24 - Obstetrics

CLINICAL PHASE

OBSTETRICS

DARWIN’S NOTEBOOK

TABLE OF CONTENTS

HISTORY & EXAMINATION IN OBSTETRICS 1

DISORDERS OF EARLY PREGNANCY 5

ANTENATAL CARE 11

INFECTIONS IN PREGNANCY 17

HYPERTENSIVE DISORDERS IN PREGNANCY 23

OTHER MEDICAL DISORDERS IN PREGNANCY 30

RED CELL ISOIMMUNISATION 44

PRETERM DELIVERY 47

ANTEPARTUM HAEMORRHAGE 52

FOETAL GROWTH, COMPROMISE & SURVEILLANCE 56

ABNORMAL LIE & BREECH PRESENTATION 61

MULTIPLE PREGNANCY 63

LABOUR MECHANISM 67

LABOUR MANAGEMENT 71

LABOUR SPECIAL CIRCUMSTANCES 79

INSTRUMENTAL & OPERATIVE DELIVERY 82

OBSTETRIC EMERGENCIES 86

THE PUERPERIUM 89

OBSTETRICS – HISTORY & EXAMINATION IN OBSTETRICS

DARWIN’S NOTEBOOK 1

Outline the relevant history in an obstetric patient

• Personal details ® name, age, occupation, gestation & parity

• Presenting complaint:

o Why is she in hospital ® e.g. hypertension, pain, antepartum haemorrhage, unstable lie or

PROM

o Has the pregnancy been uncomplicated?

• Dates:

o Spontaneous or from IVF?

o LMP, length of cycle, regular / irregular?

o Weeks’ gestation

o Expected date of delivery:

§ Subtract 3 months from date of LMP, add 7 days and one year (+ days longer than 28

days if cycle is >28 days)

§ Use USS & crown-rump length at 12-week scan

• Complications of pregnancy:

o Any bleeding, HTN, DM, anaemia, urine infections?

o Concerns about foetal growth or other problems?

o Admitted to hospital?

• Tests ® what tests have been performed (e.g. blood tests, USS, prenatal diagnostic testing)?

• Past obstetric history (chronologically):

o Most & gestation of delivery, birth weight, sex, any complications

o Parity ® number of deliveries

o Gravidity ® number of pregnancies

• Past gynaecological history:

o Last cervical smear ® treated for abnormal smear?

o Prior conception ® any problems with conception?

o Female genital mutilation ® if relevant background

• Past medical history:

o Previous operations

o Heart disease

o Hypertension

o Diabetes

o Psychiatric

o Epilepsy

o Other chronic illness

• Systemic review ® cardiorespiratory, abdominal & neurological

• Drugs:

o What drugs was she taking at conception?

o What was she taking before?

o What is she taking now?

• Family history:

o Diabetes

o Pre-eclampsia

o Autoimmune disease



o Venous thromboembolic disease

o Thrombophilia

o Mental illness

o Inherited disease

• Personal history:

o Smoking

o Drinking alcohol

o Drug sensitivity

• Social history:

o Social support

o Domestic abuse

o Child safeguarding

• Allergies ® penicillin or latex in particular

• VTE risk ® fill in routine form if it has not already been done

Outline the relevant examination in an obstetric patient

• General examination:

o Temperature, pulse rate, oedema & possible anaemia

o Booking visit ® BMI, chest, breast, CVS & legs are examined

o Blood pressure & urinalysis

• Mood ® should be assessed throughout pregnancy & postnatally

• Abdominal examination:

o Semi-prone ® avoiding aortocaval compression

o Uterus palpable abdominally from 12 weeks

o By 20 weeks the fundus is usually at the level of the umbilicus

o Before 20 weeks, a uterus that is larger than expected could be due to incorrect dates, full

bladder, multiple pregnancy, uterine fibroids or pelvic mass

o Inspection:

§ Size of uterus, linea nigra, scars (especially suprapubic area)

§ Foetal movements may be obvious in later pregnancy

o Palpation:

§ Is the foetus adequately grown?

§ Is the liquor volume normal?

§ Is the lie longitudinal?

§ Is the presentation cephalic, and is it engaged?

o Auscultation:

§ Listen over anterior shoulder ® between head & umbilicus for cephalic presentation

§ >28 weeks, it should be heard with a Pinard stethoscope

§ Normal is 110–160 beats/minute

o Step 1 ® measure the symphysis fundal height (>24 weeks, should equate to gestational

weeks ±2 cm)

o Step 2 ® palpate down the foetus towards the pelvis with two hands to palpate foetal parts &

estimate liquor volume ® determine the lie (longitudinal / transverse / oblique)

o Step 3 ® assess the presentation & engagement in fifths (if <2/5 palpable, it is engaged)



Outline the relevant history & examination in a postnatal patient HISTORY

• Number of days since delivery

• Delivery:

o Gestation

o Mode of delivery ® vaginal, instrumental or C-section ® why?

o Mode of onset ® spontaneous or induced

o Length of labour & analgesia

o Blood loss

• Infant:

o Name, sex & birth weight

o APGAR score & cord pH

o Mode of feeding

o Vitamin K given?

• History of puerperium:

o Lochia discharge ® volume & any odour?

o Have bowels opened & passing urine? ® difficulty, leaking or dysuria?

o Pain ® particularly in the perineum

• Drugs ® what is she taking, including analgesia?

• Plans for puerperium:

o Contraception ® POP if breastfeeding & COCP 4–6 weeks if bottle feeding

o Help available at home?

• History of pregnancy & obstetric history ® include parity and major antenatal complications (e.g. pre-

eclampsia, DM)

• Social / personal history ® consider home conditions for neonate

• VTE risk ® update risk assessment

EXAMINATION

• Assess mood, appearance, temperature, pulse, BP & anaemia

• Also examine chest, breasts, wound or IV site, and legs

• Look for uterine involution & palpable bladder

• Inspect the perineum if there is discomfort

Outline examination of the neonate

• General:

o Colour ® pallor / jaundice / cyanosis

o Features ® dysmorphism / evidence of trauma / birthmarks / any abnormalities

o Posture

o Behaviour & feeding movement ® abnormal / restricted

o Respiration

• Measure ® heart rate, temperature, head measurements, weight

• Examine:

o Look for primitive reflexes ® grasp, Moro, rooting

o Inspect back & spine with baby prone



o Heart, check all pulses equal ® e.g. radiofemoral delay

o Abdomen, genitalia (e.g. undescended testes / hernias / ambiguous genitalia), anus

o Look & examine for congenital dislocation of the hip & talipes

• Investigations:

o Serum bilirubin if jaundiced

o Day 7 ® Guthrie test (phenylketonuria, thyroid)

OBSTETRICS – DISORDERS OF EARLY PREGNANCY


Outline the physiology of early pregnancy

• Oocyte is fertilised in the ampulla of the Fallopian tube, and forms a zygote ® swept towards the uterus

by ciliary action & peristalsis

• Enters uterus around day 4 as a multicellular morula ® becomes blastocyst by developing fluid-filled

cavity

• Outer layer trophoblast invades the endometrium to implant between days 6–12 ® this layer forms the

placenta

o NB: 15% of embryos are lost at this stage

• Trophoblasts produce hCG, which peaks at 12 weeks ® this maintains the corpus luteum, which

produces oestrogen & progesterone, which turn secretory endometrium into decidua (rich in glycogen &

lipids)

• Trophoblastic proliferation leads to formation of chorionic villi on the endometrial surface of the

embryo® forms the surface area for nutrient transfer in the cotyledons of the placenta

• Placenta morphology is complete at 12 weeks ® a heartbeat is established at day 22, and visible on

transvaginal USS a week later

Outline the types, investigation & management of spontaneous miscarriage

• Spontaneous miscarriage ® when a foetus dies or delivers dead before 24 completed weeks of

pregnancy ® the majority occur before 12 weeks

• 15% of clinically recognised pregnancies spontaneously miscarry, and more will be so early as to not be

recognised ® rate of miscarriage increases with maternal age

• Isolated non-recurring chromosomal abnormalities account for >60% of ‘one-off’ or sporadic miscarriage

® however, if ≥3 miscarriages occur, then recurrent causes are more likely

• Usually presents with bleeding ® pain from uterine contractions can cause confusion with ectopic

pregnancy, but severe uterine tenderness is abnormal

• Uterine size & state of cervical os determine what type of miscarriage

• USS will show if a foetus is in the uterus & viable, and may also detect retained foetal products ® if any

doubt, women should be rescanned in 1 week, as very early pregnancy can be confused with non-viable

pregnancy

• USS does not always show ectopic pregnancy ® but if a foetus is seen in utero, then a concurrent

ectopic pregnancy is very unlikely

• Pregnancy of unknown location ® sometimes very difficult to differentiate between an early viable or

failed intrauterine pregnancy, a complete miscarriage or an ectopic pregnancy ® so assume ectopic

until location is determined

• hCG levels can also help differentiation:

o Blood levels normally increase >63% in 48 hrs with a viable intrauterine pregnancy

o A decline in hCG of >50% suggests a non-viable pregnancy

o A change in hCG over 48 hrs of between 50% decline and 63% rise suggests an ectopic

pregnancy

• Admission is required if ectopic pregnancy is suspected, if the woman is symptomatic, if the miscarriage

is septic, or if there is heavy bleeding ® resuscitation is sometimes needed as products of conception in

the cervical os can cause pain, bleeding & vasovagal shock ® they are removed using a speculum &

polyp forceps



• IM ergometrine will reduce bleeding by contracting the uterus ® but only used if foetus is non-viable

• If fever, then swabs & IV antibiotics given

• Rhesus negative women should be given anti-D if the miscarriage is treated surgically or medically, or if

there is bleeding >12 weeks ® reduces risk in future pregnancies

• 90% of women in whom foetal heart activity is detected at 8 weeks will not miscarry

TYPES OF MISCARRIAGE

• Threatened miscarriage:

o There is bleeding, but the foetus is alive, the uterus is of expected size, and the cervical os is

closed

o 25% will go on to miscarry

• Inevitable miscarriage:

o Bleeding is heavier

o Foetus may still be alive, but the cervical os is open

o Miscarriage is about to occur

• Incomplete miscarriage ® some foetal parts have been passed, but the os is usually open

• Complete miscarriage:

o All foetal tissue has been passed

o Bleeding has diminished, the uterus is no longer enlarged, and the cervical os is closed

• Septic miscarriage:

o Contents of the uterus are infected, causing endometritis

o Vaginal loss is offensive, uterus is tender, but fever may be absent

o If pelvic infection occurs, there is abdominal pain & peritonism

• Missed miscarriage:

o The foetus has not developed, or died in utero

o This is not recognised until bleeding occurs or USS is performed

o Uterus is smaller than expected, and the os is closed

MANAGEMENT OF NON-VIABLE INTRAUTERINE PREGNANCY

• Expectant management:

o Can be continued as long as the woman is willing & there are no signs of infection

o It is successful within 2–6 weeks in >80% of women with incomplete miscarriage, and in 30–

70% of women with missed miscarriage

o A large intact sac is associated with lower success rates

• Medical management:

o Vaginal or oral prostaglandin (misoprostol)

o It is successful in >80% of women with incomplete miscarriage, and 40–90% of women with

missed miscarriage

o Urine pregnancy test should be repeated after 3 weeks to exclude ectopic or molar pregnancy

• Surgical management:

o Surgical management of miscarriage (SMM) was previously known as ERPC

o Carried out under general anaesthetic using vacuum aspiration

o Suitable if the woman prefers it, or if there is heavy bleeding or signs of infection

o Success rates are >95% for both incomplete & missed miscarriage

o Tissue is examined to exclude molar pregnancy



• Complications:

o Vaginal bleeding in expectant or medical management may be heavy & painful ® may need

surgical management (10–40%)

o Infection (3%) are similar across all managements

o Surgical management can partly remove the endometrium causing Asherman’s syndrome, or

perforate the uterus (<1%)

Outline the causes of recurrent miscarriage

• Recurrent miscarriage is when 3 or more miscarriages occur in succession

• 1% of couples are affected, but chance of miscarrying in 4th pregnancy is still only 40%

• In early pregnancy, USS monitoring is very important ® in later pregnancy, ‘high-risk’ monitoring is

important, because late pregnancy complications are more common

CAUSES OF RECURRENT MISCARRIAGE

• Antiphospholipid syndrome:

o Thrombosis in the uteroplacental circulation is likely to be the mechanism

o Treatment is with aspirin & LMW heparin

• Parental chromosomal defects:

o Foetal miscarriage tissue is karyotyped ® if shows an unbalanced abnormality, then parental

karyotyping is performed

o Refer to clinical geneticist

o CVS & amniocentesis is offered

o Donor oocytes or sperm is an option, or PGD of IVF embryos is an alternative

• Anatomical factors:

o Uterine abnormalities are diagnosed using USS, MRI or hysterosalpingogram

o More common with late miscarriage

o Often an incidental finding, and surgical intervention may lead to uterine weakness or adhesion

formation

o Cervical problems contribute to late miscarriage, as well as preterm labour

• Infection ® not a cause of recurrent early miscarriage, but implicated in preterm labour & late

miscarriage

• Hormonal factors:

o Thyroid dysfunction (± thyroid antibodies) is associated with recurrent miscarriage ® so

should be tested & treated

o PCOS may be associated with an increased risk of pregnancy loss

• Others:

o Obesity

o Smoking

o Excess caffeine intake

o Older maternal age

Outline the methods of therapeutic abortion in unwanted pregnancy

• Rhesus negative women should receive anti-D within 72 hrs of TOP

• Contraception should be discussed at the initial consultation ® screened for STIs



• Surgical methods:

o Suction curettage is used between 7 and 12–14 weeks

o Before 7 weeks, failure rates are higher than with medical abortion

o >14 weeks, medical methods are usually employed ® although surgical abortion by dilation &

evacuation is safe & effective

o The cervix is ‘prepared’ with preoperative vaginal misoprostol, and antibiotic prophylaxis given

• Medical methods:

o Anti-progesterone (mifepristone) plus prostaglandin (misoprostol) 36–48 hrs later is the most

effective method of abortion at <7 weeks

o Can be used at any gestation as an alternative to surgical methods

o It is the usual & most effective method for mid-trimester abortions (13–24 weeks)

o From 22 weeks, feticide is performed first to prevent live birth using KCl into umbilical vein or

foetal heart ® such late terminations are usually only performed where a foetal abnormality is

detected

• Complications of therapeutic abortion:

o Haemorrhage ® 1 in 1000 women, with greater risk in later gestations

o Infection ® up to 10% of cases, but reduced by screening & prophylactic antibiotics

o Uterine perforation ® 1–4 in 1000 surgical abortions

o Cervical trauma ® at the time of surgical abortion

o Failure ® <5% of surgical & medical abortions require further intervention, and <1% fail to the

end of the pregnancy

o Preterm delivery ® associated with multiple surgical terminations

o Unsafe abortion ® 50% worldwide, with 98% of these in developing countries

Outline the clinical features, investigation & management of ectopic pregnancy

• An ectopic pregnancy is when the embryo implants outside the uterine cavity

• Occurs in 1 in 60–100 pregnancies

• Mortality rate is 16.9/100,000 estimated ectopic pregnancies

• They are more common with advanced maternal age & lower socioeconomic class

• The thin-walled tube is unable to sustain trophoblastic invasion ® it bleeds into the lumen & may

rupture, where intraperitoneal blood loss can be catastrophic

• Often no cause is evident ® any factor which damages the tube can cause fertilised oocytes to be

caught (e.g. PID from STIs)

• Additional risks:

o Assisted conception

o Pelvic surgery ® particularly tubal

o Previous ectopics

o Smoking

• The diagnosis is easily missed ® abnormal vaginal bleeding, abdominal pain, or collapse in any women

of reproductive age should have a pregnancy test

CLINICAL FEATURES

• Lower abdominal pain ® colicky pain, then constant

• Light, dark vaginal bleeding



• Syncopal episodes & shoulder tip pain ® intraperitoneal bleeding

• Amenorrhoea for 4–10 weeks previously

• Rebound tenderness

• Cervical excitation

• Adnexal tenderness

• Uterus is smaller than expected

• Cervical os is closed

INVESTIGATION

• Pregnancy test ® normally positive with ectopic pregnancy

• USS ® may not visualise ectopic, but will detect lack of intrauterine pregnancy, and may detect free

fluid in the adnexa

• Quantitative serum hCG:

o Useful if uterus is empty

o If >1000 IU/ml® then an intrauterine pregnancy will be visible on transvaginal USS

o If the level is lower but rises >63% in 48 hrs ® it is a viable early intrauterine pregnancy

o Declining or slowing levels suggest an ectopic or non-viable intrauterine pregnancy

• Laparoscopy ® most reliable but very invasive

MANAGEMENT

• Where symptoms are present, the patient should be admitted ® IV access & blood crossmatched, and

anti-D given if the patient is Rhesus negative

• Surgical management:

o Appropriate if the woman is in significant pain, adnexal mass >35 mm, visible foetal heart

activity, or a serum hCG level >5000 IU/ml

o Laparoscopy is standard and preferable to laparotomy ® the recovery is faster, and

subsequent fertility rates are equivalent or better

o The ectopic is either removed from the tube (salpingostomy), or the whole tube including the

ectopic is removed (salpingectomy)

• Medical management:

o Appropriate if the patient is able to return for follow-up, has no significant pain, has an adnexal

mass <35 mm with no foetal heart activity, plus no coexisting intrauterine pregnancy

o The lower the hCG, the higher the success rate

o Systemic single-dose methotrexate can be used without recourse to laparoscopy

o hCG levels measured to confirm removal ® but second dose (15%) or surgery (10%) may be

required

Describe hyperemesis gravidarum, including its management

• Hyperemesis gravidarum is when nausea & vomiting in early pregnancy are so severe as to cause

dehydration, weight loss & electrolyte disturbance

• Occurs in 1 in 750 women ® seldom persists beyond 14 weeks, and is more common in multiparous

women

• Predisposing condition include urinary infection & multiple or molar pregnancy



• IV rehydration is given ® anti-emetics (metoclopramide, cyclizine or ondansetron) & thiamine to

prevent neurological complications of vitamin depletion

• Steroids have been used in severe cases

Describe gestational trophoblastic disease (molar pregnancy) & outline the types

• Gestational trophoblastic disease (GTD) is where trophoblastic tissue proliferates in a more

aggressive way than normal ® proliferation can be localised and non-invasive (hydatidiform mole),

and is considered a premalignant condition

• hCG is usually secreted in excess (>5000 IU/ml)

• Hydatidiform mole can be subdivided based on genetic & histopathological features:

o Complete mole:

§ Entirely paternal in origin ® usually when one sperm fertilises an empty oocyte &

undergoes mitosis

§ There is no foetal tissue, merely a proliferation of swollen chorionic villi

o Partial mole:

§ Usually triploid ® derived from two sperms entering one oocyte

§ There is variable evidence of a foetus

• The proliferation may have characteristics of malignant tissue:

o Invasive mole ® invasion only locally within the uterus

o Choriocarcinoma ® metastasis has occurred

• The least common form of GTD is placental site trophoblastic tumour (PSTT) ® which in contrast to

other types of GTD presents an average of 3 years later

• GTD occurs in 1 in 500–1000 pregnancies ® more common at the extremes of reproductive age, and is

twice as common in Asian women

• The uterus is often large, and early pre-eclampsia & hyperthyroidism may occur ® vaginal bleeding is

usual & may be heavy, and hyperemesis may occur

• The condition may be detected on routine USS

• USS shows a characteristic ‘snowstorm’ appearance of the swollen villi with complete moles ® but the

diagnosis can only be confirmed histologically

• Trophoblastic tissue is removed by ERPC, and the diagnosis is confirmed

• Serial blood & urine hCG levels are taken ® with persistent or rising levels being suggestive of

malignancy

• Recurrence of molar pregnancy occurs in about 1 in 60 subsequent pregnancies

• Gestational trophoblastic neoplasia follows 15% of complete and 0.5% of partial molar pregnancies

OBSTETRICS – ANTENATAL CARE


Outline the aims of antenatal care

• Detect and manage pre-existing maternal disorders that may affect pregnancy outcome

• Prevent or detect & manage maternal complications of pregnancy

• Prevent or detect & manage foetal complications of pregnancy

• Detect congenital foetal problems, if requested by the parents

• Plan, with the mother, the circumstances of pregnancy care & delivery to ensure maximum safety for the

mother and baby, and maximum maternal satisfaction

• Provide education & advice regarding lifestyle and ‘minor’ conditions of pregnancy

Outline preconceptual care & counselling

• Previous pregnancies ® could have been traumatic & have implications on another pregnancy

• Health check ® assess for cardiovascular health or cervical smear abnormalities

• Rubella status ® so immunisation can occur prior to pregnancy

• Chronic condition check ® glucose control optimised in diabetes or blood pressure control

• Medication ® e.g. antiepileptics

• Folic acid supplements ® reduce the chances of neural tube defects

Describe the booking visit

• Booking is at 10 weeks’ gestation ® the purpose is to screen for possible complications that may arise

in pregnancy, labour & the puerperium

• Risk is assessed using history, examination & standard investigations

• Decisions about pregnancy care must be constantly re-evaluated as the pregnancy proceeds ® the

gestation of pregnancy should also be checked, appropriate prenatal screening is discussed, and a

general health check is done

HISTORY

• Age ® <17 yrs and >35 yrs have an increased risk of obstetric & medical complications in pregnancy

• History of presenting pregnancy ® early USS (usually 11–13+6 weeks) is used to date all except IVF

pregnancies

• Past obstetric history ® any obstetric disorders have significant recurrence rates, including:

o Preterm labour

o Pre-eclampsia

o Gestational diabetes

o Intrauterine growth restriction

o Stillbirth

o Antepartum & postpartum haemorrhage

o Congenital anomalies

o Rhesus disease

• Past gynaecological history ® past gynaecological surgery may influence delivery recommendations

or increase preterm labour risk (e.g. loop diathermy)

• Past medical history ® may cause increased risk of pregnancy problems & input from the appropriate

specialist, including:

o Hypertension

o Diabetes




o Haemoglobinopathy

o Thromboembolic disease

o Cardiac disease

o Renal disease

o Mental health problems ® increases risk of suicide

• Drugs ® contraindicated drugs should be changed to those considered safer in pregnancy

• Family history ® gestational diabetes is more common if a 1st degree relative has diabetes, and

hypertension, thromboembolic & autoimmune diseases, and pre-eclampsia are familial

EXAMINATION

• BMI is calculated ® if >30, maternal & foetal complications are more common

• Baseline BP ® enables comparison if hypertension occurs later in pregnancy

• From 12 weeks the foetal heart can be auscultated ® but abdominal palpation is hard before 3rd

trimester

• If a smear has not been performed for 3 years ® it is usually done 3 months postnatally

INVESTIGATION

• Ultrasound scan:

o 11–13+6 weeks, so foetus can be ‘dated’ using crown-rump length ® unless IVF pregnancy

o Also detects multiple pregnancy & enables screening for chromosomal abnormalities with

nuchal translucency measurement, in conjunction with b-hCG & PAPP-A as the ‘combined test’

