Women’s Health

Ectopic Pregnancy.
• Fertilised ovum implants somewhere else other than the uterine body.
o 97% in the tubes.
 Most in ampulla
 25% in isthmus.
• As narrow and inextendable, tend to present early and to
rupture.
o 3% on ovary, cervix or peritoneum.

Incidence
• In the UK, 11.1 per 1000 pregnancies
• World wide rates are higher.
• About 7% of maternal deaths are due to ectopics.
o 1.8 deaths per 1000 ectopic pregnancies.

Predisposing factors.
• Anything that slows the ovum’s passage down the tubes.
o Damage to tubes.
 Salpingitis
 Previous surgery
 Previous ectopics.
o Presence of older – style IUCD
o GIFT fertilisation
o Endometriosis.
o Progesterone only Pill

Natural History.
• Trophoblast invades tubal wall.
• Weakens it and produces haemorrhage, which dislodges the embryo.
o If embryo dislodged, then is just passed like a normal miscarriage.
o If embryo not dislodged, and tube does not rupture, embryo converted into a
tubal mole and absorbed.
o If embryo not dislodged, and tube ruptures, can be a surgical emergency.
 Can be gradual, giving increasing pain and blood loss.
 Can be sudden and catastrophic, causing shock.
• Peritoneal pregnancies can survive into the 3rd trimester, and occasionally can be
successfully delivered surgically.
Clinical presentation.
• * Abdominal pain or bleeding in sexually active woman is ectopic unless proven
otherwise *.

• Sudden Rupture presents with sudden severe pain, peritonism and shock.
• Gradual rupture is more common.
o Generally about 8 weeks of amenorrhoea.
 May present before a period is even missed.
o Pain normally precedes vaginal bleeding.
 Can be dark, and like “prune juice”
 Can be fresh.
o Bleeding into the peritoneum causes diaphragmatic irritation and shoulder tip
pain.
o Opening bowels and urinating may cause pain due to compressing the embryo.
• Presentation may just be non – specific symptoms.
o Diarrhoea.
o Vomiting.
o Nausea.
o Dizziness.

• On examination.
o Tender abdomen (95%)
o Adnexal mass (63%)
o Cervical excitation (50%)
o Enlarged uterus (30%)
• Examine gently, due to risk of rupture.
• Preferably have a large cannula in situ.

Management.
• Give anti – D prophylaxis if needed.
• Early diagnosis is vital.
o Dipstix for βHCG.
 Is sensitive to 25iu/L
o Monitoring can be done with blood βHCG & ultrasound.
 If βHCG.> 6000 iu/L, and no intrauterine gestational sac is seen on
abdominal ultrasound, an ectopic pregnancy is likely.
 If βHCG1000 – 1500 iu/L, and no intrauterine gestational sac is seen
on transvaginal ultrasound, an ectopic pregnancy is likely.
 Very high result (30 – 40,000) is likely to be a uterine pregnancy.

• Management depends on woman’s desire for future pregnancy, and chance of rupture.
• Laparotomy.
o Shock from a ruptured ectopic can be fatal.
o Immediate laparotomy is needed as only treatment is clamping of the bleeding
artery.
o If an ectopic is suspected, insert a large cannula.
o If shocked, insert 2 large cannula and group and save.
 o Until blood is available, give colloid through a pressure bag.
o Inform consultant and take immediately to theatre.

Laparotomy Laparoscopy
Recovery time Reduced
Rate of subsequent intrauterine Similar Similar
pregnancy.
Persisting trophoblast needing 1.2% 12%
further treatment.
Repeat ectopic pregnancy Slightly less common.

• In presence of contralateral, healthy tubes RCOG guidelines is that salpingotomy and

salpingectomy are as good as each other.
Salpingotomy Salpingectomy
Rate of subsequent intrauterine 49% Reduced
pregnancy.
Persisting trophoblast needing 8% 4%
further treatment.
Repeat ectopic pregnancy 18% 8%

• If other tube is unhealthy, salpingotomy is preferred but patients should be warned about
risk of future ectopics.
• Methotrexate.
o 50mg/m2 IM or intertubal injection into gestation sac.
o Can be used for small ectopics
 < 3.5 cm in greatest diameter.
 βHCG < 3000 iu/L
 Minimal symptoms.
o Visualisation of foetal heart a contraindication to treatment.
o 15% will require more than one dose
o 10% will need surgical intervention.
 7% rupture rate following methotrexate.
o Side effects.
 75% will get abdominal pain.
• Admission for observation and ultrasound is often needed to
distinguish pain from ectopic rupture from pain of tubal
abortion.
 Multiple ovarian cysts.
 Life threatening neutropaenia.
 Pneumonitis.
 Late collections of pelvic blood.
o Advise avoidance of sex during treatment, and effective contraception for the
following 3 months.
o Subsequent fertility rates seem to be increased by methotrexate treatment.
 • Expectant management.
o Some tubal ectopics resolve spontaneously, so expectant management can be
used.
 Absence of acute symptoms.
 Falling βHCG levels that are < 1000 iu/L.
 No evidence of blood.
 < 100 ml fluid in pouch of Douglas.
o Follow up twice weekly with blood βHCG and ultrasound until.
 βHCG < 20 iu/L
• Tubal rupture can occur at very low levels of βHCG.
 Adnexal mass reducing by 7 days,
o Expectant management may also be used for women with βHCG < 1500, but no
ultrasound evidence of pregnancy.
 Acutely manage if symptoms develop.
 βHCG levels plateau.
 βHCG rise at 48 – 72 hours.

• Management of persistent trophoblast.

o Occurs in 8.2% having laparoscopic salpingotomy.
 4% having open salpingectomy.
o Diagnosis by βHCG failing to fall along predicted curve.
o Surveillance regimes vary.
 Eg. <65% of pre – op value by 48 hours.
 Eg. <10% of pre – op value by 10 days.
o Treatment with IM Methotrexate.

Measures to reduced missed ectopic pregnancies.

• Always send uterine curettings to histology at evacuation of retained products (ERPC)
• If histology doesn’t confirm failed uterine pregnancy, recall the patient.
o Ensure rapid return of histology results.
• If ultrasound suggests an incomplete abortion, but no foetus has been seen, consider an
ectopic.
Hypertension in Pregnancy
Pre–existing essential hypertension.
• Drugs may need to be modified.
o Some cause IUGR.
• Risk of pre – eclampsia is raised by 500%.
o Suspect if:
 BP rises by <30/15mmHg from baseline.
 Hyperuricaemia.
 Protienuria
 Clotting activation
o If these symptoms are episodic, suspect phaeochromcyotoma.

Pre – eclampsia
• Is hypertension with protienuria induced by pregnancy.
• Eclampsia is pre – eclampsia, plus seizures.
o Affects 1:2000 pregnancies.
o Major cause of maternal and foetal morbidity and mortality.

• Multi – system disorder originating in the placenta.

• Primary defect is failure of the trophoblastic cells to properly invade spiral arteries.
o If invasion complete, makes spiral arteries unreactive to vasoconstricors and so
protects placental blood flow.
o If this fails, BP increases to compensate.
• The high blood pressure damages hepatic and renal vasculature, and also the coagulation
system.
• Develops after 20 weeks and usually resolves within 10 days after delivery.
o Be warned, 50% of eclamptic fits are postpartum and 25% are > 48 hours post
partum
• Maybe asymptomatic, so regular screening is very important.

• Risk factors.
o Maternal.
 PMHx or FHx of pre – eclampsia.
 Lack of sperm mediated partner – specific immune tolerance.
• Relationship < 4 months of duration.
• Primip/ first child with this partner
• IVF by ICSI.
• Ht < 155 cm
• Overweight
• Age < 20 or > 35
• Migraines
 • Pre – existing Hypertension
• Renal disease
• Being a Non – smoker
o Foetal.
 Increased placental bulk.
• Hydatidiform mole.
• Multiple pregnancy
• Placental hydrops (eg. rhesus disease)

• Effects of pre – eclampsia

o Reduced plasma volume.
o Increased peripheral resistance.
o Placental ischemia
o BP > 180/140 mmHg can cause microaneurysms
o Oedema may develop.
 Cause sudden weight gain of 1kg.
o Protienuria is a late sign, denoting renal involvement.
 Can be detected earlier by monitoring urate levels.
• Pre – eclampsia suggested by:
o > 0.29 mmol/L at 28 weeks
o > 0.34 mmol/L at 32 weeks
o > 0.29 mmol/L at 36 weeks
 Originally GFR is normal and only serum urate increases.
• Later urate and creatinine can be raised.
o Liver may be involved.
 Contributes to risk of DIC and HELLP syndrome.
• HELLP is Haemolysis, Elevated Liver Enzymes and Low
Platelets.
• Raised LDH
• Raised ALT < 500U/L
• Bilirubin <86 μmol/L
o Placental abruption
o Foetal asphyxia
o IUGR

• Preventing pre – eclampsia.

o Antenatal BP & urinalysis screening.
o MgSO4 prophylaxis in at risk women.
o Uterine artery scans can identify at risk women.
o Aspirin prophylaxis can cause a significant reduction in at risk women.

• Symptomatic pre – eclampsia.

o May mimic flu.
 Headache
 Chest or epigastric pain.
 Vomiting
 Tacchycardia
 o Important to recognise and treat at this stage as full blown eclampsia, with
generalised seizures, can easily develop.
o Death can occur rapidly from:
 Stroke (most commonly)
 Hepatic failure.
 Renal failure
 Cardiac failure.

• Management of early pre – eclampsia.

o Admit if:
 BP rises by > 30/20 mmHg over booking BP.
 BP > 160/110
 BP > 140/90 in presence of protienuria (however small)
 IUGR
o In hospital
 Measure BP every 2 – 4 hours.
 Weight daily
 Dipstix all urine.
 Strict fluid balance.
 Monitor.
• U&Es
• LFTs
• Urate
• Placental function
• Platelets.
o Beware falls to < 110 x 109/ L
 Regular CTG with US scan to monitor foetal growth and biophysical
profiles.

 If asymptomatic.
• Hypertension can be treated with drugs under supervision in
hospital.
o 250 mg – 1g/6h Methyldopa
• Antihypertensives alone are only appropriate if all other
variables are satisfactory.

 If symptoms worsen, discuss delivery with paediatric team.

 All labouring pre – eclamptics need H2 – blockers at onset of labour.
• Management of severe pre – eclampsia.
o Applies to those with BP > 160/110 with protienuria of > 0.5g/day.
o Also applies to those with BP> 140/90 with protienuria, plus any of the
following:
 Seizures.
 Headache or epigastric pain.
 Platelets < 100 x 109/ L
 Visual disturbances.
 Creatanine <100 μmol/ L
 ALT > 50 iu/L
 Clonus > 3 beats
 Creatanine clearance < 80 mL/min
o Continually monitor maternal O2 saturation, and take BP every 15 minutes.
o “Magpie” regimen
 4g MgSO4 (8ml of 50% solution) IV over 15minutes in 100 ml 0.9%
saline.
o Catheterize for Urine output.
o Hourly.
 Temperature.
 FBC
 U&E
 LFT
o Blood creatinine every 12 hours.
o Monitor foetal well being.
 Foetal heart rate
 Liquor volume
 Foetal growth
 Umbilical cord Doppler.
o Deliver early with senior anaesthetist, obstrician and midwife in attendance.
o Management of hypertension.
 BEWARE, automated BP devices underestimate BP.
  If BP > 160/110 mmHg or MAP > 125 mmHg, slowly give 5mg
hydralazine IV, repeating every 20 minutes to a maximum of 20 mg.
• Contraindicated if pulse > 120 bpm.
 Alternatively, give labetalol IV following the protocol..
• 0 minutes 20mg
• 10 minutes 40 mg
• 20 minutes 80 mg
 Prophylactic H2 – blockers until normal post natal care begins.
 Restrict fluids to 85 ml/hour
 Monitor urine output.
• If oligouria < 100ml/4h, consider 500 ml IV Human albumin
solution (HAS).
 Also consider HAS prior to
• Hydralazine use
• C – section
• Regional anaesthesia
 If HAS is used, consider inserting a CVP line.
• Definitely insert one if oligouria reoccurs.
• If CVP > 10 mmHg, or there is persistent oligouria, give 20mg
fruesomide.
• If CVP < 10 mmHg, consider giving 500ml IV HAS.

o Treatment of eclamptic seizures.

 Treat first seizure with 4g MgSO4 (8ml of 50% solution) IV over
5minutes in 100 ml 0.9% saline
• Maintain with 1g/h for the next 24 hours.
• Beware of respiratory depression.
 If seizures recur, give 2g MgSO4 as a bolus.
 Check tendon reflexes and respiratory rate every 15 minutes.
 Stop MgSO4 if RR < 14/min or SaO2 < 95%.
 Monitor Mg levels (therapeutic range: 2 – 4 mmol/L) if recurrent fits or
renal compromise is present.
• Have IV calcium glutonate ready in case of magnesium
toxicity.
 If fits continue, give 5 – 10mg diazepam as a slow IVI.
• Consultant level decision
 If fits still recur, consider other causes and send for CT scan.
o Pitfalls in management of pre – eclampsia and eclampsia.
 Believing the disease is predictable and that BP is a good marker of
severity.
 Ignoring mild protienuria.
• Cases of patients being 1+ in urine, and being dead 24 hours
later.
 Believing anti – hypertensives stop pre – eclampsia.
• May stop stroke, but hypertension is a symptom of the disease,
not a cause.
• Diuretics further deplete plasma volume and are
contraindicated in all but a few, rare cases.
o Left ventricular failure.
 o Laryngeal oedema complicating pre – eclampsia.
• Believing that delivery removes risk.
o 50% of eclamptic fits are postpartum
o 25% of eclamptic fits are > 48 hours post partum.
o Observe until clinically and biochemically normal.
 Giving ergometrine for the 3rd stage of labour.
• Further increases BP, so high risk of stroke.
• Oxytocin may be used.
 Not replacing significant blood loss meticulously.
• Risk of hypovolaemia or fluid overload if not done carefully.
• Sign of something going wrong is acute respiratory distress
syndrome.
• Have the most experienced person as the only one dealing
with the IVIs.
 Failure to inform and involve anaesthetists and ITU early.

Diabetes Mellitus.
• Meticulous control around conception reduces rates of malformation.
• Management of diabetes needs to be optimised pre – conception, so mention it to all
diabetics.
o Treat retinopathy pre – pregnancy.
 20% of diabetics will develop proliferative retinopathy during
pregnancy, so screen on antenatal visits.
o Check for diabetic renal disease.
 If severe, advise against pregnancy.
• Insulin demands go up during pregnancy, so doses will need reviewing regularly.

• Due to increased GFR and no scope for increase reabsorption in the proximal tubule,
glycosuria is common in pregnancy and doesn’t necessarily mean diabetes.
• In a non – diabetic, BM will remain generally stable at 3.5 – 4.5 mmol/L, but will peak
after meals.
o Foetal blood glucose will follow mothers due to free diffusion.
o Compensatory foetal hyperinsulinaemia will cause increased foetal growth.

Complications.
• Maternal.
o Polyhydramnios
 25% of mothers.
 Query due to foetal polyuria.
o Pre – term labour.
  17%.
 Associated with polyhydramnios.
o Late miscarriage and Still birth.
• Foetal.
o Malformation.
 Rates are 3 – 400% higher than the general population.
o Sacral agenesis.
 Rare.
 Almost exclusive to babies of diabetic mothers.
o CNS and CVS malformations.
o Macrosomia & IUGR.

• Neonatal.
o Hypoglycaemia.
o Slowed intrauterine maturity
 Respiratory Distress Syndrome
o Polycythaemia.
 29%
 Neonatal jaundice.
o Hypocalcaemia
o Hypomagnesaemia

Antenatal care.
• Review in joint clinic with diabetologist.
• Confirm gestation with early ultrasound.
• Detailed abnormality scan at 19 – 20 weeks
• Foetal echocardiogram at 22 weeks, if early control has been poor.
• Educate about benefits of normoglycaemia and home glucose monitoring.
o Regular postprandial monitoring prevents harm to the baby.
o Aim for
 Fasting level < 5.5 mmol/L
 1 hour post prandial level < 7.5 mmol/L
• Insulin needs increasing 50 – 100% as pregnancy progresses.
o Review regularly.
• Give glucagon kit and ensure partner knows how to use it.
• Admit if adequate control proves impossible at home.
• Oral hypoglycaemics currently avoided.
o However, glyburide does not cross the placenta and may be safe.
• Monitor foetal growth and wellbeing with ultrasound and CTG.

Delivery.
• Timing takes into account.
o Diabetes
 o Any pre – eclampsia
o Maturity
o Size of baby
• Delivery < 38 weeks may result in neonatal respiratory distress.
• Deliver baby where there are good neonatal facilities.
• Traditionally delivery was at 36 – 38 weeks to avoid risk of stillbirth.
o With careful monitoring, pregnancies can go to (but not beyond) term.

• In labour.
o Avoid acidosis.
o Monitor the foetus with CTG and Doppler.
o Avoid maternal hyperglycaemia, as risk of neonatal hypoglycaemia.
 Use extra insulin to avoid hyperglycaemia.
• May need 5 IU/h
• Particularly if β – sympathetomimetics or glucocorticoids used
for preterm labour.
o Aim for vaginal delivery with labour of < 12 hours.
o Beware shoulder dystocia with macrosomic babies.
o With elective deliveries.
 Give normal insulin night before induction.
 During labour, give 1L of 5 – 10% glucose/8h with 1 – 2 U insulin/h
via pump.
 Aim for BM = 4.5 – 5.5 mmol/L
• Check hourly.
 Insulin need falls as labour progresses and immediately post partum.
• Stop infusions at delivery.
• Return to pre – pregnancy regimen.
 Perform emergency C – section if labour prolonged.
 Clamp cord early.
• Reduces risk of polycythaemia.

