Renal disease in pregnancy

Note

Values considered normal when not pregnant may reflect decreased renal function in pregnancy. Creatinine >75mol/L and urea >4.5mmol/L merit further investigation. See p 15. Glycosuria in pregnancy may reflect altered renal physiology and not necessarily imply hyperglycaemia.

Treat asymptomatic bacteriuria in pregnancy. Check that infection and bacteriuria clear with treatment.

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Maternal mortality

Maternal mortality is defined in the UK as the death of a mother while pregnant or within 42 days of termination of pregnancy, from any cause related to or aggravated by the pregnancy or its management, but not from accidental or incidental causes (called coincidental deaths). Deaths are subdivided into those from direct causes those in which the cause of death is directly attributable to pregnancy (eg abortion, eclampsia, haemorrhage) and indirect deaths those resulting from previous existing disease or disease developed during pregnancy, and which were not due to direct obstetric causes but were aggravated by pregnancy (eg heart disease). Late deaths are those occurring between 42 days and 1 year after termination, miscarriage, or delivery that are due to direct or indirect maternal causes.

History

Since 1952 there have been 3-yearly confidential enquiries into maternal deaths. Prior to 1979, as many deaths were considered to have had avoidable factors (this term was used to denote departures from acceptable standards of care by individuals, including patients) but since 1979 the wider term of substandard care has been used to cover failures in clinical care and other factors, such as shortage of resources and back-up facilities.

Maternal mortality has almost halved every decade since reports have been issued (deaths per 100,000 maternities have been 67.1 in 1955-7, 33.3 in 1964-6, 11 in 1973-5, but 13.1 in 2000-2 of which direct deaths were 5.3 per 100,000).1 Rates are lowest for women aged 20-24 years rising markedly in the over-35s. Mortality was highest for first pregnancies. Risk of dying in pregnancy, childbirth or from abortion is 1:65 in developing countries (1:16 in some) as opposed to 1:9000 in the United Kingdom. Note: pregnancy is very protective as all-cause mortality in 15-45 year old women is 58.4:100,000/year (ie rates of death 4 × lower in pregnancy and 1y after).

In 2000-2, 391 UK deaths were recorded including 94 late deaths. Of these 106 were direct obstetric deaths; 155 were indirect and 36 were coincidental (in no way related to pregnancy, eg car accident). Death was increased in non-affluent areas (×1.45); in non-whites (×3 but ×7 if black African or asylum seeker); if both parents unemployed (×20) or single mother (×3) and in those booking late or missing 4 antenatal appointments. Of those dying 14% had reported domestic violence; 35% were obese; 8% were substance abusers.

In 2000-2 thromboembolism was the chief cause of direct death in the UK (28% of deaths). Other direct causes: early pregnancy (14.1%) (mainly ectopic pregnancy at 10.3%); hypertensive disorders (13.2%); genital tract sepsis (12%); amniotic fluid embolism (4.7%); haemorrhage (16.%); fatty liver of pregnancy (2.8%), anaesthetic deaths (5.6%). 33% died before delivery. When unreported deaths were also investigated, suicide was the commonest cause of (indirect) death overall; the mothers tending to be white, older, comfortably off, with other children, and dying by violent means.

The death rate from caesarean section for the 2000-2 period was 1 per 100 thousand operations. 4 direct deaths and 1 later were due to bowel perforation 3 due to Ogilvie's syndrome (pseudo-obstruction leading to perforation; not direct perforation), all in women who had had caesareans.

The maternal mortality rate was higher than in the previous triennium for direct deaths (5.3 vs 5:100,000), and again there were more indirect than direct deaths. Care was considered substandard in 67% of cases of direct death in 2000-2, in 47% this was major ie might have affected outcome. Substandardness includes pregnant women who refuse medical advice.

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Perinatal mortality

This is the number of stillbirths and deaths in the first week of life/1000 total births. Stillbirths only include those fetuses of >24 weeks' gestation, but if a fetus of <24 weeks' gestation is born and shows signs of life, and then dies, it is counted as a perinatal death in the UK (if dying within the first 7 days). Neonatal deaths are those infants dying up to and including the 28th day after birth. Other countries use different criteria including stillbirths from 20 weeks and neonatal deaths up to 28 days after birth, so it is not always easy to compare statistics.

Perinatal mortality is affected by many factors. Rates are high for small (61% of deaths are in babies <2500g) and preterm babies (70% of deaths occur in the 5% who are preterm). See p 50 & p 128. Regional variation in the UK is quite marked. There is a social class variation with rates being less for social classes 1 and 2 than for classes 4 and 5. Teenage mothers have higher rates than mothers aged 20 29. From 35yrs rates rise until they are 1.5-fold higher than the low-risk group (25 35 years) by the age of >40. Second babies have the lowest mortality rates. Mortality rates are doubled for fourth and fifth children, trebled by sixth and seventh (this effect is not independent of social class as more lower social class women have many children). Rates are lower for singleton births than for multiple. Rates are higher for the offspring of mothers of Pakistani (14.6:1000) and Caribbean (15.5:1000) extraction living in the UK, as opposed to those of UK extraction (7.8:1000).

Perinatal mortality rates in the UK have fallen over the years from rates of 62.5/1000 in 1930 5 to 8.3/1000 in the 2002 for England and Wales.67 Declining mortality reflects improvement in standards of living, improved maternal health, and declining parity, as well as improvements in medical care. The main causes of death were congenital abnormalities (21%), unclassified hypoxia (asphyxia) (18%) in 2002. Previously placental conditions (16%), birth problems including cord problems (11%), and maternal conditions (8%) have been other major causes.

Of neonatal deaths the main causes are prematurity (59%) and malformation (33%).

Examples of how changed medical care may reduce mortality:

• Worldwide, treatment of syphilis, antitetanus vaccination (of mother during pregnancy), and clean delivery (especially cord techniques), have the greatest influence in reducing perinatal mortality.
• Antenatal detection and termination of malformed fetuses.
• Reduction of mid-cavity procedures and vaginal breech delivery.
• Detection of placenta praevia antenatally.
• Prevention of rhesus incompatibility.
• Preventing progression of preterm labour.
• Better control of diabetes mellitus in affected mothers.
• Antenatal monitoring of at risk pregnancies.

While we must try to reduce morbidity and mortality still further, this must not blind us to other problems that remain, such as the overmedicalization of birth; the problem of reconciling maternal wishes to be in charge of her own delivery with the immediate needs of the baby; and the problem of explaining risks and benefits in terms that both parents understand, so that they can join in the decision-making process.

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Episiotomy and tears

Perineal tears

These are classified by the degree of damage caused. Tears are most likely to occur with big babies, precipitant labours, babies with poorly flexed heads, shoulder dystocia, when forceps are used, or if there is a narrow suprapubic arch. Perineal massage in pregnancy helps prevent perineal trauma but may be uncomfortable at first.

Labial tears

Common, these heal quickly and suturing is rarely helpful.

First degree tears

These tears are superficial and do not damage muscle. They may not need suturing unless blood loss is marked.

Second degree tears

These lacerations involve perineal muscle. They are repaired in a similar fashion to repair of episiotomy (see below).