• Blood tests:

o FBC ® pre-existing anaemia

o Serum antibodies (anti-D) ® intrauterine isoimmunisation

o Glucose tolerance test ® in at risk women (e.g. BMI >30, Asian)

o Syphilis ® serious implications on foetus

o Rubella immunity ® vaccination offered postnatally

o HIV & Hep B ® counselling & screening offered

o Haemoglobin electrophoresis ® for sickle cell anaemia & thalassaemias in at risk women

• Screening for infections ® chlamydia & BV can cause preterm labour

• Urine MC&S ® asymptomatic bacteriuria in pregnancy commonly leads to pyelonephritis (20%)

• Urinalysis for glucose, protein & nitrites ® underlying diabetes, renal disease & infection

HEALTH PROMOTION

• Folic acid ® 400 micrograms/day should be continued until at least 12 weeks ® increased doses of 5

mg/day in women with BMI .30, sickle cell disease, malabsorption, or if on antiepileptics

• Vitamin D ® recommended for all women (10 µg/day) or 25 µg/day in women with BMI >30, South

Asian or Afro-Caribbean origin, low sunlight exposure, or increased pre-eclampsia risk

• Aspirin ® 75mg recommended in women with increased pre-eclampsia risk

• Immunisation ® seasonal flu vaccine & >28 weeks pertussis vaccine

• Diet:

o 2500 Calories

o No alcohol or smoking



o Avoid listeriosis by drinking only pasteurised or UHT milk, avoiding soft / blue cheese, pate &

uncooked / partially cooked ready prepared food

• Exercise ® advised, with swimming being good

• Sleeping ® left lateral position from 28 weeks

• Antenatal classes ® prepare & educate women and partners about pregnancy & labour

Outline routine tests that occur in later pregnancy

• Structural abnormalities & risk assessment:

o Another USS should be offered at around 20 weeks ® this is the ‘anomaly scan’, which

enables detection of most structural foetal abnormalities

o USS cervical length measurement at around 20 weeks can be used for risk assessment of

preterm delivery ® progesterone can be given to women who have a short cervix but are

otherwise low risk

o USS measurement of uterine artery ® can be used as screening for IUGR & pre-eclampsia

• Routine later pregnancy testing:

o FBC & antibody assessment ® performed at 28 weeks

o Non-invasive prenatal testing (NIPT) ® used to determine if Rhesus negative mother is

carrying a Rhesus positive baby, and given anti-D if so

Describe the continuing antenatal care

• Women are seen at increasing intervals throughout the pregnancy, because complications are more

common later in pregnancy ® frequency depends on likelihood of complications and on foetal &

maternal health

• NICE recommends 10 appointments for uncomplicated pregnancies in a nulliparous woman, and 7

appointments for uncomplicated pregnancies in a multiparous woman ® more frequent visits are

appropriate in high-risk pregnancies

ANTENATAL VISITS

• Blood pressure & urine dipped at every antenatal visit

• Abdomen is examined ® but presentation is variable & unimportant until 36 weeks

• Listening to the foetal heart is reassuring

• Reassessment of pregnancy risk is undertaken

• 16 weeks ® results of screening tests for chromosomal abnormalities & booking blood tests ® ‘triple

test is offered for women who missed chromosomal abnormality testing

• 18–21 weeks ® anomaly scan is performed, with further scan at 32 weeks if the placenta is low

• 25 weeks ® only recommended for nulliparous women, to exclude onset of pre-eclampsia & GTT if

required

• 28 weeks ® fundal height is measured, FBC & antibodies checked, and anti-D given to Rhesus

negative women

• 31 weeks ® fundal height is measured in nulliparous women

• 34 weeks ® fundal height is measured, and FBC is rechecked if Hb was low

• 36, 38 & 40 weeks ® fundal height is measured, and foetal lie & presentation are checked ® referral

for external cephalic version (ECV) is offered if in breech position



• 41 weeks ® fundal height is measured, and foetal lie & presentation are checked ® membrane

sweeping is offered, as is induction of labour by 42 weeks

Outline the common minor conditions in pregnancy

• Itching ® common in pregnancy ® sclerae are checked for jaundice, LFTs & bile acids are assessed

• Pelvic girdle pain ® common, and causes varying degrees of discomfort in pubic / sacroiliac joints ®

physio, corsets, analgesics & even crutches may be used

• Abdominal pain ® universal to some degree in pregnancy ® usually benign & unexplained

• Heartburn ® affects 70% of women, and most marked in supine position

• Backache ® universal & may cause sciatica ® most resolve after delivery

• Constipation ® common & exacerbated by oral iron ® high fibre intake is needed

• Ankle oedema ® common, and worsens towards the end of pregnancy ® is an unreliable sign of pre-

eclampsia, and diuretics should not be given

• Leg cramps ® in 30% of women, and treatments are unproven

• Carpal tunnel syndrome ® due to fluid retention compressing the median nerve

• Vaginitis ® due to candidiasis ® imidazole vaginal pessaries (e.g. clotrimazole) used for symptomatic

infection

• Tiredness ® universal & often incorrectly attributed to anaemia

Briefly describe various methods of prenatal testing MATERANL BLOOD TESTING

• Chromosomal abnormalities:

o Levels of several blood markers can be altered ® including b-hCG, pregnancy associated

plasma protein A (PAPP-A), alpha fetoprotein (AFP, oestriol & inhibin A

o Results can be integrated with other risk factors & USS measurements (e.g. nuchal

translucency) to screen for trisomies 21, 18 & 13

• Non-invasive prenatal testing (NIPT):

o Free foetal DNA in maternal circulation allows diagnosis of chromosomal abnormalities

o Tests take >1 week and are expensive



ULTRASOUND

• USS is used to determine the gestation & pregnancy site, and exclude multiple pregnancy

• Nuchal translucency ® measures the space between the skin & soft tissue overlying the cervical

spine, and the larger it is the higher the risk

• Amniocentesis & CVS are performed under USS guidance

• Structural abnormalities are usually diagnosed at around 20 weeks at the anomaly scan:

o Congenital malformations of all organs & systems are detectable

o 25% can be identified at the time of nuchal translucency

o Heart anomalies can remain undiagnosed, even at 20 weeks

• Some abnormalities do not become evident until later, either because they are not visible, or they

develop with gestation ® development of polyhydramnios can be the result of a foetal abnormality

FOETAL MRI

• MRI scanning of the foetus in utero is used to aid diagnosis of intracranial lesion

• May also have a role as an alternative to post-mortem examination

3D / 4D ULTRASOUND

• 3D or realtime 3D (4D) uses a computer reconstructed 3D ultrasound image

• Allows better evaluation of certain abnormalities

• Being extensively used

AMNIOCENTESIS

• Diagnostic test involving the removal of amniotic fluid using a fine gauge needle under USS guidance

• Safest performed at 15 weeks ® but may be done later

• Enables prenatal diagnosis of chromosomal abnormalities, some infections (e.g. CMV & toxoplasmosis),

and some inherited disorders (e.g. sickle cell, thalassaemia & CF)

• 1% of women miscarry after amniocentesis ® most unrelated to the procedure

CHORIONIC VILLOUS SAMPLING (CVS)

• Diagnostic test involving biopsy of the trophoblast by passing a fine gauge needle through the

abdominal wall (or cervix) into the placenta ® can be done from 11 weeks

• Results can be obtained earlier than amniocentesis, and allows an abnormal foetus to be identified at a

time when termination is usually performed under GA

• Miscarriage rate is slightly higher than amniocentesis ® but performed earlier, when spontaneous

miscarriage is more common

• For both CVS & amniocentesis ® FISH, karyotyping, and microarray-CGH is used to identify

chromosomal abnormalities

PRE-IMPLANTATION GENETIC DIAGNOSIS

• In IVF, cells can be removed from a developing embryo for genetic analysis before it is transferred into

the uterus ® allows selection of only embryos that will not be affected by the disorder for which it is

being tested

• Technique is expensive & presents ethical dilemmas ® but has been used in prenatal diagnosis of sex-

linked disorders, trisomies, and autosomal dominant & recessive conditions

• It does require IVF ® even in couples who are fertile



Outline common congenital / chromosomal abnormalities & their identification

• Congenital abnormalities affect 2% of pregnancies ® they include:

o Structural deformities ® e.g. diaphragmatic hernia

o Chromosomal abnormalities ® e.g. Down’s syndrome

o Inherited disease ® e.g. cystic fibrosis

o Intrauterine infection ® e.g. rubella

o Drug exposure ® e.g. antiepileptics

• Chromosomal abnormalities affect 6 per 1000 live births ® much more common in early pregnancy, but

can cause miscarriage

• The combined test:

o Integrates the risk from maternal age with PAPP-A & b-hCG blood tests, with nuchal

translucency at dating scan

o Performance of test can be enhanced using other risk factors ® e.g. absence of nasal bone /

tricuspid regurgitation

• The quadruple test:

o Used when booking is too late for nuchal scan or it is technically not possible (e.g. high BMI)

o Comprises a blood test at 14–22 weeks ® integrating the risk from maternal age with that

calculated from AFP, total hCG, inhibin & oestriol

OBSTETRICS – INFECTIONS IN PREGNANCY


Outline the importance of infection in pregnancy

• Infections assume a particular importance in pregnancy in several ways:

o Maternal illness ® may be worse, as with varicella

o Maternal complications ® may be more common, as with pre-eclampsia in HIV positive

women

o Preterm labour ® associated with infections

o Vertical transmission ® innocuous infections can cause miscarriage, be teratogenic, or

damage developing organs

o Neurological damage ® more common in the presence of bacterial infection in both preterm &

term babies

o Antibiotics ® usage in pregnancy is occasionally limited by adverse effects to the foetus

List common viral infections in pregnancy CYTOMEGALOVIRUS

• Pathology:

o CMV is a herpesvirus, and is transmitted by personal contact

o 35% of women in the UK are immune

o 1% develop subclinical CMV infection in pregnancy

o Is a common cause of childhood handicap or deafness

• Foetal / neonatal effects:

o Vertical transmission occurs in 40%

o 10% of infected neonates are symptomatic at birth ® with IUGR, pneumonia &

thrombocytopaenia

o Most develop severe neurological sequelae ® such as hearing, visual & mental impairment

o Asymptomatic neonates are at risk of deafness (15%)

• Diagnosis:

o USS abnormalities are evident in 20% ® intracranial or hepatic calcification

o Most infections are diagnosed when being specifically tested for ® CMV IgM remains positive

for a long time after infection, and could predate the pregnancy

o If maternal infection is confirmed ® then amniocentesis at least 6 weeks after maternal

infection will confirm or refute vertical transmission

• Management:

o Most infected neonates are not seriously affected

o USS can help determine those most at risk

o No prenatal treatment ® termination may be offered

o Routine screening is not advised, and no vaccine is available

HERPES SIMPLEX

• Pathology:

o Type 2 DNA virus causes genital herpes

o <5% of pregnant women have history of prior infection ® but many have antibodies


o HSV is not teratogenic, and neonatal infection is rare but has a high mortality

o Vertical transmission occurs at vaginal delivery ® particularly if vesicles are present



o Most likely to follow recent primary maternal infection ® as the foetus will not have passive

immunity from maternal antibodies

• Diagnosis ® usually clear clinically, and swabs are of little use in pregnancy

• Management:

o Referral to GUM

o C-section is recommended for those delivering within 6 weeks of primary attack, and those with

genital lesions

o Risk is very low in recurrent herpes who do not have vesicles at the time of labour ® so C-

section is not recommended

o Daily aciclovir in late pregnancy may reduce the frequency of recurrences at term

o Exposed neonates are given aciclovir

HERPES ZOSTER

• Pathology:

o Primary infection with DNA herpesvirus causes chickenpox & reactivation causes shingles

o Women who are not immune to herpes zoster can develop chickenpox after exposure to

chickenpox or shingles

o Rare in pregnancy (0.03%) ® but can cause severe maternal illness


o Teratogenicity is rare (1–2%) in early pregnancy infection, and is treated immediately with oral

aciclovir

o Maternal infection in 4 weeks preceding delivery can cause severe neonatal infection ® most

common if delivery occurs within 5 days or 2 days before maternal symptoms

• Management:

o IVIG is used to prevent & aciclovir used to treat

o Pregnant women exposed to herpes zoster are tested for immunity, and IVIG given within 10

days if non-immune, or aciclovir given if infection occurs

o In later pregnancy, if delivery is 5 days after or 2 days before maternal symptoms ® then

neonates are given IVIG & aciclovir if infection occurs

o Vaccination is possible

RUBELLA

• Pathology:

o Rubella virus usually affects children & causes mild febrile illness with macular rash

o Congenital rubella is very rare in the UK, as there is widespread immunity

o <10 affected neonates are born every year ® immunity is lifelong


o Maternal infection in early pregnancy causes multiple foetal abnormalities ® including

deafness, cardiac disease, eye problems & mental retardation

o Probability & severity decreases with gestation

• Management:

o If a non-immune woman develops rubella <16 weeks, then termination is offered

o Screening remains routine at booking

o Vaccine is live & contraindicated in pregnancy



PARVOVIRUS

• Pathology:

o Parvovirus B19 infects 0.25% of pregnant women ® but 50% are immune

o ‘Slapped cheek’ appearance is classical, but may have arthralgia or be symptomatic

o Infection is usually from children


o Virus suppresses foetal erythropoiesis causing anaemia

o Variable degrees of thrombocytopaenia can also occur

o Foetal death occurs in 10% of pregnancies ® usually with infection <20 weeks

• Diagnosis:

o If maternal exposure or symptoms have occurred ® positive maternal IgM testing will prompt

foetal surveillance

o Anaemia is detectable on USS as increased blood flow viscosity in foetal MCA, and

subsequent oedema (hydrops fetalis) from cardiac failure

o Spontaneous resolution of anaemia & hydrops occurs in 50%

• Management:

o Mothers infected are scanned regularly to look for anaemia

o If hydrops is detected in utero ® transfusion can be given if this is severe

o Excellent prognosis in survivors

HEPATITIS B

• Pathology:

o Caused by small DNA virus & transmitted by blood products or sexual activity

o Infection resolves in 90% of adults, but persists in 10%

o Infectious state is present in 1% of women in the West

o The degree in infectivity depends on antibody status ® HBsAB positive individuals are

immunologically cured, and of low infectivity to others & foetus, but HBsAg / HBeAG positive

are more infectious


o Vertical transmission occurs in delivery

o 90% of infected neonates become chronic carriers ® compared to 10% of adults

• Management:

o Maternal screening is routine in the UK

o Neonatal immunisation reduces the risk of infection by >90%, and given to all positive women

o Women with high viral loads are treated with antiviral agents from 32 weeks, and passive

immunity given postnatally to the neonate

HEPATITIS C

• 0.5% of pregnant women are infected in the UK ® worldwide incidence of 3%, and 30% in HIV positive

• Main risk factors ® drug abuse & sexual transmission

• Hep C leads to chronic hepatitis in 80% ® but most pregnant women are asymptomatic

• Vertical transmission of HCV occurs in 3–5% ® but higher if large viral load or co-existing HIV

• Elective C-section, avoidance of breastfeeding, and administration of immunoglobulin do not reduce

vertical transmission to neonate ® screening is restricted to high-risk groups



HIV

• Pathology:

o ~1000 pregnancies a year are infected by HIV

o Heterosexual transmission is now the most important route ® with a risk of <1% per episode of

sexual intercourse

o Pregnancy does not hasten progression to AIDS

o Incidence of pre-eclampsia is greater, and may be increased by antiretroviral therapy

o Gestational diabetes may also be more common


o Stillbirth, pre-eclampsia, IUGR & prematurity are more common

o Vertical transmission is mostly beyond 36 weeks, intrapartum or during breastfeeding

o Transmission is greater with low CD4+ counts & high viral load, coexisting infection, premature

delivery, and during labour ® particularly with ruptured membranes for >4 hrs

o 25% of HIV infected neonates will develop AIDS in 1 yr and 40% in 5 yrs

• Management:

o Screening is universal® positive women should have regular CD4+ & viral load tests

o Prophylaxis against PCP is given if the CD4+ count is low

o Drug toxicity is monitored with liver & renal function, haemoglobin & blood glucose testing

o HAART reduces viraemia & maternal disease progression, and should be continued

throughout pregnancy & delivery ® with the neonate treated for the first 6 weeks

o If the woman is not receiving pre-pregnancy treatment ® then it is started at 28 weeks

o C-section is recommended if viral load is above 50 copies/ml, or there is coexistent hepatitis C

infection

o Breastfeeding is avoided

INFLUENZA

• Pathology ® the influenza H1N1 (swine flu) particularly affects pregnant women, especially those with

comorbidity (including obesity)

• Foetal / neonatal effects ® no known adverse effects

• Management:

o If symptoms are present, then oseltamivir should be prescribed, and admission considered if

there are respiratory symptoms

o Seasonal, yearly vaccination with an inactivated vaccine is strongly recommended for pregnant

women at any gestation

ZIKA

• Declared a public health emergency in 2016 following outbreaks in multiple countries

• There is a likely link with foetal CNS abnormalities in maternal infection during 1st & 2nd trimesters ®

including intracranial calcification, ventriculomegaly & microcephaly

• Transmitted by the Aedes mosquito ® maternal symptoms are mild and include rash & fever, but also

Guillain-Barré syndrome

• Virus can be detected by PCR, but antibody testing is currently unreliable due to cross-reactivity

• Pregnant women should be advised not the travel to countries affected by outbreaks



List common bacterial & parasitic infections during pregnancy GROUP A STREPTOCOCCUS

• Bacterium traditionally responsible for puerperal sepsis ® most common bacterium associated with

maternal death

• Group A strep (Streptococcus pyogenes) is carried by 5–30% of people ® most common symptom is

sore throat

• Infections during pregnancy are usually from children

• Chorioamnionitis with abdominal pain, diarrhoea & severe sepsis may occur ® infected foetus often

dies in utero, and labour will then usually ensue

• Early recognition, cultures & high dose antibiotics ± ICU is required

GROUP B STREPTOCOCCUS

• Streptococcus agalactiae is carried without symptoms by 25% of pregnant women

• Foetus can be infected during labour after the membrane ruptures ® most common with preterm

labour, if labour is prolonged, or if there is maternal fever

• Early onset neonatal GBS sepsis occurs in 0.35/1000 neonates in the UK ® causes severe illness &

has mortality rate of 6% in term infants, and 18% in preterm infants

• Vertical transmission can be mostly prevented by high dose IV penicillin throughout labour ® in the

UK, treatment is only used if risk factors for GBS vertical transmission are present, or if found

incidentally, including:

o Previous affected neonate

o Positive urinary culture for GBS

o Preterm labour

o Ruptured membranes for >18 hrs

o Maternal fever in labour

SYPHILIS

• STI due to Treponema pallidum ® rare in pregnant women in the UK (0.02%)

• Active disease in pregnancy causes miscarriage, severe congenital disease or stillbirth

• Prompt treatment with benzylpenicillin is safe and will prevent, but not reverse, foetal damage

• Screening tests (VDRL) are still in routine use

TOXOPLASMOSIS

• Due to the protozoan parasite Toxoplasma gondii ® follows contact with cat faeces or soil, or eating

infected meat

• In UK, 20% of adults have antibodies ® infection in pregnancy occurs in 0.2% of women in the UK

• Foetal infection follows in 30% ® more common as the pregnancy progresses, but earlier infection

causes more severe sequelae:

o Mental handicap

o Convulsion

o Spasticity

o Visual impairment

• USS may show hydrocephalus, but maternal infection is usually diagnosed due to exposure or anxiety

® vertical transmission is diagnosed or excluded via amniocentesis after 20 weeks



• Health education reduces maternal risk

• Spiramycin is started as soon as a woman is diagnosed ® additional combination therapy of

pyrimethamine & sulfadiazine with folinic acid is given if vertical transmission is confirmed

LISTERIOSIS

• Caused by Listeria monocytogenes (Gram positive bacillus) ® infection can follow consumption of pate,

soft cheese & prepacked meals

• Causes non-specific febrile illness ® bacteraemia occurs in pregnancy, and potentially fatal infection of

the foetus may follow

• Diagnosis is established from blood cultures ® prevention is key

CHLAMYDIA & GONORRHOEA

• Chlamydia is caused by Chlamydia trachomatis ® occurs in 5% of pregnant women

• Gonorrhoea is caused by Neisseria gonorrhoeae ® occurs in 0.1% of pregnant women

• Most women are asymptomatic, and the disease are best known as causes of PID & subfertility ® but

both have association with preterm labour & neonatal conjunctivitis

• Chlamydia is treated with azithromycin or erythromycin ® tetracyclines cause foetal tooth

discolouration

• Gonorrhoea is treated with cephalosporins

BACTERIAL VAGINOSIS

• Common overgrowth of normal vaginal lactobacilli by anaerobes ® such as Gardnerella vaginalis &

Mycoplasma hominis

• Can be asymptomatic or cause offensive vaginal discharge

• Preterm labour & late miscarriage is common

• Treatment with oral clindamycin ® reduces the risk of preterm birth if used <20 weeks

OBSTETRICS – HYPERTENSIVE DISORDERS IN PREGNANCY


Outline the normal blood pressure changes in pregnancy

• Blood pressure normally falls to a minimum level in the 2nd trimester by about 30/15 mmHg due to

reduced vascular resistance ® this occurs in both normotensive & chronically hypertensive women

• By term, the blood pressure rises again to pre-pregnancy levels

• Hypertension due to pre-eclampsia is largely caused by an increase in systemic vascular resistance

• Protein excretion is increased in normal pregnancy ® but in the absence of underlying renal disease, it

is <0.3g /day

Briefly outline the classification of hypertension in pregnancy PREGNANCY-INDUCED HYPERTENSION

• This is when the blood pressure rises above 140/90 mmHg after 20 weeks ® can be due to pre-

eclampsia or transient hypertension

• Pre-eclampsia is a disorder in which hypertension & proteinuria (>0.3g /day, or protein:creatinine

ratio >30 mg/nmol) appear in the 2nd half of pregnancy, often with oedema ® eclampsia / epileptiform

seizures are a complication

• Occasionally, proteinuria is absent in pre-eclampsia, particularly in early pregnancy ® can be hard to

distinguish from gestational hypertension

• Gestational hypertension ® new hypertension presenting after 20 weeks without proteinuria

PRE-EXISTING OR CHRONIC HYPERTENSION

• This is present when the blood pressure is >140/90 mmHg before pregnancy / before 20 weeks’

gestation, or the woman is already on hypertensive treatment

Describe pre-eclampsia and outline its clinical features, diagnosis & management

• Pre-eclampsia is a multisystem syndrome that usually manifests as new hypertension after 20 weeks

with significant proteinuria ® it is specific to pregnancy, of placental origin, and cured only by delivery