• Postnatal.
o Encourage breast feeding.
 Oral hypoglycaemics contraindicated.
o Encourage pre – pregnancy counselling before next pregnancy.
o Post partum glucose tolerance test at 6 weeks check.

Gestational diabetes.
• Diagnosed if BM > 7.8 on Oral glucose tolerance test.
• Incidence of 3% of pregnancies.
o 50% go on to develop full – blown diabetes mellitus, so give lifelong dietary
advice & follow up.
• Risk factors for development of full blown diabetes.
o High BMI pre – pregnancy
o Age > 30
o Mothers who had low birth weights or IUGR.
o 1st degree relative with diabetes.
o Unexplained stillbirth
o Gestational Diabetes before 27 weeks.
 o Insulin dependent gestational diabetes.
• All these risks can be reduced with good diet, exercise and no smoking.

Thromboembolism
• Chief cause of maternal death in the UK.
o Investigate any unexplained leg or chest symptoms as an emergency.
o VTE risk rises 6 – fold during pregnancy.
• Half of mothers with a 1st VTE during pregnancy have thrombophilia.
o Investigate all women who present with VTE.
o Some factors associated with thrombophilia are:
 Factor V Leiden mutation
• This reduces Factor V breakdown by Protein C.
• Affects 4 – 10% of the population.
• Increases thrombotic risk 3 – 8 times.
• Homozygous individuals have 80 times the risk of
thromboembolism
 Protein S deficiency.
• Affects 2% of the population.
• Increases thrombotic risk by 10 times.
 Antithrombin III deficiency.
• Affects 0.02% of the population.
• Thrombosis risk increased by 25 – 50 times.
 Lupus anticoagulant ± cardiolipin antibody.
• Women with lupus anticoagulant risk venous and arterial
emboli in atypical vessels.
o Eg. portal and arm vessels.
 G20210A mutation of the prothrombin gene.
• 2% of the population
 Homozygosity for the thermolabile variation of
methylenetetrahydrofolate reductase (C677T MTHFR)
• 10% of the population
• Leads to homocysteinaemia.
 Dysfibrinogenaemia
• Rare
• Thrombotic risk is variable.

o Pregnancy is an acquired risk factor for VTE.

 Not all women should be screened for thrombophilia.
 Screening should be performed in women with.
• History of thromboembolism.
• Family history of thromboembolism
• Those with history of 2nd trimester loss.
• Severe or recurrent pre – eclampsia.
• IUGR
o Those with thrombophilia, but no history of thromboembolism, should have an
individualised assessment of the defect and other risk factors that may be
present.
 Low molecular weight heparin prophylaxis is recommended.
• When tests for VTE is negative, but clinical suspicion is high, treat anyway.
 o Stop treating only after repeat negative tests > 1 week later.
o Before starting heparin therapy, take bloods for.
 FBC
 U&Es
 LFTs
 Coagulation & thrombophilia screen
Pulmonary embolism
• Small emboli may cause.
o Pyrexia.
o Syncopy
o Cough
o Chest pain
o Breathlessness
• Main differential of pleurisy is pulmonary embolism in the Absence of:
o High fever
o Much purulent sputum.
• Large emboli present with.
o Collapse
o Chest pain
o Breathlessness
o Cyanosis
o Raised JVP
o 3rd heart sound
o Parasternal heave
• Tests.
o CXR and ECG may be normal.
 Tacchycardia most consistent finding.
o Some ECG changes can be caused by pregnancy alone.
 Deep S – wave in Lead I
 Q – wave and inverted T – wave in Lead III
o Blood gases may be helpful.
 Low PaO2
 Low PaCO2
o CT pulmonary angiograms are better than V/Q scans.
o Scan legs for venous thrombi.

• Treatment.
o Massive emboli may require
 Prolonged cardiac massage
 Thrombolysis
 Percutaneous thrombus fragmentation
 Pulmonary embolectomy
o Give 5000U IV unfractionated heparin.
 10000U in severe cases
o Follow this with 1000U/h in 0.9% saline via syringe pump.
 o Monitor APPT at 6 hours, then at 24 hours.
o Adjust dose as needed.
 Usually 1000 – 2000U/h
o After 3 – 7 days, maintain on long term heparin with careful monitoring.
 Eg. 10000U/12h SC

• Problems with heparin treatment.

o Maternal osteopaenia.
 Reversible on discontinuing.
o Thrombocytopaenia.
o Allergic skin reactions
o Alopecia

• For less massive emboli.

o Low molecular weight heparin is an alternative.
 Eg. enoxapin.
 1 mg/kg/12h SC, based on pre – pregnancy weight.
o Warfarin is teratogenic
 64% of those who take warfarin in pregnancy have babies with Conradi
– Hunermann syndrome.
• Saddle nose
• Nasal hypoplasia
• Frontal bossing
• Short stature
• Stippled epiphyses
• Optic atrophy
• Cataracts
• Low IQ
• Flexural contractures
 Only used antenatally in those with artificial heart valves.
• Only to 36 weeks.
o Sub cutaneous heparin continued throughout labour
 Contraindicated in epidurals.
o Postpartum, heparin is reduced.
 Eg. 7500U/12h SC for unfractionated heparin.
 Treat for at least 6 weeks postpartum, or 6 months from embolus.
 Some choose warfarin from 2 days postpartum.

DVT
• Suspect if
o Leg pain/ discomfort.
 Especially left.
o Swelling oedema
o Pyrexia.
 o Increased WCC
o Lower abdominal pain.
• Tests.
o Doppler ultrasound

• Treatment.
o Elevate legs and use compression stockings.
o Give heparin throughout pregnancy.
 Eg. Enoxaparin.
o Measure peak anti – Xa activity3 hours post – injection
 Aim for level 0.4 – 1U/ml
 If above this reduce dose eg. from 80mg/12h to 60mg/12h
 Repeat anti – Xa after dose is changed to check clotting.
o Check platelets at 7 days, and then monthly.
 If heparin – induced thrombocytopaenia occurs, use danaparoid sodium
o After delivery, warfarin may be used.
 Breastfeeding is fine on warfarin.
o Monitor INR meticulously.
o Treat for at least 6 weeks post partum, and 6 months from thrombosis.
o Compression stockings should be worn for 2 years.
 Reduces port – thrombotic syndrome incidence from 23% to 11%.

• Prophylaxis.
o As pregnancy is a hypercoagulabe state, consider thromboprophylaxis at all
stages of pregnancy, labour and delivery.
o In all pregnant women avoid dehydration and immobility.
o Also assess risk factors, and treat if any two of the following are present.
 Age < 35 years
 BMI < 35 or weight < 90 kg
 Parity >3
 Gross varicose veins
 Paraplegia
 Sickle cell disease
 Nephrotic syndrome
 Previous thromboembolism
 History of thrombophilia
 Myeloproliferative disorders
 Irritable bowel disease
 Hyperemesis/ dehydration
 Pre – eclampsia
 Immobility for > 3 days
 Ovarian hyperstimulation
 Major infection (eg. pyelonephritis)
 Labour lasting > 12 hours
 Mid - cavity forceps use
 Excessive blood loss
 Evacuation of retained products of conception
 Post – partum sterilisation.

o If patient is high risk, treat with LWMH (eg. enoxaparin) as soon as possible
after delivery.
  Contraindicated in:
• Post – partum haemorrhage
• Within 4 hours of epidural insertion or removal.
• Within 6 hours of traumatic epidural insertion or removal.
 Continue for 3 – 5 days, even if discharged before then.
 Dose based on pre – pregnancy weight.
• < 50 kg 20mg/24 hours SC
• 50 – 90 kg 40mg/24 hours SC
• > 90 kg 80mg/24 hours SC
 If heparin contraindicated, use TED stockings.
o If patient very high risk ( >2 risk factors).
 Start prophylaxis antenatally and as early as possible.
 Consider normal dose prophylaxis when admitted in labour.

o Woman with a history of VTE in pregnancy or thrombophilia need slightly

different considerations.
o Action depends on whether they are very high, high or moderate risk.
 Very high risk patients are those with previous VTE, and already on
long term warfarin therapy
• Use high dose LMWH.
o 80mg/24 hours SC or 1mg/kg/h BD
o Start prenatally.
• Half dose on day of induction and day of delivery
• Revert to warfarin postpartum.

 High risk patients are ones who fall into any of the following
categories.
• Recurrent VTE
• Previous VTE and 1st degree relative with VTE or
thrombophilia
• Previous VTE with thrombophilia
• Asymptomatic thrombophilia with any of the following gene
problems.
o Antithrombin III deficiency
o Combined defects
o Homozygous factor V Lieden deficiency
o Prothrombin gene defect
• Management is to give LMWH antenatally and postpartum.
 Moderate risk patients are those with asymptomatic thrombophilia,
other than the types outlined above.
• If previous VTE in pregnancy and no other risk factors, give:
o Antenatal aspirin
o LMWH for 6 weeks postpartum.
 o Air travel while pregnant.
 For all patients until 6 weeks post partum advise.
• Isometric leg exercises during flight.
• Maintain good hydration.
o No caffeine or alcohol.
• If flight is long haul (> 4 hours) wear knee length TED
stockings.
o If additional risk factor present.
 Wear TED stockings for all flights.
 Consider LWMH 40mg/24 hours SC on day
of flight and following day.
 If heparin unsuitable, use 75 mg aspirin PO
for 3 days before flight and on day of flight.

Liver dysfunction.
• Jaundice in pregnancy requires immediate referral to an expert.
• While waiting for the expert, determine:
o Any drugs taken? What? When? How much?
o Travel history.
o Life style or occupational risks.
• About 1 in 1500 pregnancies results in jaundice.
o Viral hepatitis and gallstones are common.
o Investigation is similar to in the non – pregnant patient.
• Patients with Gilbert’s or Dublin – Johnson syndromes do well.
o Pregnancy may exacerbate Dublin - Johnson

• Tests.
o Serology
 Check HBsAg in all women with jaundice
 Look for anti – HBc IgM to check for acute infection
 Avoid contact with blood during delivery, and be extra careful with
disposal of sharps.
 Vaccinate baby at birth.
 Offer vaccination to family.
o Urine tests for bile
o LFTs
o Ultrasound

• Intrahepatic cholestasis of pregnancy.

o Incidence of 0.1 – 1.5% of pregnancies in Europeans.
o Main differential is viral hepatitis.
o Clinical picture.
 Pruritis, especially of palms and soles.
 Particularly in 2nd half of pregnancy.
o Complications are dangerous for baby, so monitor foetal wellbeing closely, and
deliver at 38 weeks.
 60% have preterm labour.
 33% have foetal distress
 2% half stillbirth
 o Tests.
 Liver transaminases mildly increased.
• About 60% sensitivity.
• Levels of < 300 U/L
 Raised billirubin.
• Sensitivity of about 25%
o Management.
 Only cure is delivery.
• Resolves within few days of delivery.
 Ursodeoxycholic acid will reduce itching and LFTs.
 At birth give Vitamin K
• 10 mg/24 PO for mother
• 1 mg IM for baby
o Contraindication for oestrogen containing contraceptives.
o Recurs in 40% of future pregnancies.

• Acute fatty liver of pregnancy.

o Incidence.
 1:6600 – 1:13000 deliveries
 Therefore condition is rare, but grave.
o Clinical picture.
 Abdominal pain
 Jaundice
 Headache
 Vomiting
 Sometimes:
• Thrombocytopaenia
• Pancreatitis
 Associated with preeclampsia in 30 – 60%
 Usually occurs after 30 weeks gestation.
 Liver steatosis with microdroplets of fat within liver cells.
o Complications
 Deep jaundice
 Uraemia
 Severe hypoglycaemia
 Clotting disorders

 Complications can result in coma and death.

o Management.
 Call haematologist
 Monitor BP
 Supportive treatment for liver and kidney failure
 Treat hypoglycaemia vigorously with CVP line.
 Correct clotting disorders
 Delivery ASAP
• Regional and epidural anaesthesia contraindicated.
 Monitor post partum, particularly for.
• Post partum haemorrhage
• Neonatal hypoglycaemia
 o Mortality can be high.
 18% maternal
 23% foetal

• Other causes of jaundice in pregnancy.

o Viral hepatitis
 Increased ALT
• > 200 U/L
 Maternal mortality increased in Hepatitis E
 Hepatitis C virus affects < 1% of woman in the UK.
 Vertical transmission affects about 5% of babies.
• Transmission is not reduced by caesarean section, except in
cases where there is also HIV.
 Passive antibodies from the mother wane by 18 months.
 Interferon treatment is generally not recommended in children under 3
years.
 Screening for viral hepatitis is currently not planned.
 Infected women should be referred for interferon and ribravarin
treatment after birth.

o Pre – eclampsia
 Severe pre – eclampsia can cause hepatic rupture or infarction.
 ALT < 500 U/L
 Bilirubin < 86 µmol/L

o Hyperemesis Gravidum.
 Rare complication.
 Often fatal
 ALT < 200 U/L

o Halothane.
 Can cause jaundice.
 Don’t use halothane in pregnant patients.

o HELLP syndrome.
 Defining characteristics.
• Haemolysis
• Elevated Liver enzymes
• Low Platelets
 Incidence.
• Wider pregnant population is 0.1 – 0.6%
• In pre – eclampsia is 4 – 12%
 Clinical picture.
• Upper abdominal pain
 • Malaise
• Vomiting
• Jaundice
• Headaches
• Microangiopathic haemolytic anaemia
• DIC
 Results.
• Raised LDH
• Raised ALT < 500 U/L
• Bilirubin < 86 µmol/L
 Recurs in 20% of patients.
 Management.
• Admit to hospital
• Get expert help
• Deliver if severe.
Bleeding in early pregnancy.
• The most common cause of bleeding in early pregnancy is miscarriage.
• Other causes include.
o Ectopic pregnancy
o Cervical problems.
• Miscarriage.
o Loss of pregnancy before 24 weeks.
 20 – 40% of pregnancies miscarry.
 Most are lost in the first trimester.
o Most present with bleeding PV.
o Diagnosis may not be straightforward.
 Consider ectopic.
 Have a low threshold for doing an ultrasound scan.
 Pregnancy tests remain positive for several days after foetal death.
o Management of early pregnancy bleeding.
 Is she shocked?
• Blood loss
• Products of conception in the cervical canal.
o Remove with sponge forceps.
 Has pain and bleeding been worse than a period?
• Have products of conception been seen?
o Clots may be mistaken for products.
 Is the os open?
• The external os of a multigravida usually admits the tip of a
finger.
 Is uterine size appropriate for dates?
 Is the bleeding from a cervical lesion or from the uterus?
 What is her blood group?
• If Rhesus – ve she will need Anti – D.
o If os is closed and symptoms are mild, it is a threatened miscarriage.
 Advise rest.
• May not actually affect prognosis..
 75% will settle.
  Threatened miscarriage, especially in the second trimester, is associated
with premature rupture of membranes and delivery.
• Book mother into hospital with good neonatal facilities.
o If symptoms are severe and the os is open, it is an inevitable, incomplete or
complete miscarriage.
 If bleeding is profuse, consider IM ergometrine.
 If bleeding or pain is unacceptable, or US shows significant retained
tissue, arrange an evacuation of retained products of conception
(ERCP).
 Expectant management is used when volume of retained products is
small.
• < 15 mm across on transvaginal US.
 When retained products are 15 – 50 mm across, consider medical
management.
• Mifepristone.
• May not give conclusive benefit.

o Missed abortion.
 Said to have occurred when the foetus dies, but is retained.
 There has usually been bleeding, and the uterus will be small for dates.
 Confirm the diagnosis with US scan.
 Attempt to induce evacuation if uterus is small.
• Mifepristone
• Misoprostol

• 50% will need surgical evacuation if products are.

o > 5 cm2 in the transverse plane.
o > 6 cm2 in the sagittal plane.
• Larger uteruses will also need surgical evacuation.

o Mid – trimester abortion.

