the booking visit and all subsequent
antenatal consultations. The cuff size used should be documented in the medical records. Women with a booking BMI 35 with
no additional risk factor can have community monitoring for preeclampsia at a minimum of 3 weekly intervals between 24 and
32 weeks gestation, and 2 weekly intervals from 32 weeks to delivery.
All pregnant women with a booking BMI 30 should be screened for gestational diabetes. Maternal obesity is known to be an
important risk factor for GDM with a number of large cohort studies reporting a three-fold increased risk compared to women
with a healthy weight.
Observational studies have shown that there is a higher incidence of intrapartum complications among women with obesity
compared to women with a healthy weight. There is an increased risk of slow labour progression, shoulder dystocia and
emergency caesarean section. There is also an increased risk of primary postpartum haemorrhage. Caesarean section can be
more technically difficult in these women and there is a higher risk of anaesthetic complications compared to healthy-weight
women. Women with a booking BMI 30 should have an individualised decision for VBAC (vaginal birth after caesarean)
following informed discussion and consideration of all relevant clinical factors.
In the absence of other obstetric or medical indications, obesity alone is not an indication for induction of labour and a normal
birth should be encouraged. The duty anaesthetist covering labour ward should be informed when a woman with a BMI 40 is
admitted to the labour ward if delivery or operative intervention is anticipated. This communication should be documented by
the attending midwife in the notes.

43

Operating theatre staff should be alerted regarding any woman whose weight exceeds 120kg and who is due to have an
operative intervention in theatre. An operating table with the appropriate safe working load and appropriate lateral transfer
equipment should be available prior to the womans transfer to theatre. Women with a BMI 40 who are in established labour
should receive continuous midwifery care. Women with a BMI 40 should have venous access established early in labour. All
women with a BMI 30 should be recommended to have active management of the third stage of labour.
Women with a BMI 30 having a caesarean section have an increased risk of wound infection, and should receive prophylactic
antibiotics at the time of surgery. Women undergoing caesarean section who have more than 2cm subcutaneous fat, should
have suturing of the subcutaneous tissue space in order to reduce the risk of wound infection and wound separation
All women with a booking BMI 30 who have been diagnosed with gestational diabetes should have a test of glucose tolerance
approximately 6 weeks after giving birth. Women with a booking BMI 30 and gestational diabetes who have a normal test of
glucose tolerance following childbirth, should have regular follow up with the GP to screen for the development of type 2
diabetes. All women with a booking BMI 30 who have been diagnosed with gestational diabetes should have annual screening
for cardio-metabolic risk factors, and be offered lifestyle and weight management advice.

RCOG Statement No. 5 Alcohol consumption & the outcomes of pregnancy

This statement addresses issues relating to fertility, early fetal development, growth and maturation and long-term
neurodevelopmental and behavioural outcomes associated with alcohol intake in pregnancy. There is an increasing body of
evidence suggesting harm to the fetus from alcohol consumption during pregnancy. While the safest approach may be to avoid
any alcohol intake during pregnancy, it remains the case that there is no evidence of harm from low levels of alcohol
consumption, defined as no more than one or two units of alcohol once or twice a week.

Binge drinking in early pregnancy may be particularly harmful and specific advice to young men and women should make
this clear. Advice on the risk of harm to an unplanned pregnancy, as well as the risk of sexually transmitted disease,
should be widely available. Access to postcoital contraception and screening for sexually transmitted infection should be
made available to those whose behaviour has put them at risk.

In antenatal clinics, effort should be made to improve objective history taken about alcohol and other substance abuse, to
attempt to identify the high-risk group of women with problem drinking or other behaviour that can be harmful to the fetus.

Counselling and detoxification programmes should be made easily available to women.

Continuing efforts should be made to identify a biochemical test that could be applied to give an objective assessment of
chronic alcohol use in pregnant and nonpregnant women.