• Blood vessel endothelial cell damage leads to vasospasm, increased capillary permeability & clotting

dysfunction ® both the foetus & mother are at risk

• Hypertension is just a sign rather than the disease itself ® both hypertension & proteinuria can be

absent until the late stages

• Two phenotypes exist:

o Early onset ® that which causes complications before 34 weeks, and typically the foetus is

growth restricted

o Late onset ® manifests at any later gestation, and not usually associated with growth

restriction, although foetal death & damage may occur

PATHOPHYSIOLOGY

• Stage 1 ® poor placental perfusion:

o In normal pregnancy, trophoblastic invasion of spiral arterioles leads to vasodilation of vessel

walls to allow adequate placental perfusion

o In early onset PE, this is incomplete, causing oxidative stress ® the effects can be detected as

high-resistance flow in uterine arteries



o In late onset PE, it occurs as growth of an apparently normal placenta reaches its limits ®

intervillous perfusion may reduce because terminals become overcrowded, causing oxidative

stress

• Stage 2:

o Both mechanisms cause the oxidatively stressed placenta to oversecrete proteins that regulate

angiogenic balance ® this can be detected as increased sFlt-1 & reduced PIGF levels in the

maternal blood

o Widespread endothelial damage may follow ® causing vasoconstriction, increased vascular

permeability & clotting dysfunction, which cause the clinical manifestations of the disease

CLASSIFICATION

• Pre-eclampsia is new hypertension presenting after 20 weeks with significant proteinuria

• Severe pre-eclampsia is pre-eclampsia with severe hypertension and/or with symptoms and/or

biochemical and/or haematological impairment

• Hypertension is classified as:

o Mild ® 140/90 – 149/99 mmHg

o Moderate ® 150/100 – 159/109 mmHg

o Severe ® ≥160/110 mmHg

• Classifications of pre-eclampsia can vary ® the ones below encompass the principles & diversity of the

disease:



o Mild or moderate ® pre-eclampsia without severe hypertension, and with no symptoms or

biochemical / haematological impairment

o Severe ® pre-eclampsia with severe hypertension and/or symptoms or biochemical /

haematological impairment

o Early ® <34 weeks

o Later >34 weeks

EPIDEMIOLOGY

• Pre-eclampsia affects 6% of nulliparous women ® it is less common in multiparous women unless

additional risk factors are present

• There is a ~15% recurrence risk ® this is up to 50% if there has been severe pre-eclampsia before 28

weeks

AETIOLOGY

• Predisposing risk factors include:

o Nulliparity

o Previous / family history of pre-eclampsia

o Long interpregnancy interval

o Obesity

o Extremes of maternal age ® e.g. >40 yrs

o Disorders characterised by microvascular disease ® e.g. chronic hypertension, chronic renal

disease, sickle cell disease, diabetes, autoimmune disease, antiphospholipid syndrome

o Pregnancies with a large placenta ® e.g. twins, hydrops fetalis, molar pregnancy

CLINICAL FEATURES

• Pre-eclampsia is usually asymptomatic ® possible symptoms include:

o Headache

o Drowsiness

o Visual disturbance

o Nausea / vomiting

o Epigastric pain ® later stage

• Hypertension is usually the first sign ® massive oedema is often found in pre-eclampsia, that is not

postural or of sudden onset

• The presence of epigastric tenderness is suggestive of impending complications

• Urine dipstick testing for protein should be considered part of the clinical examination

COMPLICATIONS

• Maternal:

o Early onset disease is more severe ® occurrence of any of the following complications (which

may occur together or up to 24 hrs postpartum) is any indication for delivery whatever the

gestation

o Eclampsia:

§ Grand mal seizure resulting from cerebrovascular vasospasm

§ Mortality can result from hypoxia & concomitant complications of severe disease

§ Treatment is magnesium sulphate & intensive surveillance for other complications



o Cerebrovascular haemorrhage:

§ Results from a failure of cerebral blood flow autoregulation at MABP >140 mmHg

§ Treatment of hypertension should prevent this

o HELLP syndrome:

§ Haemolysis, elevated liver enzymes & low platelets

§ DIC, liver failure & liver rupture may also occur

§ Treatment is supportive, and includes magnesium sulphate prophylaxis against

eclampsia

§ Liver infarction or subcapsular haemorrhage may also occur

o Renal failure:

§ Identified by careful fluid balance monitoring & creatinine measurement

§ Haemodialysis is required in severe cases

o Pulmonary oedema:

§ Severe pre-eclampsia is particularly vulnerable to fluid overload

§ Pulmonary oedema is treated with oxygen & furosemide ® assisted ventilation may

be required

§ ARDS may develop

• Foetal:

o Perinatal morbidity & mortality of the foetus are increased ® pre-eclampsia accounts for ~5%

of stillbirths, and up to 10% of preterm deliveries

o In early onset pre-eclampsia, the principle problem is growth restriction ® preterm delivery is

often required, although spontaneous preterm labour is also more common

o At term, pre-eclampsia affects foetal growth less ® but is still associated with increased

morbidity & mortality

o At all gestations, there is an increased risk of placental abruption

INVESTIGATION

• If bedside urinalysis is positive, the protein is quantified:

o 24hr urine or protein:creatinine ratio is used

o A level of 30 mg/nmol is roughly equivalent to 0.3 g/day protein excretion

o Proteinuria may be absent in early disease ® so testing for proteinuria is repeated

• Blood tests including FBC are taken to show elevation of uric acid, and the Hb is often high ® a rapid

fall in platelets due to aggregation on damaged endothelium indicates impending HELLP syndrome

• A rise in LFTs (particularly ALT) suggests impending liver damage or HELLP ® LDH levels rise with

liver disease & haemolysis

• Renal function is often mildly impaired ® a rapidly rising creatinine suggests severe complications &

renal failure

• To monitor foetal complications, USS helps estimate foetal weight at early gestations & is used to

assess foetal growth ® umbilical artery Doppler & CTG are required to evaluate foetal wellbeing

SCREENING & PREVENTION

• Early prediction:

o Most common screening test is uterine artery Doppler at 20 weeks

o The sensitivity at any stage in pregnancy is ~40% for a 5% specificity

o For early onset pre-eclampsia, the figures are much better



• Late prediction:

o The ratio of sFlt-1 to PIGF in maternal blood is used later in pregnancy ® particularly in

women with mild hypertension

o Useful in determining who will actually develop pre-eclampsia

• Prevention:

o Low dose aspirin 75mg before 16 weeks reduces the risk of pre-eclampsia & is now NICE

recommended

o High dose vitamin D with Ca±2+± supplementation might also be effective

MANAGEMENT

• Assessment:

o Women with new hypertension >140/90 mmHg are assessed in day assessment unit ®

sFlt-1:PIGF ratio assays may determine who is at higher risk

o Patients without proteinuria and with mild or moderate hypertension are usually managed as

outpatients ® BP & urinalysis repeated twice a week, and USS every 2–4 weeks unless

suggestive of foetal compromise

• Admission:

o Necessary with severe hypertension & presence of proteinuria

o If there is no hypertension, but proteinuria ≥30 mg/nmol / ≥0.3 g/day, they should be admitted

o Assessment using sFlt-1:PIGF assay may determine which women are most at risk & should

be admitted

• Medication:

o Antihypertensives:

§ Given if BP reaches 150/100 mmHg

§ Labetalol maintenance is recommended

§ For severe hypertension, nifedipine is used for initial control ® with IV labetalol as

second line

§ Aim for BP is 140/90 mmHg

§ They do not change the course of pre-eclampsia ® but increase maternal safety &

can prolong pregnancy

o Magnesium sulphate:

§ Used in both treatment & prevention of eclampsia ® increases cerebral perfusion so

treats underlying pathology of eclampsia

§ IV loading dose followed by IV infusion

§ If it is required, then delivery is indicated

§ Toxicity is severe ® resulting in respiratory depression, hypotension & loss of patellar

reflex

o Steroids ® used to promote foetal pulmonary maturity if gestation is <34 weeks

• Delivery:

o Women with pre-eclampsia should be delivered by 36 weeks ® diagnosis after this time

should prompt delivery

o Clinical deterioration, maternal complications or concerns for foetal wellbeing on CTG will

prompt delivery ® therefore can be extremely preterm



o As a general rule ® 1 or more foetal / maternal complications are likely to occur within 2 weeks

of the onset of proteinuria

o Women with gestational hypertension should be delivered by 40 weeks as usual ® as long as

foetal compromise is monitored

o C-section is usual delivery ® epidural will help reduce blood pressure:

§ Before 34 weeks

§ If severe growth restriction

§ Abnormal CTG

§ After 34 weeks ® labour can be induced with prostaglandin

o Antihypertensives should be used in labour

o Maternal pushing should be avoided in second stage if BP is ≥160/110 mmHg

o Oxytocin should be used instead of ergometrine in the third stage (as the latter can increase

BP)

• Postnatal care:

o Highest BP is usually reached 4–5 days after birth

o Postnatal treatment is with a b-blocker (e.g. nifedipine), and ACE-I as the second line

o Treatment may be needed for several weeks

Outline the causes & management of pre-existing hypertension in pregnancy

• Diagnosed when BP is already treated, or exceeds 140/90 mmHg before 20 weeks

• Underlying hypertension is present in 5% of pregnancies ® it is more common in:

o Older women

o Obese women

o Positive family history

o Developed HTN on COCP

• Primary / idiopathic hypertension is the most common cause ® secondary hypertension is commonly

associated with:

o Obesity

o Diabetes

o Renal disease ® ADPKD, renal artery stenosis or chronic pyelonephritis

o Phaeochromocytoma

o Cushing’s syndrome

o Cardiac disease

o Coarctation of the aorta

• Symptoms are usually absent

• Renal function is assessed, and renal USS performed ® phaeochromocytoma is excluded, and

quantification of any proteinuria & uric acid level allow for comparison in later pregnancy

• Ideally, medication will be changed before pregnancy:

o ACE-Is ® teratogenic & affect foetal urine production

o Labetalol ® normally used

o Nifedipine ® second line

• Medication may not be needed in the second trimester ® due to the physiological fall in BP

• If the pregnancy is treated as high risk, low dose aspirin is advised ® screening using uterine artery

Doppler & additional antenatal visits are usual



• Delivery is usually undertaken at 38–40 weeks ® although the benefits of this are debated

OBSTETRICS – OTHER MEDICAL DISORDERS IN PREGNANCY


Describe gestational diabetes, and outline its clinical features & management PHYSIOLOGY

• Glucose tolerance decreases in pregnancy due to altered carbohydrate metabolism and the antagonistic

effects of human placental lactogen, progesterone & cortisol

• Pregnancy is ‘diabetogenic’ ® women without diabetes, but with impaired or potentially impaired

glucose tolerance often deteriorate enough to be classified as diabetic in pregnancy (gestational

diabetes)

• Even slightly increased glucose levels have adverse pregnancy effects ® so the definition & diagnosis

are driven by the levels at which treatment is beneficial

• The kidneys of non-pregnant women start to excrete glucose at 11 mmol/L ® in pregnancy, this varies

more but often decreases, so urinalysis for glycosuria is not a useful diagnostic test

• Raised foetal blood glucose levels induce foetal hyperinsulinaemia ® causing foetal fat deposition &

excessive growth (macrosomia)

DEFINITIONS

• Pre-existing diabetes:

o Affects at least 1% of pregnant women

o In those on insulin, increasing amount will be required in pregnancy to maintain

normoglycaemia

• Gestational diabetes:

o ‘Carbohydrate intolerance’ which is diagnosed in pregnancy ® which may or may not resolve

after pregnancy

o Becoming more common ® largely because of increasing prevalence of obesity & varying

diagnostic thresholds

• To diagnose gestational diabetes, NICE stipulate a fasting glucose level ≥5.6 mmol/L ® or >7.8

mmol/L after a 75g glucose tolerance test

• Depending on the criteria used, up to 16% of pregnant women will develop gestational diabetes

FOETAL COMPLICATIONS

• Congenital abnormalities (particularly NTDs) ® 3–4x more common in women with established

diabetes, and related to periconceptual glucose control

• Preterm labour ® occurs in >10% of women with established diabetes

• Foetal lung maturity ® is less than with non-diabetic pregnancies

• Birthweight ® increased, which leads to increased urine & polyhydramnios

• Dystocia & birth trauma ® baby tends to be larger, particularly related to poor 3rd trimester glucose

control

MATERNAL COMPLICATIONS

• Insulin requirements ® increase by up to 300% by the end of pregnancy

• Ketoacidosis ® rare, but hypoglycaemia may result from attempts to achieve optimum glucose control

• Urinary tract infection

• Wound / endometrial infection ® are more common after delivery

• Hypertension & pre-eclampsia ® more common

• Pre-existing ischaemic heart disease ® often worsens



• C-section / instrumental delivery ® more likely because of foetal complications due to compromise &

size

• Diabetic nephropathy (5–10%) ® associated with poorer foetal outcomes, and can lead to massive

proteinuria & deterioration of maternal renal function

• Diabetic retinopathy ® often deteriorates in pregnancy

MANAGEMENT OF DIABETES IN PREGNANCY

• Precise glucose control & foetal monitoring are key in diabetes in pregnancy

• Preconceptual care:

o Glucose levels need to be optimum at conception to reduce risk of foetal complications ®

HbA1c should be <6.5%, and pregnancy is not advised if >10%

o Fasting glucose levels should be 4–7 mmol/L ® if achievable without hypoglycaemia

o Metformin & insulin are appropriate, but other hypoglycaemic agents need to be stopped

o 5mg folic acid should be given

o Statins stopped, and antihypertensives (e.g. labetalol) given instead

o Renal function (creatinine <120 µmol/L), BP & retinae are assessed

• During pregnancy, aim for a fasting level of <5.3 mmol/L, and a 1hr level of <7.8 mmol/L

• Renal function should be checked & the retinae screened for retinopathy ® if abnormal, this needs to

be repeated every trimester

• Aspirin 75mg daily from 12 weeks is advised to reduce the risk of pre-eclampsia

• Foetal monitoring:

o Foetal echocardiography is indicated

o USS to monitor growth & liquor volume at 32 & 36 weeks

• Delivery at 37–39 weeks is advised ® birth trauma is more likely, so C-section is used where estimated

foetal weight is >4 kg

• During labour, glucose levels are maintained with a sliding scale of insulin & dextrose infusion

• The neonate commonly develops hypoglycaemia, as it has been accustomed to hyperglycaemia &

therefore has high insulin levels ® blood glucose should be checked within 4 hrs, and breastfeeding is

strongly advised

GESTATIONAL DIABETES

• Screening using pre-existing risk factors ® these women are given a GTT at 24–28 weeks:

o Previously large baby (>4.5 kg)

o Unexplained stillbirth

o 1st degree relative with diabetes

o BMI >30 kg/m2

o Minority ethnic family origin

o Previous gestational diabetes

• Screening is also done in women with pregnancy factors ® e.g. polyhydramnios or persistent glycosuria

• HbA1c levels are checked to identify pre-existing diabetes ® target levels are the same as in pre-

existing diabetes

• Initially managed with diet & exercise advice ® if not maintaining glucose control (>7 mmol/L fasting

glucose), then metformin and/or insulin is added



• Women should be managed as for pre-existing diabetes ® however, well controlled gestational

diabetes do not need to deliver before 40 weeks

• Treatment should be discontinued postnatally ® but fasting glucose should be measured at 6 weeks

postnatal due to increased risk of T2DM (>50% will become diabetic within the next 10 yrs)

Outline the types of cardiac disease in pregnancy

• In pregnancy, there is a 40% increase in cardiac output ® due to increase in stroke volume & heart

rate, and a 40% increase in blood volume

• There is also a 50% decrease in systemic vascular resistance ® so BP often drops in the 2nd trimester,

but returns to normal by term

• The increased blood flow produces an ejection systolic murmur in 90% of women ® ECG is altered

during pregnancy, and shows left axis shift & inverted T waves

• Cardiac disease affects 0.3% of pregnant women, but is the leading cause of maternal death in the UK

® the maternal risk is dependent on cardiac status, and most encounter no problems

• Increased cardiac output acts as an ‘exercise test’ with which the heart may be unable to cope ® this

usually manifests >28 weeks or soon after labour, with decompensation in association with blood loss &

fluid overload

• Patients should be assessed pre-pregnancy ® cardiac assessment including echo are often required

• Some drugs are contraindicated (including ACE-I & warfarin) ® so hypertension is often managed by b-

blockers, and thromboprophylaxis by LMWH

• In labour fluid balance is important ® elective epidural analgesia reduces afterload, and elective forceps

delivery helps avoid the additional stress of pushing in severe cases

• Foetal cardiac abnormalities are common (3%) ® best detected on USS at 20 weeks’ gestation

TYPES OF CARDIAC DISEASE

• Mild abnormalities:

o E.g. mitral valve prolapse, PDA, uncomplicated VSD / ASD

o Do not usually cause complications

• Pulmonary hypertension ® because of high maternal mortality (20%), pregnancy is contraindicated,

and a termination is offered

• Cyanotic heart disease without pulmonary hypertension:

o Usually corrected, but there is a particular risk of paradoxical embolism

o Anticoagulation is advised

• Aortic stenosis:

o Severe disease causes an inability to increase cardiac output when required, and should be

corrected before pregnancy

o b-blockade is often used

o Epidural analgesia is contraindicated in the most severe cases

o Anticoagulation is required for mechanical aortic valves

• Mitral valve disease:

o Should be treated before pregnancy

o In severe cases of stenosis ® heart failure may develop late in pregnancy

o b-blockade is used

o Artificial metal valves are prone to thrombosis ® so anticoagulation is indicated



• Myocardial infarction:

o Unusual, but becoming more frequent

o Mortality is greater at later gestations

• Peripartum cardiomyopathy:

o Rare (1 in 3000) cause of heart failure & specific to pregnancy

o Develops in the last month, or first 6 months after pregnancy

o Frequently diagnosed late

o Cause of maternal death (risk 15%), and leads to LV dysfunction in >50%

o Treatment is supportive with diuretics & ACE-I

o There is a significant recurrence rate in subsequent pregnancies

Outline respiratory disease in pregnancy

• Tidal volume is increased by 40% in pregnancy ® although there is no change in respiratory rate

• Asthma is common in pregnancy ® it has a variable effect on the disease

• Drugs should not be withheld as they are safe, and a severe asthma attack is life threatening ® well

controlled asthma will have little detrimental effect

• Women on long-term steroids require an increased dose in labour ® as the chronically suppressed

adrenal cortex is unable to produce adequate steroids for the stress of labour

Outline epilepsy in pregnancy

• Epilepsy affects 0.5% of pregnant women ® seizure control can deteriorate in pregnancy, particularly

in labour

• Epilepsy is a significant cause of maternal death, and anti-epileptic treatment should be continued ®

however, the risk of congenital abnormalities (particularly NTD) is increased by 4% due to drug therapy

• The newborn has a 3% risk of developing epilepsy

• Management involves seizure control with as few drugs as possible at the lowest dose ® together with

5mg folic acid

• Sodium valproate should be avoided ® lamotrigine & carbamazepine are the safest

• Vitamin K is given orally from 36 weeks for women on enzyme inducing anti-epileptics

Outline thyroid disease in pregnancy

• Thyroid status does not alter in pregnancy, although iodine clearance is increased ® but goitre is more

common

• Foetal thyroxine production starts at 12 weeks ® before that, it is dependent on maternal thyroxine, so

maternal TSH is increased in early pregnancy

• Hypothyroidism:

o Affects 1% of pregnant women, and commonly due to Hashimoto’s thyroiditis or thyroid

surgery

o Untreated disease is rare, as it leads to anovulation ® but is associated with a high perinatal

mortality

o Even subclinical hypothyroidism is associated with miscarriage, preterm delivery, and

intellectual impairment in childhood

o Also associated with an increased risk of pre-eclampsia ® particularly if anti-thyroxine

antibodies are present



o Replacement with thyroxine is important, and TSH levels are monitored every 6 weeks ® in

normal pregnancy, TSH levels are decreased

• Hyperthyroidism:

o Affects 0.2% of pregnant women, and commonly due to Graves’ disease

o Untreated disease is rare as anovulation is usual ® but inadequately treated disease

increases perinatal mortality

o Anti-thyroid antibodies can cross the placenta and cause neonatal thyrotoxicosis & goitre

o For the mother, thyrotoxicosis may improve in late pregnancy ® but poorly controlled disease

can lead to a thyroid storm

o Hyperthyroidism is treated with propylthiouracil (PTU) in the 1st trimester (rather than

carbimazole) ® but it can cross the placenta & cause neonatal hypothyroidism

o Graves’ disease often worsens postpartum

• Postpartum thyroiditis:

o This is common (5–10%) and a cause of postnatal depression

o Risk factors include anti-thyroid antibodies & T1DM

o There is usually a transient & subclinical hyperthyroidism at around 3 months postpartum ®

followed by about 4 months of hypothyroidism

o Hypothyroidism is permanent in 20%

Outline liver disease in pregnancy ACUTE FATTY LIVER

• Very rare (1 in 9000) but serious condition that is part of the spectrum of pre-eclampsia

• Acute hepatorenal failure, DIC & hypoglycaemia lead to a high maternal & foetal mortality

• There is extensive fatty change in the liver ® malaise, vomiting, jaundice & vague epigastric pain are

early features, while thirst may occur weeks earlier

• Early diagnosis & prompt delivery are essential ® correction of clotting defects & hypoglycaemia are

needed first

• Treatment is then supportive ® further dextrose, blood products, careful fluid balance & occasionally

dialysis

• The recurrence rate is low

INTRAHEPATIC CHOLESTASIS OF PREGNANCY

• Multifactorial condition characterised by:

o Unexplained pruritus

o Abnormal LFTs

o Raised bile acids

o Resolves after pregnancy

• Due to abnormal sensitivity to the cholestatic effects of oestrogen ® occurs in 0.7%, is familial & tends

to reoccur (50%)

• Traditionally associated with increased risk of stillbirth, meconium passage & postpartum haemorrhage

® stillbirth is thought to be due to the toxic effects of bile salts

• Ursodeoxycholic acid (UDCA) helps relieve itching & may reduce the obstetric risks by reducing bile

acid levels

• Due to high risk of maternal & foetal haemorrhage ® vitamin K 10 mg/day is given from 36 weeks



• Induction of labour is often offered ® no clear guidance exists on delivery, but induction at 40 weeks is

common (or 38 weeks if bile acid levels are high)

• Six week follow-up is indicated to ensure liver function returns to normal

Outline renal disease is pregnancy

• In pregnancy, the GFR increases by 40% ® causing urea & creatinine levels to decrease

CHRONIC KIDNEY DISEASE

• Affects 0.2% of pregnant women

• Foetal & maternal complications are dependent on the degree of hypertension & renal impairment ®

pregnancy is considered very high risk if the creatinine level is >200 mmol/L

• Renal function often deteriorates late in pregnancy ® this is more common in severe disease, and can

lead to permanent deterioration

• Proteinuria can cause diagnostic confusion with pre-eclampsia ® but is normally present <20 weeks

• Foetal complications:

o Preterm delivery

o Pre-eclampsia

o IUGR

o Polyhydramnios

• Management involves USS for foetal growth, measurement of renal function, screening for urinary

infection & control of hypertension ® in severe cases, dialysis is necessary

URINARY TRACT INFECTION

• Urine infection is associated with:

o Preterm labour

o Anaemia

o Increased perinatal morbidity & mortality

• Asymptomatic bacteriuria affects 5% of women ® but in pregnancy, it is more likely to lead to

pyelonephritis (20%)

• Urine should be cultured at booking visit, and asymptomatic bacteriuria treated