Third degree tears

Damage involves the anal sphincter. If rectal mucosa is involved it is a fourth degree tear. See p 91. Repair by an experienced surgeon, under epidural or GA in theatre with intra-operative antibiotic cover. Rectal mucosa is repaired first using absorbable suture from above the tear's apex to the mucocutaneous junction. Muscle is interposed. Vaginal mucosa is then sutured. Severed ends of the anal sphincter are apposed using figure-of-eight stitches. Finally skin is repaired. Avoid constipation postoperatively by using a high-fibre diet and faecal softeners for 10 days.

Episiotomy

This is performed to enlarge the outlet, eg to hasten birth of a distressed baby, for instrumental or breech delivery, to protect a premature head, and to try to prevent tears (but anal tears are not reduced by more episiotomies in normal deliveries). Rates: 8% Holland, 12% England, 50% USA.

The tissues which are incised are vaginal epithelium, perineal skin, bulbo-cavernous muscle, superficial, and deep transverse perineal muscles. With large episiotomies, the external anal sphincter or levator ani may be partially cut, and ischiorectal fat exposed.1

Technique

Hold the perineal skin away from the presenting part of the fetus (2 fingers in vagina). Infiltrate area to be cut with local anaesthetic, eg 1% lidocaine (=lignocaine). Still keeping the fingers in the introitus, cut mediolaterally towards the ischial tuberosity, starting medially (6 o'clock), so avoiding the Bartholin's glands. (Midline episiotomy is ineffective at protecting perineum and sphincters and may impair anal continence).2

Repair

(See diagrams.) NB: use resorbable suture polyglactin 910 recommended.3 In lithotomy, and using good illumination, repair the vaginal mucosa first. Traditional method: start above the apex using interlocking stitches 1cm apart, 1cm from wound edges. Tie off at mucocutaneous junction of fourchette. Then repair muscles with interrupted stitches to obliterate any dead spaces. Finally close the skin (subcutaneous stitch is more comfortable than interrupted stitches). A loose continuous non-locking suturing technique to appose each layer is associated with less short-term pain compared with traditional interrupted method.

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Anaemia in pregnancy

Even a small PPH may become life-threatening if the mother is anaemic. Anaemia predisposes to infection, and makes heart failure worse. Worn-out, anaemic mothers may not cope with their offspring. Anaemia is the main cause of perinatal problems associated with malaria; above all, anaemia is a leading mechanism by which poverty exacts its morbid toll in pregnancy.

WHO definition of anaemia of pregnancy

Hb <11g/dL. By this standard 50% of women not on haematinics become anaemic. The fall in Hb is steepest around 20 weeks' gestation, and is physiological (p 6); indeed failure of Hb to fall below 10.5g/dL (but not further than ~9.5g/dL) indicates ↑risk of low birth weight or premature delivery.

Who is prone to anaemia?

Those who start pregnancy anaemic, eg from menorrhagia, hookworm, malaria, with haemoglobinopathies; those with frequent pregnancies, twin pregnancy, or a poor diet.

Antenatal screening

includes Hb estimation at booking, at 28 and 36 weeks. In black patients do sickle-cell tests, in others of foreign descent consider Hb electrophoresis for other haemoglobinopathies. From malarious areas consider malaria, and thick films. See p 27.

Treatment

Pregnancy increases iron needs by 700 1400mg (per pregnancy), provided for by a pregnancy-induced 9-fold increase in iron absorption. Iron and folate supplements (and prevention against hookworm and malaria) are recommended in many developing countries.13

Offer iron to those likely to be iron deficient (see above) or who would refuse transfusion if haemorrhaging (p 85). Parenteral iron may be given (to those with iron deficiency anaemia not tolerating oral iron) as iron dextran or iron sucrose. Beware anaphylaxis. Use only if cardiopulmonary rescuscitation facilities to hand. Hb rises over 6 weeks, so late severe anaemia (Hb <9g/dL) may need blood transfusion. One unit of blood increases the Hb by ~0.7g/dL.

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Tests to detect Down's syndrome

The first antenatal diagnosis of Down's syndrome was made in 1968. Initially there was amniocentesis for older mothers (Penrose noted association with maternal age in 1933; rates of Down's are 1:1500 babies if mother aged 20, 1:800 if aged 30, 1:270 if aged 35, 1:100 if aged 40, 1:50 if aged 45 or older.) Then screening by blood test was introduced, and nuchal screening (p 11). By 2007 the UK plans nationwide screening with tests giving detection rates of 75% with a false positive rate of <3% (and aims for 60% detection with <5% false positive from 2005). Tests aim to estimate the risk of Down's taking into consideration information from nuchal scanning, blood tests and the woman's age. Where risk of Down's is >1:250 (high risk-estimated to be 5% of pregnancies) she will be offered further tests such a chorionic villus sampling (p 46) and amniocentesis (p 10). Early ultrasound is vital for dating pregnancies for these tests.

The combined test

This combines nuchal translucency (NT)+ free Î-human chorionic gonadotrophin (ÎHCG) + pregnancy associated plasma protein PrAP-A + the woman's age. Used between 10 weeks 3 days and 13 weeks 6 days. It can achieve detection rates of 95% of all aneuploides, 86% trisomy-21, and 100% of trisomy-18 and trisomy-13. In one study (n=4190), 97.6% took up screening; false positive screening occurred in 6.7%: 7 cases had neural tube defects, and 2 ventral wall defects were picked up on scan. 200 accepted chorionic villus sampling: there was fetal demise in 2 in next 28 days 1 of which had Down's.1

The integrated test

This is better than the combined test if there are good facilities for nuchal translucency measurements available and the woman is prepared to wait for 2nd trimester results. It involves NT+ PrAP-A in the first trimester + the quadruple test in the 2nd trimester.

The quadruple test

This combines maternal α-fetoprotein (AFP) + unconjugated estriol + free ÎHCG or total ÎHCG + inhibin-A + the woman's age in the second trimester. This test is useful for women presenting in the second trimester.

The emotional cost to the mother is impossible to calculate

From the parents' point of view, a telling statistic is that 56 out of every 57 women under 37yrs old who had a +ve test, proved, after amniocentesis, not to have an affected fetus. Amniocentesis causes fetal loss, and these losses will usually be of normal babies. New screening regimens in the 1st trimester go some way to mitigating distress and anxiety.

We have no idea of the best way of counselling parents before the test. If you just hand out a leaflet, few will read it, and then when it comes to amniocentesis and termination, many will refuse”and the screening test wastes money, as well as laying health authorities open to litigation: I never understood that I might lose a normal baby The alternative is to provide full details at the time of the initial blood test. The irony is that gaining informed consent is then the most expensive part of the test, and one which itself could cause much distress. Imagine an overjoyed expectant mother arriving in the clinic serenely happy in fulfilling her reproductive potential: the quintessence of health. She leaves only after being handed ethical conundrums of quite staggering proportions, involving death, disease, and human sacrifices, and a timetable for their resolution that would leave even the most fast-moving philosopher breathless and disorientated, and which may leave her forever bereft of one of Nature's most generous gifts: the fundamental belief in one's own wholeness.