 Usually due to mechanical causes.
• Cervical incompetence.
o Results in rapid, painless delivery of a live foetus.
o Can be strengthened by cervical encirclage suture at
16 weeks.
o Stitch is removed prior to labour.
• Uterine abnormalities.
• Chronic maternal disease.
o Diabetes mellitus
o SLE

o After a miscarriage.
 Miscarriage may be a bereavement.
• Give parents space to
o Grieve
o Ask why it happened
o Ask if it will happen again.
 • Foetal products are normally incinerated.
o Allow parents to arrange their own burial if they
wish.
• Most early pregnancy losses are due to aneuploidy and
abnormal foetal development.
o 10% is due to maternal illness.
 Eg. Pyrexia.
o Second trimester losses are often due to infection.
 CMV
 Bacterial vaginosis
• Most subsequent pregnancies will be normal, but at increased
risk.

o Recurrent miscarriage.
 Defined as loss of 3 or more consecutive pregnancies.
 Affects 1% of women
 Prognosis is affected by.
• Number of previous miscarriages.
• Maternal age.
 Possible causes.
• Endocrine.
o Polycystic ovaries.
 Found in 41% on ultrasound.
 Polycystic pathology does not predict
increased risk of pregnancy loss in women
with recurrent miscarriage who conceive
naturally.
o Infection.
 Bacterial vaginosis.
• Associated with 2nd trimester
losses.
• Screening and treatment is
recommended for those with
o Previous mid – trimester
losses
o Pre – term births.
o Parental chromosome abnormality
 4% of recurrent miscarriage.
 Usually a balanced reciprocal or
Robertsonian translocation.
 Refer to clinical geneticist.
  Genetic counselling offers:
• Prognosis for future pregnancies.
• Familial chromosome studies.
• Appropriate advice for subsequent
pregnancies.
o Risk may be 5 – 10% of
an unbalanced
translocation.
o Uterine abnormalities.
 Uncertain as to how much effect these have
on recurrent miscarriage.
 Not known if hysteroscopic correction of
abnormality contributes to successful
pregnancy.
 Open uterine surgery increases chance of
uterine rupture in pregnancy.

o Antiphospholipid antibodies.
 Antibodies.
• Anti – cardiolpin.
• Lupus anticoagulant.
• Anti – phospholipid
 Present in 15% of women with recurrent
miscarriage.
 Most miscarry in the first trimester.
 Can be controlled by.
• Low – dose aspirin prophylaxis
throughout pregnancy.
• Heparin as soon as foetal heart
appears (about 5 weeks) until 34
weeks.
 Get expert advice.
 Subsequent pregnancies need special
surveillance as they are at increased risk of.
• Repeated miscarriage
• Pre – eclampsia
• Foetal growth restriction
• Pre – term birth.
o Autoimmune.
 Suggested that women who have the same
HLA alleles as their partner don’t mount the
 satisfactory protective response to the
foetus.
 Immunotherapy has not been shown to
increase live birth rate.
• Potentially dangerous.
• Should not be offered.
o Recommended investigations.
 Karyotyping of peripheral blood of both
parents.
 Karyotyping foetal products.
 Pelvic US to assess ovaries and uterus.
 Test for Antiphospholipid antibodies.
• Take 6 weeks apart.
• Take a third set if discordant
results.
o Septic/ backstreet abortion.
 Presents as acute salpingitis.
• Treated similarly.
 Start broad – spectrum antibiotics 1 hour prior to uterine curettage.
• Co – amoxiclav IV
• Metronidazole PR.

• Cervical ectropion.
o Often called erosions
 Sounds alarming, but is a normal phenomenon.
o Red ring around the os due to endocervical territory over the paler epithelium of
the ectocervix.
o Ectropions extend temporarily under hormonal influence.
 Puberty
 COCP
 Pregnancy.
o As columnar epithelia is got and glandular, ectropium is prone to.
 Bleeding
 Excess mucous production
 Infection.
o Treatment.
 Cryocautery if it is a problem.
 Otherwise is self limiting and requires no treatment.
• Nabothian cysts.
o Mucous retention cysts.
o Found on the cervix.
o Harmless
o Management.
  Cryocautery if they are discharging.
• Cervical polyps.
o Pedunculated, benign tumours of endocervical epithelium.
o May cause.
 Increased mucous discharge.
 Post – coital bleeding.
o Treatment.
 In younger women, can be avulsed.
 In older women, D&C to rule out intrauterine pathology.
• Cervicitis.
o May be follicular or mucopurulent
 Mucopurulent will present with discharge.
o Causes.
 Chlamydia
• Up to 50%
 Gonococci
 Herpes.
• Look for vesicles.
o Chronic cervicitis is usually a mixed infection.
 May respond to antibacterial cream.
o Be cautious when cervicitis is found on a smear.
 May mask neoplasia.

Antepartum Haemorrhage.
• This is bleeding after 24 weeks gestation.
• All bleeding during pregnancy is associated with increased perinatal mortality.
• Severe bleeding can cause maternal death.
• If patient is bleeding during pregnancy, avoid doing a vaginal exam until placenta praevia
has been rule out by ultrasound.

• Dangerous causes.
o Abruption
 “accidental haemorrhage”
 Occurs when part of the placenta comes away from the uterine wall.
 Consequences depend on how much placenta comes away, and the
degree of bleeding.
 Cause.
• Unknown.
• Associated with pre – eclampsia
• May occur in future pregnancies (6% of patients)
• More common in smokers
  Can complicate external cephalic version
 Bleeding may localise to one placental area.
• Can cause bleeding to go undiscovered for a period of time.
 Consequences.
• Placental insufficiency.
o Foetal anoxia, which can cause foetal death
• Compression of uterus by blood can cause tenderness.
o Prevents good quality contractions in all stages.
o 25% risk of post – partum haemorrhage.
• Conversely, can cause uterine hypercontractility.
> 7 contractions in 15 minutes.
• Posterior abruptions may cause backache.
• 10% of patients will get DIC due to Thromboplastin release.
• Concealed losses can cause shock in the mother
o Renal failure.
o Sheehan’s syndrome.
 Also called Simmon’s disease.
 Pituitary hypoperfusion can cause necrosis
of the gland.
 Lack of pituitary hormones, causing.
• Primary Hypothyroidism
• Primary Addison’s disease
• Genital atrophy
o Placenta praevia
 Occurs in 0.5% of pregnancies.
 Where the placenta lies in the lower segment.
 Depending on exactly where the placenta lies, the placenta praevia is
classified as either.
• Minor
o Type I and II in old classification
o Placenta in lower segment, but more than 2 cm from
internal os.
o Aim for vaginal delivery.
• Major.
o Type III and IV in old classification
o Placenta encroaches on internal os.
o Require C – section for delivery.
 Risk of significant haemorrhage by both mother and foetus.
 Associations.
• Large placenta (eg. twins).
• Uterine abnormalities and fibroids
• Uterine damage.
o Multiparity
o Caesarean sections
o Myomectomy
o Previous infection.
 Diagnosis.
• Ultrasound at 24 weeks shows that 28% of placentas are low
lying at this time.
 • Due to the fact that the uterus grows from the bottom up, only
3% of these end up having placenta in the lower segment.
• Transvaginal ultrasound is superior to abdominal ultrasound in
determining exact position of placenta.
• If combined with Doppler can diagnose.
o Vasa previa
o Placenta accrete.
• Has not been shown to increase risk of bleeding.
 Common presentations.
• Antepartum haemorrhage.
o Placenta comes away as lower segment stretches.
• Failure of head to engage
o Diagnosed as high presenting part.
 Problems.
• Bleeding.
• Difficult delivery due to obstruction of os.
• Placenta accreta in 5% of cases.
o When placenta inserts into myometrium, rather than
endometrium.
o Makes disattachment very difficult.
o In about 24% who have had previous C – section.
• Poor lower segment contractility predisposes to Post partum
haemorrhage.
 C – sections should be performed by the consultant obstetrician and
consultant anaesthetist
 The old practice of admitting major placenta praevia at 35 weeks for
constant observation is controversial and not often practiced.
• Hospitalisation is recommended if there is any history of APH
in this pregnancy.
 Distinguishing placenta praevia from abruption.
Placenta praevia Abruption
Shock in proportion to visible loss Shock out of proportion to visible loss
No pain Constant pain
Uterus non – tender Tender, tense uterus
Both lie and presentation may be abnormal Lie and presentation normal
Foetal heart normally normal Foetal heart rate absent or showing distress
Coagulation problems are rare Associated with coagulation problems
Starts with small bleeds, that gradually Beware pre – eclampsia, DIC, anuria
increase

o Vasa praevia
 This occurs when foetal vessels run in the membranes crossing, or
close to the internal os.
 The vessels are not protected by being enclosed in the umbilical or
placental tissues, so are at risk of rupturing during delivery when the
membranes break.
• This is why it is important to check liquor for staining with
blood.
  Risk factors.
• Velamentous insertion of the umbilical cord into the chorion,
rather than the placenta.
• Accessory placental lobes.
• Multiple pregnancies.
 Diagnosis.
• Rarely confirmed before delivery.
o May be suspected if antenatal sonogram with colour
flow Doppler shows vessels crossing the internal os.
• Diagnosis is normally confirmed after delivery by examining
the placental and foetal membranes.
 Prognosis if foetus is delivery vaginally is very poor.
• Most foetuses will die due to haemorrhaging the majority of
their blood volume before delivery is complete.
• Can take as little as 300 ml to kill a foetus.
• Blood volume is about 80 – 100 ml/kg.
 Management.
• Planned C – section if vasa praevia suspected in utero.
• Immediate emergency C – section if waters break and baby
haemorrhaging.

• Other causes.
o Uterine
 Circumvalate placenta
 Placental sinus
o Lower genital tract
 Cervical polyps
 Cervical carcinoma
 Cervical erosions
 Cervicitis
 Vaginitis
 Vaginal varicosities

• Management of APH.
o Always admit.
o If bleeding is severe.
 Call 999.
 Put up IV fluids through a large bore cannula in each dorsum.
 Take bloods.
  Raise legs
 Give 15 L/min oxygen through a face mask.
 On admission.
• If shocked, give 6 Units of blood quickly, until systolic BP >
100 mmHg.
• Send bloods for clotting screen.
• Catheterise bladder.
o Keep urine output > 30 ml/hour
• Call anaesthetist to monitor fluids.
o CVP lines help.
• Call obstetric and paed crash teams.
• If bleeding is severe, deliver.
o Consider need for C – section.
• Beware risk of PPH.
o If bleeding is less severe.
 Set up IV fluids.
 Take blood for
• FBC
• Crossmatch.
• Coagulation studies.
• U&Es
 Regularly monitor.
• BP
• Pulse.
• Blood loss.
 Establish diagnosis.
• Ultrasound of placenta.
• Speculum examination.
 If placenta praevia diagnosed
• Admit until delivery.
• Delivery normally by C – section at 35 – 37 weeks.
 If pain and bleeding from a small abruption settles and foetus is not
compromised, woman can be discharged home.
• May require anti –D before discharge.
• To be treated at high risk pregnancy from then on
• Arrange follow up.

Premature labour.
• Leading cause of perimortal mortality and morbidity.
• Premature infants are those born before 37 weeks gestation.
• Prevalence.
o 6% of singletons
o 46% of twins
o 79% of triplets or higher order.
• About 2% are before 32 weeks.
o Causes greatest neonatal problems.
• Aetiology.
o 25% are due to
 APH.
 Cervical incompetence
 Amnionitis
 Uterine abnormalities
 Diabetes
 Polyhydramnios
 Pyelonephritis
 Other infections
o 40% have unknown cause.
 Factors implicated as risk factors or risk markers include.
• Bacterial vaginosis
• Ureaplasma
• Mycoplasma hominis.
o Consumption of fish oil during pregnancy decreases risk of pre – term labour,
and so increases birth weight.
• Managing premature rupture of membranes (PROM).
o Complicates 2 – 4% of term births.
o Admit.
o Do observations.
 Temperature.
 MSU
 High vaginal swab.
o Assess for causes/ association.
 Abruption
 Twins
 Polyhydramnios
o If liquor isn’t obvious, check with nitrazine sticks.
 pH sensitive.
 Turn black.
 False positives with.
• Infected vaginal discharge.
• Semen
• Blood
• Urine
o In 80%, rupture of membranes will initiate labour.
o In the 20% who don’t enter labour, balance risks of remaining in utero (Infection
causes 20% of neonatal deaths after PROM) against benefits (maturity and
surfactant).
 Intrauterine infection occurs after rupture of membranes in.
• 10% by 48 hours
• 26% by 72 hours
• 40% by > 72 hours.
  Prophylactic antibiotics may allow labour to be delayed.

o If infection does develop.

 Blood cultures.
 IV Ampicillin + netilmicin
 Expedite labour.
o Antibiotics for 24 hours before labour reduces rate of.
 Intraventricular haemorrhage
 Periventricular malacia.
o If it is decided to induce labour.
 Dinoprostone PV
 Oxytocin IV
 Misoprostol PO

 Induction doesn’t reduce sectioning rate, does decrease time to delivery

o If labour supervenes, allow it to progress.
o If liquor stops draining, slowly mobilize the mother.
 This is rare.

• Management of pre – term labour.

o In 50%, contractions stop spontaneously.
o Treating the cause (eg. Pyelonephritis) may stop the contractions.
o Attempts to stop contractions (tocolysis) are unlikely to work if.
 Membranes ruptured.
 Cervix > 4 cm dilated.
o Consider transfer to hospital with SCBU facilities.
o Call paediatrician to attend to the baby when it is born.

o Tocolytic drugs.
 The idea behind tocolysis is to delay preterm labour to improve foetal
outcome, without harming the mother or foetus.
 Only use between 24 – 33 weeks.
 Trials have shown that only nifedipine has clinical benefit in improving
foetal outcome.
 It is quite reasonable to not attempt tocolysis.
• May be desirable if giving corticosteroids or performing in
utero transfer.
 Absolute contraindications.
• Chorioamnionitis
• Foetal death
• Lethal abnormalities
• Foetal or maternal condition requiring immediate delivery.
 Relative contraindications.
• Foetal growth restriction/ distress
• Pre – eclampsia
• Placenta praevia
• Abruption
• Cervix dilated to > 4 cm.
 β – sympathomimetics aren’t used.
 • Maternal fluid overload.
• Pulmonary oedema.

 Atosiban.
• Less maternal effects.
• No real foetal benefit.
• Expensive.
 Nifedipine.
• Associated with reduced rates of admission to SCBU and
reduced respiratory distress.
• Side effects.
o Hypotension
o Flushing
o Tachycardia
 Transiently
o MI
 Rarely.

o Glucocorticoids.
 Betametasone IM.
• Followed by repeat dose 12 hours later.
• An alternate regimen is 4 doses of Dexamethasone
 Promotes surfactant production.
• Halves mortality
• Reduces complications of respiratory distress syndrome.
 Helps close patent ductuses.
 Protects against periventricular malacia.
• A cause of cerebral palsy.
 Use between 24 – 34 weeks.
 If diabetic, monitor glucose carefully.
 Benefit is maximal after 24 hours.
• Benefit lasts a week.

• Survival and disability.

o The main question is whether gestation is less than 28 weeks.
o Disability rate at < 28 weeks is 25%
o By 29 weeks, it is only 12%
o 10% of those born at < 28 weeks will never have
 Independent mobility
 Intelligible communication.
o 4% of babies born before 24 weeks will survive.
 > 50% of these will be severely disabled.
o Use of surfactant in babies born at < 28 weeks hasn’t reduced.
 Viability threshold.
 Rates of severe disability.
o Babies born at > 30 weeks with no deformity all survive.
Multiple pregnancies.
• Monozygous twins are always.
o Same sex
o 1 chorion
o 2 amnions.
• Incidence.
o Twins: 3/200 pregnancies.
o Triplets: 1/10,000 pregnancies.
• Predisposing factors.
o Previous twins.
o Family history of dizygotic twins.
o Increasing maternal age.
 < 20 years: 6.4/1000
 > 25 years: 16.8/1000
o Induced ovulation.
o In vitro fertilisation.
 1% of all UK pregnancies.
o Racial origin.
 1/150 pregnancies in Japanese omen.
 1/36 in Nigerian Igbo women.
o Worldwide rate for monozygotic twins is constant at 3 – 5/1000.

• Features.
o Early pregnancy.
 Uterus too large for dates.
 Hyperemesis
o Later.
 Polyhydramnios
 More than 2 poles palpable.
 Extra foetal parts felt.
 2 foetal heart rates heard.
• Reliable if rates differ by > 10 bpm.
 US confirms diagnosis.
• Can distinguish monochorionic from dichorionic twins by 10
– 14 weeks.
• Complications.
o Polyhydramnios.
o Pre – eclampsia.
 30% of multiple pregnancies.
 10% of singleton pregnancies.
o Anaemia.
 Iron and folate requirements are increased.
o Antepartum haemorrhage.
  6% of multiple pregnancies.
 4.7% of singleton pregnancies.

 Due to abruption and placenta praevia (due to large placenta).

• Foetal complications.
o Increased perinatal mortality.
 8/1000 for singletons.
 36.7/1000 for twins
 73/1000 for triplets.
 204/1000 for higher order pregnancies.
o Prematurity.
 Mean gestation for twins is 37 weeks.
 Mean gestation for triplets is 32 weeks.
o Growth restriction.
 Same as singletons up to 24 weeks.
 May be slower thereafter.
o Malformations.
 Increased 2 – 4 times.
 Especially in monozygotic twins.
 Severe disability rate.
• 1.5% for singletons.
• 3.4% for twins.
 US is main diagnostic test.
• Selective foeticide is best performed before 20 weeks if
indicated.
o Intracardiac potassium chloride.
o Plethora/ Anaemia.
 With monozygotic twins, intermingling blood supply may result in
disparate twin sizes.
 One may be born plethoric, and develop jaundice later.
 One may be born anaemic.
• If one foetus dies in utero, it may become foetus papyraceous.
o May deliver prematurely
o May be aborted.