• Pyelonephritis affects 1–2% of women, causing loin pain, rigors, vomiting & fever ® requires treatment

with IV antibiotics

o NB: E. coli accounts for ~75% of cases & is often amoxicillin resistant

Outline the thrombophilias & the antiphospholipid syndrome ANTIPHOSPHOLIPID SYNDROME (APS)

• This is when lupus anticoagulant, anti-apolipoprotein antibodies and/or anticardiolipin antibodies

occur in association with adverse pregnancy complications or thrombotic events

• Foetal loss is high, and complications include:

o Placental thrombosis

o Recurrent miscarriage

o IUGR

o Early pre-eclampsia

• Low levels of antibodies are also present in nearly 2% of all pregnant women ® but treatment should be

restricted to those with the syndrome



• The pregnancy is managed as high risk:

o Serial USS & elective induction of labour

o Treatment with aspirin & LMWH

o Postnatal anticoagulation is recommended to prevent VTE

OTHER PROTHROMBOTIC DISORDERS

• Other prothrombotic conditions can also cause increased risk of pregnancy complications, as well as

VTE, including:

o Antithrombin deficiency

o Protein S or C deficiency

o Prothrombin gene mutation

o Factor V Leiden heterozygosity

• Risk is greater where these conditions co-exist, or if there have been previous complications

• Hypohomocysteinaemia:

o Also associated with increased pregnancy loss & pre-eclampsia

o Treatment is usually high dose folic acid

o Women with prothrombin tendencies & an adverse pregnancy history are usually treated as for

antiphospholipid syndrome ® although the effectiveness of this is not proven

SYSTEMIC LUPUS ERYTHEMATOSUS

• SLE affects 0.1–0.2% of pregnant women

• In the absence of lupus anticoagulant or anti-apolipoprotein / anticardiolipin antibodies ® the risks to

pregnancy are largely confined to those with active disease or associated hypertension, renal or

cerebral disease

• Maternal symptoms often relapse after delivery

Outline venous thromboembolic disease in pregnancy

• Pregnancy is prothrombotic, and incidence of VTE is increased 6x ® blood clotting factors are

increased, fibrinolytic activity is reduced, and blood flow is altered by mechanical obstruction &

immobility

• Women with inherited prothrombotic conditions or those with a family / personal history are particularly

prone to thromboses

• Pulmonary embolism:

o Leading direct cause of maternal death in the UK

o Embolism occurs in <0.3% ® with a mortality of 3.5%

o Chest pain & dyspnoea are common ® along with tachycardia, raised RR & JVP, and chest

abnormalities

o Diagnosis using CXR, ABG & CT, or with VQ scan

§ NB: ECG changes of normal pregnancy can mimic a PE

• Deep vein thrombosis:

o Occurs in 0.1% of pregnant women

o Thromboses are more often iliofemoral & on the left

o Doppler examination & venogram or pelvic MRI are used

• Cerebral venous thrombosis:

o Occurs in 1 in 10,000 pregnancies ® particularly during the puerperium



o Present as headache and/or stroke

o Imaging with MRI is best

• A thrombophilia screen is performed before treatment with subcutaneous LMWH ® dosing is weight

based and adjusted according to anti-Factor Xa level, and more is needed than in a non-pregnant

woman as clearance is rapid

• If possible, treatment is stopped shortly before labour ® but restarted & continued into the puerperium

• Warfarin is teratogenic & may cause foetal bleeding, so seldom used antenatally ® both LMWH &

warfarin can be used in breastfeeding women

• Every woman requires an early antenatal risk assessment ® reviewed according to subsequent events

• General measures are required for all (e.g. mobilisation & maintenance of hydration) ® compression

stockings are useful for those in whom LMWH is contraindicated

• Antenatal prophylaxis is restricted to women at very high risk ® e.g. previous VTE

• Postpartum prophylaxis is more frequently used ® if it has been used antenatally it is continued, or if

there is one major or intermediate, or two or more minor risk factors ® then LMWH is prescribed for at

least 10 days, and can usually be given 12 hrs after delivery

Outline the risks of obesity in pregnancy • Up to 20% of pregnant women now have a MBI >30 ® most risks are linearly related to BMI

• Obese women have a higher risk of:

o Thromboembolism

o Pre-eclampsia

o Diabetes

o C-section

o Wound infection

o Difficult surgery

o Postpartum haemorrhage

o Maternal death



• There is a higher rate of congenital abnormalities (e.g. NTDs) & USS are less accurate ® diabetes &

pre-eclampsia contribute to a 2–3x increase in perinatal mortality

• High dose folic acid (5mg) is recommended, as is vitamin D

• The pregnancy should be considered high risk, particularly if BMI ≥35 ® screening for diabetes & closer

BP surveillance are required

• A formal anaesthetic risk assessment & antenatal thromboprophylaxis are recommended if BMI ≥40

• There is an increasing trend towards elective C-section in very obese women

Outline mental illness in pregnancy & the postnatal period

• Early postnatal period represents the highest risk period for women developing new onset mental illness

• Mental illness & postnatal depression are major risk factors for maternal suicide ® 23% of women who

die between 6 weeks & 1 yr postpartum are from psychiatric causes

• Red flag signs that need referral for senior psychiatric assessment are:

o Recent significant change in mental state

o Emergence of new symptoms

o New thoughts

o Acts of violent self-harm

o New & persistent expressions of incompetency as a mother

o Estrangement from the infant

BIPOLAR AFFECTIVE DISORDER

• Lifetime risk is up to 1% ® onset most commonly during childbearing age

• Characterised by episodes of depression or mania which persist for several weeks at a time ®

sometimes with psychotic symptoms

• Delivery can precipitate relapse in women with bipolar ® and condition is a major risk factor for

postpartum psychosis

• Treatment includes mood stabilisers, antipsychotics, anticonvulsants & lithium (cardiac defects) ®

treatment decisions must weigh the risks to the foetus against increased risk of relapse or postpartum

psychosis

POSTPARTUM PSYCHOSIS

• Severe mental illness than can affect 1–2 in 1000 women ® it is a psychiatric emergency

• Presents suddenly in the early postnatal period, with psychotic & severe mood symptoms

• There may be an acute risk of suicide, self-harm or neglect, or neglect of the baby ® intentional harm to

the baby is rare

DEPRESSION

• Depression affects 10–15% of pregnant & postnatal women

• Incidence of severe depression in women is highest in the postnatal period, affecting 3% of mothers ®

symptoms are similar to those in non-pregnant women

• Treatment in pregnant & postnatal women generally follows guidelines of depression in non-pregnant

women:

o CBT should be sought as first line in mild to moderate depression

o Antidepressants are effective in severe depression ® SSRIs & TCAs

• NB: Withdrawal & short-term side effects of antidepressants have been seen in the neonate



ANXIETY DISORDERS

• These include:

o Generalised anxiety disorder

o Panic disorder

o Phobias

o Obsessive compulsive disorder

o Post-traumatic stress disorder

• Anxiety disorders are common in the perinatal period, and may also be prominent symptoms in

depression ® prevalence rates are similar to the general population

• Incidence of OCD may increase in the perinatal period ® the content of obsessive thoughts may involve

the baby, but are not usually associated with risk of intentional harm

• PTSD may be triggered by traumatic experience during delivery ® particularly instrumental delivery

• Tokophobia (fear of childbirth) can cause great distress to pregnant women ® in severe cases, it may

constitute an indication for elective C-section

• Treatment guidelines broadly follow those for the general population:

o Psychological therapies as first line

o Medications should be reserved for severe cases ® SSRIs

o Benzodiazepines are not recommended in pregnancy due to the risk of dependence, neonatal

withdrawal & oversedation

SCHIZOPHRENIA

• Affects up to 1% of women over the course of a lifetime ® most common during childbearing age

• Majority of people with schizophrenia require long-term treatment with antipsychotics ® these have not

been shown to be teratogenic, but olanzapine & quetiapine are associated with weight gain & therefore

gestational diabetes

• Treatment is usually continued due to the high risk of relapse if medication is stopped ® relapse of

schizophrenia in the perinatal period is associated with poor outcomes for the mother & child

RECREATIONAL DRUG USE

• Women abusing drugs in pregnancy are often vulnerable personally & socially ® and at an increased

risk of other illnesses (e.g. STIs, HIV, Hep C)

• Pregnancy care should be MDT, the newborn may be subject to a care order, and the foetus may also

be at risk of congenital abnormalities ® so the pregnancy should be considered high risk, especially for

IUGR & preterm delivery

• Opiates:

o Not teratogenic ® but use is associated with preterm delivery, IUGR, stillbirth, developmental

delay & SIDS

o Methadone maintenance is advised

o Some neonates experience severe withdrawal symptoms & convulsions

• Cocaine:

o Probably teratogenic

o Can cause childhood intellectual impairment ® but is particularly associated with IUGR,

placental abruption, preterm delivery, stillbirth & SIDS

o Pregnancy monitoring is required



• Ecstasy:

o Teratogenic with an increased risk of cardiac defects & probably gastroschisis

o Pregnancy complications are similar to cocaine

• Benzodiazepines:

o Associated with foetal clefts

o Can cause neonatal hypotonia, as well as withdrawal symptoms

• Cannabis:

o Abuse of other drugs makes attribution of risk difficult ® but may cause IUGR & affect later

childhood development

• Alcohol:

o 50% of women drink no alcohol at all in pregnancy

o 10% admit to drinking more than 3 units per week ® below this level, there is no consistent

evidence of harm

o May cause miscarriage in the first 12 weeks

o At higher levels, the incidence of IUGR & birth defects increases

o Alcohol abuse in pregnancy greatly increases risk ® associated with foetal alcohol

syndrome, with an incidence of 0.6 per 1000

o Affected individuals have facial abnormalities, growth restriction, a small / abnormal brain &

developmental delay (>18 units per week)

o Alcohol spectrum disorder (9 in 1000) encompasses lesser variants of the syndrome ® USS

may not detect the syndrome, but is used to monitor foetal growth

• Tobacco:

o Smoking in pregnancy is related to social class ® about 1 in 3 women smoke during

pregnancy, and 10% of pregnancies are exposed to environmental smoke

o Smoking is probably not teratogenic ® associated in a dose-response manner with an

increased risk of:

§ Miscarriage

§ IUGR

§ Preterm birth

§ Placental abruption

§ Stillbirth

§ SIDS

§ Associated with a variety of childhood illnesses

o Pre-eclampsia is less common ® but more severe if it does occur

o Women should be encouraged to stop or at least cut down smoking ® nicotine replacement is

effective & preferable to smoking

o Pregnancy should be considered high risk

Outline the types of anaemia that occur in pregnancy

• There is a 40% increase in blood volume in pregnancy, which is relatively greater than the increase in

red cell mass ® so the result is a net fall in Hb concentration, such that the lower limit of normal is 110

g/dL in the first trimester, and 95 g/dL in the third trimester

• Iron & folic acid requirements increase ® iron absorption is increased 3x



• A high Hb level is associated with an increased risk of pregnancy complications (e.g. preterm & IUGR)

® possibly because it reflects low blood volume (as found in pre-eclampsia) & because of its

association with smoking

IRON DEFICIENCY ANAEMIA

• Affects >10% of pregnant women ® although 80% of women not receiving iron have depleted stores by

term

• May coexist with folic acid deficiency

• Symptoms are usually absent unless Hb is <90 g/dL ® the MCV reduces, but is often initially normal,

and ferratin levels are reduced

• Treatment is with oral iron (achieving an increase of up to 8 g/dL/week, but can cause GI upset ® in

severe cases, IV iron is quicker & may prevent the need for blood transfusion

FOLIC ACID & VITAMIN B12 DEFICIENCY ANAEMIA

• Folic acid deficiency is more common than that of vitamin B12

• The MCV is usually increased, and red cell folic acid & vitamin B12 levels are low

• Folic acid deficiency should always be considered if anaemia is present without marked microcytosis

• Treatment is with oral folic acid & vitamin B12

PROPHYLAXIS AGAINST ANAEMIA

• Routine iron supplements reduce the incidence of anaemia without affecting perinatal outcome ®

postnatal blood transfusion is less frequently required

• Further foetal & neonatal anaemia have adverse outcomes ® although their relationship to maternal

iron stores is unknown

• Iron is often poorly tolerated, and routine supplementation is not universal ® all women are given

dietary advice, and the Hb is check at booking, 28 & 34 weeks

• Iron ± folic acid is given if the Hb is <110 g/dL in the 1st & 3rd trimesters, and if <105 g/dL in the 2nd

trimester

• In those with epilepsy, diabetes, obesity, or previous history of NTD ® a 5mg dose of folic acid is given

Outline influenza in pregnancy

• Influenza accounted for 10% of all maternal deaths in the UK during the 2009–10 swine flu ® in 2011–

13, it accounted for 4%

• Pregnancy, particularly with comorbidity, increases susceptibility to severe disease

• Presentation is typical, and early use of zanamivir is recommended ® with more severe or pre-existing

chest disease, then oseltamivir is recommended

• ICU & ECMO may be required in severe cases

• The best management is prevention ® vaccination of pregnant women at any stage of pregnancy is

strongly advised during winter months

• The vaccine has not known adverse foetal effects, and will reduce both maternal & foetal mortality

Outline haemoglobinopathies in pregnancy • The adult Hb molecule (HbA) is made of two a chains & two b chains bound together to form a tetramer

® foetal Hb (HbF) is normally replaced with HbA after birth, and is made of two a chains & two g chains



SICKLE CELL DISEASE

• Recessive disorder due to abnormal b chain formation (S chain) ® results in an abnormal Hb molecule

made of two a chains bound to two S chains

• Found in people with Afro-Caribbean ancestry

• In the UK there are 100–200 pregnancies in homozygotic individuals every year ® but 300,000 affected

individuals born worldwide every year

• Heterozygous have 35% HbS and usually have no problems ® Hb electrophoresis now performed in

the UK on all pregnant women

• Homozygous individuals are often affected with sickle cell crises of bone pain & pulmonary symptoms

® pulmonary hypertension & proliferative retinopathy may occur

• Homozygous individuals will have chronic haemolytic anaemia for life

• Maternal complications in pregnancy include:

o Acute painful crises (35%)

o Pre-eclampsia

o Thrombosis

• Foetal complications in pregnancy include:

o Miscarriage

o IUGR

o Preterm labour

o Death

• Management should be in conjunction with a haemoglobinopathy specialist ® advice on avoiding

dehydration & seeking help early is important

• Other management options include:

o Hydroxycarbamide is probably teratogenic & so stopped

o Penicillin V is continued

o High dose folic acid

o Aspirin & LMWH are often indicated

o Monthly urine culture

o Iron is avoided to prevent overload

• Crises are managed with hydration, analgesia, and often antibiotics & anticoagulation

• USS every 4 weeks, and delivery is normally indicated by 38 weeks

THALASSAEMIAS

• Alpha thalassaemia:

o Results from impaired synthesis of the a chain in the Hb molecule

o Occurs in largely South East Asian origin

o 4 genes are responsible for chain synthesis ® individuals with all 4 gene deletions die in utero,

those with 3 gene deletions have lifelong requirement for transfusions, and those with 1 or 2

deletions are carriers, usually with mild anaemia

• Beta thalassaemia:

o Results from impaired synthesis of the b chain in the Hb molecule

o Occurs in largely South East Asian origin & Mediterranean ancestry

o Recessive disorder, and the heterozygous state causes little illness ® although there is a

chronic anaemia which can worsen during pregnancy



o Homozygous beta thalassaemia in pregnancy is rare in the UK ® but 70,000 individuals

affected worldwide every year

• A chronic haemolytic anaemia is present, and multiple transfusions cause iron overload ® therefore

causing hepatic & cardiac dysfunction, endocrine disease (thyroid & parathyroid), and diabetes

• Monitoring for effects of iron overload & use of chelation therapy have been key to reducing mortality

• Maternal complications ® fertility is reduced, and liver disease, cardiac failure & diabetes are common


o Growth restriction & foetal death are more common

o Prenatal diagnosis is offered if the partner is heterozygous for either the beta or alpha form

• Preconceptual planning is crucial ® primarily because chelation therapy is probably teratogenic, and

avoided in the 1st trimester ® deferoxamine is used after this time, and USS is used 4-weekly

Outline female genital mutilation (FGM) & the impact on pregnancy

• This practice involves partial or total removal of the external female genitalia, or injury to the female

genital organs for non-medical reasons

• It is classified into four types:

o Type 1 (clitoridectomy) ® partial or total removal of the clitoris or of the prepuce

o Type 2 (excision) ® partial or total removal of the clitoris & labia minora ± labia majora

o Type 3 (infibulation) ® narrowing of the vaginal opening by cutting & repositioning the labia,

with or without removal of the clitoris

o Type 4 (other) ® all other procedures to the female genitalia for non-medical purposes

• FGM is practiced in many countries in Africa, the Middle East, Malaysia & Indonesia ® communities

practice it for different reasons, including:

o Ideas of preservation of virginity

o Promoting hygiene

o Adherence to cultural norms

o Religion ® not condoned in Bible or Quran

• FGM is performed from infancy to 15 yrs, depending on the country & culture ® it is a violation of

human rights, child abuse, and has no health benefits

• Complications include:

o Pain

o Bleeding

o Infection

o Urinary retention

o Damage to pelvic organs

o Death

• Longer term complications include:

o Failure to heal

o Urinary tract infections

o Difficulty urinating or

menstruating

o Chronic pelvic infection

o Vulval pain due to cysts or

neuromas

o Pain during sex

o Infertility

o Fistulae

o Severe perineal trauma during

childbirth

• FGM is illegal to perform in the UK, and illegal to arrange in the UK to happen abroad

OBSTETRICS – RED CELL ISOIMMUNISATION


Outline the pathophysiology of red cell isoimmunisation

• Red cell isoimmunisation occurs when the mother mounts an immune response against antigens on

foetal red cells in her circulation ® the resulting antibodies then cross the placenta & cause foetal red

cell destruction

BLOOD GROUPS

• Blood is classified according to its ABO & Rhesus genotype ® Rhesus consists of three linked gene

pairs, and one allele of each pair is dominant to the other:

o C/c

o D/d

o E/e

• An individual inherits one allele of each pair from each parent in a Mendelian fashion ® the most

significant in isoimmunisation is the D gene

• Only individuals who are DD or Dd express the D antigen & are therefore D Rhesus positive ® people

who have dd are D Rhesus negative, and their immune systems will recognise the D antigen as foreign

if they are exposed to it

SENSITISATION

• Small amounts of foetal blood cross the placenta & enter the maternal circulation during uncomplicated

pregnancies ® particularly at sensitising events, such as delivery

• If the foetus is D Rhesus positive & the mother is D Rhesus negative ® the mother will mount an

immune response & therefore create anti-D antibodies

HAEMOLYSIS

• Immunity is permanent ® so if the mother’s immune system is again exposed to the antigen (e.g. in a

subsequent pregnancy), large numbers of antibody are created

• These antibodies can cross the placenta & bind to foetal RBCs, which are then destroyed in the foetal

reticuloendothelial system ® this can cause haemolytic anaemia & ultimately death, called Rhesus

haemolytic disease of the newborn

• A similar immune response can be mounted against other RBC antigens ® the principal antibodies

affecting the foetus are anti-C, anti-E & anti-Kell

EPIDEMIOLOGY

• 15% of Caucasian women, but fewer African or Asian women, are D Rhesus negative

• The use of anti-D, smaller family size & good management of isoimmunisation has resulted in perinatal

death attributed to Rhesus disease becoming extremely rare

• About 1% of D Rhesus negative women have been sensitised in the UK ® mostly as a result of omitted

or inadequate anti-D

PREVENTION

• Production of maternal anti-D can be prevented by the administrations of exogenous anti-D to the

mother ® this mops up the foetal RBCs that have crossed the placenta by binding to their antigens,

thereby preventing recognition by the mother’s immune system

• If both parents are known to be D Rhesus negative ® there foetus must also be D Rhesus negative,

and therefore will be unaffected



• Routine NIPT for foetal Rhesus type, using maternal blood, is now recommended in the UK ® anti-D is

pointless if maternal anti-D is already present, as sensitisation has already occurred

• Anti-D should be given to all women who are Rhesus negative if foetal status is unknown or the baby is

Rhesus positive at 28 weeks ® this alone will reduce the rate of isoimmunisation in a first pregnancy to

0.2%

• Anti-D is also given to such women within 72hrs of a sensitising event ® including amniocentesis &

ECV, foetal death, or antepartum haemorrhage

• It is also given after in utero events ® such as miscarriage or threatened miscarriage, if the uterus is

instrumented (ERPC), termination of pregnancy, or ectopic pregnancy

• Postnatally, the neonate’s blood group is checked ® if Rhesus positive, then anti-D is given to the

mother within 72hrs

• A Kleihauer test to assess the number of foetal cells in the maternal circulation is also performed within

2hrs of birth to detect occasional larger foetomaternal haemorrhages that require larger doses of anti-D

to mop up

MANIFESTATIONS OF RHESUS DISEASE

• As antibody levels rise & cross the placenta ® they cause haemolysis in the foetus

• In mild disease, this may lead to neonatal jaundice only ® or there may be sufficient haemolysis to

cause neonatal anaemia (haemolytic disease of the newborn)

• More severe disease causes in utero anaemia ® as this worsens, it causes cardiac failure, ascites &

hydrops fetalis, and foetal death follows

• Rhesus disease usually worsens with successive pregnancies ® as maternal antibody production

increases

Describe the management of red cell isoimmunisation

• The management of Rhesus isoimmunisation varies widely ® but comprises:

o Identification of women at risk of foetal haemolysis & anaemia

o Assessing if / how severely the foetus is anaemic

o Blood transfusion in utero or delivery for affected foetus

IDENTIFICATION

• Foetal Rhesus status:

o Unsensitised women are screened for antibodies at booking & at 28 weeks’ gestation

o If antibodies are found ® the foetal genotype needs to be determined

• Maternal antibody level:

o If anti-D levels are <10 IU/ml & there is no previous history of an affected baby ® a significant

foetal problem is very unlikely, and levels are subsequently checked every 2–4 weeks

o When anti-D levels are >4 IU/ml ® the foetus is investigated for anaemia using USS

o If there is previous history of foetal effects ® antibody levels are less predictive

ASSESSING SEVERITY OF FOETAL ANAEMIA

• Pregnancies at risk of foetal anaemia are assessed using USS ® Doppler USS of the peak velocity in

systole of the foetal MCA has a high sensitivity for anaemia before 36 weeks, and it is used at least

fortnightly in high-risk pregnancies



• Very severe anaemia is detectable as foetal hydrops or excessive foetal fluid ® if anaemia is

suspected, foetal blood sampling is performed under USS using a needle in the umbilical vein at the

cord insertion in the placenta, or in the intrahepatic vein

• The risk of foetal loss is 1%, and after 28 weeks it should be performed with facilities for immediate

delivery if complications arise

TREATMENT OF FOETAL ANAEMIA

• Foetal blood sampling is performed with Rhesus negative, high haematocrit, CMV negative blood ®

which can be injected into the umbilical vein if anaemia is confirmed

• The process of quantification of anaemia & transfusion will need to be repeated at longer intervals until

about 36 weeks ® after which time delivery is undertaken

• Blood can be administered to the neonate ® both top up (anaemia) or exchange (hyperbilirubinaemia)

transfusions may be required

• All neonate born to Rhesus negative bothers should have their blood group checked ® an FBC, blood

film & bilirubin may detect mild degrees of isoimmunisation

OBSTETRICS – PRETERM DELIVERY


Define preterm delivery

• Preterm delivery occurs between 24–37 weeks’ gestation

• Most important before 34 weeks ® as neonatal risk is highest

• <24 weeks it is thought of as miscarriage ® although some babies have survived

• 5–8% of deliveries are preterm ® 6% present with contractions preterm, but deliver at term