Preimplantation genetic diagnosis1

Preimplantation genetic diagnosis (PGD) is an early form of prenatal diagnosis in which embryos created in vitro are analysed for well-defined genetic defects. Defect free embryos are then used for implantation.

It is used in those with high risk of genetic disease eg carriers of monogenic disease or chromosome structural abnormalities (eg translocations) who have repeatedly terminated pregnancies due to prenatal tests showing abnormality, who have concurrent infertility, who have had recurrent miscarriage (as occurs with translocation carriers), and for those with moral or religious objections to termination.

It may also be used to screen for aneuploidy (PDG-AS) in those undergoing in vitro fertilization to enhance chance of ongoing pregnancy (sometimes the case for women >37“40 years old).

Pioneered in the early 1990s, by mid 2001, 3000 PGD cycles had been performed resulting in 700 pregnancies (pregnancy rate 24%), of which 5% of babies had some kind of abnormality. PGD selection of embryos by HLA type so that a child born after using this technology can be used as a stem cell donor to save a sibling from certain conditions is controversial but possible.

Genetic analysis at the single cell level occurs using 1st polar body of an egg, or 2nd polar body (extruded after fertilization and completion of second meiotic division), or using blastomeres from cleavage-stage embryos. The blastocyst is the latest stage from which cells can be used but is little used as it leaves little time for analysis as embryos must be transferred before day 5 or 6. Biopsied surplus embryos can be cryopreserved but implantation rate for these is only 12%.

Fluorescence in situ hybridisation (FISH) is used for analysis of chromosomes and polymerase chain reaction (PCR) for analysis of genes in monogenic diseases. PGD can currently be applied for detecting 33 monogenic diseases. Gene analysis for X-linked conditions has the advantage that healthy male embryos and non-carrier female embryos can be transferred. Sexing embryos for X-linked conditions remains useful for conditions where the single gene is not known (eg non-fragile-X X-linked mental retardation), has been judged too difficult a search, and for women eg over 37 who do not wish to wait for specific tests to be developed.

Pregnancy rates are 17% after testing for structural chromosome abnormality (including translocations), 16% after sexing, 21% after testing for monogenic diseases. This is lower than the expected rate of 20“25% expected for regular IVF. For PGD-AS 25% pregnancy rates are achieved overall for women of previously poor prognosis due to advanced maternal age, repeated IVF failure (but only 8% do get pregnant) and recurrent miscarriage (28% pregnancy rate achieved).

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HIV in pregnancy and labour

Many babies are not infected in utero but become so during parturition. Most mothers at risk of passing on HIV to the next generation (vertical transmission) do not want to know their HIV status, or cannot afford to find out. (If their husband is uninfected, what is the chance of him remaining loyal?) In our section on perinatal HIV (p 34) we comment that anti-retrovirals and caesarean section can prevent vertical transmission but this is not much help if the nearest hospital is 3h away by wheelbarrow, and has only basic drugs. What is needed is much more cost-effective advice.

• Only give blood transfusions if absolutely necessary.
• Avoid any procedure likely to lead to maternal cells contacting fetal blood eg external cephalic version, and amniocentesis.
• In instrumental deliveries, try to avoid abrasions of the fetal skin. Vacuum extractors may be preferable to forceps.
• When you clamp the cord, ensure there is no maternal blood on it.
• Artificial rupture of membranes and episiotomies should be left to the last possible moment, or avoided altogether.
• Avoid fetal scalp electrodes, and doing fetal scalp blood samples.
• If the membranes have ruptured, avoid long labours transmission risk doubles after ruptured for 4h and increases by 2%/h thereafter up to 24h.MET14
• During caesarean sections, open the last layer by blunt dissection, to avoid minor cuts to the baby from the scalpel.
• Rinse the baby after birth; wipe the face away from mouth, eyes, and nostrils.
• Unless there is apnoea, avoid suction catheters to aspirate mucus from the nostrils. The baby's face is likely to be covered with the mother's blood at this stage, and you do not want to force HIV into nostrils.
• Health programmes are likely to end up encouraging breast feeding if there is no satisfactory alternative. Humanized milk is expensive, and may indicate to the mother's neighbours that she is HIV+ve. Using humanized milk might also compound problems by removing the one free method of contraception: lactational amenorrhoea. But studies from Nairobi showed 70% formula fed babies alive and disease-free at 2yrs vs 58% if breast fed. Most transmission occurred in the first 6 months. These babies had access to the city water supply.RCT15 Breast milk transmission was 16%. Also HIV+ve mothers in developing countries who breast feed may die sooner.
• Offer advice on avoiding future pregnancies. This is not an easy area. Encouraging the use of condoms is fine, but many will want the added protection of the Pill. IUCDs promote bleeding, and may increase spread to men. This may also be a problem with the progestogen-only Pill, but note that the latter may cause less ectropion than the combined Pill, and this might be advantageous. Sterilization is the hardest choice, especially when the mother now has no living children because of HIV.

Traditionally, drug therapy for HIV in pregnant patients consisted of mono-therapy with zidovudine in contrast to non-pregnant women treated with combination therapy. Combination therapies are recommended in pregnancy.1 Antiretrovirals are becoming more available in many developing countries but there is a long way to go before all infected mothers will have access to them. Get expert advice.

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Normal labour

is that occurring after 37 weeks' gestation. It should result in the spontaneous vaginal delivery of the baby within 24h of the onset of regular spontaneous contractions. It is often heralded by ashow, ie a plug of cervical mucus and a little blood as the membranes strip from the os. The membranes may then rupture.

The first stage of labour

is the time from the onset of regular contractions until the cervix is fully dilated (no cervix felt around the head). The cervix initially effaces (becomes shorter and softer) before it dilates. A satisfactory rate of dilatation from 3cm dilated is 1cm/h. The first stage generally takes up to 12h in a primip, and 7.5h in a multip. During the first stage check maternal pulse, BP, and T° half-hourly; assess the contractions every 15min, their strength (you should not be able to indent the uterus with the fingers during a contraction) and their frequency (ideally 3-4 per 10min, lasting up to 1min). Carry out vaginal examination eg every 4h to assess the degree of cervical dilatation, the position and the station of the head (measured in cm above the ischial spines) and note the degree of moulding (p 42). Note the state of the liquor (see p 72). Test maternal urine 4-hourly for ketones and protein. If the mother becomes ketotic set up an IVI and give her 10% dextrose.1 Measure the fetal heart rate (if not being continuously monitored) every 15min. Note the rate before, during, and immediately after a contraction.

The second stage

is the time from complete cervical dilatation until the baby is born.

The mother has an urge to push and uses abdominal muscles and the Valsalva manoeuvre to help move the baby. As the head descends, the perineum stretches and the anus gapes. Normal time for second stage is 45-120min in a primip, and 15-45min in a multip. Prevent a precipitate delivery (and so intracranial bleeding) by pressure over the perineum.

Delay in clamping the cord for 30sec and holding the baby 20cm below the introitus results in higher haematocrit levels, so reducing transfusion and oxygen supplement requirements in premature babies.