It is quite likely that many cases of fetal alcohol spectrum disorder (FASD) are being missed and training in the
recognition of this disorder and the availability of tertiary referral for confirmation of the diagnosis should be made more
widespread in the UK through community and hospital based paediatric clinics.
Alcohol consumption is usually reported in units: the amount of alcohol found in many standard drinks (one small glass of wine,
one measure of spirits, half pint of beer/lager) and is measured at 7.9 g or 10 ml of ethanol. International comparisons are
difficult because of different alcohol contents of units and uncertainties introduced by self-reporting of drinks. That most
women who are suffering from problem drinking have other behaviours (such as smoking, drug abuse, poor nutrition). Alcohol
may be exerting toxic effects throughout the reproductive process from infertility through miscarriage, aneuploidy, structural
congenital anomaly, disordered fetal growth, perinatal death, developmental delay and indeed susceptibility to disease in adult
life. Another effect of alcohol on reproductive health is the relationship between binge drinking and unprotected sexual activity.
Alcohol consumption is associated with an increased rate of miscarriage. In continuing pregnancies, major structural
malformations are seen about three times more commonly in women drinking more than 35 g a day compared with those
consuming less or none at all.
Diagnostic criteria for fetal alcohol syndrome (Stratton et al.): 1.) Confirmed maternal alcohol exposure. 2.) Evidence of a
characteristic pattern of facial anomalies that includes features such as short palpebral fissues and abnormalities in the
premaxillary zone (e.g. flat upper lip, flattened philtrum and flat midface). 3.) Evidence of growth restriction as in at least
one of the following: low birth weight for gestational age, decelerating weight over time not due to nutrition, disproportionally
low weight to height 4.) Evidence of central nervous system neurodevelopmental abnormalities, as in at least one of the
following: decreased cranial size at birth or structural brain abnormalities (e.g. microcephaly, partial or complete agenesis of
the corpus callosum, cerebellar hypoplasia) or neurological hard or soft signs) such as impaired fine motor skills,
neurosensory hearing loss, poor tandem gait, poor eyehand coordination. The consumption of alcohol offers no benefits in
relation to the outcomes of pregnancy. Under reporting of alcohol consumption is thought to be widespread, such that adverse
effects in the offspring may not always be recognised. It is important for GPs, obstetricians and midwives to devise ways of
identifying women who may suffer from problem drinking, during or before any pregnancy, at a time when potentially beneficial
interventions can be offered. On the other hand, there is considerable doubt as to whether infrequent and low levels of alcohol
consumption during pregnancy convey any long-term harm, in particular after the first trimester of pregnancy.

Cervical cancer

44

The TNM staging system for cervical cancer is analogous to the FIGO stage.
Stage 0
Stage I
limited to
the cervix
Stage
II
beyond
cervix
Stage III Stage IV

full-thickness involvement of the epithelium without invasion into the stroma (carcinoma in situ)
IA1 - stromal invasion less than 3 mm in depth and 7 mm or less in horizontal spread
IA2 - stromal invasion between 3 and 5 mm with horizontal spread of 7 mm or less
IB - visible lesion or a microscopic lesion with more than 5 mm of depth or horizontal spread of more than 7 mm
IB1 - visible lesion 4 cm or less in greatest dimension
IB2 - visible lesion more than 4 cm
IIA - without parametrial invasion, but involve upper 2/3 of vagina
IIB - with parametrial invasion
IIIA - involves lower third of vagina
IIIB - extends to pelvic wall and/or causes hydronephrosis or non-functioning kidney
IVA - invades mucosa of bladder or rectum and/or extends beyond true pelvis
IVB - distant metastasis

Microinvasive cancer (stage IA) is usually treated by hysterectomy (removal of the whole uterus including part of the vagina).
For stage IA2, the lymph nodes are removed as well. An alternative for patients who desire to remain fertile is a local surgical
procedure such as a loop electrical excision procedure (LEEP) or cone biopsy.[52]
If a cone biopsy does not produce clear margins,[53] one more possible treatment option for patients who want to preserve
their fertility is a trachelectomy.[54] This attempts to surgically remove the cancer while preserving the ovaries and uterus,
providing for a more conservative operation than a hysterectomy. It is a viable option for those in stage I cervical cancer which
has not spread; however, it is not yet considered a standard of care,[55] as few doctors are skilled in this procedure. Early
stages (IB1 and IIA less than 4 cm) can be treated with radical hysterectomy with removal of the lymph nodes or radiation
therapy. Radiation therapy is given as external beam radiotherapy to the pelvis and brachytherapy (internal radiation). Patients
treated with surgery who have high risk features found on pathologic examination are given radiation therapy with or without
chemotherapy in order to reduce the risk of relapse.
Larger early stage tumors (IB2 and IIA more than 4 cm) may be treated with radiation therapy and cisplatin-based
chemotherapy, hysterectomy (which then usually requires adjuvant radiation therapy), or cisplatin chemotherapy followed by
hysterectomy.
Advanced stage tumors (IIB-IVA) are treated with radiation therapy and cisplatin-based chemotherapy.
With treatment, 80 to 90% of women with stage I cancer and 50 to 65% of those with stage II cancer are alive 5 years after
diagnosis. Only 25 to 35% of women with stage III cancer and 15% or fewer of those with stage IV cancer are alive after 5
years