• Preterm delivery can be spontaneous, but at later gestations is more likely to be iatrogenic ® most

common example is pre-eclampsia, as delivery is the only cure

• Late miscarriage is between 16–23+6 weeks ® overlaps with preterm if the foetus is born alive

Outline the complications of preterm delivery NEONATAL

• Prematurity accounts for ~80% of neonatal ICU admissions, 20% of perinatal mortality, and up to 50%

of cerebral palsy

• Other long-term morbidity is common, including:

o Chronic lung disease

o Blindness

o Minor disability

• At 24 weeks, approximately 1/3 of babies will be handicapped, and 1/3 will die ® by 32 weeks, these

risks are 5%

• Even between 34–37 weeks, there is increased respiratory distress & infant mortality, and an increased

risk of subtle cognitive & behavioural problems

MATERNAL

• Infection is associated with preterm labour ® occasionally causes severe maternal illness & death

• C-section is more commonly used

Describe the risk factors, clinical features & management of spontaneous preterm labour RISK FACTORS

• Previous history

• Lower socioeconomic class

• Extremes of maternal age

• A short interpregnancy interval

• Maternal medical disease ® e.g. renal failure, DM, thyroid

• Pregnancy complications ® e.g. pre-eclampsia, IUGR

• Male foetal gender

• High haemoglobin

• Sexually transmitted & vaginal infections ® e.g. BV

• Previous cervical surgery

• Multiple pregnancy

• Uterine abnormalities

• Fibroids

• Polyhydramnios

• Congenital foetal abnormalities

• Antepartum haemorrhage



MECHANISMS

• Multiple pregnancy is an increasing contributor due to assisted conception ® delivery before 34 weeks

occurs in 20% of twins & is the mean time for twins

• Polyhydramnios has the same effect ® probably largely mediated by increased stretch

• Can be due to the foetal survival response, which is more common where the foetus is at risk ® e.g.

pre-eclampsia, IUGR, infection, or placental abruption ® iatrogenic preterm delivery attempts to

improve upon this mechanism

• Can be due to uterine abnormalities ® such as fibroids or congenital (e.g. Müllerian duct) abnormalities

• Can be caused by cervical impotence, when the cervix painlessly dilates & precedes some preterm

deliveries ® some cervical surgery (e.g. for CIN) or multiple dilations of the cervix may be a cause

• Infection is implication in 60% of preterm deliveries & is often subclinical ® BV is a known risk factor,

but GBS, Trichomonas, Chlamydia & commensals have also been implicated ® manifestations include:

o Chorioamnionitis

o Offensive liquor

o Neonatal sepsis

o Endometritis

• Urinary tract infection & poor dental hygiene are also risk factors

PREDICTION & PREVENTION OF PRETERM LABOUR

• Cervical length on transvaginal USS is both a sensitive & specific indicator of preterm labour risk

• Prevention strategies are limited to women at high risk, and should begin at 12 weeks ® most

frequently women who have previously delivered between 16–34 weeks

• Cervical cerclage:

o Insertion of one or more sutures in the cervix to strengthen it & keep it closed

o Commonly used, and vaginal route is usual ® but can be placed abdominally if the cervix is

very short or scarred, or if previous vaginal cerclage has failed

o Usually pre-pregnancy, and can be laparoscopic

o Cerclage is used in 3 situations:

§ Elective at 12–24 weeks

§ Cervix can be scanned & only sutured if significant shortening ® usual policy

§ Rescue suture ® prevent delivery even when the cervix is widely dilated in up to 50%

of suitable women

• Progesterone supplementation ® suppositories in early pregnancy reduce the risk of preterm labour

in women at high risk

• Infection ® screening and treatment of STIs, UTIs & BV (before 16 weeks) is beneficial, although the

role of antibiotics for other bacteria is disputed

• Foetal reduction ® reduction of higher order multiples is offered at 10–14 weeks

• Treatment of polyhydramnios:

o Polyhydramnios can be treated by needle aspiration (amnioreduction) or NSAIDs (foetal

surveillance)

o These reduce foetal urine output ® but can occasionally cause (reversible) premature closure

of the foetal ductus arteriosus



• Treatment of medical disease:

o The prevention of placental disease associated with autoimmune disease reduces the risk of

preterm delivery

o Women with thyroid antibodies may also benefit from thyroxine

CLINICAL FEATURES & INVESTIGATION

• Women present with painful contractions ® but >50% will spontaneously resolve & not result in delivery

until term

• Cervical incompetence is painless cervical dilation ® women may experience a dull suprapubic ache or

increased discharge

• Antepartum haemorrhage & fluid loss are common ® latter suggests ruptured membranes

• Fever & severe sepsis may occur ® vaginal exam is performed (unless membranes have ruptured),

and dilated cervix confirms diagnosis

• A negative foetal fibronectin assay means preterm delivery within the next week is unlikely ® TV USS

of cervical length is also predictive, with delivery unlikely if >15 mm

• CTS & USS are used to assess the foetal state

• Vaginal swabs should be taken ® maternal CRP usually rises with chorioamnionitis, and WCC is

useful (but steroids also cause it to rise)

MANAGEMENT

• Steroids & tocolytics:

o Steroids are given between 23–34 weeks in women who are presenting with contractions ®

can be restricted to those who are fibronectin positive or have a short cervix

o Steroids reduce perinatal morbidity & mortality by promoting pulmonary maturity ® do not

increase risk of infection, but additional insulin will need to be given to diabetic patients

o Take 24 hrs to work, so delivery is artificially delayed using tocolytics ® only 1 course is

advised

o Tocolytics:

§ Nifedipine or oxytocin receptor antagonists (e.g. atosiban) can be given to allow

steroids time to act, or allow in utero transfer to a unit with NICU

§ It delays (rather than stops) preterm labour, and should not be used for more than

24hrs or in the presence of an infection

• Detection & prevention of infection:

o Sepsis requires full rapid evaluation & treatment ® may occur even when the membranes

have not ruptured

o Chorioamnionitis warrants IV antibiotics & immediate delivery ® antibiotics should not be

administered to non-infected women, as long-term cognitive impairment is increased

• Magnesium sulphate:

o Magnesium sulphate is neuroprotective for the neonate if given <12hrs prior to anticipated or

planned preterm labour

o Single dose of 4g by slow IV infusion is used prior to delivery between 23–34 weeks ® care is

required as it is toxic in overdose



• Transfer:

o Extremely premature (<27 weeks) or small (<800g) neonates have a better survival rate if born

in a unit with NICU ® the effect is probably a result of both improved antenatal & postnatal

care

o If delivery is not imminent or the mother unstable ® urgent in utero transfer should be

arranged

• Delivery:

o Vaginal delivery reduces incidence of neonatal respiratory distress syndrome ® C-section

is only undertaken for the usual obstetric indications, but most preterm are in breech position,

so C-section is common

o Paediatric facilities are mobilised ® membranes may not rupture in labour (at least up to 32

weeks), so labour may be slow, allowing steroids to act

o Forceps (rather than ventouse) are used only for the usual obstetric indications

o Unless immediate neonatal resuscitation is required ® the cord should not be clamped for 45

seconds to reduce neonatal morbidity

o Antibiotics for delivery are recommended for women in actual preterm labour ® because of the

increased risk & morbidity of GBS

Describe the clinical features, investigation, complications & management of prelabour

rupture of membranes DEFINITION

• PROM ® this is when membranes rupture before labour at <37 weeks

• Often the cause is unknown ® but all the causes of preterm labour may be indicated

• It occurs before 1/3 of preterm deliveries

COMPLICATIONS

• Preterm delivery is the principal complications ® follows within 48hrs in >50% of cases

• Infection of foetus, placenta (chorioamnionitis), or cord (funisitis) are common, and may occur before

(and be the cause) or after membrane rupture ® the earlier the gestation at membrane rupture, the

higher the risk of pre-existing infection

• Prolapse of the umbilical cord may rarely occur ® absence of liquor can result in pulmonary hypoplasia

& postural deformities

CLINICAL FEATURES

• Presents with a gush of clear fluid ® followed by further leaking

• A pool of fluid in the posterior fornix on examination is diagnostic ® digital examination is avoided for

fear of infection

• Chorioamnionitis is characterised by contractions or abdominal pain, fever or hypothermia, tachycardia,

uterine tenderness, and coloured or offensive liquor ® although clinical signs often appear late

INVESTIGATION

• ‘Point of care’ tests are available in doubtful cases ® but not entirely reliable

• USS may reveal reduced liquor ® but the volume can also be normal as foetal production continues

• High vaginal swab, FBC & CRP are taken to look for infection ® lactate assesses severity of sepsis



• Foetal wellbeing is assessed by CTG ® a persistent foetal tachycardia is suggestive of infection

MANAGEMENT

• Risk of preterm delivery is balanced against risk of infection ® the woman is admitted for at least 48hrs

& given steroids

• Close maternal & foetal surveillance is performed ® if the gestation reaches 34–36 weeks, then

normally delivery is undertaken

PREVENTION OF INFECTION

• Prophylactic use of erythromycin in women even without clinical evidence of infection is usual

• Co-amoxiclav is contraindicated ® as the neonate is more prone to necrotising enterocolitis

OBSTETRICS – ANTEPARTUM HAEMORRHAGE


Define antepartum haemorrhage & outline the causes

• Antepartum haemorrhage (APH) is bleeding from the genital tract after 24 weeks’ gestation

• Causes include:

o Placenta praevia

o Placental abruption

o Uterine rupture

o Ruptured vasa praevia

o Bleeding of undetermined origin

o Bleeding of gynaecological origin

Describe placenta praevia and outline the investigation & management

• Placenta praevia occurs when the placenta is implanted in the lower segment of the uterus ®

complicates 0.4% of pregnancies at term

• At 20 weeks, the placenta is ‘low-lying’ in many pregnancies, but appears to move upwards as the

pregnancy continues ® this is due to the formation of the lower segment of the uterus in the 3rd

trimester, and the myometrium where the placenta is implanted moves away from the internal cervical

os

• Placenta praevia is classified according to the proximity of the placenta to the internal os ® it may be

predominantly on the anterior or posterior uterine wall:

o Marginal ® placenta in lower segment, not over os

o Major ® placenta partially or completely covering os

• Aetiology is unknown ® but is slightly more common in:

o Twins

o High parity

o Increased maternal age

o Scarred uterus

• The placenta in the lower segment obstructs engagement of the head ® this necessitates C-section,

and may also cause transverse lie

• Haemorrhage can be severe ® may continue during & after delivery, as the lower segment is less able

to contract & constrict the maternal blood supply

• If a placenta implants in a previous C-section scar ® it may be so deep as to prevent placental

separation (placenta accreta) or penetrate through the uterine wall into surrounding structures such as

the bladder (placenta percreta)

o Placenta accreta occurs in 10% of women who have both a placenta praevia & a single

previous C-section

o This may provoke massive haemorrhage at delivery & often requires a hysterectomy

• Presents with intermittent painless bleeds, which increase in frequency & intensity over several weeks

® however, 1/3 of women do not experience bleeding before delivery

• Breech position & transverse lie are common, and the foetal head is not engaged & high ® vaginal

exam is never performed unless placenta praevia has been excluded

• USS is used to make the diagnosis ® if a low-lying placenta is detected at 2nd trimester scan, then it is

repeated at 32 weeks to exclude placenta praevia (vaginally if placenta is posterior)

• Placenta <2cm from internal cervical os is likely to be praevia at term ® if it is anterior & under C-

section scar, 3D USS is used to exclude placenta accreta



• Where presentation is with bleeding, CTG, FBC, clotting & crossmatch are completed ® foetal

distress is uncommon

• Women are admitted if there is bleeding from placenta praevia ® steroids are administered if <34

weeks

• Delivery is by elective C-section at 39 weeks ® intrapartum & postpartum haemorrhage are common,

and emergency C-section is required if there is severe bleeding before this time

• Placenta accreta or percreta should have been anticipated, and a clear plan made for elective delivery

with interventional radiology and expert surgical & anaesthetic support:

o Uterine incision is made away from the placenta ® which can be left in situ or removed with

the entire uterus

o Partial separation or transection during uterine incision may lead to massive haemorrhage

o Treatment involves compression of the inside of the scare after removal of the placenta with an

inflatable balloon, excision of the affected uterine segment, or frequently total hysterectomy

Describe placental abruption and outline the clinical features, investigation & management

• Placental abruption is when part (or all) of the placenta separates before delivery of the foetus

• It occurs in ~1% of pregnancies ® however, it is likely that many antepartum haemorrhages of

‘undetermined origin’ are small placental abruptions

• When the placenta separates, considerable maternal bleeding may occur behind it ® this can have

several consequences:

o Further placental separation ® acute foetal distress

o Antepartum haemorrhage ® tracks down between membranes & myometrium

o Blood enters the liquor or myometrium

• Foetal death is common (30% of proven abruptions) ® haemorrhage often necessitates blood

transfusion, and DIC & renal failure may lead to maternal death

• Many affected women have no risk factors ® however, there are several associated factors:

o IUGR

o Pre-eclampsia


o Maternal smoking

o Cocaine usage

o Previous history of placental abruption (6% risk)

o Multiple pregnancy

o High maternal parity

o Trauma

o Sudden reduction in uterine volume ® e.g. membrane rupture

• Presents with painful bleeding ® pain is due to blood behind the placenta & in the myometrium

• Blood is often dark ® the degree of vaginal bleeding does not reflect true severity of the bleed

• Tachycardia suggests profound blood loss ® hypotension only occurs after massive blood loss

• The uterus is tender & often contracting, so labour ensues ® foetal tones are often abnormal or absent

• Diagnosis is made on clinical judgment ® ICU for the mother may be necessary

• Foetus is monitored using CTG & uterine activity ® USS is used to exclude praevia & estimate foetal

weight



• Admission is required, as resuscitation may be necessary, and delivery depends on foetal state &

gestation ® if foetal distress, then emergency C-section, but if not then labour is induced with

amniotomy

• If no foetal distress, the pregnancy is preterm & the degree of rupture is minor, then steroids can be

given ® patiently is closely monitored and discharged if all symptoms settle, but the pregnancy is now

high risk

• Whatever the mode of delivery ® postpartum haemorrhage is a major risk

Outline other causes of antepartum haemorrhage BLEEDING OF UNDETERMINED ORIGIN

• When APH is small & painless, but the placenta is not praevia

• May be impossible to find a cause

• Many episodes are likely to be minor degrees of placental abruption

RUPTURED VASA PRAEVIA

• Vasa praevia occurs when a foetal blood vessel runs in the membranes in front of the presenting part ®

occurs in 1% of pregnancies

• These vessels usually result from the umbilical cord being attached to the membranes rather than the

placenta (velamentous insertion), or where the placenta is in parts

• Rupture is more likely with vessels closer to the cervix ® occurs in 1 in 5000 pregnancies (usually when

the membranes rupture), and massive foetal bleeding follows

• Typical presentation is painless, moderate vaginal bleeding at rupture of membranes, which is

accompanied by severe foetal distress ® C-section is often not fast enough to save the foetus



UTERINE RUPTURE

• Significant antenatal rupture of a lower segment C-section scar is very rare

• Very occasionally, rupture occurs before labour in women with other uterine scars, or a congenitally

abnormal uterus

BLEEDING OF GYNAECOLOGICAL ORIGIN

• Cervical cancer can present in pregnancy ® if a cervical smear is overdue, then women with small

recurrent or postcoital haemorrhage should undergo speculum examination & colposcopy

• Cervical polyps, ectropion or vaginal lacerations may also be evident ® but bleeding should not

usually be attributed to them

OBSTETRICS – FOETAL GROWTH, COMPROMISE & SURVEILLANCE


Outline disorders of foetal health & growth SMALL FOR GESTATIONAL AGE (SGA)

• This means that the weight of the foetus is less than the 10th centile for its gestation ® if at term this is

2.7kg, but other cut-off points may be used

• Traditionally, small size was felt to reflect chronic illness due to placental dysfunction ® these babies

are at increased risk of complications because they are more likely than normal birthweight babies to be

growth restricted ® but many are simply constitutionally small, have grown consistently & are not

compromised

• Assessment of foetal weight is better at identifying IUGR if customised according to what would be

expected for the individual, rather than the overall population

INTRAUTERINE GROWTH RESTRICTION (IUGR)

• Describes foetuses that have failed to reach their own growth potential ® their growth in utero has

slowed, and they may end up being SGA

• If a foetus was genetically determined to be 4kg at term & delivers weighing 3kg ® its growth has been

restricted, and it may have placental dysfunction

FOETAL DISTRESS

• This refers to an acute situation that may result in foetal damage or death if it is not reversed, or if the

foetus is not delivered urgently (e.g. hypoxia)

• It is usually seen in labour ® however, most babies that subsequently develop cerebral palsy were not

born hypoxic

FOETAL COMPROMISE

• This describes a chronic situation and should be defined as when conditions for the normal growth &

neurological development are not optimal

• Most identifiable causes involve poor nutrient transfer through the placenta (placental dysfunction)®

commonly there is IUGR, but this may also be absent (e.g. maternal diabetes or prolonged pregnancy)

Outline the aims & methods of foetal surveillance AIMS OF FOETAL SURVEILLANCE

• Identify the high-risk pregnancy using history or events during pregnancy, or using specific

investigations

• Monitor the foetus for growth & wellbeing ® the methods used will vary according to pregnancy risks &

events during the pregnancy

• Intervene (usually expedite delivery) at an appropriate time, balancing the risks of in utero compromise

against those of intervention & prematurity ® the latter is itself a major cause of morbidity & mortality

IDENTIFICATION OF PREGNANCY RISKS

• Pre-pregnancy risks ® there are no specific risk factors that can be detected in pre-pregnancy

• Early pregnancy risks:

o Pregnancy-associated plasma protein A (PAPP-A):

§ This is a placental hormone, and the level is reduced in the 1st trimester with

chromosomal abnormalities

§ It is therefore used in screening for Down’s syndrome



§ A low level also indicates a high risk for IUGR, placental abruption & consequent

stillbirth

o Maternal uterine artery Doppler:

§ Uterine circulation normally develops a very low resistance in normal pregnancy

§ Abnormal wave forms suggesting failure of development of a low resistance

circulation identifies 75% of pregnancies at risk of adverse neonatal outcomes in the

early 3rd trimester ® particularly early pre-eclampsia, IUGR or placental abruption

§ The test is less predictive of later problems ® so is most sensitive at 20–23 weeks,

but can be used from 12 weeks to term

• Later pregnancy risks:

o With the occurrence of pre-eclampsia or vaginal bleeding, or if a routine abdominal palpation

suggests an SGA foetus ® more close examination is required, and the risk level will change

METHODS OF FOETAL SURVEILLANCE

• The tests outlined below are not routine for low-risk pregnancies ® they are centred around

identification of the small or compromised foetus by taking serial measurements of the symphyseal-

fundal height, and other aspects of antenatal visits

• Ultrasound assessment:

o USS is used to measure foetal size after the 1st trimester ® particularly the abdominal & head

circumference, and these are recorded on centile charts

o Three factors help to differentiate between the healthy small foetus and the growth-restricted

foetus:

§ The rate of growth can be determined by previous scans or a later examination at

least 2 weeks apart

§ The pattern of ‘smallness’ may help ® the foetal abdomen will often stop enlarging

before the head, which is spared, resulting in a thin foetus or asymmetrical growth

restriction ® a reduction in the rate of growth of the abdominal circumference by

>30% is suggestive of IUGR

§ Allowance for constitutional non-pathological determinants of foetal growth enables

‘customisation’ of individual foetal growth ® assessing actual growth according to

expected growth

o Serial USS is sage & useful in confirming consistent growth in high risk & multiple pregnancies

® one-off USS in later pregnancy is of limited benefit in low-risk pregnancies

o Mothers with diabetes often have large babies, particularly with a large abdominal

circumference ® although these babies are still more vulnerable

• Doppler waveforms of the umbilical artery:

o Doppler is used to measure velocity waveforms in the umbilical arteries ® evidence of high

resistance circulation suggests placental dysfunction (e.g. reduced / absent flow in foetal

diastole compared to systole)

o Resistance is described according to end-diastolic flow ® high (>95th centile), absent (ADEF),

or reversed (REDF), with the latter two findings indicating severe placental dysfunction

o Umbilical artery waveforms help identify which small foetuses are actually growth restricted &

therefore compromised ® best performed before 34 weeks as not sensitive alone, unless used

in conjunction with MCA or cerebroplacental ratio



o Its usage improves perinatal outcomes in high-risk pregnancies, while reducing intervention in

those not compromised ® the absence or reversal of slow in diastole usually predates CTG

abnormalities, and correlates well with severe compromise

o It is not useful in low-risk pregnancies ® less effective at identifying the normal weight but

compromised foetus

• Doppler waveforms of the foetal cerebral circulation:

o Doppler is used to assess the resistance or velocity of the MCA ® with foetal compromise, the

MCA often develops a low resistance pattern in comparison to the thoracic aorta or renal

vessels (this reflects a head-sparing effect)

o The velocity of MCA flow also increases with foetal anaemia

o The ratio of the pulsatility index (PI) of this vessel compared to the umbilical artery

(cerebroplacental ratio) is currently the best method of assessing chronic placental dysfunction

>34 weeks

• Doppler waveforms of the foetal venous circulation:

o All major foetal vessels can be seen, but the most commonly measured is the ductus venosus

® this is a measure of cardiac function, and used to assess extremely preterm foetuses (<28

weeks) as an alternative to CTG

o It is useful in assessing disease severity in babies with heart failure or TTTS

• Cardiotocography:

o Foetal heart rate is recorded electronically for up to 1hr

o Accelerations & variability >5 bpm should be present, decelerations should be absent, and the

rate should be 110–160 bpm

o CTG gives immediate information about foetal status at >26 weeks ® but are of no use as an

antenatal screening test

• Kick chart:

o The mother records the number of individual movements that she experiences every day

o Most compromised foetuses have reduced movements in the hours before death ® however,

they only stop moving shortly before death, so should not be used routinely

Outline the causes, diagnosis & management of a small for gestational age foetus &

intrauterine growth restriction CAUSES

• Small for gestational age usually means <10th centile

• Foetal size & health are determined by a combination of genetic & acquired factors

• Constitutional determinants ® these affect growth & birth weight without causing IUGR:

o Low maternal height & weight

o Nulliparity

o Asian ethnic group

o Female foetal gender

• Pathological determinants ® these can cause IUGR, and include:

o Pre-existing maternal disease ® e.g. renal / autoimmune disease

o Maternal pregnancy complications ® e.g. pre-eclampsia

o Multiple pregnancy

o Smoking



o Drug usage

o Infections ® e.g. CMV

o Extreme exercise

o Malnutrition

o Congenital abnormalities

• Complications of SGA include stillbirth, foetal distress in labour, admission to NICU, and long-term

handicap

• Up to 50% of ‘unclassified’ stillbirths are SGA or have IUGR

• Preterm delivery is more common ® including iatrogenic

• Maternal risk is also higher, as pre-eclampsia may coexist & C-section is often used