• Complications of labour.
o PPH is more common.
 4 – 6% in singletons.
 10% in twins.
o Malpresentation is common.
 40% are cephalic/cephalic.
 40% are cephalic/ breech.
 10% are breech/breech
  5% are cephalic/transverse
 4% are breech/transverse
 1% are transverse/transverse
o Rupture of vasa praevia.
o Increased rates of cord prolapse.
 0.6% in singletons.
 2.3% in twins.
o Increased risks in monozygotic twins.
 Premature separation of placenta
 Cord entanglement.
o Undiagnosed twins.
 In spite of modern technology, this sometimes happens.
 Staff are unprepared.
 Syntometrine may be used inappropriately, delaying delivery of second
twin.
o Epidural anaesthesia is helpful for versions.
• Management.
o Ensure adequate rest.
 Need not entail admission.
o Use ultrasound for.
 Diagnosis
 Monthly checks on foetal growth.
o Give additional iron and folate.
o More antenatal visits.
 Weekly from 30 weeks.
 Monitoring for increased risk of pre – eclampsia.
o Tell mother how to identify preterm labour, and what to do.
o Consider induction at 40 weeks.
 Have IV infusion running during labour.
 Have anaesthetist available at delivery.
 Have paediatricians in attendance.
• Ideally one for each baby.
• Babies may need resuscitation.
• Second twins have higher risk of asphyxia.

o Warn parents that, with more babies, it gets exponentially harder and more tiring
to raise them.
 In one study, at 4 years, all mothers suffered exhaustion and emotional
distress.
 One third required antidepressants.
 One third spontaneously reported regretting having triplets.

 It may not be a good idea to perform selective foeticide.

 If one triplet is selectively aborted in utero, one – third of mothers will
suffer emotional problems (guilt, persistent sadness.
• Adjustment has occurred in 90% by 2 years post – natally.

 Legislation has limited number of embryos that we implant to reduce

incidence of higher order pregnancies.
• >2 embryos in mothers < 40 years.
• >3 embryos in mothers > 40 years.
Normal and Abnormal labour.
• From the first trimester, the uterus has Braxton – Hicks contractions.
o Classically painless.
o 15 mmHg pressure increase.
o In labour, pressure increases to 60 mmHg.
• Normal labour.
o Occurs after 37 weeks gestation.
o Should result in spontaneous, vaginal delivery of the baby within 24 hours of
onset of regular spontaneous contractions.
o Often heralded by a show.
 Plug of cervical mucous.
 Small amount of blood.
 Sign of membranes stripping from the os.
o Show is followed by membranes rupturing.
o First stage.
 Time from onset of regular contractions until cervix fully dilated.
• No cervix is felt around the head.
 Cervix normally effaces before it dilates.
• Becomes shorter and softer.
 A satisfactory rate of dilatation from 3 cm dilated is 1 cm/h.
 The first stage generally takes.
• 12 hours in a primip.
• 7.5 hours in a multip.
 During the first stage, monitor.
• Every half an hour
o Pulse
o BP
o Temperature
• Every 15 minutes.
o Contraction strength.
 Shouldn’t be able to indent the uterus with a
finger during a contraction
o Contraction frequency.
  Ideally 3 – 4 every 10 minutes.
 Lasting up to 1 minute.
 Foetal heart rate.
• Before, during and after contraction

• Every 4 – 6 hours.
o Vaginal exam to look for.
 Degree of cervical dilatation
 Position and station of the head.
• Measure in centimetres from the
ischial spines.
 Degree of moulding.
o Urine Dipstix.
 Ketones
• If mother becomes ketotic, give IV
infusion of 10% Dextrose.
 Proteins

• Monitor state of liquor.

o Dull – green meconium stained liquor is normal in
late pregnancy.
o Passage of fresh, lumpy, sticky meconium during
labour can be a response to labour stress, or could be
a sign of distress.
 Transfer to consultant led unit.
 Start continuous foetal monitoring.
 Aspiration of fresh meconium can cause
severe pneumonitis.
• Suction nose and oropharynx at
delivery.
• Have paediatrician in attendance to
suction pharynx and trachea under
laparoscopy.
o Meconium stained liquor at ARM suggests placental
insufficiency.
 Indication for.
• Foetal scalp blood sampling
• Scalp clip electronic monitoring.
o Consider emergency C – section if.
 Foetal blood pH is very low.
 Meconium is very thick.

 Second stage.
• Time from complete dilatation until delivery of baby.
• Mother has urge to push.
o Uses abdominal muscles and Valsalva manoeuvre to
help move the baby.
• As head descends.
 o Head rotates at level of ischial spines to occipital –
anterior alignment.
o Perineum stretches.
o Anus gapes.
o In late second stage, head will broach the vulval ring
(“crowning”).
• Normal time for second stage is.
o 45 – 120 minutes for a primip
o 15 – 45 minutes for a multip.
• Prevent a precipitate delivery (and so intracranial bleeding) by
pressure over the perineum.
• Delay clamping the cord, and hold the baby 20 cm below the
introitus, for 30seconds before clamping the cord.
o Increases neonatal haematocrit levels.
o Reduces requirement for transfusion and oxygen
supplements in premature babies.

 Third stage.
• Delivery of placenta.
• Us the uterus contracts to a < 24 – week size after baby is
born, placenta separates from uterus through spongy layer of
deciduas basalis.
• Then buckles, and a small amount of retroperitoneal
haemorrhage aids it removal.
• Examine placenta after delivery to check that it is intact and
there is none retained.
• Consider need for thromboprophylaxis.

• Signs of separation.
o Cord lengthening
o Rush of blood PV
o Uterus rises
o Uterine contracts in the abdomen.
 Felt in abdomen as a globular mass.

• Routine use of syntometrine (ergometrine maleate + oxytocin)

as the anterior shoulder is born decreases third stage time to
about 5 minutes.
o Decreases incidence of PPH
o May cause problems in undiagnosed twins.
o Can precipitate MI
o Contraindicated in
 Pre – eclampsia
 Severe hypertension
  Severe liver disease
 Renal impairment
 Severe heart disease
 Familial hypercholesterolemia

• Induction.
o 5 – 20% of UK labours are artificially induced.
 Usually because it is more dangerous to remain in utero than to be
born.
 Sometimes because there is a risk to the mother.
o 75% of inductions are for.
 Hypertension
 Pre – eclampsia
 Prolonged pregnancy
• Inducing mothers at 41 weeks reduce stillbirth rates.
 Rhesus disease.
o Other indication are
 Diabetes
 Previous stillbirth
 Abruption
 Foetal death
 Placental insufficiency.

o Contraindications.
 Cephalopelvic disproportion
 Malpresentations, other than.
• Breech
• Face
 Cord presentation
 Foetal distress
 Placenta praevia
 Vasa praevia
 Pelvic tumour
 Previous cervical repairs
• Be cautious if previous cone biopsy.

o Cervical ripeness.
 When induction is planned, state of cervix is assessed.
 In 95% of women at term, the cervix is ripe.
 If primips are induced with a Bishop’s score of < 3, there is increased
rates of.
• Prolonged labour.
• Foetal distress
• C – sections.
 • Increase is less marked in multips.

Modified 0 1 2
Bishop’s score
Cervical 0 1–2 3–4
dilatation (cm)
Length of >2 1–2 <1
cervix (cm)
Station of head –3 –2 –1
(cm above
ischial spines)
Cervical Firm Medium Soft
consistency
Position of Posterior Middle Anterior
cervix

 A score of > 5 is ripe.

• An unripe cervix may be ripened using prostaglandin (PGE2)
vaginal gel or misoprostol on the morning of induction, or the
evening before.
o Use higher doses for primips.
o Prostaglandins shorten time to delivery.
 May result in higher C – section rate.
o Prostaglandin may precipitate labour in itself.
• If antenatal foetal distress, set up continuous monitoring
before prostaglandin inserted.
• In Dublin, patients are returned to antenatal ward to await
onset of labour.
• If there is failure to ripen (occurs in 12%), prostaglandin can
be repeated 6 – 8 hours later.
o If still fails to ripen, consider C – section.
 Once cervix is ripe.
• Rupture membranes (amniotomy)
• Start intrapartum foetal heart monitoring.
o Scalp clip
o Pulse oximeter.
• Start oxytocin IV infusion until effective uterine contraction
o Beware uterine hyperstimulation
o Beware use of large volumes of IV fluids.
 Risks water intoxication.
• Confusion
• Convulsions
• Coma
• When cervix 5 cm dilated, it is more sensitive to oxytocin.
o Turn down infusion rate.
• Dublin regimen results in most women going into spontaneous
labour.
o Based on titration of oxytocin to give a rate of
dilatation of 1 cm per hour.
o If rate drops to 0.5 cm dilatation per hour there is an
association with premature intervention.
 o Progression is plotted on a partogram.
 Also records.
• Heart rate
• State of liquor
• Analgesia
• Oxytocin use.

 Problems of induction.
• Iatorgenic prematurity.
• Infection.
o Use antibiotic cover in women with heart lesions, due
to risk of endocrditis.
• Bleeding.
o Vasa praevia
• Cord prolapsed.
o When high head at amniotomy.
• 19% go to C – section.
o Compared to 11% without induction.
• 14% require instrumental delivery.
o Compared to 11% without induction.

• Dublin is a centre of excellence for reducing caesarean rates.

o 5% compared to 14% for other centres.
o This is achieved by.
 Only admitting women who are actually in labour.
 Regular assessment to check cervical dilation is progressing.
• Take action if it isn’t.
• Primips with single, cephalically presenting babies who aren’t
achieving satisfactory cervical dilatation are given oxytocin to
augment contractions.
• C – sections are performed on those whom delivery isn’t
imminent at 12 hours after admission to the ward.
 Results in.
• C – section rate of 5%.
• Forceps rate of 10%
• Active management of labour.
o Augmentation.
  Recognition that
• Primiparous uterus is an inefficient organ of birth that is
unlikely to rupture.
• Multiparous uterus is an efficient organ which is prone to
rupture.
 Oxytocin may be used in primips to improve efficiency, without
maternal risk.
• Maximum of 5 units in 24 hours.
 Oxytocin should not be routinely given to speed up multips.
• Delay is likely to be due to obstructed labour.
• If obstructed, oxytocin can precipitate rupture.
• Oxytocin can be given to multips, but only by a consultant.

o Examination.
 Women are examined at admission and hourly for the first 3 hours.
• Important that the examiner is constant.
 Progress is assessed at 1 hour.
 ARM can be performed to
• Aid progress.
• Allow liquor viewing.
 Examination at 2 hours.
• If primips haven’t dilated by an extra 1 cm, consider
augmentation with oxytocin.
• Also consider oxytocin if there is delay in descent in second
phase.

Foetal monitoring.
• High risk pregnancies require monitoring to detect intrauterine hypoxia with.
o Cardiotocography.
o Biophysical profiling with ultrasound.
• Cardiotocography (CTG).
o Doppler US detects foetal heartbeat.
o Tocodynamometer over uterine fundus records any contractions.
o Continuous trace is printed over 30 minutes.
 Ie. A paper speed of 1 cm/minute.
o Mother has to lie either.
 Semi – recumbent
 Left lateral position.
o Normal trace in afebrile mother at term, who is not having any drugs.
 Base rate of 110 – 160 bpm.
  Variability of > 5 bpm
 At least 2 accelerations of amplitude > 15 bpm over 20 minute period.
• Common response to movement or noise.
o Foetal heart rate falls by about 1 bpm from 28 weeks.
o Tests need to be done every 24 hours antenatally to identify changing foetal
heart rate pattern associated with hypoxia.
 Loss of baseline variability
 Decelerations.

o Intrapartum monitoring.
 Death and disability due to complications of labour occur in <1:300
labours.
 Intrapartum foetal heart monitoring aims to detect patterns known to be
associated with foetal distress.
• Diagnosis is supported by foetal hypoxia and acidosis found
on blood sampling.

o Intermittent auscultation.
 Performed at the end of a contraction.
 Aim is to listen for decelerations.
 Performed with Doppler scanner or Pinard stethoscope.
 Used every.
• 15 minutes in 1st stage
• 5 minutes throughout 2nd stage
 If abnormality noticed, or intrapartum problems occur, start continuous
CTG monitoring.
• Poor predictive value for foetal distress.
• Tends to over diagnose, even when combined with foetal
blood monitoring.
• Its value is uncertain, even in high – risk pregnancies.
o Used throughout.
o Combined with scalp electrodes and pulse oximetry.

o Foetal electrocardiogram.
 Can be derived from scalp electrode.
 ST wave form analysis is associated with.
• Fewer babies with severe metabolic acidosis
• Less foetal blood sampling
• Fewer operative interventions.
 Main use may be for labours with worrying CTG patterns.
 Indications.
• High – risk pregnancy.
• Use of oxytocin.
 • Abnormalities on intermittent auscultation.
o Bradycardia < 100 bpm
o Tachycardia > 16 bpm.
• Fresh meconium passed.
 Disadvantages.
• Limits maternal mobility
• Uncomfortable.

• Foetal blood sampling.

o Take samples from scalp.
o Foetal acidosis reflects hypoxia.
 7.3 – 7.4 Normal
 7.25 – 7.29 Repeat after 45 minutes.
 7.2 – 7.24 Consider C – section
 < 7.2 Urgent delivery needed, unless in second stage.

 In second stage, levels as low as 7.15 can be acceptable.

o Contraindications.
 Maternal infection.
• HIV
• Viral hepatitis
• Herpes
 Suspected foetal clotting disorder.
 < 34 weeks gestation.
• Management of a poor trace.
o Lie patient on her side.
o Give oxygen
o Stop oxytocin
o If there is uterine hypercontractility.
 SC terbutaline.
o Take foetal blood sample.
 Consider rapid delivery if bloods not available and trace doesn’t
improve.

• Foetal heart patterns and their significance.

o Accelerations suggest intact sympathetic activity, and are rarely associated with
hypoxia.
o Loss of baseline variability.
 Baseline variability of > 5 bpm shows response to.
• Vagal tone
• Sympathetic stimuli
 • Catecholamines
 This demonstrates activity in a well oxygenated foetal brainstem.
 Loss of baseline variability may reflect.
• Sleeping preterm foetus
• Drug effects.
o Diazepam
o Morphine
o Phenothiazine
• Hypoxia.
o Baseline tachycardia.
 Heart rate > 170 associated with.
• Maternal fever
• β – sympathomimetics
• Chorioamnionitis.
o Also causes loss of variability.
• Acute or subacute hypoxia.
 Persistent rates > 200 bpm are associated with foetal cardiac
arrhythmias.
o Baseline bradycardia.
 Heart rate < 110 bpm is rarely associated with foetal hypoxia.
• Except in placental abruption.
 May reflect
• Increased foetal vagal tone.
• Foetal heart block
• Cord compression.
o If spasmodic.
o Early deceleration.
 Coincide with contractions
 Due to increased vagal tone as foetal intracranial pressure increases
with contraction.
o Late decelerations.
 When nadir of deceleration develops 30 seconds after peak of uterine
contraction.
 Reflects foetal hypoxia.
 Degree and duration of deceleration related to severity of hypoxia.
o Variable decelerations.
 In degree and relation to contractions.
 May represent umbilical cord compression around limbs or presenting
part.

o Pathological CTG pattern.

 Either has 2 suspicious features.
• Baseline rate either 100 – 109 bpm or 161 – 180 bpm.
 • Variability of < 5 bpm for 40 – 90 minutes.
• Early, variable or prolonged decelerations of < 3 minutes.
 Or has 1 abnormal feature.
• Baseline rate < 100 bpm or > 180 bpm.
• Sinusoidal pattern for > 10 minutes.
• Variability of < 5 bpm for > 90 minutes.
• Atypical variable decelerations
• Single deceleration of > 3 minutes.

• Ultrasound scan.
o In each US examination, look at.
 Placental site & structure.
 Liquor volume
 Foetal structure & wellbeing.

o Early pregnancy.
 If there is bleeding and pain, US can confirm intrauterine pregnancy.
• At 4 + 3 weeks for regular 28 day cycle with transvaginal
scan.
• Can also detect ectopic pregnancy and assess viability of the
foetus.
 Where there is discrepancy between uterine size and dates, gestation
can be estimated.
 Can also diagnose.
• Viable foetus
• Twins
o Monochorionic
o Dichorionic
 Especially useful after use of fertility drugs, or in presence of
hyperemesis gravidarum.
• Also exclude hydatidiform mole.
o Estimation of gestational age.
 Crown – rump length is measured from 6 – 12 weeks.
• 10 mm at 7 weeks
• 55 mm at 12 weeks.
 From 12 weeks, the biparietal diameter can be measured.
 Femur length can be measured from 14 weeks.
• Enables 2 independent estimations with each procedure.
 Biparietal diameter measurements to estimate age is most accurate up
to 20 weeks.
• Unreliable from 34 weeks.
 Knowledge of gestational age is important in management of.
• Rhesus disease
• Diabetes in pregnancy
• Dating the pregnancy if.
o LMP is unknown
o Cycle is irregular.
o Foetal abnormality scan.
 Many units offer routine abnormality scan at 18 – 20 weeks.
 With modern machines and skilled sonographers, increasing range of
markers of abnormality can be detected.
• Nuchal thickness in Down’s syndrome
o Also positive in 6% of normal pregnancies.
 Due to greater range of abnormalities, it is more and more likely that
false positive results will be found.
 It is difficult to know how to counsel these women before scanning.
• Informed consent in itself can cause psychopathology.
 Also, many foetuses with chromosomal abnormalities will
spontaneously miscarry.
• Will have overburdened the mother needlessly.
 Specific indications for abnormality scanning include.
• Family history of neural tube defects
• Maternal diabetes or epilepsy.
• AFP abnormal.
• Oligohydramnios.
• Twins.
• Polyhydramnios.
o Foetal echocardiography.
 Offered to high risk groups.
• Personal or 1st degree relative with history of heart disease
associated with increased nuchal thickening.
• Traditionally offered at specialist centres at 22 – 24 weeks.
• Scanning at 12 – 15 weeks at these centres may exclude most
major abnormalities.
o Biophysical profile scoring.
 US of the foetus in the womb over a period of up to 30 minutes.
 Aims to assess if the foetus is being affected by acute or chronic
asphyxia.
 With acute asphyxia.
• Foetus loses active biophysical variables regulated by central
nervous system outflow.
o Foetal breathing
o Gross body movement
o Foetal flexor tone
o Heart rate accelerations with foetal body movements.
 Reduction in amniotic fluid demonstrated by pockets of fluid, less than
1 cm deep measured in 2 perpendicular planes.
 By use of specific criteria for these 5 variables a wellbeing score can be
reached.
 Management protocols according to score help obstetrician decide
when intervention should take place.
o US is used as an adjunct to diagnostic procedures of.
 Amniocentesis
 Foetoscopy
 Cordocentresis
 Chorionic vilus biopsy.
o In pregnancy where foetal growth is of concern, growth can be monitored with
regular scans.
 Abdominal to skull circumference ratio is of particular use.
o Foetal weight can be estimated when planning vaginal deliveries of breech
presentations.
 Less accurate for larger foetuses.
o In later pregnancy.
 Lie and presentation of foetus can be determined by US.

o If there is APH,
 Placenta praevia can be excluded.
 Abruption can be visualised
o With secondary postpartum haemorrhage, retained products of conception can
be visualised.

o Doppler US and foetal well being.