The third stage

is delivery of the placenta. As the uterus contracts to a <24-week size after the baby is born, the placenta separates from the uterus through the spongy layer of the decidua basalis. It then buckles and a small amount of retroplacental haemorrhage aids its removal.

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Multiple pregnancy

Features

Early pregnancy: uterus too large for dates; hyperemesis. Later there may be polyhydramnios. The signs are that >2 poles may be felt; there is a multiplicity of fetal parts; 2 fetal heart rates may be heard (reliable if heart rates differ by >10 beats/min). Ultrasound confirms diagnosis (and at 10-14 weeks, can distinguish monochorionic from dichorionic twins).1

Complications during pregnancy

Polyhydramnios; pre-eclampsia is more common (10% in singleton pregnancies; 30% in twins); anaemia is more common (iron and folate requirements are increased). There is an increased incidence of APH (6% for twins, vs 4.7% for singletons) due to both abruption and placenta praevia (large placenta).

Fetal complications

Perinatal mortality for twins is 36.7/1000 (8/1000 if single; 73/1000 for triplets; and 204 for higher multiples). The main problem is prematurity. Mean gestation for twins is 37 weeks, for triplets 33 weeks. Growth restricted babies (p 52) are more common (growth the same as singletons up to 24 weeks but may be slower thereafter). Malformation rates are increased 2-4 times, especially in monozygotic twins. Severe disability rate 1.5% for singletons, 3.4% for twins. Ultrasound is the main diagnostic test. Selective fetocide (eg with intracardiac potassium chloride) is best used before 20 weeks if indicated. With monozygotic twins, intermingling blood supply may result in disparate twin size and one being born plethoric (hence jaundiced later), the other anaemic. If one fetus dies in utero it may become a fetus papyraceous which may be aborted later or delivered prematurely.

Complications of labour

PPH is more common (4-6% in singletons, 10% in twins). Malpresentation is common (cephalic/cephalic 40%, cephalic/breech 40%, breech/breech 10%, cephalic/transverse (Tv) 5%, breech/Tv 4%, Tv/Tv 1%). Rupturing of vasa praevia, increased rates of cord prolapse (0.6% singleton, 2.3% twins), premature separation of the placenta and cord entanglement (especially monozygous) may all present difficulties at labour. Despite modern technology some twins remain undiagnosed, staff are unprepared, and syntometrine may be used inappropriately, so delaying delivery of the second twin. Epidural anaesthesia is helpful for versions.

Management

• Ensure adequate rest (need not entail admission).
• Use ultrasound for diagnosis and monthly checks on fetal growth.
• Give additional iron and folate to the mother during pregnancy.
• More antenatal visits, eg weekly from 30 weeks (risk of eclampsia↑).
• Tell the mother how to identify preterm labour, and what to do.
• Consider induction at 40 weeks. Have an IVI running in labour and an anaesthetist available at delivery. Paediatricians (preferably one for each baby) should be present at delivery for resuscitation should this be necessary (second twins have a higher risk of asphyxia).

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Minor symptoms of pregnancy

Symptoms and signs in the first 10 weeks

Early symptoms are amenorrhoea, nausea, vomiting, and bladder irritability. Breasts engorge, nipples enlarge (darken at 12 weeks), Montgomery's tubercles (sebaceous glands on nipples) become prominent. Vulval vascularity increases and the cervix softens and looks bluish (4 weeks). At 6 10 weeks the uterine body is more globular. Temperature rises (<37.8 °C).

Headaches, palpitations, and fainting are all commoner in pregnancy. Sweating and feeling hot are also common, due to a dilated peripheral circulation. Management: Increase fluid intake and take showers.

Urinary frequency is due to pressure of the fetal head on the bladder in later pregnancy. Exclude UTI.

Abdominal pain

Breathlessness is common.

Constipation tends to occur as gut motility decreases. Adequate oral fluids and a high fibre diet help combat it. Avoid stimulant laxatives they increase uterine activity in some women. Increased venous distensibility and pelvic congestion predispose to haemorrhoids (if they prolapse, rest the mother head down, apply ice packs and replace them), and varicose veins. Resting with feet up, and properly worn elastic stockings help.

Reflux oesophagitis and heartburn occur as pyloric sphincter relaxation allows irritant bile to reflux into the stomach. Cigarettes and spices should be avoided, small meals taken, and antacids may be used. Use more pillows, and a semi-recumbent position.

Third trimester backache

Due to pelvic ligament and muscle relaxation, pain tends to be worse at night. A firm mattress, flat shoes, standing with back straight, and pelvic support from physiotherapy all help.

Carpal tunnel syndrome (p 714) in pregnancy is due to fluid retention. Advise wrist splints until delivery cures the problem.

Itch/itchy rashes are common (up to 25%) and may be due to the usual causes (OHCM p 76, check LFT see p 26) or to pruritic eruption of pregnancy (PEP = prurigo of pregnancy) an intensely itchy papular/plaque rash on the abdomen and limbs. PEP is most common in first pregnancies beyond 35 weeks' gestation. Emollients and weak topical steroids ease it. Delivery cures it. If vesicles are present, think of pemphigoid gestationis (PG): a rare (1:50,000) condition which may cause fatal heat loss and cardiac failure; the baby may be briefly affected; refer early (prednisolone may be needed). PG may recur in later pregnancies.

Ankle oedema

This is very common, almost normal manifestation of pregnancy. Measure BP and check urine for protein (pre-eclampsia, p 48). Check legs for DVT. It often responds to rest and leg elevation. Reassure that it is harmless (unless pre-eclampsia).

Leg cramps 33% get cramp, the latter half of pregnancy, severe in 5%, often worse at night. Raising the foot of the bed by 20cm will help.

Chloasma

This is a patch of darker pigmentation.
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Epilepsy in pregnancy

Epilepsy de novo is rare in pregnancy. Epilepsy affects ~0.5% of women of child-bearing age so a unit with 3000 deliveries per year has ~15 pregnant epileptic women at any one time. Seizure rates worsen in most women having >1 seizure/month. Sleep deprivation in the last month of pregnancy may contribute to seizures. It is unusual for seizures to recur in pregnancy when preceded by a long seizure-free period.

Complications

Maternal

Risk of 3rd trimester vaginal bleeding. 1% convulse in labour.

Fetal:

• Haemorrhagic disease of newborn can occur with enzyme inducers (below).
• Congenital malformation (UK register suggests 5.9% affected with sodium valproate, 2.3% with carbamazepine, 2.1% with lamotrigine). Malformation is commoner if 2 anticonvulsants are used and with higher doses.