DIAGNOSIS

• Reduced foetal movements are not consistent with IUGR ® as this is a very late stage

• Serial measurements of the symphyseal-fundal height may be reduced or slow down

• The BP & urinalysis must be checked ® as pre-eclampsia often coexists with IUGR, esp. <34 weeks

• The diagnosis of SGA is made using USS, and investigations are to determine both the cause & the

severity of the compromise ® the anomaly scan is repeated to look for malformations, and testing for

CMV or chromosomal abnormalities with NIPT / amniocentesis should be considered

• To tell which SGA foetuses are actually IUGR & how severely ® USS & umbilical artery Doppler

(combined with MCA as the CPR when >34 weeks) are used

• A reduction in growth velocity by >30% of the abdominal circumference also suggests IUGR ® the

amniotic fluid volume is often reduced (oligohydramnios)

• CTG is also used ® but will become abnormal usually only when severe compromise or foetal distress

is present

MANAGEMENT

• Small for gestational age:

o Growth is rechecked with USS at 2–3 weekly intervals

o At gestation >37 weeks, delivery should be arranged ® however, in some foetuses that are not

very small, with normal umbilical artery & CPR Dopplers, it may be more appropriate to wait

until 40–41 weeks to allow labour to be spontaneous

• Intrauterine growth restriction:

o Gestation <34 weeks:

§ The aim is to prevent in utero foetal death or neurological damage associated with

ongoing placental dysfunction, whilst maximising the gestation to avoid complications

of prematurity

§ An estimated foetal weight for intervention needs to be >500g, and the gestation >25–

26 weeks for a foetus to be viable once delivered

§ An IUGR foetus with abnormal umbilical artery Doppler values is reviewed at least

twice a week ® if AEDF is seen, the mother is admitted & given steroids ® if

gestation is >32 weeks, as C-section is usual, but if <32 weeks then a daily CTG is

performed & delivery only arranged if this is abnormal

§ The severely IUGR foetus is usually delivered by C-section ® delivery <34 weeks

should be immediately preceded by maternal administration of magnesium sulphate



o Gestation 34–37 weeks:

§ At this gestation, delivery can sometimes be deferred in the absence of severely

abnormal Doppler values

§ Delivery can be by induction or C-section if the CTG is abnormal

o Gestation >37 weeks ® delivery is indicated by induction or C-section if the CTG is abnormal

Define stillbirth & outline its possible causes

• Stillbirth occurs when a foetus is delivered after 24 completed weeks of gestation showing no signs of

life

• Occurs in 1 in 200 pregnancies ® women who have had one stillbirth are 3–5x more likely to have

another

• Possible causes include:

o IUGR ® the most common, with smoking & multiple pregnancy as important risk factors

o Unexplained cases ® often due to the pathology behind IUGR

o Foetal & chromosomal congenital abnormalities ® vary in incidence according to the level

of prenatal diagnosis

o Pregnancy related maternal disease ® much of the risk is via placental disease (e.g. pre-

eclampsia, gestational diabetes)

o Infection ® GBS, parvovirus or CMV


o Intrapartum ® usually due to hypoxia

o Rare ® foetal exsanguination (as foetomaternal haemorrhage or vasa praevia), fatty liver &

cholestasis

• The majority of antepartum stillbirths present as reduced or absent foetal movements ® the diagnosis is

made using USS

Define the prolonged pregnancy & outline its management

• A pregnancy is prolonged if >42 weeks ® the risks of perinatal morbidity & mortality rapidly rise

between 41–42 weeks

• ~6% of pregnancies reach 42 weeks ® it is more common if previous pregnancies have been

prolonged, and in nulliparous women

• The rate of stillbirth per 1000 continuing pregnancies rises from 0.35 at 37 weeks to 2.12 at 43 weeks ®

neonatal illness & encephalopathy, meconium passage, and a clinical diagnosis of foetal distress are

more common

• The aim of management is to balance the risks of obstetric intervention against those of prolonged

pregnancy ® by 41–42 weeks, induction of labour is favoured & prevents 1 foetal death in every 500

women induced

• Sweeping of the cervix usually occurs at 40–41 weeks & helps to spontaneously start labour

OBSTETRICS – ABNORMAL LIE & BREECH PRESENTATION


Describe the aetiology, complications & management of abnormal (transverse / oblique) lie DEFINITION

• The lie of the foetus describes the relationship of the foetus to the long axis of the uterus

• If lying longitudinally ® the lie is longitudinal & the presentation is cephalic or breech

• If neither is palpable at the pelvic inlet ® then the foetus must be lying across the uterus with the head

in one iliac fossa (oblique lie) or in the flank (transverse lie)

• Abnormal lie occurs in 1 in 200 births ® more common earlier in pregnancy, and before term it is

normal

AETIOLOGY

• Preterm labour is more commonly complicated by an abnormal lie than labour at full term

• Circumstances that allow the foetus to turn are the most common cause (e.g. polyhydramnios or high

parity) ® frequently resulting in an unstable or continuingly changing lie

• Conditions that prevent turning may also cause persistent transverse lie ® e.g. foetal or uterine

abnormalities, or twin pregnancy

• Conditions that prevent engagement include placenta praevia, pelvic tumours & uterine deformities

COMPLICATIONS

• If the head or breech cannot enter the pelvis ® the labour cannot deliver the foetus

• An arm of the umbilical cord may prolapse when the membranes rupture ® if neglected, the obstruction

eventually causes uterine rupture

• Both foetus & mother are at risk

MANAGEMENT

• No action is required for transverse or unstable lie <37 weeks ® unless the woman is in labour

• >37 weeks, the woman is often admitted to hospital in case the membranes rupture ® USS is

performed to exclude particular identifiable causes (e.g. polyhydramnios / placenta praevia)

• External cephalic version (ECV) is unjustified, because the foetus normally turns back

• If spontaneous version occurs & persists for >48 hrs ® then the mother is discharged

• In the absence of pelvic obstruction ® an abnormal lie will usually stabilise before 41 weeks

• At 41 weeks, or if the woman is in labour ® the persistently abnormal lie is delivered by C-section

Outline breech presentation including the management

• Presentation refers to the part of the foetus that occupies the lower segment of the uterus or pelvis

• Breech presentation occurs in 3–4% of term pregnancies ® but more common if the labour is preterm

(25%)

• Types of breech:

o Extended breech (70%) ® has both legs extended at the knee

o Flexed breech (15%) ® has both legs flexed at the knee

o Footling breech (15%) ® has one or both feet present below the buttocks

• Prematurity is commonly associated with breech presentation ® conditions that prevent movement or

that prevent head engagement are more common

• Breech presentation is commonly missed (30%) ® but diagnosis is only important from 37 weeks or if

the woman is in labour

OBSTETRICS – ABNORMAL LIE & BREECH PRESENTATION


• Upper abdominal discomfort is common, and USS confirms diagnosis ® ensures the prerequisites for

ECV are met

• Perinatal & long-term morbidity & mortality are increased ® foetal abnormalities are more common, and

labour also has additional hazards of hypoxia & birth trauma

EXTERNAL CEPHALIC VERSION

• From 37 weeks, an attempt is made to turn the baby to a cephalic presentation ® this reduces breech

presentation at term, and therefore C-sections

• Success rate is 50%, but approximately 3% of those will turn back ® where ECV fails, only 3% will turn

spontaneously before delivery

• ECV is done by administering a tocolytic (uterine relaxant) to the mother ® it is performed under USS

guidance & in hospital to allow immediate delivery if complications occur

• CTG is performed straight after, and anti-D given if required

• Lower success rates are seen in:

o Nulliparous women

o Caucasians

o Engaged breech

o Head is not easily palpable

o High uterine tone

o Obese women

o Reduced liquor volume

• ECV is not performed if:

o The foetus is compromised

o Vaginal delivery is contraindicated ® e.g. placenta praevia

o There are twins

o The membrane has ruptured

o There has been a recent antepartum haemorrhage

MODE OF DELIVERY

• In the West, most breech presentations will undergo elective C-section ® however, women can deliver

vaginally if they wish, and this is particularly common if it is a late presentation or a 2nd twin

• Vaginal birth is probably riskier with a foetus >3.8 kg ® or with evidence of foetal compromise, an

extended head, or footling legs

• Pushing is discouraged until the buttocks are visible, and CTG is advised ® in 30% of cases there is a

slow 1st stage or 2nd stage, so C-section is advised

OBSTETRICS – MULTIPLE PREGNANCY


Outline the types of multiple pregnancy, and their aetiology TYPES OF MULTIPLE PREGNANCY

• Twins occur in 1 in 80 pregnancies, and triplets in 1 in 1000 ® there is considerable geographical

variation

• The incidence of twins is increasing because of subfertility treatment & the increasing number of older

mothers ® although in the UK, triplets & higher order pregnancies have become fewer, again with

better fertility treatment regulation

• Dizygotic twins:

o 2/3 of all multiple pregnancies

o Result from fertilisation of different oocytes by different sperm

o Such foetuses may be of different sex, and are no more genetically similar than siblings from

different pregnancies

• Monozygotic twins:

o Result from mitotic division of a single zygote into ‘identical twins’

o Whether they share the same amnion or placenta depends on the time at which division into

separate zygotes occurs:

§ Division before day 3 ® dichorionic diamniotic (separate placenta & amnions)

§ Division between day 4–8 ® monochorionic diamniotic (shared placenta but

separate amnions)

§ Division between day 9–13 ® monochorionic monoamniotic (shared placenta &

amnion)

§ Incomplete division ® conjoined twins

AETIOLOGY & DIAGNOSIS

• Most important factors ® largely affecting dizygotic twins:

o Assisted conception

o Genetic factors

o Increasing maternal age

o High parity

• ~20% of all IVF conceptions & 5–10% of clomiphene assisted conceptions are multiple ® embryo

transfer of more than two fertilised ova at IVF is now only performed in the UK in exceptional

circumstances

• Vomiting may be more marked in early pregnancy ® the uterus is also larger than expected for the

dates, and palpable at <12 weeks

• Later in pregnancy, there will be 3 or more foetal poles ® but most are diagnosed only at USS

Outline the complications of multiple pregnancy MATERNAL

• All obstetric risks are exaggerated in multiple pregnancies ® gestational diabetes & pre-eclampsia

are particularly more frequent

• Anaemia is common ® partly because of a greater increase in blood volume causing dilutional effect,

and partly because more iron & folic acid are needed



FOETAL ANTENATAL

• All multiples:

o Twins have greater mortality (6x) & long-term handicap (5x)

o Triplets fare even worse ® with an 18x increase in handicap

o The major risk factors are:

§ Preterm delivery

§ IUGR

§ Monochorionicity

o Miscarriage:

§ One of a twin pregnancy can ‘vanish’ where there is a 1st trimester death

§ Late miscarriage is also more common ® particularly in monochorionic twins as a

complication of twin-twin transfusion syndrome

o Preterm labour:

§ Main cause of perinatal mortality

§ 40% of twins & 80% of triplet pregnancies deliver before 36 weeks

§ 10% of twins deliver before 32 weeks

o IUGR ® much more common

o Congenital abnormalities:

§ Not more common per baby in dichorionic ® but they are in monochorionic

pregnancies

• Monochorionic pregnancies:

o These largely result from the shared blood supply in the single placenta

o Twin-twin transfusion syndrome (TTTS):

§ Occurs only in MCDA twins (the most common form of identical twins), and in about

15%

§ Results from unequal blood distribution through vascular anastomoses of the shared

placenta

§ One twin (donor) is volume depleted and develops anaemia, IUGR &

oligohydramnios ® the other twin (recipient) becomes volume overloaded and may

develop polycythaemia, cardiac failure & massive polyhydramnios (causing

distension of the uterus)

§ Disease is staged according to Quintero stages 1–5

§ Both twins are at very high risk of in utero death or severely preterm delivery

o Twin anaemia polycythaemia sequence (TAPS):

§ Occurs where there are marked Hb differences between monochorionic twins ® but

in the absence of the liquor volume changes characteristic of TTTS

§ Occurs as a consequence of small placental anastomoses

§ Can occur following incomplete laser ablation for TTTS

o Twin reverse arterial perfusion (TRAP):

§ Rare abnormality of MC twins

§ An abnormal, often acardiac foetus is perfused by a normal ‘pump’ twin ® therefore, it

is at risk of cardiac failure

o Intrauterine growth restriction (IUGR):

§ More common in MC twins, in the absence of clear blood volume discordancy



§ A particular problem is where the umbilical artery waveform of the smaller twin is very

erratic ® this may be the result of the superficial artery-artery anastomoses

§ Sudden in utero death occurs in up to 20%, and handicap in 8%

o Co-twin death:

§ If one of an MC twin pair dies due to TTTS or any other cause ® the drop in its blood

pressure allows acute transfusion of blood from the other twin

§ This rapidly leads to hypovolaemia ® and in 30% of cases, death or neurological

damage

o Monoamniotic twins:

§ The cords are always entangled

§ In utero death is common ® probably because of this and/or sudden acute shunting

of blood between the two babies in anastomoses between the close cord insertions

INTRAPARTUM

• Malpresentation of the 1st twin occurs in 20% ® this is an indication for C-section

• Foetal distress:

o Common in labour

o The 2nd twin delivered has a 5x increased risk of death because of hypoxia, cord prolapse,

tetanic uterine contraction, or placental abruption ® the second twin may present as breech

• Postpartum haemorrhage ® more common (10%)

Outline the management of multiple pregnancy ANTEPARTUM MANAGEMENT

• The pregnancy should be considered high risk ® iron & folic acid supplements are prescribed & low-

dose aspirin is advised if there are other factors (to prevent pre-eclampsia)

• Multiple pregnancies increase maternal tiredness & anxiety

• NICE recommends specialist & MDT supervised pregnancy care

• Chorionicity is most accurately ascertained in the 1st trimester:

o DC twins ® dividing membrane is thicker as it meets the placenta (lambda sign)

o MC twins ® dividing membrane is thinner & perpendicular to the shared placenta (T sign)

• IUGR is harder to detect in multiple pregnancies ® serial USS for growth are routinely performed at 28,

32 & 36 weeks (more often in MC twins)

• Delivery is at 37 weeks for DC, and 36 weeks for uncomplicated MC twins

• Monochorionic pregnancies:

o USS surveillance for MC twins starts by 12 weeks ® USS is advised every 2 weeks until 24

weeks, and every 2–3 weeks thereafter

o TTTS is most commonly diagnosed between 16–24 weeks, as growth & liquor volume

discordances with polyhydramnios are evident ® laser ablation of the entire placental

interface using USS & fetoscopy is the preferred treatment

§ Even with optimal treatment ® survival of both twins is 50% & one twin is 80%, but

10% of survivors have neurological disability

§ Pregnancies complicated by TTTS after 26 weeks are usually delivered

o IUGR is managed by careful surveillance & iatrogenic preterm delivery ® occasionally laser

ablation or umbilical cord occlusion are appropriate if at pre-viable gestations



• Higher order multiple pregnancy:

o Selective reduction to a twin pregnancy at 12 weeks should be discussed with women with

triplets or higher order pregnancies ® while is slightly increases early miscarriage rates, it

reduces the chances of preterm birth & therefore cerebral palsy ® it is safest before 14 weeks

o Surveillance is according to the chorionicity ® delivery by 36 weeks is usually advised

• Foetal abnormality:

o Before 14 weeks, intracardiac injection of KCl can be used in DC twins ® it can be offered up

to 32 weeks if alte termination of pregnancy is legal

o In MC twins, the cord must be occluded using bipolar diathermy, or its insertion ablated (as the

circulation is shared)

INTRAPARTUM MANAGEMENT

• Mode of delivery:

o If the presenting twin is cephalic, C-section does not improve perinatal outcome ® it is only

indicated if the 1st twin is breech or transverse lie, with higher order multiples, or if there have

been antepartum complications

o Vaginal delivery when the 1st foetus is cephalic is commonplace ® whatever the presentation

or lie of the 2nd

• Method of delivery:

o Induction is usually at 37 weeks (DC twins) or 36 weeks (MC twins) ® after which time

perinatal mortality is increased

o CTG monitoring is advised ® risk of intrapartum hypoxia is increased, particularly in 2nd twin

o Epidural analgesia is not mandatory ® but helpful if difficulty is encountered with the 2nd twin

o Contractions often diminish after the 1st twin ® usually these return within a few minutes, but if

not then oxytocin can be started

o The lie of the 2nd twin is check, and ECV performed if it is not longitudinal

o Excessive delay between twins is associated with increased mortality for the 2nd twin ® but

excessive haste is equally dangerous

o After delivery, a prophylactic oxytocin infusion is used to prevent postpartum haemorrhage

OBSTETRICS – LABOUR MECHANISM


Outline the mechanical factors of labour

• Three mechanical factors determine progress during labour:

o Power ® the degree of force expelling the foetus

o Passage ® the dimensions of the pelvis & the resistance of soft tissue

o Passenger ® the diameters of the foetal head

POWER

• Once labour is established, the uterus contracts for 45–60 secs every 2–4 minutes ® this pulls the

cervix up (effacement) & causes dilation, aided by the pressure of the head as the uterus pushes it

down into the pelvis

• Poor uterine activity is a common feature of nulliparous women & induced labour ® it is rare in

multiparous women

PASSAGE

• The bony pelvis:

o This has 3 principal planes:

§ Inlet ® 13cm transverse diameter

§ Mid-cavity

§ Outlet ® 12.5cm AP diameter

o Ischial spines are landmarks by which to assess the descent of the head on vaginal

examination ® the level of descent is called the station, and is crudely measured in cms in

relation to the spine ® station 0 means the head is at the level of the spines, while +2 is 2cm

below, and -2 is 2cm above

o A variety of pelvic shapes are described ® but diagnoses & therefore description of these are

seldom useful in clinical practice



• Soft tissues:

o Cervical dilation is a prerequisite for delivery ® it is dependent on contractions, the pressure of

the foetal head on the cervix, and the ability of the cervix to soften & allow distension

o The soft tissues of the vagina & perineum need to be overcome in the 2nd stage ® the

perineum often tears or is cut (episiotomy) to allow the head to deliver

PASSENGER

• The head is oblong in transverse section ® its bones are not yet fused, and spaces between them are

palpable as sutures & fontanelles

• The anterior fontanelle (bregma) lies above the forehead ® the posterior fontanelle (occiput) lies on the

back of the top of the head ® between these two is the vertex

• In front of the bregma is the brow ® because the head is not round, several factors determine how

easily it fits through the pelvic diameters

• Attitude ® extended / flexed:

o The attitude is the degree of flexion of the head on the neck

o The ideal attitude is maximal flexion, keeping the head bowed ® this is called vertex

presentation, and the presenting diameter is 9.5cm running from the anterior fontanelle to

below the occiput

o A small degree of extension results in a larger diameter:

§ Extension of 90o causes a brow presentation & a much larger diameter of 13cm

§ A further 30o extension is a face presentation

o Extension of the head can mean that the foetal diameters are too large to deliver vaginally

• Position ® rotation:

o The position is the degree of rotation of the head on the neck

o If the sagittal suture is transverse ® the oblong head will fit the pelvic inlet best

o But at the outlet, the sagittal suture must be vertical for the head to fit ® the head must

therefore rotate 90o during labour

o It is usually delivered with the occiput anterior (OA) ® in 5% of deliveries it may be OP, and

more difficulty may be encountered ® persistence of the OT position implies non-rotation, and

delivery without assistance is impossible

• Size of the head:

o The head can be compressed in the pelvis as the sutures allow the bones to come together &

even overlap ® this slightly reduces the diameters of the head, and is called moulding

o Pressure of the scalp on the cervix or pelvic inlet can cause localised swelling or caput

o It is relatively unusual for a normally formed head to be too big to pass through the bony pelvis

® although a larger head may cause a longer & more difficult labour

Describe the stages of labour INITIATION & DIAGNOSIS OF LABOUR

• Involuntary contractions of uterine smooth muscle occur throughout the 3rd trimester ® often felt as

Braxton Hicks contractions

• It is not fully understood how it is achieved, but the foetus has a role, and prostaglandin production is

important in both reduction of cervical resistance & increasing release of oxytocin from the posterior



pituitary ® this aids stimulation of contractions, which arise in one of the

pacemakers situated at each cornua of the uterus

• Labour is diagnosed when painful regular contractions lead to

effacement & dilation of the cervix

• Effacement is when the normally tubular cervix is drawn up into the

lower segment until it is flat ® this is commonly accompanied by a

‘show’, or a pink / white mucous plug from the cervix and/or rupture of

the membranes, causing release of liquor

• Labour in multiparous women is often much faster than in nulliparous

ones

THE FIRST STAGE

• This lasts from the diagnosis of labour until the cervix is dilated to 10cm

(fully dilated)

• The descent, flexion & internal rotation described above occur to varying

degrees

• If the membranes have not already ruptured ® they normally do now

• The latent phase ® where the cervix dilates slowly for the first 4cm &

may take several hours

• The active phase follows ® average cervical dilation is at the rate of

1cm/hr in nulliparous women, and 2cm/hr in multiparous women ® the

active first stage should not normally last longer than 16hrs

THE SECOND STAGE

• This lasts from full dilation of the cervix to delivery ® descent, flexion &

rotation are completed, and followed by extension as the head delivers

• The passive stage:

o This lasts from full dilation until the head reaches the pelvic

floor & the woman experiences the desire to push

o Rotation & flexion are commonly completed

o This stage may last a few minutes ® but it can be much longer

• The active stage:

o When the mother is pushing

o The presence of the head on the pelvic floor produces an irresistible desire to bear down ®

although spinal analgesia may prevent this

o The woman gets in the most comfortable position for her (but not supine) and pushes with

contractions

o The foetus is delivered, on average, after 40 minutes (nulliparous) or 20 minutes (multiparous)

o This stage can be much quicker ® but if it takes >1hr then spontaneous delivery becomes

increasingly unlikely

DELIVERY

• As the head reaches the perineum, it extends to come up out of the pelvis ® the perineum begins to

stretch & often tears, but can be cut if progression is slow or foetal distress is present



• The head then restitutes, rotating 90o to adopt the transverse position in which is entered the pelvis

• With the next contraction, the shoulders deliver ® the anterior shoulder comes under the symphysis

pubis first, usually aided by lateral body flexion in a posterior direction

• The posterior shoulder is aided by lateral body flexion in an anterior direction

• The rest of the body follows

THE THIRD STAGE

• This is the time from delivery of the foetus to delivery of the placenta ® it normally lasts about 15 mins

• Normal blood loss is <500 ml

• Uterine muscle fibres contract to compress the blood vessels formerly supplying the placenta ® which

shears away from the uterine wall

PERINEAL TRAUMA

• The perineum is intact in about 1/3 of nulliparous women & 1/2 of multiparous women