 Can be used to assess circulation on both sides of the placenta.
 Been shown to be of use as a screening tool in routine antenatal care.
• Also use in high – risk pregnancies.
 Waveform outlines (velocimetry) have been seen to be abnormal in
• Small babies who have poor outcomes.
 Babies who are small on US, but have normal umbilical flow, have no
increased risk of poor outcome.
• If end – diastolic signals are absent, baby is likely o be
hypoxic and acidotic.
 In growth – retarded babies with no other obstetric complications.
• Doppler velocimetry is more cost – effective than CTG.
• May be sufficient as sole means of surveillance in addition to
biophysical parameters.

 Consider C – section if umbilical artery Doppler velocimetry shows

absent or reversed end diastolic velocities in pregnancies complicated
by intrauterine growth retardation and hypertension.
• Prevents postnatal problems like
o Cerebral haemorrhage.
o Anaemia
o Hypoglycaemia.
• These changes correlate with placental intervillous space
ischaemia and spasm or occlusion of tertiary stem arterioles on
the foetal side of the circulation.
o Leads to centralisation of foetal circulation.
o Blood returned from the placental is shunted to.
 Foetal brain
 Coronary arteries.
 Adrenal glands.
 Intervention based on knowledge of abnormal umbilical waveform
patterns have resulted in a 500 g mean increase in weight of growth
retarded babies.
• Low dose aspirin is given.
o Low dose aspirin also delays onset of hypertension and reduces its severity in
primips whose babies have abnormal umbilical waveforms.
  However, no demonstrated benefit in low – risk pregnancies.

Caesarean section.
• Incidence.
o 23% of UK labours.
o 9% pre – labour
• Maternal mortality is 1:100,000.
o 9:1000 will require admission to ITU.
• Morbidity is moderate.
o Infection
o Illeus
o Thromboembolism.
• For a first C – section.
o 25% are due to failure to progress.
o 28% are due to foetal distress.
o 14% are for breech presentation
• Incidence of C – section is reduced by.
o Support in labour.
o Induction at 41 weeks.
o Consultant decision in discussion of need for section
o Foetal blood sampling
o 4 hour partogram with an action line
• Lower uterine segment incisions.
o Straight incision 3 cm above pubis symphysis.
 Joel Cohen incision.
o Blunt dissection thereafter.
o This approach reduces blood loss.
o 2% of foetuses get lacerated.
• Classical C – section.
o Involves vertical incision.
o Rarely used these days.
o Indications include.
 Very premature foetus.
 Poorly formed lower segments.
 Transverse lying foetus, with ruptured membranes and draining liquor.
 Structural abnormalities making lower segment incision impossible.
 Constriction ring present.
 Fibroids.
• Sometimes.
 Anterior placenta praevia.
• Lower segment is abnormally vascular.
 Mother is dead, and rapid birth desired.
• Before an emergency section.
o Explain to mother what is about to happen.
o Activate.
 Anaesthetics.
 Theatre staff.
 Porters
 Paediatrics
o Put mother on 100% oxygen if foetal distressed.
o Neutralise gastric contents.
 Sodium citrate
 Metoclopramide.
 Consider pre – operative gastric emptying.
• Drain stomach prior to any extubation.
o Crossmatch 2 units of blood.
 6 units if previous section and anterior placenta.
o Catheterise bladder.
o Tip table to 15o to left side.
o Use pulse oximetry pre and post – operatively if dark skinned patient.
 Cyanosis difficult to see in dark skin.
o Warn paediatrics about any opiates given in the last 4 hours.
o Remember thromboprophylaxis.

• Anaesthetic complications.
o Vomiting on induction.
o Light anaesthesia
 Out of concern for baby.
 Causes paralysed awareness.

• Indications for elective C – section.

o Known cephalo – pelvic disproportion.
o Placenta praevia
o Breech presentation.
 Offer version at 36 weeks.
o Twins, where 1st twin not cephalic.
o Some malpresentations
o After vaginal surgery.
 Suburethral repair.
 Vesio – vaginal fistula repair.
o Some maternal infections.
  3rd trimester herpes
 HIV

• If repeat C – section is planned.

o Localise placenta and rule out placenta praevia.
o Increased risk due to adhesion to old scar.
o Also risk of placenta accrete.
 Risk of massive haemorrhage.

• Emergency C – section.
o May be needed due to antenatal complications.
 Severe pre – eclampsia.
 Abruptio placentae.
• Baby still alive.
o May also be needed due to problems in labour.
 Foetal distress.
 Prolapsed cord.
 After failed induction or failure to progress.

• At C – section.
o Remove placenta by controlled cord traction.
 Reduces endometritis compared to manual removal.
o In rhesus –ve mothers.
 Remove all excess blood from peritoneal cavity.
 Use Kleihauer test to determine dose of anti – D.

• After C – section
o Give one to one support in recovery.
o Closely monitor
 Pulse
 Respiratory rate
 BP
 Sedation levels
o Remove catheter.
o Mobilise early.
o Remove wound dressing at 24 hours.
o Give analgesia.
 Ibuprofen
 Codeine
 Paracetamol.

• Complications.
o Antibiotic prophylaxis is recommended.
 Cefradine.
 Reduces rate of wound infection, UTI and endometritis.
 o Bleeding
 Women on thrombolysis should have their dose halved the day before
C – section.
 Omit dose on the day of operation.
 Give normal dose 3 hours post – op.
• Unless epidural anaesthetic used.
 2% of women will get wound haematoma.

• Thromboprophylaxis.
o If low risk.
 No drugs.
 Just early mobilisation and good hydration.
o If moderate risk.
 Age > 3555 years.
 Obesity/> 80kg
 Para 4+
 Pre – eclampsia
 Emergency section in labour
 Gross varicose veins
 Current infection
 Immobility for > 4 days previously.
 Major current illness
 Labour lasting > 12 hours.

 Heparin prophylaxis or TED stockings.

o If high risk.
 Any >3 risk factors.
 Extended pelvic or abdominal surgery.
• Eg. Caesarean hysterectomy.
 FH or PMH thromboembolism or thrombophilia.
 Paralysed lower limbs.
 Antiphospholipid syndrome

 Heparin until 5 days post – op or fully mobilised.

• Whichever is longer.
 TED stockings.
 If previous thromboembolism.
• Thromboprophylaxis for 6 weeks postpartum.
The Puerperium.
• The period to 6 weeks post delivery.
• Uterus involutes.
o From 1kg at delivery down to 100 g.
o Felt at umbilicus after delivery
o Pelvic organ at 10 days
o After - pains are felt as it contracts.
 Especially while suckling.
• Cervix becomes firm over 3 days.
o Internal os closes by day 3
o External os closes by 3 weeks.
o Lochia passed PV for first 10 days.
 Endometrial slough.
 Red cells
 White cells
o Discharge becomes white by day 10.
 Lochia alba
 Continues until week 6.
• Breasts produce milky discharge and colostrums during last trimester.
o Milk replaces colestrom by day 3.
o By day 3 – 4, breasts become
 Physiologically engorged.
 Swollen
 Red
 Tender

• Management in the first days.

o If Rhesus –ve, give anti – D within 72 hours.
o Check.
 Temperature
 BP
  Breasts
 Legs
 Lochia
 Fundal height
o Teach pelvic floor exercises.
o Persistent red lochia suggests
 Failure of uterine involution
 PPH.
 Retained products.
o Check rubella immunity.
 Vaccinate if non – immune.
 Delay until postnatal exam if anti – D given.
o Check haemoglobulin on day 1 and again on day 7.
 Postpartum physiological haemodilution occurs from day 2 – 6.

• Puerperal pyrexia.
o Temperature > 38 oC in the first 14 days after delivery or miscarriage.
o Examine fully.
 Chest
 Breasts
 Legs
 Lochia
 Bimanual vaginal examination.
o Investigations.
 MSU culture
 High vaginal swab culture
 Blood culture
 Sputum culture.
o 90% will be due to infection of the urinary or genital tract.
o Superficial perineal infections occur around day 2.
o Puerperal infection can be reduced by leaning the vaginal canal with 0.25%
chlorhexidine after every vaginal exam.

• Endometriosis
o Causes.
 Lower abdominal pain.
 Offensive lochia
 Tender uterus
• On bimanual examination
o Management.
 IV flucloxacillin
 IV + PO metronidazole.
 Uterine curettage.
  Prevents abscesses.
o Suckling or milk expression will prevent stagnantation.

• Superficial thrombophlebitis.
o Affects 1% of women.
o Presents with vein that is.
 Painful
 Tender
 Usually varicose.
o Management.
 Anti – inflammatories
 Bandage and elevate leg.
 Recovery is usual within 4 days.

• Puerperal psychosis.
o Affects 1:500 births.
o Symptoms.
 Persistent crying
 Sleeplessness
 Feelings of inadequacy.
 Tends to resolve within 6 months.
• This is a very long time when you’re suddenly this depressed
and psychotic.
• Suicide rate is unacceptably high.
• Watchful waiting is not an option.
o Distinguished from mild depression that often follows birth due to.
 High suicidal drive.
 Severe depression
 Mania
 Schizophrenic symptoms.
• Rarely.
 Delusions that the child is malformed.
o If an acute, organic reaction is present, suspect puerperal infection.
o Screen all post – natal women at 6 – 8 weeks with Edinburgh postnatal
depression scale (EPDS)
 Score of 12/30 diagnoses depression with a.
• Sensitivity of 77%
• Specificity of 93%
 o Management.
 Explain to mother that
• Puerperium isn’t always a time of joy.
• It’s OK to feel low.
• Should talk to GP, midwife or health visitor about negative
feelings.
 Fluoxetine
• As effective as CBT in the short – term
• Rarely detectable in breast milk.
• Observe baby for side effects.
• Consider stopping breast feeding if large doses used.
 Lithium.
• May help as second line.
 ECT.
 Transdermal oestrogen.
• Partially effective in severe postnatal depression.

• 6 – week postnatal exam.

o Gives a chance to.
 See how mother and baby relate.
 Check BP & weight.
 Do FBC if anaemic postnatally.
 Arrange cervical smear.
• If not done antenatally.
 Check contraceptive plans are enacted.
 Ask about.
• Depression
• Back ache
• Incontinence
• Resumption of intercourse.
o Sexual problems are common and prolonged.
o 50% report intercourse less satisfying than pre
pregnancy.
o Major complaints are.
 Loss of libido
 Dyspareunia.
 Vaginal exam to check healing is not normally needed.
Contraception after a baby.
• Lactation amenorrhoea.
o 98% effective.
o Breastfeeding delays return of ovulation.
 Suckling disrupts frequency and amplitude of gonadotrophin surges.
 Although there is gonadotrophin rise in response to falling placental
sex hormones after delivery, ovulation does not occur.
o Women who are fully breastfeeding, day & night are amenorrhoeic at 6 months.
o Average first menstruation in breast feeding mother is at 28.4 weeks.
 Range 15 – 48 weeks.
o Contraceptive efficacy is reduced if.
 Night feeding stops
 Separation from the baby
 Baby receiving supplements
 Mother or baby become stressed or ill
o In the UK.
 69% initiate breastfeeding
 21% still breastfeeding at 6 months.
o Aim for additional contraception once decreased efficacy is anticipated.
• Progesterone only Pill (PoP)
o May be started at any time post – partum.
o If started after day 21, additional protection is needed for 2 days.
o No effect on breast milk production
o Low doses (<1%) of hormones are secreted in milk, but have no effect on baby.
• Combined Pill.
o Start at 3 weeks if not breast feeding.
o Affect early milk production.
 Not recommended in breast feeding until 6 months.
 Can be used from 6 weeks if other contraception not acceptable.
o Levels of hormones in milk similar to those during normal ovulatory cycles.
• Emergency contraception.
o Progesterone method is suitable for all.
o Not needed until 21 days post partum.
• Depot injection.
o Not normally recommended until 6 weeks in those breast feeding.
 Theoretical risk of sex steroids insulting baby’s immature nervous
system and liver.
o Depo – Provera (Medroxyprogesterone acetate) can be given from 5 days post
partum.
o Noristerat (Norethisterone enanthate) can be given immediately post natally,
 When Depo – Provera would cause severe bleeding.
• Progesterone implants.
o Not recommended until 6 weeks post natally in those breast feeding.
 Hormone can enter breast milk.
o If bottle feeding, can implant at 21 – 28 days.
• Intrauterine device (IUCD).
o Should be inserted within first 48 hours post partum
 Or delayed until 4 weeks.
o This minimises risk of uterine rupture at insertion.
o Levornogestrel – releasing devices are inserted at 4 weeks.
 • Diaphragms and cervical caps.
o Women needs to be fitted at 6 weeks.
 Different sizes may be required from previously.
o Alternative contraception is needed from day 21 until the new ones are
confidently handled.
• Sterilization.
o Unless sterilization high recommended at C – section, it is best to wait an
appropriate interval.
 Immediate post partum tubal ligation has
• Possible increased failure rate.
• More chance of being regretted.
o Indications for sterilization at C – section include.
 Repeated section
 Family complete.

Small for dates.

• Growth restricted neonates are those that are below the 10th percentile for their gestational
age.
• When talking to parents, avoid the term growth retardation.
o Will invariably make them think of mental handicap, which is not necessarily
the case.
• Important to distinguish premature babies from those that are small for gestational age
(SGA).
o They are at risk of different problems.

• Causes.
o Multiple pregnancy
o Malformation
o Infection
o Smoking
 o Diabetes
o Hypertension
o Anaemia
o Pre – eclampsia
o Heart disease
o Renal disease
o Asthma
o Idiopathic.
 10% are to mothers who will always have small babies.

• Asymmetric growth retardation.

o Where placental insufficiency was the cause, head circumference is relatively
spared.
o Growth retardation was due to baby being starved.

• Antenatal diagnosis.
o 50% are undetected before birth.
o Many babies suspected of having IUGR don’t have it.
o Measuring fundal height progress from symphysis pubis is a reasonable measure
of growth.
 Especially if used with centile charts.
o Other signs of placental insufficiency include.
 Oligohydramnios
 Poor foetal movements.
o If IUGR is suspected, growth can be measured with serial US of.
 Head circumference
 Abdominal circumference
 Umbilical Dopplers.
• If normal, out come of IUGR tends to be better.
o Fewer stillbirths
o Fewer premature births.
• If abnormal, may benefit from low dose aspirin
o Advise mother.
 Stop smoking
 Get plenty of rest.
o In labour, presence of hypoxia and need for urgent delivery is measured by.
 Biophysical profiling
 CTG

• Labour and aftercare.

o Growth restricted foetuses are more susceptible to hypoxia.
 Monitor in labour.
o After birth problems include
 Hypothermia.
• Ensure a warm welcome.
• If < 2kg, nurse in an incubator
 Jaundice.
• Relative hypoxia in utero causes high Hb.
• Breaks down after birth to cause jaundice.
 Hypoglycaemia.
 • Small amount of glycogen stores.
• Feed within 2 hours of birth
• Measure BM before each 3 – hourly feed.
• If hypoglycaemia, in spite of regular feeds, transfer to SCBU
• More susceptible to infection
o Birth reveals those for whom abnormality was the cause of the IUGR.

• Distinguishing IUGR from prematurity.

o Before 34 weeks there is no breast bud tissue.
 From 34 weeks it develops at 1 mm diameter per week.
o Ear cartilage develops from 35 – 39 weeks.
 Premature babies’ ears don’t spring back when folded.
o Testes lie in the inguinal canal at 35 weeks.
 Should have descended to the scrotum by 37 weeks.
o Labia minora are exposed in premature girls.
o Skin creases on anterior third of the foot appear by 35 weeks.
 Anterior two – thirds have creases by 39 weeks.
 Whole foot has creases by term.
o Premature babies have red, hairy skin.
o Vernix is made from 28 weeks.
 Maximal at 36 weeks.
o All limbs are flexed from 36 weeks.

• Effects of IUGR in adult life.

o Increased risk of.
 Hypertension
 Coronary artery disease
 Non – Insulin dependent diabetes mellitus.
 Autoimmune thyroid disease.
o Specific early deficiencies can cause long term problems.
 Iron
 Iodine.

Large for gestational age.