Endometrial cancer:

Risks: obesity, nulliparity, late menopause/ early menarche, prolonged irregular bleeding, PCOS, unopposed
oestrogen therapy or endogenous oestrogen from granulosa cell tumour, tamoxifen therapy, diabetes mellitus,
hypertension, personal are family history of breast cancer or colon cancer, high fat / low carbohydrate diet,
sedentary lifestyle.
Reduced rate associated with: COCP, physical exercise, smoking, late age at last birth. Diet high in fruit and
vegetables.
Incidence rises dramatically between the ages of 40 and 55 years and levels off after the menopause at about
44/100,000. Median age of presentation is 61 years. 73% 5 year survival. Endometroid adenocarcinoma is the
commonest histological type. Overall lifetime risk is 1.4%
81% of women have no lymph node involvement at diagnosis. In 9% there is pelvic node involvement, in 7%
pelvic and para-aortic node involvement, and in 3% para-aortic node involvement.
There is associated between the depth of myometrial invasion and the presence of nodal metastases.
In women with metastic disease, spread to the ovaries is common. Direct spread to the cervix.
Direct metastatic spread to the para-aortic nodes without pelvic node involvement occurs. Supra-clavicular
and inguinal are rarely involved.
The histopathology of endometrial cancers is highly diverse. The most common finding is a welldifferentiated endometrioid adenocarcinoma, which is composed of numerous, small, crowded glands with
varying degrees of nuclear atypia, mitotic activity, and stratification. This often appears on a background of
endometrial hyperplasia.

Endometrial cancer: FIGO

Stage 1
1a confined to the endometrium
1b <50% myometrial invasion
1c >50% myometrial invasion
Stage 2
IIa endocervical glandular involvement

80% present. 90% 5 year survival

10% present. 70% 5 year survival

45

IIb endocervical stromal involvement

IIIa invades serosa or adnexae or positive peritoneal cytology
6% present. 40% 5 year survival
IIIb vaginal metastasis
IIIc pelvic or para-aortic nodes
Stage 4
IVa invades bladder or bowl mucosa
2% present. 25% 5 year survival
IVb distant metastases inguinal nodes
If there is involvement of the endocervical stroma or glands BSO radical hysterectomy with bilateral salphingoophorectomy and pelvic lympadenopathy is the recommended operation. +/- omentectomy
Direct spread to the cervix. Direct spread to the para-aortic nodes without pelvic node involvement occurs. Supraclavicular and inguinal nodes are rarely involved. Often metastasis to ovaries.
Stage 3

Ovarian Cancer:

Risks include; early menarch, late menopause, nulliparity or having first pregnancy after 30 years. Family history is
associated with increased risk, ovarian, colorectal or breast. About 10% of ovarian cancers are hereditary, mainly
associated with BRCA 1 and 2 is increased with women with blood group A (low risk in group 0)
Most ovarian cancers develop after menopause; increased risk with obesity (50%), fertility drugs, personal history of
breast cancer.
Decreased risk associated with OCP use, TL, multiparity, breastfeeding, blood group O. prophylactic oophorectomy
reduces but does not eliminate the risk of ovarian cancer, primary peritoneal carcinomatosis may still occur.
Hysterectomy and ovarian conservation is associated with a reduction in ovarian cancer risk.
First degree cousin 3.6 fold risk, second-degree cousin 2.9 fold risk.