• There are different degrees of perineal tear:

o 1st degree ® minor damage to the fourchette

o 2nd degree & episiotomies ® involving perineal muscle

o 3rd degree ® involving anal sphincter (1%)

o 4th degree ® involving anal mucosa

OBSTETRICS – LABOUR MANAGEMENT


Describe the general care of a woman in labour

• Temperature & BP should be monitored every 4hrs ® pulse should be monitored every hour in the

first stage, and then every 15 minutes in the second stage ® contraction frequency should be noted

every 30 mins

• Position:

o Most deliver in a semi-recumbent position ® e.g. squatting, kneeling or left-lateral position

o Supine is avoided ® as it can lead to compression of main blood vessels, leading to reduced

cardiac output, hypotension & foetal distress

• Eating is appropriate in labour ® unless high risk, as may need a general anaesthetic

• Pyrexia in labour is >37.5oC, and is associated with an increased risk of neonatal illness ® it is more

common with epidural & prolonged labour ® paracetamol is administered, and IV antibiotics & CTG

monitoring are warranted if fever reached 38oC

• Neglected retention of urine can cause irreversible damage to the detrusor muscle ® frequent

micturition is encouraged in labour

o NB: Catheterisation is required if an epidural is in situ

• Fear & anxiety can cause adrenaline secretion, which slows labour ® the continued presence of a

caregiver is reassuring

Outline the management of slow progression of labour

• Progress in labour is dependent on power, passage & passenger ® dilation of the cervix & progression

of the head are assessed on vaginal examination & recorded

• After the latent phase (4cm dilated) ® the unusual minimum rate of dilation is 1cm/hr

POWER

• Inefficient uterine action is the most common cause of slow progression ® it is common in nulliparous

women & induced labour

• Persistently slow progress is treated with augmentation ® initially with amniotomy, and then oxytocin

• Hyperactive uterine action occurs with excessively strong, frequent or prolonged contractions

• Foetal distress occurs as placental blood flow is diminished, and labour may be very rapid ® associated

with placental abruption, too much oxytocin, or a side effect of prostaglandins administered to induce

labour

• If no abruption, it can be treated with a tocolytic (e.g. IV salbutamol) ® but C-section is often

indicated because of foetal distress

• Nulliparous women:

o Slow progress in the nulliparous woman is usually due to inefficient uterine action ®

augmentation can rectify this problem, and involves artificial rupture of membranes

(amniotomy) or IV oxytocin with a gradually increasing dose ® CTG is required

o Oxytocin usually increases cervical dilation within 4hrs if it is going to be effective ® if full

dilation is not imminent within 12–16hrs, then a C-section is performed

o If descent is poor, oxytocin infusion should be started ® pushing it not encouraged until the

woman feels the urge (epidural diminishes this urge)

o Pushing need not be directed unless ineffective, or an epidural is present

o If active 2nd stage lasts longer than 1–2hrs ® then instrumental delivery is often required due

to maternal exhaustion, foetal hypoxia & maternal trauma



• Multiparous women ® augmentation of labour in a multiparous woman must be preceded by exclusion

of malpresentation

PASSENGER

• The foetus can contribute to poor progress in labour

• OP position:

o Often combined with varying degrees of extension, causing a larger diameter

o Labour is often longer & more painful, with backache and an early desire to push

o If labour is slow, augmentation is used

o If position is persistent (5%) ® then delivery will be face to pubis, and completed by flexion

rather than extension over the perineum

o If it is associated with a prolonged active 2nd stage ® then instrumental delivery is usually

achievable with rotation to OA position using ventouse, manual rotation, or Keilland’s forceps

• OT position:

o This occurs when normal rotation has been incomplete

o Occiput lies on the left or right

o Only if vaginal delivery has not been achieved after 1hr of pushing in the 2nd stage is the

position significant ® this is common & usually associated with poor power

o Rotation with traction is required for delivery to occur, and is achieved with a ventouse

• Brow presentation:

o Rare, occurring in 1 in 1000 labours

o Extension of the foetal head on the neck results in a large presenting diameter that will not

normally deliver vaginally

o Anterior fontanelle, supraorbital ridges & nose are palpable vaginally

o C-section is required

• Face presentation:

o Rare, occurring in 1 in 400 labours

o Complete extension of the head results in the face being the presenting part

o Foetal compromise in labour is more common

o Presenting diameter is 9.5cm, allowing vaginal delivery in most cases ® as long as the chin is

anterior, delivery is completed by flexion over the perineum

o If the chin is posterior ® then a C-section is indicated

PASSAGE

• Cephalo-pelvic disproportion:

o This is when the pelvis is too small to allow passage of the head ® but can almost never be

diagnosed with certainty

o Depends on foetal & pelvic size

o It is most commonly a retrospective diagnosis ® defined as the inability to deliver a particular

foetus despite:

§ The presence of adequate uterine activity

§ The absence of a malposition or presentation

o Cephalo-pelvic disproportion is more likely with a large baby, with very short women, or where

the head in a nulliparous woman remains high at term



• Pelvic variants & deformities:

o The gynecoid pelvis is found in 50–80% of Caucasian women

o The anthropoid pelvis is found in 20% of women ® it has a narrower inlet, with a transverse

diameter often less than the AP diameter

o The android pelvis is found in 5% of women ® it has a heart-shaped inlet & a funnelling shape

to the mid-pelvis

o The platypelloid pelvis is found in 10% of women ® the oval shape of the inlet persists within

the mid-pelvis

o Abnormal pelvises are usually confined to the developing world, due to poor health & nutrition

o Rarely, a pelvic mass blocks engagement & descent of the head (e.g. ovarian tumour or

uterine fibroid) ® this is palpable vaginally, and a C-section is indicated

Outline the care of the foetus during labour

• Permanent foetal damage attributable to labour is uncommon ® e.g. only 10% of cases of cerebral

palsy are attributed solely to intrapartum problems

• There are several causes of damage:

o Foetal hypoxia ® commonly described as foetal distress

o Infection / inflammation in labour ® e.g. GBS

o Meconium aspiration ® leading to chemical pneumonitis

o Trauma ® commonly due to obstetric intervention (e.g. forceps)

o Foetal blood loss

FOETAL DISTRESS & HYPOXIA

• Foetal distress is hypoxia that might result in foetal damage or death if not reversed, or the foetus

delivered urgently

• Foetal scalp blood with pH <7.2 indicates significant hypoxia ® however, it is only when pH <7 that

neurological damage is considerably more common, and even then most babies with neurological

damage had a normal pH at birth (suggesting other influences, such as IUGR / maternal fever)

• Contractions temporarily reduce placental perfusion, and may compress the umbilical cord ® so longer

labours & those with excessive time spent pushing are more likely to produce hypoxia

• Acute hypoxia in labour can be due to:


o Hypertonic uterine states

o Use of oxytocin

o Prolapse of the umbilical cord

o Maternal hypotension

• Intrapartum risk factors include:

o Long labour

o Meconium

o Epidurals

o Oxytocin

• Antepartum risk factors include:

o Pre-eclampsia

o IUGR



• Diagnosing foetal distress:

o Colour of the liquor:

§ Meconium is the bowel contents of the foetus that stains the amniotic fluid

§ Rare in preterm foetuses, but common after 41 weeks

§ Meconium very diluted in amniotic fluid is not significant ® but undiluted, it shows a

4x increase in perinatal mortality (but is not a reliable indicator of foetal wellbeing

§ It is an indication for caution because:

§ Foetus may aspirate it ® causing meconium aspiration syndrome

§ Hypoxia is more likely

o Foetal heart auscultation:

§ The heart is auscultated every 15mins during the 1st stage, and every 5mins during

the 2nd stage using a Pinard’s stethoscope of handheld Doppler

§ Distressed foetuses normally exhibit abnormal heart rate patterns

§ Used in low-risk pregnancies ® but if abnormalities are heard or risk factors develop,

then a CTG is indicated

o Cardiotocograph (CTG):

§ This records the foetal heart rate on paper / electronically ® either from a transducer

on the mother’s abdomen, or from a probe attached to the foetal scalp

§ Another transducer records the uterine contractions

o Foetal blood sampling ® Blood is taken from the scalp, and if pH <7.2 then delivery is

expedited in the fastest possible way

CTG MONITORING IN FOETAL DISTRESS

• CTGs are classified as normal, non-reassuring, or abnormal, according to four key features:

o Baseline rate:

§ Should be 110–160 bpm

§ Tachycardias are associated with fever, foetal infection & potentially foetal hypoxia

§ A steep, sustained deterioration in rate suggests acute foetal distress

o Baseline variability:

§ The short-term variation in FHR should be >5bpm ® except during episodes of foetal

sleep (which usually last less than 45 minutes)

§ Prolonged reduced variability, particularly with other abnormal features, suggest

hypoxia

o Accelerations ® increases in the FHR with movements or contractions are reassuring

o Decelerations:

§ Early decelerations ® synchronous with a contraction as a normal response to head

compression, and therefore are usually benign

§ Variable decelerations ® vary in timing & classically reflect cord compression, which

can ultimately cause hypoxia

§ Late decelerations ® persist after the contraction is completed & are suggestive of

foetal hypoxia

§ NB: The depth of the deceleration is usually unimportant

• Indications for using a CTG:

o Pre-labour ® pre-eclampsia, IUGR, previous C-section, or induction



o In labour ® presence of meconium, use of oxytocin, temperature >38oC, or epidural

anaesthesia

OTHER CAUSES OF FOETAL DAMAGE

• Foetal infection & inflammation:

o GBS affects 1.7 per 1000 live births

o Fever is a strong risk factor for seizures, foetal death & cerebral palsy ® even in the absence

of evidence of infection

o Treated with antibiotics & antipyretics

• Meconium aspiration:

o When aspirated into the lungs, it causes severe pneumonitis

o More common in the presence of foetal hypoxia ® but can occur without it

o If meconium is thick, it can be diluted in the uterus to reduce the risk of aspiration ® but

maternal safety is unproven

• Foetal trauma ® trauma may be iatrogenic (instrumental delivery) or from shoulder dystocia

• Foetal blood loss ® this is rare and due to vasa praevia, foetomaternal haemorrhage, or occasionally

placental abruption

Outline the care of the mother in labour PAIN RELIEF IN LABOUR

• Non-medical:

o Preparation at antenatal classes, presence of birth attendant & maintenance of mobility all help

women cope with pain

o Immersion in water at body temperature helps

o Other possible unscientific methods include:

§ TENS

§ Hypnotherapy

§ Localised pressure on

back

§ Acupuncture

§ Superficial heat or cold

§ Massage

§ Aromatherapy

• Inhalation agents:

o Entonox is an equal mix of nitrous oxide & oxygen

o Rapid onset & mild analgesia

o Insufficient for most mothers ® and can cause lightheadedness, nausea & hyperventilation

• Systemic opiates:

o Pethidine & meptid are widely use IM injections

o Analgesic effect is small, and woman may become sedated, confused, or feel out of control

o Anti-emetics are normally needed

o Can also cause respiratory depression in the newborn

• Epidural analgesia:

o Combination of an opiate (fentanyl) with a local anaesthetic (bupivacaine / ropivacaine)

o Delivered to an indwelling catheter in the epidural space between L3–4 or L4–5

o Given as a loading dose, with intermittent low dose top-ups

o Should remove pain sensation, but may also cause motor blockade

o Can be used for the entire labour, and in obstetric procedures if topped up



ANAESTHESIA FOR OBSTETRIC PROCEDURES

• Spinal anaesthesia:

o Local anaesthetic is injected as a single shot through the dura mater into the CSF

o This rapidly produces a short-lasting but effective local analgesia (& motor blockade) that is

suitable for both C-section or mid-cavity instrumental vaginal delivery

o Complications include hypotension

• Epidural anaesthesia:

o Higher dose epidural analgesia can be used for both instrumental delivery & C-section

o For the latter, a combination of spinal & epidural is best ® allowing rapid onset (due to spinal)

and longer lasting anaesthesia, with the opportunity for top-ups due to the epidural

• Pudendal nerve block:

o Local anaesthetic is injected bilaterally around the pudendal nerve where it passes the ischial

spine

o This is suitable for low-cavity instrumental vaginal deliveries

Describe the appropriate conduct for each stage of labour INITIATION & DIAGNOSIS OF LABOUR

• The woman is advised to contact maternity services if contractions are regular, painful, lasting at least

30secs, and occurring every 3–4 minutes, or if the membranes rupture

• Presentation is checked & vaginal examination looks at cervical effacement & dilation to confirm

diagnosis of labour ® the degree of descent is also assessed, and the colour of leaking liquor is noted

• Every 15mins, the foetal heart is listened to for 1min following a contraction ® if the pregnancy is high

risk or meconium is seen, or if there is maternal fever, a CTG is started

• At this stage, account must be taken of the woman’s wishes for labour, and the birth plan should be

read

FIRST STAGE OF LABOUR

• The mother is made comfortable, and encouraged to remain mobile ® supine position is avoided

• If analgesia is requested, then entonox can be used for short-term relief ® but commonly an epidural

is used

• Catheterisation will be required if an epidural is given ® but not otherwise routine

• The foetal heart is auscultated every 15mins or monitored on a CTG ® if abnormal & delivery needs to

be expedited, the only option is a C-section

• Progress is assessed every 4hrs by vaginal examination ® dilation & descent are estimated digitally in

centimetres

• Slow dilation after the latent phase can be treated with amniotomy ® if progress continues to be slow,

oxytocin is used in both a nulliparous woman & a multiparous woman (if malpresentation has been

excluded)

• If the cervix is not fully dilated by 12–16hrs, then a C-section is appropriate ® unless delivery can be

anticipated in the next hour or two

SECOND STAGE OF LABOUR

• If there is no epidural ® pushing is encouraged when the mother has the desire to push or the head is

visible



• If an epidural is in situ ® then at least an hour is waited before pushing, and oxytocin is administered

to a nulliparous woman, or if descent is poor

• Directed pusghing ® if an epidural is in situ, the woman is instructed to push three times for about 10

seconds during each contraction

• Foetal distress is normally diagnosed the same as in the 1st stage ® using FHR & scalp blood

sampling

• If delivery is not imminent after 2hrs of pushing (1hr in multiparous) or there is foetal distress ®

expedition of delivery is usually recommended with ventouse or forceps

• Episiotomy should be reserved for when there is foetal distress, where the head is not passing over the

perineum despite paternal effort, or if a large tear is likely ® if it is performed, the perineum is infiltrated

with local anaesthetic, and a 3–5cm cut is made from the centre of the fourchette at a 45o angle to the

(mother’s) right side of the perineum

• When the head starts to deliver, the mother is asked to stop pushing & to pant slowly ® the attendant

may press on the perineum & the head to prevent a rapid delivery & perineal damage ® the head then

restitutes

• With the next contraction, maternal pushing & gentle downward traction on the head leads to delivery of

the anterior shoulder ® traction is then directed upward to deliver the posterior shoulder

• Unless requiring resuscitation, the baby is delivered onto the mother’s chest & wrapped to keep warm

® the umbilical cord should not be clamped for at least a minute (unless resuscitation is urgently

required)

THIRD STAGE OF LABOUR

• IM oxytocin is administered to help the uterus contract once the shoulders are delivered ® a

combination of ergometrine & oxytocin is often used, but frequently leads to maternal vomiting

• Active management of the 3rd stage can be unpopular ® but reduces the incidence of PPH & the need

for blood transfusion

• Once placental separation is evident from lengthening of the cord & the passage of blood ® continuous

gentle traction on the cord allows delivery of the placenta, and at the same time the left hand pushes

down suprapubically to prevent uterine inversion

• The placenta is checked for missing cotyledons, and the vagina & perineum are checked for tears

• Once these are sutured, a check has been performed & blood loss is recorded ® the mother can be

cleaned, made comfortable, and encouraged to breastfeed

• Maternal observation should be continued for at least 2hrs

• Retained placenta:

o A 3rd stage longer than 30 minutes ® occurs at 2.5% of deliveries

o Partial separation may provoke considerable blood loss into the uterus ® causing it to enlarge

& leading to hypovolaemia

o In the absence of bleeding, 1hr is given for natural separation ® after which the placenta is

manually removed

o Blood is crossmatched, and IV antibiotics given

Outline the principles of perineal repair

• First & second degree tears / uncomplicated episiotomies:

o Sutured under local anaesthetic



o Failure to suture reduces healing, and may cause more pain

o Absorbable synthetic material is used ® continuous sutures for the muscle & subcuticular

sutures for the skin

o Rectal & vaginal examination excludes sutures that are too deep, and retained swabs

• Third & fourth degree tears:

o Occur in 1–3% of deliveries

o The sphincter is repaired under epidural or spinal anaesthesia ® with the visualisation &

asepsis of an operating theatre

o The torn ends of the external sphincter are mobilised & sutured ® with the internal sphincter

sutured separately if damaged

o Antibiotics & laxatives are given, as well as analgesia

o A physiotherapy assessment is required

o Up to 30% of women have long-term sequelae ® including incontinence or urgency

OBSTETRICS – LABOUR SPECIAL CIRCUMSTANCES


Outline the methods, complications, indications & contraindications for induction of labour METHODS OF INDUCTION

• Success of induction depends on the state or ‘favourability’ of the cervix

• Often scored out of 10, as the Bishop’s score ® the lower the score, the more unfavourable the cervix

• Bishop’s score is related to:

o ‘Consistency’

o Degree of effacement or early dilation

o How low the head is in the pelvis ® the station

o Cervical position ® anterior / posterior

• Induction with prostaglandins (PGE2):

o Gel or slow-release preparation is inserted into the posterior vaginal fornix

o Best method for nulliparous women & multiparous women (unless the cervix is favourable)

o It either starts labour, or the ‘ripeness’ of the cervix is improved to allow amniotomy

• Induction with amniotomy ± oxytocin:

o Forewaters are ruptured with an amnihook

o Oxytocin infusion is then started within 2hrs if labour has not ensured

o Oxytocin is often used alone if spontaneous rupture of the membranes has already occurred ®

although PGs are as effective

• Natural induction by cervical sweep:

o Cervical sweeping involves passing a finger through the cervix and ‘stripping’ between the

membranes & the lower segment of the uterus

o At 40 weeks, this increases the chance of induction & reduces postdates pregnancy ® but can

be uncomfortable

INDICATIONS FOR INDUCTION

• Foetal indications ® high-risk situations, including:

o Prolonged pregnancy

o Suspected IUGR or compromise

o Antepartum haemorrhage

o Poor obstetric history

o Prelabour rupture of membranes

• Maternofoetal indications ® pre-eclampsia & maternal disease (e.g. diabetes)

• Maternal indications ® social reasons & in utero death

• Routine indications ® studies show lowest perinatal & infant mortality rate is achieved by delivery at 38

weeks

CONTRAINDICATIONS FOR INDUCTION

• Absolute contraindications:

o Acute foetal compromise ® e.g. abnormal CTG

o Abnormal lie

o Placenta praevia

o Pelvic obstruction

o ≥2 C-sections

• Relative contraindications ® 1 C-section & prematurity



MANAGEMENT & COMPLICATIONS OF INDUCTION

• Foetus is at increased risk in labour, due to indications & drugs used ® CTG should be used for 1hr

• Oxytocin is commonly required in labour, and also warrants CTG monitoring

• Induction commonly increases the time spent in early labour ® and the woman should be warned of this

• Labour may fail to start or be slow due to inefficient uterine activity

• Paradoxically, overactivity of the uterus can occur ® this hyperstimulation is rare, but causes foetal

distress & even uterine rupture

• Other complications include:

o PPH

o Intrapartum / postpartum infection

o Prematurity

o Instrumental delivery or C-section

Outline the factors involved in labour & vaginal birth after a previous Caesarean section

• Vaginal birth after Caesarean (VBAC) can often be safely achieved ® contraindications include:

o All absolute indications for C-section

o Vertical uterine scar

o Previous uterine rupture

o Multiple previous C-sections (≥2)

• If VBAC is attempted, 72–75% of women will deliver vaginally ® the rest will require an emergency C-

section in labour

• Factors associated with increased success:

o Spontaneous labour

o Interpregnancy interval <2yrs

o Low age & BMI

o Caucasian race

o Previous vaginal delivery

o Previous elective C-section, or due to foetal distress (not dystocia)

• Risk of maternal death is approximately 13 in 100,000 ® double planned C-section

• Uterine rupture occurs in 0.5% of VBAC attempts after 1 C-section & 1.3% after 2 C-sections ® these

amount to 0.04% risk of deliver-related death with planned VBAC

• The overall risk of foetal mortality with VBAC is roughly the same risk as found in a first labour

• Delivery in hospital & with CTG monitoring is advised because of the risk of scar rupture ® induction is

usually avoided as it is associated with a higher risk of rupture, and augmentation also increases the

risk of rupture

• Scar rupture usually presents as:

o Foetal distress

o Scar pain

o Cessation of contractions

o Vaginal bleeding

o Maternal collapse



Describe the presentation & management of prelabour rupture of membranes

• In 10% of women after 37 weeks, the membranes rupture before the onset of labour ® 60% will start

labour within 24hrs

• Typically, there is a gush of clear fluid, which is followed by an uncomfortable intermittent trickle (so it is

occasionally initially confused with urinary incontinence) ® ‘point of care’ tests (e.g. Actim PROM) may

help where the diagnosis is not clear

• A few only have hindwater rupture ® liquor leaks, but the membranes remain intact in front of the foetal

head

• Risks of PROM:

o Cord prolapse ® rare & usually a complication of transverse lie or breech position

o Neonatal infection ® small but definite risk, increased by vaginal examination, presence of

GBS, and increased duration of rupture

• Lie & presentation need checking, and foetal auscultation or CTG are performed ® vaginal

examination is usually avoided, but may be performed in a sterile manner if there is risk of cord prolapse

• Management options:

o Spontaneous labour:

§ Wait for <24hrs

§ Presence of meconium or evidence of infection warrants immediate induction

§ After 18–24hrs, prophylactic antibiotics given against GBS, and labour is induced

o Induced labour ® does not increase risk of C-section, and associated with a lower chance of

maternal infection

OBSTETRICS – INSTRUMENTAL & OPERATIVE DELIVERY


Describe forceps & ventouse delivery and their indications

• Allows the use of traction if delivery needs to be expedited in the 2nd stage

• The shape of the pelvis will only allow delivery if the occiput is anterior (occasionally posterior) ®

rotation may be required, and in the absence of rotation instrumental delivery adds power

• The aim is to prevent foetal & maternal morbidity associated with a prolonged 2nd stage, or expedite

where the foetus is compromised

• In the UK, approximately 20% of nulliparous & 2% of multiparous women are delivered by forceps or

ventouse

VENTOUSE

• Consists of a plastic, rubber or metal cap connected to a handle ® the cap is fixed near the foetal

occiput by suction

• Traction during maternal pushing will deliver the OA positioned head ® also often allows the shape of

the pelvis to simultaneously rotate a malpositioned head to the OA position

OBSTETRIC FORCEPS

• Come in pairs that fit together ® each has a blade, shank, lock & handle, and when assembled the

blade fits around the foetal head and the handles fit together, and the lock prevents them from slipping

apart

• Non-rotational forceps (e.g. Simpson’s):

o Grip the head in whatever position it is in & allows traction

o Only suitable for OA position

o Have a cephalic curve for the head & a pelvic curve which follows the sacral curve