• These are babies who are above 90th centile weight for gestation.
• Caused by.
o Constitutionally large.
 Usually familial
 Largest 10% of the population.
o Maternal diabetes
o Hyperinsulinaemia
 o Beckwith – Wiedemann syndrome.
• Labour and aftercare.
o At risk of birth trauma.
 Especially shoulder impaction and dystocia.
o Prone to
 Immaturity of suckling and swallowing.
• May need temporary tube feeding.
 Hypoglycaemia
 Hypocalcaemia
 Jaundice.
• Polycythaemia can cause large babies.
 Left colon syndrome.
• Self – limiting condition
• Clinically mimics Hirschprung’s disease.
• Temporary bowel obstruction ± meconium plug.
• Risk of renal vein thrombosis.
o Rarely.

Neonatal life support.

• Most neonates are born perfectly healthy.
o Best management is a quick return to mother for bonding and warmth.
• A paediatrician, or neonatal – resus nurse, should attend all high risk births.
o Emergency C – section.
o Breech
o Twins
o Forceps for foetal distress
o Intrapartum bleeding
o Prematurity
o Hydrops foetalis
o Eclampsia.
• Before birth.
o Check equipment
o Get a warm blanket
o Warm crib.
• At birth.
o Assess Apgar.
Apga Pulse Respirations Muscle Colour On
r tone suction
2 > Strong, Active Pink Coughs
100 crying well
1 < Slow, Limb Blue Depressed
100 irregular flexion limbs cough
0 0 Nil Absent All No
blue response
or
white

o Set clock in motion and start resus if

 Pulse < 100
 Poor colour
 No respiratory effort.
o Be alert to.
 Hypothermia.
• Use heat lamp.
 Hypoglycaemia.
• Dextrose 10% 5 ml/kg IV
 Pethidine toxicity.
• Naloxone IM.
• Contraindicated in opiate abuse.
 Anaemia.
• Worry about heavy foetal blood loss.
• Blood 20 ml/kg
• 4.5% albumin
 Lung disease/ cyanotic heart disease.
• Transfer to NICU/SCBU for monitoring.
 Only suction oropharynx if meconium aspiration is suspected
 Breathing air is better than 100% oxygen

o Resus
 Dry the baby.
• Remove any wet clothes or cloths.
 Initial assessment.
• Colour
• Tone
• Breathing
• Pulse
 If not breathing.
• Head in neutral position
• 5 inflation breaths, 2 – 3 seconds long.
o Confirm response with chest movements or increased
heart rate.
• If no response.
o Perform jaw thrust and repeat inflation breaths.
• If still no response.
o Get an assistant to assist with airway and repeat
inflation breaths.
 Directly visualise the oropharynx.
 Repeat inflation breaths
 Insert oro – pharyngeal airway.
 Repeat inflation breaths.
o Consider intubations.
 Confirm placement with chest movements
or increases heart rate.
• Once chest is moving, continue with ventilation breathing if
no spontaneous breathing.
  Check heart rate.
• If < 60 and not rising 9or undetectable), start chest
compressions.
o 3 compressions to 1 breath.
o Continue for 30 seconds.
• Reassess pulse.
o If improving, stop chest compressions.
o If nor breathing, continue ventilation.
o If heart rate still slow, continue ventilation and chest
compressions.
 Consider IV or umbilical access and drugs.
• Adrenaline.
• IV or inhaled through endotracheal tube.

o Intubating the neonate.

 Is a key skill.
 Use uncuffed, unshouldered tubes on term infant
• 3.5 mm Term infants.
• 3.0 mm 1.25 – 2.5 kg.
• 2.5 mm < 1.25 kg.
 Have many sizes to hand.
 Learn from an expert.
 Practice on models.

• Prognosis.
o Mortality for prems based on 5 – minute Apgar score is
 315/1000 if score is < 3
 5/1000 if score is > 7.
o Mortality for term infants based on 5 – minute Apgar score is.
 244/1000 if score is < 3
 0.2/1000 if score is > 7.
o If a term infant with Apgar < 3 has arterial pH < 7, risk of death increases 8 –
fold.
o Survival in those weighing 0.5 – 1.5kg is
 66% if needing CPR
 88% if not needing CPR
o Risk of intracranial haemorrhage is.
 15% in those needing CPR.
 5% in those not needing CPR.
Neonatal intensive care.
• Monitor.
o Temperature
o Pulse
o BP.
 Intra – arterial if critical
o Respirations.
 Continuous read – out device.
o Blood gases.
 Transcutaneous oximetry and carbon dioxide monitoring.
 Intra – arterial electrode.
o FBC
o U&E
o Bilirubin
o Weight.
 Daily
o Head circumference
 Weekly.

• Baby is normally premature, the things that are going to kill them quickest are.
o Hypothermia.
 Nurse in incubator
o Hypoxia
 Nurse in incubator with FiO2 = 60%
o Hypoglycaemia
o Respiratory distress syndrome
o Infection
o Intraventricular haemorrhages
o Necrotizing entrocolitis
o Apnoea
 Incidence.
• 25% neonates < 2.5kg
• 90% neonates < 1kg
 Causes.
• Respiratory centre immaturity
• Aspiration
• Heart failure
• Infection
• Hypoxia
• Hypoglycaemia
• Hypocalcaemia
• Patent ductus arteriosus
• Seizures
• Temperature disturbances
• Exhaustion
• Airway obstruction
 If stimulating the baby doesn’t restore breathing.
• Suction pharynx
• Use bag and mask ventilation
• Avoid wide fluctuations in PaO2 to avoid retinopathy of
prematurity.
 Investigations.
• CXR
• U&Es
• Infection screen
• Glucose
• Serum calcium
• Serum magnesium
 Management.
• If aspiration is the problems.
o Small frequent feeds
o Continuous tube feeding
• Monitor SaO2 continuously.
o If hypoxic in spite of FiO2 > 40, start CPAP or IPPV.
• Give caffeine citrate IV.
o Fewer side effects than theophylline.
• Nasal CPAP and doxopram may prevent hypoventilation.
o If apnoea is seizure related.
 Weaning.
• Try 4 – 5 days after apnoea has stopped.
 Prevention.
• Beclamethasone intrauterine maturation
o Over – zealous investigation & handling.
• Retinopathy of prematurity.
o Retinal vessels in prems react badly to fluctuating SaO2.
 Eg. Resuscitation leads to retinal fibrosis, retinal detachment and visual
loss.
o Prevalence.
 53% of those < 1kg
 43% of those < 1.25kg
 35% of those <1.5kg
o Classification.
 5 stages.
 Depends on.
• Site involved.
• Degree of retinal detachment.
• Extent (measured in clock hours) in each eye.
o Treatment.
 Diode laser therapy.
• Causes less myopia than cryotherapy.
o Screening.
 If < 1500 g or < 31 weeks gestation.
 If < 25 weeks.
• Screen opthalmosopically under 0.5% cyclopentolate pupil
dilatation at 6 weeks old.
• Screen every 2 weeks until 36 postmature weeks.
 Often one eye exam is enough if 26 – 31 weeks gestation.
• Must be done by an experienced ophthalmologist.

• Intraventricular haemorrhage.
o Occurs in 40% if birth weight < 1.5kg.
o Risk factors.
 Hypoxia
 Hypercarbia
 Hypotension
 Bleeding disorders
 Birth trauma
 C – section
 Apgar < 4 at 1 minutes/ Apgar < 8 at 5 minutes.
 Low birth weight
 Respiratory distress
 PDA
 Anaemia
 Umbilical artery catheterization.
 o Suspect in.
 Rapid deterioration.
• Especially in 1st week of life.
 Opithotonus.
 Cerebral irritability
 Shock
 Decreased feeding skills
 Bulging fontanelle, with rapidly expanding head
 Exaggerated Moro reflex
 Fits
 Somnolence

 50% may be silent.

o Investigations.
 US
 CT
o Complications.
 Mental retardation
 Cerebral palsy
 Hydrocephalus

 Unknown if late learning and behavioural problems occur.

o Treatment.
 Supportive or preventative.
 Rest
 Head elevation
 Seizure control.

• Pulmonary hypertension.
o Arises as a consequence of disturbed first breath and conversion from foetal to
adult circulation.
 Meconium aspiration
 Pneumonia/ Group B strep. Infection
 Respiratory distress syndrome
 Diaphragmatic hernia
 Pulmonary hypoplasia.
o Can also be due to hypertrophy of muscular layer in pulmonary arteries.
 Primary pulmonary hypertension.
o Diagnosis.
 Background of adverse event mentioned above.
 Persisting desaturation, in spite of intensive oxygen therapy.
o When it is suspected
Arrange immediate echocardiogram.
• Will show right – to – left shunting in ductus arteriosus or
foramen ovale.
• Absence of structural heart disease.
 Get expert help.
o Management.
 Inhaled Nitric oxide.
 • Promotes adult circulation.
• Decreases need for dramatic intervention, such as ECMO.
• Relaxes smooth muscle.
o Increased production of cGMP.
o Sildenafil inhibits cGMP degradation, so may also be
indicated.
 Alternative drugs are.
• Adenosine
• Tolazoline
• Inhaled prostacyclin.
 When arranging ECMO.
• Ventilate.
• Treat contributory factors.
o Hypothermia
o Polycythaemia
o Hypocalcaemia
o Hypoglycaemia
 There may be a role for hyperventilation.
o Extracorporeal membrane oxygenation (ECMO)
 Complex procedure done in specialised units.
 Dramatically reduces death from respiratory failure in neonates.
 No apparent impact on severe disability due to respiratory failure.
 Criteria which may make ECMO cost effective are.
• Weight > 2 kg
• No major congenital abnormalities
• No CNS abnormalities on US
• Gestation > 34 weeks
• Oxygen index > 40, and resistant to nitric oxide therapy.
 More premature babies may have some benefit.
• Eg. When problems with circuitry and heparinization are
solved.
 Need for ECMO may be as high as 1/4000 live births.

FiO2 × MAP
Oxygen index (OI ) =
PaO2
Gynaecology.

Chronic Pelvic Pain..

• Causes much misery to reproductive aged women.

• History is usually of:
o Longitudinal pelvic pain
o Secondary dysmenorrhoea
o Deep dyspareunia
o Symptoms may cause, or be exacerbated by, emotional problems.
o Can cause depression
• Laparoscopy can reveal the cause of the problem.
o Chronic pelvic inflammatory disease
o Endometriosis
o Adenomyosis
o Adhesions
o Congested pelvic veins
• In laparoscopy does not revel the answer, then the cause may be gastrointestinal in origin.
o Consider irritable bowel disease.

Pelvic congestion.
• Lax pelvic veins become painfully congested with blood.
• The pain is worse when:
o Standing
o Walking
o Pre - menstrually
• Typically.
o Variable in site and intensity
o Unpleasant ache postcoitally
• Maximally tended to deep palpation over the ovaries.
• Vagina and cervix may become blue due to congestion.
 • May be associated posterior leg varices
• Dilate veins may be demonstrated by venography or laparoscopically.

• Treatment.
o Relief may be difficult.
o Thorough examination helps.
 ‘Pelvic migraine’
o Medroxyprogesterone for 3 months reduces pain
 50mg/24h PO
o Migraine remedies and relaxation may be tried.
o Severe symptoms may require
 Bilateral ovarian vein ligation or embolisation radiologically.
 Hysterectomy, with bilateral salpingo – oophrectomy, with HRT.

• Mittleschmerz.
o Mid – cycle menstrual pain.
o Occurs at beginning and end of menstrual life.
o From the German for “Middle Pain”

Fibroids.

• AKA uterine leiomyomata.

• Benign smooth muscle tumours of the uterus.
• Often multiple.
• Vary in size from seedling to ones occupying large proportion of abdomen.
• Begin as lumps in the uterine wall.
o May grow to bulge out of the wall to lie.
o Under peritoneum
• Subserosal
• 20%
o Under endometrium
• Submucosal
• 5%
o In uterine cavity on a stalk.
• Pedunculated.
• Fibroids are very common.
o 20% of women have them.
o Higher proportions in older women and non – Caucasians.

• Associated with mutation in gene for fumarate hydratase.

• Rare association between skin & uterine leiomyomata and renal cell carcinoma.

Natural history.
• Oestrogen dependant tumours.
• Therefore enlarge in pregnancy and on the combined pill.
• Also atrophy post – menopause.
 • May degenerate gradually or suddenly.
o Sudden degeneration is known as “Red degeneration” due to the appearance on
hystoscopy.
o Thrombosis of the blood supply.
o Venous engorgement and inflammation.
o Causes
• Abdominal pain.
• Localised peritonism
• Vomiting
• Low grade fever.
o Usually occurs in 2nd half of pregnancy or the periperium.
o Treatment.
• Expectant, with resolution over 4 – 7 days.
o Bed rest
o Analgesia
o Most fibroids arise from the body of the uterus, and so do not obstruct
labour.
• Tend to rise away from pelvis throughout pregnancy.
o If large pelvic fibroid masses noticed before pregnancy, C – section
should be planned.
o Obstruction of labour also requires C – section.
• Occasionally fibroids calcify to become “womb stones”
• Very occasionally they become sarcomas, which causes:
o Pain
o Malaise
o Bleeding
o Increased size in post – menopausal women.
Presentation
• Many are asymptomatic.
• However can cause:
o Menorrhagia
o Fertility problems
o Pain
o Mass

• Menorrhagia.
o Often produce heavy and prolonged periods.
o Do not generally cause intermenstrual or post – menopausal bleeding
• Fertility problems.
o Submucosal fibroids may interfere with implantation.
o “Natural IUCD”
o Large, or multiple, tumours can distort the uterus, provoking miscarriage should
pregnancy occur.
• Pain.
o May be due to torsion of pedunculated fibroid.
o Symptoms similar to torsioned ovarian cyst.
o Causes an acute abdomen and requires urgent surgery.
o Red degeneration following thrombosis of fibroids blood supply.
o Requires only analgesia until symptoms settle
 • Mass
o Large fibroids may be felt abdominally.
o May press on bladder causing frequency.
o May press on pelvic veins causing.
o Oedematous legs.
o Varicose veins
o Pelvic pain
o May obstruct labour or cause retention of urine.

Treatment
• In many women, no treatment is needed.
• Menorrhagia due to fibroids responds poorly to:
o Anti – prostaglandins.
o Progesterone
o Danazol
• Women who have completed their families may opt for hysterectomy.
• Younger women can be temporarily put into a menopausal state by use of a LHRH
analogue.
o Eg Goserelin
o Buserelin is not as good.
• A single dose of LHRH analogue of 10.8 mg SC reduces bulk by about 50%.
• Bone demineralisation can occur.
o Can be ameliorated by concurrent raloxifene, which also shrinks fibroids.
• LHRH analogues and raloxifene can be used pre – op as debulking agents.
• Side effects are menopausal symptoms.
• Fertility (and fibroids) will return when drugs are stopped.

• Alternatively, fibroids may be surgically shelled out (myomectomy).

• Complications of this include:
o Torrential bleeding, requiring hysterectomy.
o Post – op adhesions.
• Pregnancy rates may increase dramatically post – op.
• Laparoscopy ± laser use is possible.
o Requires much skill and patience.
• Fibroids can also be embolized.
o Part of interventional radiology.
o Can shrink fibroids, so reducing menorrhagia
o Involves only a short hospital stay, but is not widely available.
o As it induces red degeneration, can be immensely painful.

Fibroids during pregnancy.

• 5/1000 Caucasian women have fibroids during pregnancy.
o Commoner in Afro – Caribbean women.
• May cause miscarriage.
• Increase in size during pregnancy.
o Particularly in the 2nd trimester.
• Ultrasound aids diagnosis
• Peduculated fibroids may torsion.

Endometriosis
 • Foci of endometrial glandular tissue occurring beyond uterine cavity.
o Looks like the head of a burnt match.
• Tends to occur:
o Ovary.
o “Chocolate cyst”
o Rectovaginal pouch.
o Urosacral ligament
o Pelvic peritoneum
• Rarely occurs.
o Umbillicus
o Lower abdominal scars.
o Distant organs, such as lung
• If foci are found within the uterine wall, it is known as adenomyosis.
o Prevalence of 10% of all women
o Prevalence of 30 – 50% of women with infertility.

Cause
• Possibly due to cell rests.
• Sampson’s theory is currently popular.
o Retrograde menstruation.
o Explains its positive association with:
o Age
• Typically 40 – 44 years
o Long duration of IUCD and tampon use
o Explains its negative association with:
o Pregnancy
o Pill use
o Pelvic distribution
o Doesn’t explain how foci can be found outside the abdominal cavity.
• It is known that there are various associations.
o Genetic
o Autoantibodies
o Environmental factors

• Endometrial foci are under hormonal control.

o Wanes at pregnancy and menopause
o Bleeding during menstruation.
• Free blood irritates diaphragm and other tissues.
o Causes:
o Pain
o Fibroids
o Infertility
o Adhesions

Clinical picture.
• Can be asymptomatic
o Even in extensive disease
• Most commonly causes pain.
o Often cyclical with periods
o Can be constant if due to adhesions.
 o Deep dyspareunia is common.
o Can radiate to thighs.
o Can be provoked by opening bowels.
• Common differential of secondary dysmenorrhoea.
o Also tends to make periods heavier.
• Can cause bleeding from sites of endometrial foci during menstruation.
o Haemothorax.
o Haematuria.

Diagnosis.
• On PV.
o Fixed, retroverted uterus.
o Uterosacral ligament nodules with generalised tenderness.
o Enlarged, boggy, tender uterus suggests adenomyosis
• MRI can be useful
• Laparoscopy shows cysts and peritoneal deposits.
o Distinguishes endometriosis from chronic infection.