Endometrial cancer: FIGO

Stage 1
Ia one ovary, capsule intact, no ascites
Ib both ovaries, capsule intact, no ascites
Ic capsule breaches or ascites
Stage 2
IIa peritoneal deposits on uterus and tubes
IIb on other pelvic organs
IIIc with ascites
Stage 3
IIIA - microscopic peritoneal metastases beyond pelvis
IIIB - macroscopic peritoneal metastases beyond pelvis less
than 2 cm in size
IIIC - peritoneal metastases beyond pelvis > 2 cm or lymph
node metastases
Stage 4
IV distant or intrahepatic metastases

80% 5 year survival. Surgery

60% 5 year survival. Surgery and
chemotherapy
25% 5 year survival. Surgery and
chemotherapy

5-10% 5 year survival. Sugery for

palliation only then chemo

Yolk sac tumours secrete AFP

Granulosa cells secrete oestrogen (associated with precocious puberty and PMB)
Choriocarcinomas produce HCG
Struna ovarii produce thyroxine
CEA is elevated most often in mucinous cystadenocarcinomas, levels higher in poorly differentiated tumours.
The risk of ovarian cancer: nulliparous, early menarche, late menopause, first baby after 30. Family history is associated with
increased risk: ovarian cancer, breast cancer, or colorectal cancer. About 10% of ovarian cancers are hereditary, mainly
associated with BRCA 1 and BRCA 2. most ovarian cancers develop after menopause, obesity the risk is increased by 50%.
Personal history of breast cancer
Lynch type 1 syndrome: site-specific colorectal cancer
Lynch type II syndrome: autosomal dominant predisposition to colorectal cancer in addition to endometrial, ovarian, stomach,
pancreatic, renal tract and small bowel cancers. Prophylactic oophorectomy reduces but does not eliminate the risk of ovarian
cancer and primary peritoneal carcinomatosis may still occur.
A family history of ovarian cancer is not associated with an increased risk of developing ovarian cancer.
BRCA Genes:

BRCA1 germline mutations are thought to be responsible for 90% of hereditary ovarian cancer and 50% of
hereditary breast cancers. Carrier rate in the population is 1:800. Located on 17q21, a tumour suppressor gene. Males carriers
have a 30% life time risk of breast cancer.

BRCA2 gene is located on 13q12. Mutations are thought to be responsible for 40% of hereditary breast cancers and
5-10% of hereditary ovarian cancers. Carries a risk of breast cancer of 7% in males carriers.

Contraindications to COCP

46

Previous thrombosis, ischaemic heart disease, cardiomyopathies, active Kawasaki disease

BMI > 39, BP > 160/100; severe diabetes mellitus; focal migraine, thrombophilia,
4 weeks before major surgery, And 2 weeks post mobilisation
Active liver disease; undiagnosed genital tract bleeding; pregnancy Acute phorphoryia, SLE; uncorrected valvular heart disease
TIAs, cerebral haemorrhage, altitude > 4,500m Trophoblastic disease until HCG undectable hyperprolactinoma
Drugs that reduce efficacy of COCP: carbamazepine, phenytoin (not valproate), griseofulvin, Phenobarbital, primidone,
rifampicin (and rifabutin), modafinil so take additional contraception and upto 7 days after
Increased CA 125:
Malignant
Non-malignant

Ovarian cancer, liver cancer, lung cancer, breast cancer, colon cancer, pancreatic cancer, endometrial
cancer, cervical cancer
Endometriosis, PID, uterine fibroids, pregnancy, liver cirrhosis, tuberculous peritonitis, pelvic irradiation

Methyldopa side effects:

CVS bradycardia, exacerbations of anginam postural hypotension, oedema, myocarditis/ pericarditis.
CNS sedation, headache, nightmares, depression / mild psychosis, parkinsonism, Bells palsy.
Blood haemolytic anaemia (direct Commbe test is positive), bone marrow suppression

Causes of non-immune hydrops:

Idiopathic 30%, infections (parvovirus B19, syphilis, CMV, toxoplasmosis, herpes simplex, leptospirosis, Chagas disease),
anaemia (secondary to fetal infection, homozygous alpha-thalassaemia (not beta thalassaemia) chronic feto-maternal
haemorrhage, twin-twin transfusion.
.
Congenital
adrenal
hyperplasia:
Fetal hydantoin
syndrome
Fetal
warfarin
syndrome

raised ACTH, 17-hydroxprogesterone, progesterone, androstendione, testosterone ; salt losing syndrome

may be present due to aldosterone deficiency. Missing 21-hydroxylase deficiency. 17-hydroxprogesterone
and progesterone levels are increased and subsequently converted to androstendione and testosterone
with resulting masculinisation of the female fetus
result of phenytoin use: intrauterine growth restriction with microcephaly and develop minor dysmorphic
craniofacial features and limb defects including hypoplastic nails and distal phalanges. A smaller
population will have growth problems and developmental delay, or mental retardation. Rare side effects
include methemoglobinemia. Heart defects and cleft lip may also be featured.
Nasal hypoplasia, stippled epiphyses/ malformated vertebral bodies. Hydrocephalus, microcephaly, IUGR,
eye abnormalities and post-natal developmental delays

Cause of raise maternal AFP: wrong dates, multiple pregnancy, abdm=ominal wall defects, upper GI obstruction, congenital
nephrosis, placental/cord tumours, obstructive uropathy, feto-maternal haemorrhage, CAMLsacro-coccyteal teratoma, maternal
liver disease, smoking, afro0caribbean background
Drugs that cause exacerbation of muscle weakness in myasthenia gravis: magnesium salts, aminoglycosides, propanolol,
tetracycline, barbiturates, lithium salts, penicillamine, quinine, procainamide, halothane, polymxin B
Trisomy 18 early onset IUGR, rockerbottom feet, clench fist, overlapping fingers, choroid plexus cysts, 2 vessel cord,
increased NT, oligohydrmanious, polyhydramnious, renal/cardiac/CNS/ skeletal anomalies.
Tetralogy of Fallot: ventricular septal defect, right ventricular outflow obstruction, overriding aorta, right ventricular hypertrophy.
Thyroxine does not cross the placenta in significant amounts and does not cause fetal toxicity. Maternal thyroid-stimulating
antibodies in Graves disease cross the placenta and cause fetal thyrotoxicosis with heart failure and hydrops. Hypothyroidism
causes creatinism.

Oxybutynin

Uses
Anticholinergic, used in
urge incontinence

Clomiphene citrate

Ovulation induction agent

Nifedipine

Hypertension, PET

Side effects
Nausea, constipation, diarrhoea, dry mouth, blurred vision, voiding
difficulties and urinary retention, dizziness, restlessness, headache, rash,
dry skin, photosensitivity, arrhythmia, angioedema
Visual disturbance, OHSS, hot flushes, depression, insomnia,
convulsions, dizziness, breast tenderness, intermenstrual bleeding, hair
loss, vomiting abdominal discomfort.
Nausea, constipation, gum hyperplasia. Increase frequency, impotence,

47

Danazol (use for 6

months longest)
Gestrinone

Anti-oestrogen
and
progesterone
Endometriosis;
shrink
uterine fibroids and to
reduce menorrhagia

gynaecomastai, tachycardia, palpitations, dizziness, oedema, eye pain,

visual disturbance, paraesthesia, tremor
Androgenic side effects: weight gain 2-4kg, acne, hirsuitism, seborrhoea,
irritability, fatigue muscle pain, hot flushes, breast atrophy.

Parvovirus: rash does not occur until 17-18 days post infection and about 5 days after the disappearance of the virus from
serum and respiratory droplets. Patients presenting with symptoms are no longer infectious. IgG detected by the 7 day illness
and persists for life. IgM is detectable 3 days after the onset of symptoms and may persist for 6 months. If the first IgM is
negative repeat after 2-3 weeks. If maternal infection occurs screen with US for hydrops for up to 12 weeks.
VDRL/RPR (rapid plasma regain) cardiolipin tests). Positive in untreated secondary/latent/ tertiary syphilis, becomes negative
with treatment. Treponema antibody tests TPHA and FTA-ABS remain positive even with adequate treatment.
Indication for fetal echo:

Meigs syndrome: pelvic mass, ascites and right pleural effusion.

48