Fetal valproate syndrome

Signs: major organ system anomalies ± autism ± small ears, small broad nose, a long upper lip, shallow philtrum & micro/retrognathia.1

Cleft lip

Associated with maternal epilepsy only, the relative risk for a fetus having clefts compared to the non-epileptic population is 1.0 if the mother develops epilepsy after the pregnancy; 2.4 if she develops it after conception (but has no drugs); 4.7 if fetus is exposed to anticonvulsants. Phenytoin and phenobarbital cause clefts and congenital heart disease. Neural tube defects are commoner with valproate (& carbamazepine) so screen for these (p 10). Neurodevelopmental delay is seen with valproate, seen as lower verbal intelligence quotient (also seen in the offspring of those having frequent tonic clonic seizures in pregnancy.2

Management

Get expert help (refer to epilepsy specialist to optimize and monitor medication: only make antiepileptic changes on expert advice). Avoid trimethadione and paramethadione (both very teratogenic). Where anticonvulsants are needed keep the dose of the chosen drug as low as possible. Aim for 1 drug only. Give folic acid supplements, eg 5mg/24h PO from prior to conception. Give vitamin K1 20mg/24h PO to the mother from 36 weeks if she is taking enzyme inducers ie carbamazepine, ethosuximide, phenytoin, primidone, phenobarbitone (oxcarbazine and topiramate are subjects of debate).3 Screen for neural tube defects and heart disease if relevant (above). Treat status epilepticus as in the non-pregnant but monitor the fetus. It is associated with significant fetal and maternal mortality. Deliver in hospital with resuscitation facilities (1-2% epileptic women convulse in labour and the subsequent 48 hours)-and avoid early discharge. Give baby vitamin K 1mg IM at birth. If seizures are likely, to avoid dropping the baby during a seizure, advise changing the baby on mat on floor, and feeding sitting on floor supported by cushions, and only bath the baby with supervision. Mothers may breast feed (phenobarbital can cause drowsiness in the baby). Ask for review of epilepsy drugs postnatally eg at 12 weeks.

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The placenta

The placenta is the organ of respiration, nutrition, and excretion for the fetus. It produces hormones for maternal wellbeing and immunologically protects the fetus by preventing rejection and allowing the passage of IgG antibodies from the mother.

Development

At term the placenta weighs 1/7th the weight of the baby. It has a blood flow of 600mL/min. The placenta changes throughout pregnancy as calcium is deposited in the villi and fibrin on them. Excess fibrin may be deposited in diabetes and rhesus disease, so fetal nutrition.

Placental types

Battledore insertion is where the umbilical cord inserts into the side of the placenta. Velamentous insertion (1%) is where the umbilical vessels pass within the membranes before insertion. If these vessels break (as in vasa praevia) it is fetal blood that is lost. Placenta succenturia: (5%) There is a separate (succenturiate) lobe away from the main placenta which may fail to separate normally and cause a PPH or puerperal sepsis. Placenta membranacea (1/3000) is a thin placenta all around the baby. As some is in the lower segment it predisposes to APH. It may fail to separate in the third stage of labour. Placenta accreta: There is abnormal adherence of all or part of the placenta to the uterus, termed placenta increta where there is placental infiltration of the myometrium or placenta percreta if penetration reaches the serosa. These latter 3 types predispose to PPH and may necessitate hysterectomy.

Placenta praevia

The placenta lies in the lower uterine segment. It is found in ~0.5% of pregnancies. Risks are of significant haemorrhage by mother and fetus. Associations: Large placenta (eg twins); uterine abnormalities and fibroids; uterine damage, eg multiparity; former surgery (caesarean section, myomectomy); past infection. Ultrasound at <24 weeks' gestation shows a low-lying placenta in 28% but lower segment development later in pregnancy results in only 3% being low-lying at term. Transvaginal ultrasound is superior to transabdominal for localizing placentas accurately, and, if combined with Doppler, diagnose vasa praevia and placenta accreta. It has not been shown to increase bleeding.

Major (old III and IV degrees) with placenta covering the internal os requires caesarean section for delivery. Minor (old I and II) where the placenta is in the lower segment but not across the internal os: aim for normal delivery unless the placenta encroaches within 2cm of the internal os when vaginal delivery is contraindicated.1 Presentation may be as APH (separation of the placenta as the lower segment stretches causes bleeding) or as failure for the head to engage ie a high presenting part. Problems are with bleeding and with mode of delivery as the placenta obstructs the os and may shear off during labour, or may be accreta (5%), especially after previous caesarean section (>24%). Poor lower segment contractility predisposes to postpartum haemorrhage. Caesarean section should be consultant-performed or supervised with consultant anaesthetic attendance. The rule of admitting those with major placenta praevia at ≤35 weeks' gestation so that immediate help is available, is controversial, and not practiced by many UK units.2 Hospitalization is preferable if there is bleeding.3

After delivery Examine the placenta for abnormalities (clots, infarcts, amnion nodosum, vasa praevia, single umbilical artery). Weigh the placenta (weight >25% of the baby suggests congenital nephrotic syndrome). Blood may be taken from the cord for Hb, Coombs test, LFTs, and blood group (eg for rhesus disease), or for infection screens, if needed.

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Forceps

Forceps are designed with a cephalic curve, which fits around the fetal head, and a pelvic curve which fits the pelvis. Short-shanked (eg Wrigley's) forceps are used for lift out deliveries, when the head is on the perineum; long-shanked (eg Neville Barnes) for higher deliveries, when the sagittal suture lies in the AP diameter. Kielland's forceps have a reduced pelvic curve, making them suitable for rotation (only in experienced hands).

Conditions of use

The head must be engaged; the membranes ruptured; the position of the head known and the presentation suitable, ie vertex or face (mentoanterior); there must not be cephalo pelvic disproportion (moulding not excessive); the cervix must be fully dilated and the uterus contracting, and analgesia adequate (perineal infiltration for the episiotomy; pudendal blocks may be sufficient for mid-cavity forceps and ventouse deliveries but not for Kielland's). The bladder must be empty.

Indications for use

Forceps may be used when there is delay in the second stage: this is frequently due to failure of maternal effort (uterine inertia or just tiredness), epidural analgesia, or malpositions of the fetal head. They may be used when there is fetal distress or a prolapsed cord, or eclampsia— all occurring only in the second stage. They are also used to prevent undue maternal effort, eg in cardiac disease, respiratory disease, pre-eclampsia. They are used for the after-coming head in breech deliveries.

Technique

Learn from demonstration. The following is an aide-m moire for non-rotational forceps. Place the mother in lithotomy position with her bottom just over the edge of the delivery bed. Use sterilizing fluid to clean the vulva and perineum; catheterize; check the position of the head. Insert pudendal block and infiltrate the site of the episiotomy (not necessary if she has an epidural). Assemble the blades to check they fit, with the pelvic curve pointing upwards. The handle which lies in the left hand is the left blade and is inserted first (to the mother's left side) and then the right: the handles should lock easily. Traction must not be excessive (the end of bed is not for extra leverage!). Synchronize traction with contractions, guiding the head downwards initially. Do a large episiotomy when the head is at the vulva. Change the direction of traction to up and out as the head passes out of the vulva. If baby needs resuscitation, give to paediatrician. Give vitamin K (p 120). Is thromboprophylaxis needed? See p 16.

Forceps complications

Maternal: Trauma (commoner than with ventouse). Fetal: facial bruising, VII paralysis (usually resolves); brachial plexus injury.