Complications.
• Obstruction.
o GI
o Uteric
o Fallopian
• Low grade malignancy.
o Rare.
o Genes coding β catenin implicated.
o Site of origin is most commonly ovary.
 63% of the time.
o Other sites of origin include:
 Vagina
 Fallopian tubes
 Mesosalpix
 Pelvic wall
 Colon
 Parametrium

Management
• If asymptomatic, don’t treat.
• Encourage to join a support group.
o Treatment can be long and difficult.
• Investigate stress in patient’s life which can aggravate and precipitate symptoms.
• First line therapy with simple analgesia and NSAIDs.
• If resistant to first line therapy.
o Hormones.
o Aim is to suspend menstruation for 6 – 12 months to allow time for
lesions to atrophy.
• Only really effective for non – GI lesions.
o COCP at low dose can be effective.
 o If COCP contraindicated, ineffective or bad side effects try
progestogens.
• Mirena coil
• Continuous norethisterone
• Depo Provera injection
o For short term treatments, can try gonadotrophic releasing hormone
agonists.
• Eg. leuproprelin
o Studies suggest that GnRH agonists are most effective, but are
expensive and can only be used short term due to loss of bone density.
o Side effects of these therapies are those of premature menopause, eg.
loss of bone density.
o Oestrogen add back can alleviate these risks, but possibly reduce
efficacy.
o Surgery.
o Excision of foci is more effective, but less safe than ablation by
diathermy or laser.
o Can go for total hysterectomy with bilateral salpingo – oophrectomy.
• Depends on lesion site and wishes for fertility.
o Surgery may be better than hormones if symptoms are severe and
impact on quality of life, however:
• Relapse is common.
• Repeat surgery is often needed.

Prognosis.
• Endometriosis is normally chronic or relapsing.
• Is progressive in 50% of cases.
• Surgery minimally helps fertility, but is recommended by NICE.

Pelvic inflammatory disease.

• Pelvic infection affects the fallopian tubes (salpingitis)
o May involve ovaries and parametra.
• 90% are sexually acquired.
o Mainly Chlamydia
o 60% of these are asymptomatic.
o Affects males and females equally.
 o Can result in.
o Infertility.
o Ectopic pregnancy.
• 14% are due to bacteria such as gonococci.
o Retest after treatment.
• 10% follow childbirth or instrumental delivery.
o Also
o Insertion of IUCD
o TOP
o Often streptococcal
• Infection can be transmitted from the intestinal tract during appendicitis.
o Often Gram –ve anaerobes
• Can be blood bourn.
o Eg. Tuberculosis.
• Organisms cultured from endocervix are often
o Different from those found in the fallopian tubes
o Multiple organisms.

• Acute salpingitis.
o Clinical picture.
o Very unwell
o Fever
o Spasm of lower abdominal muscles.
• May be most comfortable lying on her back with legs flexed.
o Cervicitis.
• Profuse, purulent or bloody discharge.
o Heavy menstrual loss.
• Suggests endometriosis.
o Nausea & vomiting.
• Suggests peritonitis.
o Suprapubic tenderness
o Cervical excitation
o Tender fornices
o Bilateral.
• May be worse on one side.
• Sub – acute infection.
o Can be easily missed
o Laparoscopy may be needed to diagnose.

• Chronic salpingitis.
o Chronic inflammation results if infection is
o Unresolved
o Unrecognised
o Inadequately treated.
o Clinical picture.
 o Pelvic pain
o Menorrhagia
o Secondary dysmenorrhoea
o Discharge
o Deep dyspareunia
o Depression
o Signs.
o Tubal masses
o Tenderness
o Fixed, retroverted uterus
o Distinguished from endometriosis by laparoscopy.
o Treatment.
o Often unsatisfactory.
o Consider.
• Long term, broad – spectrum antibiotics.
o Eg. 3 – months of oral tetracycline.
• Short – wave diathermy
• Analgesia
• Counselling
o Only cures are.
• Menopause
• Surgical removal of infected tissue.
o Complications.
o Fibrosis and adhesions between pelvic organs
o Pyosalpinx.
• Pus – filled tubes
o Hydrosalpinx
• Fluid – filled tubes.

• Management.
o Minimise complications.
o Prompt treatment.
o Contact – tracing.
• Any sexual contacts from past 6 months.
• Ensure that they seek treatment.
o Advise avoidance of intercourse until patient and partner treatment is complete.
o Swabs, if practical
o Endocervix
o Urethra
o Admit if very unwell.
o Blood cultures.
o IV antibiotics if very unwell.
o Ceftriaxone + doxycycline
o Doxycycline + metronidazole
o If gonorrhoea isolated, get microbiologist advice.
o If less ill, give oral antibiotics.
o Ofloxacin
o If very unwell, remove IUCD if in situ.
o Don’t need to if symptoms are mild.
• Complications.
o If response to antibiotics is slow, consider possibility of an abscess.
 o Perform laparoscopy to diagnose.
o Drain via posterior fornix with laparotomy to prevent.
• Perforation
• Peritonitis
• Septicaemia
o If treatment is inadequate or delayed, it may lead to chronic infection and tubal
block..
o 8% are infertile after first episode.
o 19.5% are infertile after second episode.
o 40% are infertile after third episode.
o Ectopic pregnancy is 10 – times higher in those that do conceive.

• Screening for Chlamydia pelvic infection.

o Thought that prevalence for under – 20 year olds is.
o 8.1% in the GP setting.
o 17.37% in genitor – urinary clinics
o 12.1% in antenatal clinics
o 12.7% in TOP clinics.
o Suggested that we opportunistically screen.
o Family planning clinics
o TOP clinics
o GP appointments
o For all sexually active women aged up to 25 years.
o This may miss up to 20% of infections.
o Increasing the age limit to 30 may reduce this to 7% missed.
o It is unclear how we can work this into already busy appointments, or whether
patients will find it acceptable.
o Boots offers NHS – funded screening kits for those who are.
o 16 – 24 years old
o Have a positive partner, regardless of age.
o There is a national screening program that operates in.
o Colleges
o Prisons
o The armed forces
o Uncomplicated Chlamydia infection can be treated with a single dose of
azithromycin.
Uterine prolapse.
• Occurs when supporting structures are weak, allowing pelvic organs to sag within the
vagina.
• Weakness can be congenital.
o Normally results from child birth.
o Poor repair of perineal damage reduces strength of supporting structures.
• Weakness is exacerbated by.
o Menopausal atrophy
o Coughing
o Straining
• May cause.
o Incontinence
o Nuisance
o Uterine obstruction.
o Third degree uterine prolapse with cystocoele.
• The types of prolapsed are named with reference to the structures that are sagging.
• Several types may co – exist in the same patient.
o Cystocoele.
o The bladder sags against the upper front wall of the vagina, which
bulges in.
o Residual urine within the cystocoele may cause.
• Dysuria
• Frequency
o Urethrocele.
o Bulging of lower, anterior vaginal wall will displace the urethra.
o Results in disruption of sphincters.
o Leads to stress incontinence
o Rectocele.
o Middle posterior wall, which is attached to the rectum, bulges through a
weak levator ani.
o Often symptomless.
o May require reduction with a finger in the vagina before defecation.
o Enterocele.
o Bulges of upper posterior wall may contain loops of bowel from the
Pouch of Douglas.
o Uterine prolapse.
o First degree.
• Cervix remains in the vagina.
o Second degree.
• Cervix protrudes from the intraoitus when standing or
straining.
o Third degree (procidentia).
• Uterus lies in the vagina.
• Vagina becomes keratinized.
• Cervix may ulcerate.
• Symptoms.
o Feeling of “dragging” or “something coming down”.
o Worse during the day.
o Depending on the type of prolapsed, there may be.
o Cystitis
o Frequency
o Dysuria
o Problems with defecation.

• Signs.
o Examine vaginal walls in left lateral position using a Sims speculum.
o Ask patient to strain and bear down to demonstrate prolapsed.
o Perform urodynamic studies to
o Exclude detrusor overactivity
o Assess voiding.

• Prevention.
o Lower parity
o Better obstetric practices
o Pelvic floor exercises.

• Treatment.
o Mild disease may respond to reduction in intra – abdominal pressure.
o Lose weight
o Stop smoking
o Reduce straining.
• Consider laxatives.
o Improve muscle tone with.
• Pelvic floor exercises.
• Physiotherapy.
• 0.1% estriol cream.
o If post – menopausal
o PRN, but start twice weekly.
o Severe symptomatic disease.
o Best treated surgically.
o Any incontinence needs its cause discovered before surgical treatment
can go ahead.
• Perform urodynamic studies to determine best type of surgery.
o Repair operations.
• Excises redundant tissue, so strengthens support.
• Reduces vaginal width.
• Check whether woman is sexually active.
o If so, have to balance degree of narrowing and
strengthening against need for sufficient width to
allow intercourse.
o Manchester repair.
• AKA Fothergill’s operation.
 • Perform for uterine prolapsed.
• Pregnancy is still possible after this operation.
• Cervix is amputated, and uterus is supported by shortening
ligaments.
o Marked uterine prolapsed is best treated with hysterectomy.

o As temporary measure, or in those too frail for surgery, try ring

pessaries.
• Select size according to vaginal diameter at level of fornices.
• It will only stay in situ if the vagina narrows nearer the
introitus
• Insert in posterior fornix, and tuck above the pubic bone.
o Easier if the ring has been softened in hot water first.
• Complications include.
o Discomfort.
o Infection
o Ulceration.
 Change every 6 – 12 months.
o Displacement.
 If recurrent, try a shelf pessary.

Voiding difficulties.
• Control of bladder function
o Continence in women is maintained in the urethra by
o External sphincter.
o Pelvic floor muscles maintaining urethra pressure > bladder pressure.
o Urination occurs when these structures relax, and detrusor muscle contracts.
• Incontinence, or the threat of incontinence, can be severely limiting.
o Ask about.
o Incontinence impact.
o Role limitations.
o Physical & social limitations.
o Personal relationship impact.
o Emotions
o Sleep/ energy
o Symptoms severity.

• Urge incontinence.
o Needing to go immediately, otherwise is incontinent.
o Bladder is “unstable”.
o High detrusor muscle activity.
o Occurs equally in nulliparous and parous women.
o Usually no organic cause is found.
o Rarely is neurogenic.
• Stress incontinence.
o Small quantities of urine escape as intra – abdominal pressure rises.
o Eg. During sneezing.
o More common in parous than nalliparous women.
o Pregnancy in itself is the risk factor, not mode of delivery.
o Examination may reveal prolapsed or incontinence.
 o Revealed by getting her to cough.
• Detrusor overactivity.
o Usually presents with urge incontinence.
o 25% present with stress symptoms.
o Is a common cause of incontinence.
o In the UK population of 3.5 million incontinents, it is the cause in.
• 50% of men.
• 33% of women.

• Management.
o Exclude.
o UTI
o Diabetes.
o Cystoscopy.
o If stress incontinent.
o Diagnosis can not be made even from best history.
o With history alone, 5 – 10% of detrusor overactivity is missed.
o Mild stress incontinence.
o Responds well to pelvic floor exercises
o Physiotherapy is also good.
• Eg. Weighted vaginal cones.
o Heaviest that can be tolerated.
o Base up
o 15 minutes BD
o Graduate up to 100 g as tone improves.
o Insert vaginal tampon when stress is likely.
• Eg. When playing sport.
• Supports bladder neck.
• Prevents leaks.
o Severe stress incontinence.
o Surgery aims to
• Increase urethral pressure.
• Reduce prolapse.
o Examples of surgical techniques used include.
• Bringing upper urethra above pelvic floor, so increased
abdominal pressure also increases urethral pressure.
• Urethroplasty
• Transabdominal colposuspension
o Most effective.
• Periurethral tension free tape.
o Can be performed under local anaesthetic.
o Also very effective.
• Periurethral bulking.
o Effects may wear off after 1 – 2 years.
o Serotonin/ noradrenaline uptake inhibitors can help.
• Eg. Duloxetine.
• Licensed for use in moderate to severe stress incontinence.

o In some post – menopausal women, estriol 0.1% cream may help with.
 • Urgency
• Increased frequency
• Nocturia.
o If mixed stress – urge incontinence, rule out detrusor overactivity
before doing anything else.
• Operations for stress incontinence can worsen symptoms of
detrusor overactivity.

o Detrusor overactivity.
o Refer is any.
• Neuropathy.
• Prolapse
• Pelvic mass
• Haematuria.
o Avoid caffeine.
• Mild diuretic.
• Stimulates detrusor muscle.
o Bladder training.
• Increases time between voiding.
• Keep bladder diary.
o Pelvic floor muscle physiotherapy.
• If stress incontinence symptoms.
o Antimuscarinic drugs.
• May be effective.
• Oxybutynin BD.
• Lyrinel XL.
o Once daily tablet.
o Reduced side effects.
• Tolterodine BD.
o Lesser side effect profile, in spite of being BD.
• Solifenacin.
o Increases bladder capacity
o Reduces episode of incontinence by 50%
• Side effects.
o Dry mouth
o Blurred vision
o Nausea
o Headache
o Constipation or diarrhoea.
o Abdominal pain.
• Nocturia may respond to desmopressin.
o Unlicensed use.

• True incontinence.
 o Continuous leakage may be due to.
o Congenital problems.
• Eg. Ectopic ureters.
o Acquired problems.
• Vesicovaginal fistulas following trauma.
o In developed countries: Post – abdominal
hysterectomy.
o In other areas: Following long labours
with vertex
presentation
• Malignancy
• Radiotherapy
o If surgery not possible, seek advice of continence advisor.

• Interstitial cystitis.
o Pathogenesis may involve
o Loss of bladders glycosaminoglycan protective layer.
o Activation of high number of bladder mast cells.
o Symptoms.
o Lasting > 6 months.
o Frequency
o Urgency
o Bladder pain.
o Dyspareunia.
o Exacerbations include.
o Stress
o Ovulatory hormones
o Certain foods.
o Treatment.
o Dietary modification.
o Bladder training.
o Biofeedback.
o Antidepressants.
o Anticholinergics.
o NSAIDs.
o Bladder hydrodistension.

• Voiding difficulties.
o Rarer in women than detrusor overactivity.
o Symptoms.
o Poor flow
o Intermittent stream
o Retention.
• Can be acute or chronic.
o Hesitancy
o Straining to void
o Incontinence.
 • Due to overflow.
o Incomplete emptying
• Can result in UTI.
o May also be symptoms of faecal impaction.
• Faecal impaction can result in voiding difficulties.

o Causes.
o CNS.
• Suprapontine.
o Eg. stroke
• Cord lesions.
o Cord injury
o MS
• Peripheral nerves.
o Prolapsed disc
o Diabetic neuropathy
o Other neuropathy.
• Reflex.
o Due to pain.
o Eg. Herpes infection.
o Obstructive.
• Early oedema.
o Following bladder neck repair.
o Common cause.
• Others.
o Uterine prolapsed.
o Retroverted gravid uterus
o Fibroids
o Ovarian cysts
o Urethral foreign body
o Ectopic uterocele
o Bladder polyps
o Cancer
o Bladder over distension.
• Eg. Following epidural for childbirth.
o Detrusor weakness or myopathy.
 o Drugs.
• Epidural anaesthesia
• Tricyclic antidepressants
• Anticholinergics.

• Investigations.
o MSU.
o For ?query UTI.
o US.
o Residual urine
o Bladder wall thickness.
• > 6 mm on transvaginal scan is associated with detrusor
overactivity.
o Cytourethroscopy.
o Urodynamic studies.
o Uroflowmetry.
• Flow of < 15 mL/second for volume of > 150 ml is abnormal.
• Do this before any surgery is contemplated.
o Subtraction cystometry.
o
Detrusor pressure = (Vesicular pressure) − ( Intra − abdo min al pressure)
• Treatment of acute retention.
o Consider catheterization.
o Suprapubic if needed for several days.
o Long term conditions may require self catheterisation to be taught.

• Detrusor weakness or myopathy.

o Causes.
o Neurological problems
o Interstitial cystitis
o Symptoms..
o Incomplete emptying
o Dribbling
o Overflow incontinence
o Diagnosis.
o Cystometry
o Electromyography
o Complications.
o Contracted bladder.
• May require substitution enterocystoplasty.
o
• Detrusor weakness.
o May respond to drugs that.
o Relax urethral sphincter.
o Stimulate detrusor muscle.

o α – blockers.
o Eg. Tamsulosin.
o Relaxes the bladder neck.
o Diazepam.
o Relaxes urethral sphincter.
 o Surgery.
o May overcome obstructive causes.
o Eg. Urothrotomy for distal urethral stenosis.
o Uncommon for surgery to be indicated.

Ovarian lumps.
• Any of the ovary’s many tissues may become neoplastic.
• Benign tumours.
o 94% of tumours.
o Usually cystic.
o 24% of all ovarian tumours are functional cysts.
o Others include.
o Endometriotic cysts.
• “chocolate cysts”
• 5%
o Theca – lutein cysts.
• Hydatiform mole
• Choriocarcinoma.
o Germ cell tumours.
• Serous and mucinous cystadenomas.
• 40%
o Mature teratomas.
• From germ cells.
• 20%
o Fibromas.
• Solid lumps.
• 5%

• Malignant tumours.
o 5% are cystadenomas that have become malignant.
o 0.5% are rare germ cells or sex cord malignancies.
o 0.5% are secondaries.
o Uterus
o Stomach
• Krukenberg tumours.
• Spread is transcoelomic along the peritoneum.