• Rotational forceps (e.g. Keilland’s) ® have no pelvic curve, and enable a malpositioned head to be

rotated by the operator to an OA position before traction is applied

SAFETY OF VENTOUSE & FORCEPS

• Both methods of delivery can fail ® this is more common with ventouse, as the cup can be placed

inaccurately

• Maternal complications ® there is a greater need for analgesia with forceps, and use of either

instrument can cause vaginal lacerations, 3rd degree tears & PPH


o Slightly worse with ventouse

o Chignon (swelling on scalp) is usual as it is drawn in with suction of the cup

o Scalp lacerations, cephalohaematomata & neonatal jaundice are more common with ventouse

o Facial bruising, facial nerve damage & skull fracture can occasionally occur with injudicious

use of forceps, and prolonged traction with either instrument is dangerous

• Changing instrument is associated with increased foetal trauma ® usually only appropriate (and only

once) if the ventouse has achieved descent to the pelvic outlet, but then comes off the head and is

replaced by a low cavity forceps delivery

• If moderate traction with either instrument does not produce immediate & progressive descent ® then

C-section is indicated



INDICATIONS FOR INSTRUMENTAL VAGINAL DELIVERY

• Prolonged 2nd stage:

o Most common indication

o Usual if 1–2hrs of pushing has failed to deliver the baby

o If mother is exhausted. It may be performed earlier


o More common in 2nd stage

o Delivery can be expedited

• Prophylactic use ® indicated to prevent pushing in women with medical problems (e.g. severe cardiac

disease or hypertension)

• Breech delivery ® forceps are occasionally applied to the after-coming head

PREREQUISITES FOR INSTRUMENTAL VAGINAL DELIVERY

• The head must not be palpable abdominally

• On vaginal examination, the head must be at or below the level of the ischial spines

• The cervix must be fully dilated

• The position of the head must be known

• There must be adequate analgesia

• The bladder should be empty

LOW & MID-CAVITY DELIVERY

• Low-cavity delivery:

o Head is well below the ischial spines, usually OA position

o Bony prominences are palpable vaginally on the lateral wall of the mid-pelvis

o Forceps or ventouse are appropriate ® the latter is better if maternal effort is poor

o Pudendal block with perineal infiltration is usually sufficient analgesia

• Mid-cavity delivery:

o Head is engaged, but at or just below the level of the ischial spines

o Epidural or spinal anaesthesia is usual

o If there is any doubt that delivery will be successful ® it is attempted in the operating theatre,

with full preparations for a C-section

o OA position ® forceps or ventouse can be used

o OT position:

§ Usually the result of insufficient descent of the head to make it rotate

§ Descent is achieved with ventouse

§ Rotation in situ followed by descent can also be achieved by manual rotation or

Keilland’s rotational forceps

o OP position:

§ Often accompanied by extension of the foetal head ® making the presenting

diameter too large for the pelvis

§ Traction of a baby in this position may fail or cause severe perineal damage

§ Rotation of 180o can be achieved manually or with the ventouse / Keilland’s forceps



Describe Caesarean section, and outline the indications & complications

• Delivery by C-section occurs for about 25% of births in the developed world

• The usual operation is the lower segment Caesarean section (LSCS) ® the abdominal wall is opened

with a suprapubic transverse incision (Pfannenstiel incision), and the lower segment of the uterus is also

incised transversely to deliver the baby

INDICATIONS FOR EMERGENCY C-SECTION

• Usually performed in labour ® but may also occur with acute antepartum problems (e.g. placental

abruption)

• Prolonged 1st stage:

o Diagnosed when full dilation is not imminent by 12–16hrs, or earlier if labour was initially rapid

o Occasionally full dilation is achieved, but not all the criteria for instrumental delivery are met

o Most commonly, it is due to abnormalities of power ® e.g. insufficient uterine action

o The passenger or passage may also contribute


o Diagnosed from abnormalities of the foetal heart rate ® normally in conjunction with blood

sampling

o C-section is performed if it is the quickest route of delivery

INDICATIONS FOR ELECTIVE C-SECTION

• Performed to avoid labour ® normally at 39 weeks, as this reduces the risk of transient tachypnoea of

the newborn (retained foetal lung fluid) from 6% (38 weeks) to 4% ® if earlier, administration of

steroids should be considered

• Absolute indications:

o Placenta praevia

o Severe antenatal foetal compromise

o Uncorrectable abnormal lie

o Previous vertical C-section

o Gross pelvic deformity

• Relative indications:

o Breech presentation

o Severe IUGR

o Twin pregnancy

o Certain medical disorders ® e.g. pre-eclampsia

o Previous C-section

o Older nulliparous mothers

• When delivery is needed before 34 weeks, it is usual to perform C-section rather than induce labour ®

most common indications are severe pre-eclampsia & severe IUGR

SAFETY & COMPLICATIONS OF C-SECTION

• Maternal:

o Complications are more common when the procedure is in labour than when it is elective ®

may also be related to the indication for the C-section

o Complications include:

§ Haemorrhage



§ Need for blood transfusion

§ Infection of the uterus or wound

§ Rare visceral complications ® e.g. bladder or bowel damage

§ Postoperative pain & immobility

§ Venous thromboembolism

o Preoperative prophylactic antibiotics reduce the incidence of infection, and

thromboprophylactic measures are routine

o Approximately 1 in 5000 women will die after C-section

• Foetal:

o An elective procedure increases the risk of foetal respiratory morbidity at any given gestation

® in uncomplicated pregnancy, it is not recommended before 39 weeks

o Foetal lacerations are rare & usually minor

o Bonding & breastfeeding are particularly affected by emergency procedures

• Subsequent pregnancies:

o The incidence of placenta praevia is more common in pregnancies after a C-section

o The placenta may implant more deeply than normal in the myometrium (placenta accreta), or

through into surrounding structures (placenta percreta)

o Having a single C-section makes it less likely to deliver vaginally in subsequent pregnancies

(72–75%) ® ≥2 C-sections are an absolute contraindication to vaginal delivery

OBSTETRICS – OBSTETRIC EMERGENCIES


Describe shoulder dystocia & its management

• When additional manoeuvres are required after normal downward traction has failed to deliver the

shoulders after the head has been delivered

• Occurs in 1 in 200 deliveries ® requires urgent & skilled help

• Delay in delivery combined with unskilled attempts at delivery may cause brain injury or death

• Excessive traction of the neck damages the brachial plexus (Erb’s palsy) ® which is permanent in 10%

• The principal risk factor is macrosomia (>4kg) ® maternal diabetes doubles the risk at any given

birthweight, and other antenatal factors include previous shoulder dystocia & obesity

• Intrapartum risk factors are dystocia (obstructed deliver) & instrumental delivery ® antenatal prediction

is difficult

• Management is gentle downward traction ® legs are hyperextended onto the abdomen (McRobert’s

manoeuvre), and suprapubic pressure is applied

• If this fails, internal manoeuvres are required (via episiotomy) to rotate the shoulders into an oblique

position, or even 180o ® alternatively, the posterior arm is grasped and by flexion of the elbow, the hand

is brought down, narrowing the obstructed diameter by the width of the arm

• Last resort is symphysiotomy, or the Zavanelli manoeuvre ® involves replacement of the foetal head

& a C-section, but by this time foetal damage is usually irreversible

Outline cord prolapse & its management

• Occurs when the membranes have ruptured & the umbilical cord descends below the presenting part of

the foetus

• Untreated, the cord will be compressed or go into spasm, and the baby will rapidly become hypoxic

• Occurs in 1 in 500 deliveries ® the diagnosis is usually made at vaginal examination after the

identification of foetal distress

• Risk factors include:

o Preterm labour

o Breech presentation

o Polyhydramnios

o Abnormal lie

o Twin pregnancy

• Management:

o Involves initially pushing the cord up by the examining finger, or tocolytics (e.g. terbutaline)

are given to prevent compression of the cord

o If the cord is out of the introitus, it should be kept warm & moist, but not forced back inside ®

the patient is asked to go on all fours while preparations for delivery by the safest route are

undertaken

o Immediate C-section is normally used ® but instrumental vaginal delivery can be attempted if

the cervix is fully dilated & the head is low

Outline amniotic fluid embolism & its management • This is when liquor enters the maternal circulation, causing anaphylaxis with sudden dyspnoea, hypoxia

& hypertension ® often accompanied by seizures & cardiac arrest, and acute heart failure is evident

• It is extremely rare, but an important cause of maternal mortality ® accounted for ~5% of maternal

deaths in the UK between 2011–13



• If the woman survives for 30 mins, she will rapidly develop DIC, and often pulmonary oedema & ARDS

® in a few, haemorrhage from DIC is the first presenting feature

• Traditionally occurs when the membranes rupture ® but may occur during labour, at C-section, and

even at termination

• There are multiple predisposing factors, and prevention is impossible

• Diagnosis is easily confused with other causes of collapse & eclampsia ® often only made at post-

mortem

• Management involves resuscitation & supportive treatment as for any cause of collapse ® bloods for

clotting, FBC, electrolytes & crossmatch are taken, and treatment of massive obstetric haemorrhage will

be required

Describe uterine rupture, including risk factors & prevention

• The uterus can tear de novo, or an old scar can open

• The foetus is extruded, and the uterus contracts down & bleeds from the rupture site ® causing acute

foetal hypoxia & massive internal maternal haemorrhage

• Rupture of a lower transverse C-section scar is usually less serious than a primary rupture or one from a

vertical scar ® the lower segment is not very vascular, and heavy blood loss / extrusion of foetus into

the abdomen is less likely

• Nevertheless, the neonatal mortality from a lower segment uterine scar rupture is ~10%

• Rupture occurs in 1 in 1500 pregnancies ® including in 0.5% of women who attempt a vaginal delivery

after a previous LSCS

• The diagnosis is suspected from foetal heart rate abnormalities, or a constant lower abdominal pain ®

vaginal bleeding, cessation of contractions & maternal collapse may also occur

• Risk factors include:

o Labours with a scarred uterus ® vertical C-section or deep myomectomy carries higher risk

than previous LSCS

o Neglected obstructed labour ® rare in the West, but a common obstetric emergency in

developing countries

o Congenital uterine abnormalities ® occasionally cause rupture before labour

• Prevention measures include avoiding induction, and caution when using oxytocin in women with

previous C-section

• The foetus will very rapidly die if extruded from the uterus, and blood loss may be faster than can be

replaced

• The uterus is either repaired or removed

• It has a high recurrence in subsequent pregnancy, and early C-section is required

Outline the other obstetric emergencies UTERINE INVERSION

• When the fundus inverts into the uterine cavity ® usually follows traction on the placenta

• Occurs in 1 in 20,000 deliveries

• Haemorrhage, pain & profound shock are normal

• A brief attempt is immediately made to push the fundus up via the vagina ® if impossible, a GA is given,

and replacement performed with hydrostatic pressure of several litres of warm saline, which is run past

a clenched fist at the introitus into the vagina



EPILEPTIFORM SEIZURE

• Most commonly the result of maternal epilepsy or eclampsia ® can also be due to hypoxia from any

cause

• In the absence of cardiopulmonary collapse, diazepam will stop the seizure ® but it is wise to assume

the cause is eclampsia until it is excluded

• Magnesium sulphate is not useful in non-eclamptic seizures ® therefore, it is inappropriate where the

diagnosis is uncertain

LOCAL ANAESTHETIC TOXICITY

• Excessive doses or inadvertent IV doses of local anaesthetic can cause transient cardiac, respiratory &

neurological consequences ® occasionally resulting in cardiac arrest

• Prevention is more important ® treatment involves resuscitation & even intubation, until the effects have

worn off

OBSTETRICS – THE PUERPERIUM


Outline the physiological changes that occur in the puerperium

• Puerperium ® the 6-week period following delivery, when the body returns to its pre-pregnancy state

GENITAL TRACT CHANGES

• As soon as the placenta has separated, the uterus contracts & the fibres of the myometrium occlude the

blood vessels that formerly supplied the placenta

• Uterine size reduces over 6 weeks ® within 10 days, the uterus is no longer palpable in the abdomen

• Contractions or ‘after-pain’ may be felt for 4 days ® the internal cervical os is closed by day 3

• Lochia (uterine discharge) may be bloodstained for 4 weeks ® but thereafter is yellow or white

• Menstruation is usually delayed by lactation ® but occurs at about 6 weeks if there is no lactation

CARDIOVASCULAR SYSTEM CHANGES

• Cardiac output & plasma volume decrease to pre-pregnancy levels within a week

• Loss of oedema can take up to 6 weeks

• If transiently elevated ® BP is usually normal within 6 weeks

URINARY TRACT CHANGES

• Physiological dilation of pregnancy reduces over 3 months

• GFR decreases

HAEMATOLOGICAL CHANGES

• U&Es return to normal ® due to the reduction in GFR

• In the absence of haemorrhage ® Hb & haematocrit rise with haemoconcentration

• WCC falls ® platelets & clotting factors rise, predisposing to thrombosis

Outline the general postnatal care • Counselling & practical help with breastfeeding are often required

• Uterine involution, lochia, BP, temperature, pulse & any perineal wounds are checked daily

• Careful fluid balance check should prevent retention in women who have had an epidural

• Analgesics may be required for perineal pain ® also helped by pelvic floor exercises

• Psychiatric referral is suggested in women with a psychiatric history ® a postnatal plan including the GP

should be drawn up

Describe the physiology & process of lactation • Lactation is dependent on prolactin & oxytocin:

o Prolactin from the anterior pituitary stimulates milk secretion ® levels are high at birth, but it is

the rapid decline in oestrogen & progesterone after birth that cause milk to be secreted (as

prolactin is antagonised by them)

o Oxytocin from the posterior pituitary stimulates milk ejection in response to nipple suckling ®

which also stimulate prolactin release, and therefore more milk secretion

• As much as 1L of milk per day can be produced, depending on demand

• Since oxytocin release is controlled via the hypothalamus ® lactation can be inhibited by emotional or

physical stress



• Colostrum ® a yellow fluid containing fad-laden cells, proteins (IgA) & minerals that is passed for the

first 3 days (before milk comes in)

• Women should be gently encouraged to breastfeed when the baby is ready ® early feeding should be

on demand

• Correct positioning is vital ® the baby’s lower lip should be planted below the nipple at the time that the

mouth opens in preparation for receiving milk, so that the entire nipple is drawn into the mouth

• This could largely prevent the main problems of:

o Insufficient milk

o Engorgement

o Mastitis

o Nipple trauma

Describe the causes, clinical features & management of primary postpartum haemorrhage

• Primary postpartum haemorrhage (PPH) is the loss of >500ml of blood <24hrs after delivery ® or

>1000ml after C-section

• Occurs in 10% of women, and remains a major cause of maternal mortality

• Massive obstructive haemorrhage (MOH) is best defined as blood loss of >1500ml which is

continuing

AETIOLOGY

• Retained placenta:

o Occurs in 2.5% of deliveries

o Partial separation can cause blood to accumulate in the uterus, which will rise

o Collapse by occur in the absence of external loss

• Uterine causes:

o Account for 80%

o Uterus fails to contract properly ® either because it is atonic or because there is retained

placenta

o Uterine atony is more common with prolonged labour, grand multiparity, fibroids, and with

overdistension of the uterus (e.g. polyhydramnios or multiple pregnancy)

• Vaginal causes:

o Account for 20%

o Bleeding from the perineal tear or episiotomy is obvious

o High vaginal tears must be considered ® particularly after instrumental vaginal delivery

• Cervical tears ® rare, but associated with precipitate labour (<3hrs) & instrumental delivery

• Coagulopathy:

o Rare, but congenital disorders, anticoagulant therapy & DIC all cause PPH

o If prescribed, antenatal thromboprophylaxis should be stopped at least 12hrs before labour or

delivery ® but seldom causes haemorrhage

PREVENTION OF PPH

• The routine use of oxytocin in the 3rd stage of labour reduces the incidence of PPH by 60%

• Oxytocin is as effective as ergometrine ® which often causes vomiting & is contraindicated in

hypertensive women



CLINICAL FEATURES OF PPH

• Blood loss should be minimal after delivery of the placenta

• An enlarged uterus suggests a uterine cause

• The vaginal walls & cervix should be inspected for tears

• Very occasionally, blood loss may be abdominal ® there is collapse without overt bleeding

MANAGEMENT

• The priorities are:

o Support

o Restoration of blood volume

o Treatment of any developing coagulopathy

o Cessation of the blood loss

• Where blood loss is >1500ml and is ongoing, a MOH protocol should be activated ® it has clear

algorithms, including the use of non-crossmatched blood and anaesthetic, haematological & senior

obstetric help

• Resuscitation:

o Nursed flat

o Oxygen is given

o IV access is obtained ® blood is crossmatched

o Fluid ± blood is given

• Prevent / treat coagulopathy:

o FFP & cryoprecipitate may be required

o Tranexamic acid also reduces bleeding

• Retained placenta ® should be removed manually if there is bleeding, or if it is not expelled by normal

methods within 60mins of delivery

• Identify & treat cause:

o Vaginal examination is performed to exclude rare uterine inversion

o Vaginal lacerations are often palpable

o Uterine causes are common ® oxytocin and/or ergometrine are given IV if trauma is not

obvious

o If this fails ® an examination under anaesthesia is performed

o If uterine atony persists ® prostaglandin F2a (PGF2a) is injected into the myometrium

• Persistent haemorrhage:

o Continuation despite medical treatment requires surgery

o Bleeding from placental bed may respond to placement of a Rusch balloon

o If other methods fail ® then hysterectomy should not be delayed

Describe common psychiatric problems of the puerperium ‘THIRD DAY BLUES’

• Consist of temporary emotional lability

• Affects 50% of women

• Support & reassurance are required



POSTNATAL DEPRESSION

• Affects 10% of women ® but most do not present & receive no help

• Edinburgh Postnatal Depression Scale (EPDS) is helpful in identifying the problem ® but screening

is difficult

• Depression is more common in women who:

o Are socially or emotionally isolated

o Have a previous history

o Have other postnatal complications

• Postpartum thyroiditis should always be considered

• The severity is variable ® symptoms include tiredness, guilt & feelings of worthlessness

• Treatment involves social support & psychotherapy ® antidepressants are used in conjunction with

these

• Postnatal depression frequently recurs in subsequent pregnancies ® associated with depression later

in life (70% risk)

• Suicide is a major cause of death postpartum ® most women have a history of depressive or other

psychiatric illness, and this must be recorded at the booking visit

• In general, psychiatric drugs should be continued in pregnancy ® but this decision should be made

after assessment of the risks & benefits

o NB: For depressive illness, SSRIs (e.g. fluoxetine) are preferred

• Women with a history of mental illness should be seen by a psychiatrist before delivery ® an MDT post-

discharge should be arranged

• Urgent referral is indicated if there is:

o Recent significant change in mental state

o Emergence of new symptoms / thoughts / acts

o Estrangement from infant

o Persistent expression of incompetence as a mother

PUERPERAL PSYCHOSIS

• Affects 0.2% of women

• Characterised by an abrupt onset of psychotic symptoms ® usually around the 4th day

• More common in primigravid women with a family history

• Treatment involves psychiatric admission & major tranquilisers ® after exclusion of organic illness

• There is usually full recovery, but some develop mental illness in later life ® 10% relapse after a

subsequent pregnancy

Outline other common problems of the puerperium SECONDARY PPH

• This is excessive blood loss occurring between 24hrs and 6 weeks after delivery

• Due to endometritis (± retained placental tissue), incidental gynaecological pathology, or

gestational trophoblastic disease

• The uterus is enlarged & tender, with an open internal os

• Vaginal swabs & FBC are taken, with crossmatch in severe cases ® USS may help detect retained

products, although differentiation from blood clots is difficult



• If bleeding is heavy, then ERPC is used ® if bleeding is more chronic, then antibiotics are initially used

alone

• Characteristically, endometritis due to retained tissue causes bleeding that slows but does not stop with

antibiotics ® and gets worse again after the course is finished

POSTPARTUM PYREXIA

• This is a maternal fever of ≥38oC in the first 14 days ® infection is the most common cause

• Genital tract sepsis is a major cause of maternal mortality:

o It is most common after C-section ® but prophylactic antibiotics have considerably reduced

this

o Group A streptococcus, staphylococcus & E. coli are the most important pathogens in severe

cases

o Lochia may be offensive, and the uterus enlarged & tender

• Other common infections include:

o Urinary traction infection (10%)

o Chest infection

o Mastitis

o Perineal infection

o Wound infection after C-section

• Deep vein thrombosis can also cause low-grade pyrexia

THROMBOEMBOLIC DISEASE

• Deep vein thrombosis & pulmonary embolism is a leading cause of maternal mortality ® although

less than 0.5% of women are affected

• 1/2 of the deaths are postnatal ® usually after discharge from hospital

• Early mobility & hydration are important for all women

HYPERTENSIVE COMPLICATIONS

• Pre-eclampsia & its complications are a major cause of maternal mortality ® most deaths occur

postpartum

• Although delivery is the only cure for pre-eclampsia, it often takes at least 24hrs before the illness

improves ® BP usually peaks 4–5 days after delivery, and may need treatment for weeks

• In all pre-eclamptic patients ® attention is paid to fluid balance, renal function & urine output, BP, and

the possibility of hepatic & cardiac failure

• Blood pressure measurements continue for 5 days postnatally

THE URINARY TRACT

• Retention of urine:

o Common after delivery & usually painful

o May present with frequency, stress incontinence or severe abdominal pain ® but the women

or staff may not notice a lack of voiding

o Infection, overflow incontinence & permanent voiding difficulties may follow

o Postmicturition USS can be used to assess the residual volume non-invasively

o Treatment is catheterisation for at least 24hrs



• Urinary infection:

o Occurs in 10% of women

o Usually asymptomatic ® but often leads to symptomatic infection or pyelonephritis

o Routine urine culture is advised

• Incontinence:

o Occurs in 20% of women

o Overflow & infection should be excluded using postmicturition USS and catheterisation &

mid-stream urine sample respectively

o Obstetric fistulae are very rare in developed countries

o Symptoms of stress incontinence usually improve ® particularly with formal pelvic floor

exercises (but these has little preventative role)

PERINEAL TRAUMA

• Perineal trauma is repaired after delivery of the placenta

• Pain can persist for >8 weeks in 10% of women

• Superficial dyspareunia is common

• NSAIDs are best ® USS, salt baths & ‘Megapulse’ are of no benefit

• Paravaginal haematoma:

o Rarely, a woman experiences excruciating pain in the perineum a few hours after delivery

o This is almost always due to paravaginal haematoma ® which is usually identifiable only on

vaginal examination

o It is drained under anaesthesia

BOWEL PROBLEMS

• Constipation & haemorrhoids both occur in 20% of women ® laxatives are helpful

• Incontinence of faeces or flatus:

o Underreported symptom affecting 4% of women ® mostly transiently

o Both pudendal nerve & anal sphincter damage may be responsible

o Forceps delivery, large babies, shoulder dystocia & persistent OP positions are the main risk

factors

o Affected women are evaluated using anal manometry & USS ® and managed according to

symptoms

o Formal repair may be required ® after which all pregnancies should be by C-section

24 - Obstetrics

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Transcript of 24 - Obstetrics