Ventouse

The ventouse, or vacuum extractor, associated with less maternal trauma than forceps is preferred worldwide, but not in the UK. It may be used in preference to rotational forceps because, as traction is applied, with the cup over the posterior fontanelle, rotation during delivery will occur. It can be used through a partially dilated cervix (primips should be almost fully dilated, multips >6cm), but should not be used if the head is above the ischial spines. It is contraindicated for face presentations and for premature babies. A cup is applied with a suction force of 0.8kg/cm2. The baby's scalp is sucked up to form a chignon, which resolves in 2 days. There is increased rate of fetal cephalhaematoma (p 90) and neonatal jaundice so give vitamin K (p 120). Maternal trauma still occurs in ~11%.

If ventouse, low forceps, or mid forceps are needed for 1st delivery, spontaneous rates for 2nd delivery are 91%, 88%, 82% respectively in the absence of induction or augmentation.60 Women having vaginal delivery are more satisfied with the birth, less anxious about the baby, and more likely to breast feed. Only about a third will have vaginal delivery after previous Caesarean Section.

Indications for forceps delivery1

Relative indications (ventouse or Caesarean an alternative)

• Delay or maternal exhaustion in second stage.
• Dense epidural block with diminished urge to push.
• Rotational instrumental delivery for malposition of head.
• Suspected fetal distress.

Specific indications for forceps (forceps delivery is usually superior to ventouse or Caesarean in these circumstances)

• Assisted breech delivery, forceps to deliver head.
• Assisted delivery of preterm infant <34 weeks gestation.
• Controlled delivery of head at Caesarean section.
• Assisted delivery with face presentation.
• Assisted delivery with suspected coagulopathy or thrombocytopenia in fetus.
• Instrumental delivery where maternal condition precludes pushing (eg cardiac disease, respiratory disease).
• Cord prolapse in second stage of labour.
• Instrumental delivery under GA.

1 R Patel 2004 BMJ 328 1303

Obstetric brachial plexus palsy (OBPI)

OBPI complicates <0.5% of live births.

Risk factors

Large birth weight; shoulder dystocia with prolonged 2nd stage of labour; forceps delivery; vacuum extraction; diabetes mellitus; breech presentation. Formerly, the cause of OBPI was excessive lateral traction applied to the fetal head at delivery, in association with anterior shoulder dystocia.

Instrumental-associated OBPI may arise because of nerve stretch injuries after rotations of >90° or from direct compression of the forceps blade in the fetal neck.61 Not all cases of brachial plexus palsy are attributable to traction. Intrauterine factors may play some role.62

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Dystocia

Dystocia is difficulty in labour. There may be problems with the passenger (large baby, see impacted shoulders = shoulder dystocia p 72, or an abnormal presentation), the passages (for ideal pelvis, see p 42 note that cervical dystocia may be a problem after biopsy of the cervix, or a consequence of female genital mutilation p 246) or of propulsion (the uterine powers). Cephalopelvic disproportion results if diameters are unfavourable (p 42).

The pelvis

The ideal pelvis has a round brim (ie gynaecoid), but 15% of women have a long oval brim (anthropoid). A very flat brim is less favourable (platypoid); occurring in 5% of women over 152cm (5ft), it occurs in 30% of women <152cm. Spinal scoliosis, kyphosis, sacralization of the L5 vertebra, spondylolisthesis and pelvic fractures may all affect pelvic anatomy. Rickets and polio were formerly important causes of pelvic problems. Suspect pelvic contraction if the head is not engaged by 37 weeks in a Caucasian primip (after excluding placenta praevia).

The presentation

Cephalic presentations are less favourable, the less flexed the head. Transverse lie and brow presentations will always need caesarean section: face and OP (p 71) presentations may deliver vaginally but are more likely to fail to progress. Breech presentation is particularly unfavourable if the fetus >3.5kg.

The uterine powers

Contractions start in the fundus and propagate downwards. The intensity and duration of contractions are greatest at the fundus, but the contraction reaches its peak in all parts of the uterus simultaneously. Normal contractions occur at a rate of 3 per 10min, they should last up to 75sec, the contraction peak usually measures 30“60mmHg, and the resting uterine tone between them should be 10“15mmHg. Uterine muscle has the property of retraction. The shortening of the muscle fibres encourages cervical dilatation.

Uterine dysfunction

Contractions may be hypotonic (low resting tone, low contraction peaks) or they may be normotonic but occur too infrequently. These dysfunctions can be corrected by augmentation with oxytocin (p 64). Whenever oxytocin is used discuss with a senior obstetrician. Pain and fear cause release of catecholamines which can inhibit uterine activity. Thus adequate analgesia is needed (p 66) and may speed the progress of labour.

Cervical dystocia

Failure of cervical dilatation may be due to previous trauma, repair, cone biopsy, and cauterization. It is difficult to distinguish from failure to dilate due to uterine dysfunction though the latter should respond to oxytocin (note the important difference between primips and multips, p 64). The treatment for cervical dystocia is delivery by caesarean section.

Consequences of prolonged labour

Neonatal mortality rises with prolonged labour as does maternal morbidity (especially infection). With modern management of labour, careful monitoring of progress in labour (p 64) takes place to diagnose delay early, and treat it as necessary, to prevent prolonged labour occurring.

When there is dystocia, ask ˜is safe vaginal delivery possible?

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Prematurity

Premature infants are those born before 37 weeks' gestation. Prevalence: ~6% singletons, 46% of twin, 79% of triplet or higher order deliveries. About 2% are before 32 weeks when neonatal problems are greatest. In 25%, delivery is elective (p 62). 10% are due to multiple pregnancy; 25% are due to APH, cervical incompetence, amnionitis, uterine abnormalities, diabetes, polyhydramnios, pyelonephritis, or other infections. In 40% the cause is unknown, but abnormal genital tract colonization (bacterial vaginosis) with ureaplasma and Mycoplasma hominis is implicated, either as a risk factor or risk marker. We also know that consumption of fish oil in pregnancy can ‘birth weight by “risk of recurrence of preterm delivery.1

Managing preterm rupture of membranes (PROM)

Admit; do T° MSU, and HVS using a sterile bivalve speculum. Assess for causes/associations: eg abruption, twins, and polyhydramnios. If liquor is not obvious its presence is suggested if nitrazine sticks (pH-sensitive) turn black (false +ve with infected vaginal discharge, semen, blood, and urine). In 80%, membrane rupture initiates labour. The problem with the 20% who do not go into labour is balancing advantages of remaining in utero (maturity and surfactant‘) against the threat of infection (causes 20% of neonatal deaths after PROM). Intrauterine infection supervenes after membranes have ruptured in 10% by 48h, 26% by 72h, 40% by >72h. Prophylactic antibiotics may allow labour to be delayed. If infection develops, do blood culture and give IV antibiotics (eg ampicillin 500mg/6h IV + netilmicin 150mg/12h IV) and expedite labour (p 62). Antibiotics for ~24h pre-labour, “rates of intraventricular haemorrhage and periventricular malacia (below) in the baby. If labour supervenes, allow it to progress. If liquor stops draining for >48h (rare) slowly mobilize the mother.42

Management of preterm labour

In 50% contractions cease spontaneously. Treating the cause (eg pyelonephritis) may make it cease. Attempts to suppress contractions (tocolysis) are unlikely to succeed if membranes are ruptured or the cervix >4cm dilated. The rationale for tocolytic use was that delay of preterm labour would improve fetal outcome without causing harm to mother or fetus. Trials have shown them to be of almost no clinical benefit, and only nifedipine is associated with improvement of fetal outcome. It is quite reasonable not to use tocolytic drugs; though they may be considered desirable in certain circumstances eg to give time for corticosteroids to work; or for in utero transfer.2 Use only between 24"33 weeks. Consider transfer to hospital with SCBU facilities. Call paediatrician to attend to the baby at birth. See cord-cutting recommendations p 58.

Tocolytic drugs

Absolute CI: chorioamnionitis, fetal death or lethal abnormality, condition (fetal or maternal) needing immediate delivery. Relative CI: fetal growth restriction or distress, pre-eclampsia, placenta praevia, abruption, cervix >4cm. β-sympathomimetics, associated with maternal fluid overload and pulmonary oedema are not recommended. Atosiban (licensed in Europe) has less maternal effects, has not been shown to benefit the fetus, and is expensive. Nifedipine is as effective, and associated with less newborn respiratory distress and admission to intensive care. Regimen: nifedipine 20mg PO then 10"20mg/6"8h PO according to uterine activity (unlicensed indication). SE: “BP; headache; flushing; pulse‘ (transient); myocardial infarction (very rare).43

1

S Olsen 2002 BMJ i447 If fish oil intake is low, small amounts of n-3 fatty acids provided as fish or fish oil may protect against prematurity & low birth weight.

2

K Groom 2004 The Obstetrician and Gynaecologist 6 41

Glucocorticoids

Betametasone 12mg IM followed by a second dose 12 hours later, (or, less favoured dexamethasone 6mg/12h × 4 doses) promote fetal surfactant production, lowering mortality and complications of RDS (p 118) by 40"50%. They also help close patent ductuses and protect against periventricular malacia, a cause of cerebral palsy. Use between 24 and 34 weeks. Avoid if maternal systemic infection eg TB.

If diabetic, monitor glucose. Benefit is maximal after 24h; effects last a week.

Prematurity, survival, and disability the figures

ne major, landmark question is: Is the baby over 28 weeks' gestation?

• The disability rate is 25% if gestation is <28 weeks but half this if gestation is 28"29 weeks.
• 10% of those who survive at gestations <28 weeks will never be independently mobile, or communicate intelligibly with others.
• Only 4% of babies born before 24 weeks will survive, and of survivors, >50% will be severely disabled.
• Use of surfactant (p 118) has not reduced the viability threshold, or rates of severe disability in babies born at <28 weeks' gestation.
• Of babies born >30 weeks' gestation, in the absence of deformity, ~100% now survive.

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Thromboprophylaxis

Pregnancy is a hypercoagulable state: consider need for thromboprophylaxis pre-pregnancy, at booking, throughout the antenatal period, at start of labour and once delivered. See below. For caesarean section

Thromboprophylaxis after vaginal delivery:

In all pregnant women avoid immobility and dehydration.

Risk factors: (Thrombophilia/past thromboembolism considered separately). Women with any two of the risk factors opposite (RED BOX):

Treatment: Treat with low molecular weight heparin (LMWH) eg enoxaparin starting as soon as possible after delivery (as long as no postpartum haemorrhage and ≥4h after epidural catheter siting or removal—6h if that was traumatic). Continue for 3–5 days even if at home. Dose of enoxaparin: if the early pregnancy weight (EPW) is 50–90kg, give 40mg/24h SC; if EPW <50kg, give 20mg/24h SC; if EPW >90kg give 40mg/12h SC. If heparin is contraindicated, use TED compression stockings (TED = transverse elastic graduated). For women with ≥3 persisting risk factors consider antenatal and postnatal prophylaxis, starting as early in pregnancy as possible as risk throughout. Continue normal dose prophylaxis when admitted in labour.

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Physiological changes in pregnancy

Hormonal changes

Progesterone, synthesized by the corpus luteum until 35 post-conception days and by the placenta mainly thereafter, it decreases smooth muscle excitability (uterus, gut, ureters) and raises body temperature. Oestrogens (90% oestriol) increase breast and nipple growth, water retention and protein synthesis. The maternal thyroid often enlarges due to increased colloid production. Thyroxine levels, see p 25. Pituitary secretion of prolactin rises throughout pregnancy. Maternal cortisol output is increased but unbound levels remain constant.

Genital changes

The 100g non-pregnant uterus weighs 1100g by term. Muscle hyperplasia occurs up to 20 weeks, with stretching after that. The cervix may develop ectropion (‘erosions’). Late in pregnancy cervical collagen reduces. Vaginal discharge increases due to cervical ectopy, cell desquamation, and ↑ mucus production from a vasocongested vagina.

Haemodynamic changes

Blood

From 10 weeks the plasma volume rises until 32 weeks when it is 3.8 litres (50% >non-pregnant). Red cell volume rises from 1.4 litres when non-pregnant to 1.64 litres at term if iron supplements not taken (↑18%), or 1.8 litres at term (↑30%) if supplements are taken—hence Hb falls due to dilution (physiological ‘anaemia’). WCC (mean 10.5 × 109/L), platelets, ESR (up 4-fold), cholesterol, β-globulin, and fibrinogen are raised. Albumin and gamma-globulin fall.

Cardiovascular

Cardiac output rises from 5 litres/min to 6.5–7 litres/min in the first 10 weeks by increasing stroke volume (10%) and pulse rate (by ~15 beats/min). Peripheral resistance falls (due to hormonal changes). BP, particularly diastolic, falls during the first and second trimesters by 10–20mmHg, then rises to non-pregnant levels by term. With increased venous distensibility, and raised venous pressure (as occurs with any pelvic mass), varicose veins may form. Vasodilatation and hypotension stimulates renin and angiotensin release—an important feature of BP regulation in pregnancy.

Other changes

Ventilation increases 40% (tidal volume rises from 500 to 700mL), the increased depth of breath being a progesterone effect. O2 consumption increases only 20%. Breathlessness is common as maternal PaCO2 is set lower to allow the fetus to offload CO2. Gut motility is reduced, resulting in constipation, delayed gastric emptying, and with a lax cardiac sphincter, heartburn. Renal size increases by ~1cm in length during pregnancy.

Frequency of micturition emerges early (glomerular filtration rate↑ by 60%), later from bladder pressure by the fetal head. The bladder muscle is lax but residual urine after micturition is not normally present. Skin pigmentation (eg in linea nigra, nipples, or as chloasma—brown patches of pigmentation seen especially on the face), palmar erythema, spider naevi, and striae are common. Hair shedding from the head is reduced in pregnancy but the extra hairs are shed in the puerperium.

Pregnancy tests

Positive eg from two weeks post-conception (or from the first day of the first missed period), until ~20 weeks of pregnancy, they remain positive for ~5 days after abortion or fetal death. Otherwise, the false +ve rate is low. They detect the Ã’-subunit of human chorionic gonadotrophin in early morning urine, so are positive in trophoblastic disease (p 264).

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Diabetes mellitus in pregnancy

Meticulous control around conception 'malformation rates. Tell all diabetics about preconception services; they must know before pregnancy. Preconception change to insulin may help control. Treat retinopathy pre-pregnancy. Up to 20% may develop proliferative retinopathy so screen twice in pregnancy. If severe renal involvement; avoid pregnancy. DM may be pre-existing or appear in pregnancy; glycosuria unrelated to DM is common (glomerular filtration ' and tubular glucose reabsorption'). Non-diabetic blood glucose levels in pregnancy are constant (3.5 4.5mmol/L) except after meals. Fetal glycaemia follows maternal, but compensatory fetal hyper-insulinaemia promotes fetal growth.

Complications

Maternal

Hydramnios (25% ?due to fetal polyuria), preterm labour (17% associated with hydramnios). Stillbirth near term was common.

Fetal

Malformation rates '3 4-fold. Sacral agenesis, almost exclusive to diabetic offspring, is rare (CNS & CVS malformations are much commoner). Babies may be macrosomic (too large) or sometimes growth restricted.

Neonatal risks

Hypoglycaemia, Ca2+', Mg2+', and RDS (p 118). They may be polycythaemic (29%) so more neonatal jaundice.

Antenatal care

Review in joint clinic with diabetologist. Confirm gestation with early ultrasound. Detailed abnormality scan at 19 20 weeks. Fetal echo at 22 weeks if early control poor. Educate about benefits of normoglycaemia and home glucose monitoring: regular postprandial monitoring does prevent harm to the baby. Insulin needs increase by 50 100% as pregnancy progresses so review regularly. Aim for fasting level <5.5mmol/L; 1h post-prandial level <7.5mmol/L. Give glucagon kit and ensure partner knows how to use it. Admit if adequate control impossible to achieve at home. Oral hypoglycaemics are currently avoided though glyburide does not cross placenta and may be safe.16

Monitor fetal growth and wellbeing by ultrasound and cardiotocography.

Delivery

Timing takes into account control of diabetes, any pre-eclampsia, maturity and size of the baby, and with attention to fetal wellbeing. Delivery before 38 weeks may result in neonatal respiratory distress. Deliver the baby where there are good neonatal facilities. Traditionally, delivery was at 36 38 weeks to avoid stillbirth; but with close supervision pregnancies may go nearer to (but not beyond) term.

In labour

Avoid acidosis and monitor the fetus (p 44). Avoid maternal hyperglycaemia (causes fetal hypoglycaemia). Monitor glucose; prevent hyperglycaemia with extra insulin (may need 5U/h) if β-sympathomimetics or glucocorticoids are used in preterm labour. Aim for vaginal delivery with a labour of <12h. Beware shoulder dystocia with macrosomic babies. With elective delivery, give normal insulin the evening before induction. During labour give 1L of 5 10% glucose/8h IVI with 1 2U insulin/h via a pump. Aim for a blood glucose of 4.5 5.5mmol/L (check hourly). Insulin needs fall as labour progresses and immediately postpartum. Stop infusions at delivery. Return to pre-pregnancy regimen. Do a caesarean section if labour is prolonged. Clamp cord early (as polycythaemia risk).

Postnatal

• Encourage breast feeding (oral hypoglycaemics contraindicated).
• Encourage pre-pregnancy counselling before next pregnancy (p 2) to transfer to insulin.
• Do a postpartum glucose tolerance test at 6 weeks.

Gestational diabetes

(OGTT glucose ‰ 7.8, OHCM p 294) Incidence: 3%.17 50% get full DM, so give lifelong dietary advice & follow-up.18 Equations exist for giving risk of post-pregnancy DM from pre-pregnancy BMI (p 530), fasting plasma glucose, and months since delivery.19 Other risk factors: age >30yrs; mothers who themselves have had low birth weights or IUGR (p 52); 1st-degree relative with DM; unexplained stillbirth;20 gestational DM before 27 weeks (or if needing insulin).21 22 [n=1636]

™£ Exercise, a good diet, and no smoking all help lower this risk.

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Pre-pregnancy counselling

Pre-pregnancy counselling

The aim is to help prospective parents embark upon pregnancy under conditions most likely to ensure optimal wellbeing for the fetus. Babies conceived 18–23 months after a live birth have the lowest rate of perinatal problems.₃ Ensure that a woman is rubella (and chickenpox, p 144) immune prior to pregnancy and all women should have their need for thromboprophylaxis in pregnancy considered (p 16). Other areas covered include:

• Optimal control of chronic disease (eg diabetes) before conception. This is also important for hypothyroidism as the fetus cannot make thyroxine until 12 weeks and under-replacement may affect neurodevelopment. Strict diet is essential peri-conceptually for women with phenylketonuria (PKU).
• Stop teratogens or seek expert advice prior to conception (p 29).
• Medication to protect the fetus from abnormality (eg folate supplements for neural tube defects, p 140 and below).
• Provide expert information for those at ↑risk of abnormality so pregnancy or its avoidance is an informed choice, and any tests needed (eg chorionic villus sampling, p 10) are planned. Regional genetic services give detailed pre-pregnancy counselling. See p 154. In relevant ethnic populations, take blood for thalassaemia and sickle-cell tests (p 22).
• If past/family history of thromboembolism, screen for thrombophilia.

Diet

To prevent neural tube defects and cleft lip, all should have folate-rich foods and folic acid 0.4mg daily (eg Preconceive®) from before conception—until 13 weeks' gestation (5mg/day PO if history of neural tube defect, some epileptic drugs p 29). These foods have >0.1mg of folic acid per serving: Brussels sprouts, asparagus, spinach, blackeye beans, fortified breakfast cereals. Avoid liver and vitamin A (vitamin A embryopathy risk).

Smoking

decreases ovulations, causes abnormal sperm production (± less penetrating capacity), ↑rates of miscarriage (×2), and is associated with preterm labour and lighter-for-dates babies (mean is 3376g in non-smoker; smoker: 3200g). Reduced reading ability in smokers' children up to 11yrs old shows that long-term effects are important. ~17% of smoking mothers stop before or in pregnancy.

Alcohol consumption

High levels of consumption are known to cause the fetal alcohol syndrome (p 138). Moderate drinking has not been shown to adversely affect the fetus but alcohol does cross the placenta and may affect the fetal brain. Miscarriage rates are higher among drinkers of alcohol. NICE recommends <1unit/24h. To cut consumption: see p 513.

Spontaneous abortion (SA)

At least 12% of first pregnancies spontaneously abort. Rates after 1 SA are increased to ~24%; after 2 SA to ~36%; after 3 to ~32% and after 4 to ~25%, so chances of a future pregnancy succeeding are ~2 in 3. Pregnancy order of SA/live pregnancies is also relevant: the more recent a live birth the more likely next time will be successful.

Recurrent spontaneous abortion/miscarriage

See p 261.

Search for those who need counselling most:
Diabetes mellitus Tropical travellers Frequent abortion Hypothyroidism Epilepsy Rubella-susceptible Pet-owners (toxoplasmosis risk is ↑) Phenylketonuria BP↑ SLE Genetic history, eg: Spina bifida etc. Thalassaemia Duchenne's Cystic fibrosis Many others

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