• Risk factors.
o Nulliparity.
o Risk increased 1.5 times.
o Infertility
o Early menarche
o Positive family history
o No past use of COCP
o High total fat intake.
o Increases risk by 24%.

• Presentation.
o Varied, depending on.
o Size
 o Form
o Histological type.

o Asymptomatic.
o Found as incidentaloma
• Eg. On bimanual exam during smear test.
o Swollen abdomen.
o Palpable mass arising from pelvis.
o Dull to percussion.
o Doesn’t disappear when bladder is catheterised.
o Pressure effects.
o Eg. On bladder, causing urinary frequency.
o |Infarction/ haemorrhage.
o Mimics ovarian torsion.
o Rupture.
o May cause local peritonism.
o Rupture of a large cyst may cause peritonism and shock.
o Rupture of a malignant cyst may disseminate cancerous cells
throughout abdomen.
o Rupture of mucinous cystadenoma may disseminate mucin – secreting
cells throughout abdomen.
• Causes pseudomyxoma peritoni
• Causes death by binding the viscera.
• Treat with surgical debulking.
• 10 – year survival is 30 – 50%.
o Ascites.
o Shifting dullness suggests.
• Malignancy
• Meig’s syndrome.
o If ascites is tense, it may be difficult to distinguish it from a mass.

o Torsion.
o To twist, a tumour must be.
• Small
• Free on a pedicle
o Twisting occludes venous return, but not the arterial supply.
• Engorgement
• Pain
• High WCC
o Tumours may untwist.
• Results in history of intermittent pain.
o If pain is not too severe, a firm, tender, adnexal mass may be felt.

• Pathology.
o Functional cysts.
o Enlarged or persistent follicular or corpus luteum cysts.
o Very common.
• May be considered a normal finding if < 5 cm diameter,
o May cause pain by.
 • Rupture
• Failure to rupture at ovulation
• Bleeding.
o Serous cystadenomas.
o Develop papillary growths.
• May be so prolific that they cause the cyst to appear solid.
o Commonest in women aged 30 – 40 years.
o About 30% are bilateral.
o About 30% are malignant.
o Mucinous cystadenomas.
o Commonest large ovarian tumours.
• May become enormous.
o Are filled with mucinous material.
• Rupture rarely causes pseudomyoxoma peritoni.
o May be multilocular.
o Most common in 30 – 50 year age range..
o About 5% will be malignant.
o At surgery also remove appendix for histology.

o Men can also get pseudomyxoma from intestinal and appendicular

neoplasms.
o Most women do not have overt rupture of ovarian tumour causing their
pseudomyxoma peritoni.
• About 90% will have concurrent intestinal or appendicular
tumours, which cause both the pseudomyxoma and the ovarian
tumours as secondaries.
o Fibromas.
o Small, solid, benign fibrous tissue tumours.
o Associated with Meig’s syndrome.
• Pleural effusion
• Benign ovarian fibroma or thecoma.
• Ascites.
o Not always present.

o Teratomas.
o Arise from primitive germ cells.
o Benign, mature teratomas are known as dermoid cysts.
• May have well differentiated tissues.
o Hair
o Teeth
o Etc.
• 20% are bilateral.
• Most common in young women.
o Poorly differentiated, malignant teratomas are rare.
o Other germ cell tumours.
o All are malignant.
o All are rare.
o Examples.
• Nongestational choriocarcinoma.
 o Secrete HCG.
• Ectodermal sinus tumours.
o Yolk sac tumours.
o Secrete α – foetoprotien.
• Dysgerminomas.
o Sex – cord tumours.
o Rare
o Usually of low – grade malignancy.
o Arise from cortical mesenchyme.
o Some secrete oestrogen
• Granulosa – cell tumours
• Theca – cell tumours.
o Oestrogen secreting tumours may present with.
• Precocious puberty
• Menstrual problems
• Post – menopausal bleeding.
o Arrhenoblastomas secrete androgens.

o Gestational trophoblastic neoplasia (GTN).

o Consists of.
• Hydatiform mole
• Choriocarcinoma.
o Fertilized ovum forms abnormal trophoblastic tissue.
• Usually no foetus.
o Growth may appear.
• Benign (hydatiform mole)
• Malignant (choriocarcinoma)

• Difficult to determine, as even normal pregnancies show

invasion and metastases.
 o Common to find trophoblastic tissue in the mother’s
lungs.
o May be better to think of tissue as failed pregnancy,
rather than a true neoplasm.
o In GTN, the trophoblast is usually.
• Genetically paternal
• Has a 46XX karyotype.
o Rarely a foetus may be found with a mole that is.
• Triploid
• Partial
o Foetus is generally abnormal.
o Partial moles generally don’t become choriocarcinoma.

o Hydatiform mole.
o Tumour consists of proliferative chorionic villi.
• May have swollen up and degenerated.
o Derived from chorion.
• So produces HCG in large quantities.
• May give rise to
o Exaggerated pregnancy symptoms.
o Strongly positive pregnancy test.
o Incidence.
• 1.54:1000 UK births.
 • Most common in
o Extremes of maternal age.
o Those with a previous mole
 Increased risk of 0.8 – 2.9% after 1 previous
mole.
 Increased risk of 15 – 28% after 2 previous
moles.
o Non – Caucasians.
o Presentation.
• Most present with early pregnancy failure.
o Failed miscarriage
o Embryonic pregnancy seen on ultrasound.
• Bleeding.
o May be heavy.
• Passage of molar tissue.
o May look like frogspawn.
• Ultrasound may show “snowstorm effect” in a uterus that is
large – for – dates.
• Rarely there may be.
o Severe morning sickness
o Pre – eclampsia in the 1st trimester.
• Abdominal pain.
o Huge theca – lutein cysts in both ovaries.
o May rupture or tort.
o Take about 4 months to resolve after evacuation.
• Hyperthyroidism.
o HCG is similar to TSH, so can stimulate the thyroid.
o Warn anaesthetist, as risk of thyroid storm during
evacuation.

o Management.
• If twin pregnancy s present, can continue without increasing
risk of persisting neoplasia or adversely impacting on
treatment.
o 40% chance that baby is viable.
• Evacuation.
o Gentle suction can be used to remove molar tissue
from the soft uterus.
  Risk of perforation with other evacuation
methods.
• Pregnancy should be avoided for 12 months after evacuation
while HCG levels are monitored.
o Levels should return to normal within 6 months.
o If levels drop rapidly to normal, COCP may be used
for 6 months.
o If levels don’t drop, it suggests that.
 Mole has invaded the myometrium.
• May metastasise to.
o Lung
o Vagina
o Brain
o Liver
o Skin
 Mole has given rise to a choriocarcinoma.
• Responds well to chaemotherapy.

o Choriocarcinoma.
o Highly malignant tumour.
o Occurs in 1:40000 deliveries.
• 50% follow a benign mole.
• 20% follow abortions
• 10% follow normal pregnancy.
o Presentation.
• May be years after pregnancy.
• General malaise.
o Malignancy
o Raised HCG.
• Uterine bleeding.
• Signs and symptoms of metastases.
o May be very haemorrhagic.
 Haematoperitoneum
 Nodules on CXR
o Tumour emboli.
 Pulmonary artery obstruction may lead to
pulmonary artery hypertension.
• Haemoptysis
• Dyspnoea.
• Persistent PV bleeding after pregnancy requires investigation
to rule out choriocarcinoma.
o Management.
• Managed in 3 specialist centres nationally.
• Very good response to chemotherapy.
o Methotrexate based.
• Prognosis is good if not metastasised.
o Fertility is usually retained.
Ovarian tumours in pregnancy.
• Complicate about 1:1000 pregnancies.
o Torsion.
o Cyst rupture
 o Haemorrhage into cyst.
o Obstruction of labour.
o Malignancy.
• Easier to distinguish them in an anteverted uterus than a gravid retroverted one.
Due to the tumour lying in the rectovaginal pouch.
• Clinical suspicion of a tumour can be confirmed with ultrasound.
• Some complications are more common in pregnancy than at other times.
o Torsion of an ovarian cyst/ tumour
• Some complications are no more common in pregnancy than at other times.
o Cyst rupture
o Haemorrhage into cyst.
• Torsion may present with.
o Abdominal pain.
o Nausea
o Shock
o Local tenderness.
o Usually at 8 – 16 weeks.
• 2 – 5% of tumours are malignant.
o Will be dysgerminomas.
o Suspect malignancy if cyst ruptures.
o Biopsy other ovary as well.
• Tumours can become necrotic due to pressure on them during labour.
• Tumours in the pelvis can obstruct labour.
o C – section may be needed.
o Can avoid C – section if cyst can be drained under US guidance before labour.
• Some cysts can be left alone until after delivery.
o Asymptomatic
o < 5 cm diameter.
o Monitor with ultrasound.
• Tumours that are 5 – 10 cm diameter should be aspirated under US guidance.
o Send aspirate for cytology.
• Other tumours need removing at 16 weeks gestation.
o Complex multilocular.
o Solid portions on ultrasound.

o By 16 weeks, the foetus is not dependent on the corpus luteum.

o Miscarriage is less likely to result.
o Removal.
o Investigates for carcinoma.
o Prevents development of complications.
• If diagnosis is made late at pregnancy, and tumour not obstructing delivery, leave it alone
until after delivery.
o Remove early in the puerperium due to the high risk of torsion during this
period.

Post –menopausal ovarian tumours.

• Aim is to identify those at high risk of cancer.
o Refer these to a specialist centre.
• 21% of post – menopausal women have ovarian cysts on US screening.
• In terms of detecting cancer, US is:
o 89% sensitive.
o 73% specific.
• Monitoring CA – 125 levels to detect cancer is.
o 81% sensitive.
o 75% specific.
o CA – 125 > 30 u/mL is positive in 80% of malignancy.
o Only 50% of Stage I tumours.
• Risk of malignancy can be calculated.
o RMI < 25 has a cancer risk of < 3%
o RMI > 250 has a cancer risk of 75%.
o Manage at a specialist cancer centre.
o RMI = 3 × [CA − 125] × U
o CA – 125 concentration is in units/ml.
o U is ultrasound score.
• U = 1 if there is one feature present from the list below.
• U = 3 if there are 2 – 5 features present from the list below.

• Multilocular cysts.
• Solid area in cyst.
• Bilateral lesions
• Evidence of metastases.
• Ascites present.

• Some cysts can be managed conservatively with US every 4 months for 1 year.
o Unilocular.
o < 5 cm diameter.
o Normal CA – 125.
• Low risk cysts may be removed by bilateral laparoscopic oophrectomy.
o Post menopausal cysts should not be aspirated.
• High risk cysts require a combination of.
o Total abdominal hysterectomy.
o Bilateral slapingo – oophrectomy.
o Infracolic omentectomy.
o Cytology of.
o Ascites
o Washings
o Biopsy of suspicious areas and adhesions
o Selective pelvic/ para – aortic lymphadenectomy.
Ovarian carcinoma.
• Rare
• Fourth most common cause of cancer death in Western women.
o More deaths than cancer of cervix and cancer of uterus combined.
o In 80% there are no symptoms until there are metastases.
o Often to pelvis, with omental and peritoneal seedings.
o Lymphatic spread, via para – aortic nodes.
o Cystadenocarcinoma accounts for 80%.

• Incidence.
o 1:2500 women > 55 years.
o 1:3800 women < 25 years.
o If two close relatives have ovarian CA, lifetime risk is 40%.
o Liaise with gynaecologist.
o 10% of North American women have BRCA mutations.
o BRCA1 carriers have 40% lifetime risk.
o BRCA2 carriers have 25% lifetime risk.
o More common in those with many ovulations.
o Early menarche
o Nullparity
o Infertility treatment.
o Risk reduced by COCP use.

• Presentation.
o Vague and insidious onset.
o Abdominal pain or discomfort.
o Abdominal distension

• Screening.
o No good quality screening test.
o Transvaginal US + tumour blood flow measurement can distinguish malignant
from benign growths at an early stage.
o Doesn’t appear to have much impact on mortality.
o Plasma levels of CA – 125 are neither specific enough, nor sensitive enough, to
be a good screening tool.

o Consider prophylactic oopherectomy in older women having hysterectomy.

o Definitely in those with BRCA mutations.
o Tubal ligation is also useful if BRCA positive.
o COCP reduces risk by up to 40%

• Diagnosis.
o Suggested by
o Histology
o Ascites
o US/CT abdomen
o Raised CA – 125.
• Staging at laparotomy.
o Stage I: Disease limited to ovaries.
o Stage II: Disease confined to the pelvis.
o Stage III: Peritoneal implants outside the pelvis.
o Stage IV: Distant metastases.
o Often liver parenchyma.

o 80% present with Stage III or IV disease.

o 5 – year survival.
o Stage I: 67%
o Stage II: 42%
o Stage III or IV: 14.4%

• Management.
o Depends on tumour type.
o Surgery
o Removal of more tumour improves response to chemotherapy..
o Young women may have their fertility retained by leaving an
unaffected ovary in situ.
o If both ovaries are involved, remove.
• Both ovaries
• Uterus
• Omentum.
o Chemotherapy.
o Usual to continue for 6 months post – op.
o Carboplatin + paclitaxel.
• Better response rate and higher survival than carboplatin
alone.
• Used for both initial therapy and recurrence.
o Radiotherapy may have a role.
o Ascites can be treated with colloid gold.
o Further management can involve.
o “second – look” laparotomy.
o Further chemotherapy.
o Radiotherapy.
o Advanced or relapsed ovarian CA.
o Management changing rapidly, so check with NICE.
o Options include.
• Paclitaxel
• Pegylated liposomal doxorubicin
• Topotecan.
o Palliative care.
o Generally involves relief of symptoms due to extensive peritoneal
disease.
Polycystic ovarian syndrome (PCOS).
• Better described as polyfollicular ovary syndrome.
• Stein – Leventhal syndrome.
o Obese
o Hirsute
o Polycystic ovaries.
• PCOS comprises of.
o Hyperandrogenism
o Oligo – ovulation
o Polycystic ovaries on US.
o Absence of underlying cause for the polycystic ovaries.
o Late onset adrenal hyperplasia
o Cushing’s syndrome.
• Underlying cause is unknown.
o Results in a vicious cycle of dysfunction of
o Ovaries
o Hypothalamic – pituitary axis
o Adrenals
o Disruption of hormonal cycling causes ovarian follicles to grow, but not rupture,
enlarging the ovary.
• Affects 5 – 20% of premenopausal women.
• Clinical picture.
o Subfertility.
o Acne
o Male pattern baldness
o Hirsuitism
o Acanthosis nigricans
o Neck
o Skin flexures
o Represents hyperinsulinaemia.
o Hypertension.
o Especially in older, post – menopausal women.
o Increased risk of cancer of the
o Ovary
o Endometrium.
• Investigations.
o LH is raised in 40%
o Testosterone is raised in 30%
o Hyperinsulinaemia.
o 40% have diabetes or impaired glucose tolerance by the age of 40
years.
o Obese are at greatest risk, but slim patients also are at risk.
o Obese patients are likely to have metabolic syndrome.
 • Waist > 80 cm
• Any 2 of.
o Triglycerides > 1.7 mmol/L
o HDL cholesterol < 1.1 mmol/L
 Males < 0.9 mmol/L
o BP > 130/85
o Fasting glucose > 5.6 mmol/L
• Rate is trebled for.
o MI
o Stroke
o TIA

• Diagnosis.
o Increased LH:FSH ratio.
o May reverse to about 3:1
o Raised testosterone
o Raised prolactin
o US evidence of ovaries containing > 5 follicles that are > 5 mm
o Laparoscopy demonstrates enlarged ovaries.
• Management.
o Stop smoking.
o Detect and treat,
o Diabetes
o Hypertension
o Hyperlipidaemia
o Encourage weight loss and increased exercise.
o Increases insulin sensitivity.
o Metformin may
o Increase insulin sensitivity
o Improve menstrual disturbances.
o Improve ovulatory function.
o Recommended by NICE for those of BMI > 25 who are trying to
conceive.
o Clomifene usually induces ovulation.
o 50 – 60% will conceive within 6 months of starting treatment.
o Get specialist advice before using.
o Offer as first line.
o Warn of risk of.
• Multiple pregnancy
• Ovarian CA
o Monitor response with US during at least one cycle.
o Those who don’t respond to clomifene are at increased risk of ovarian
hyperstimulation in response to assisted conception.
o Ovarian drilling.
o Using diathermy to burn holes in ovaries to reduce steroid production.
o Recommended by NICE when clomifene doesn’t work.
• May also be used as first – line treatment.
o 65% will go on to conceive.
o No increased risk of multiple pregnancy.
o Combined oral contraceptive pill.
o Reduces bleeding.
 o Reduces risk of unopposed oestrogen action on endometrium.
• Reduces risk of endometrial CA.
o Consider need for annual US to look for evidence of endometrial
thickening
• Also consider endometrial biopsy.
o Recommend regular withdrawal bleeds every 3 months.
• Induce with dydrogesterone on days 11 – 25 of the cycle.
• Mainly used in women for whom oestrogen is not wanted or
contraindicated.
o Hirsutism.
o Cosmetic treatments.
o Anti – androgens.
• Avoid in pregnancy as teratogenic.
• Cyproterone.
• Spirinolactone (Unlicensed use).
o Finasteride has also been tried.
Ovarian hyperstimulation.
• Sudden multiplication of follicles in response to drugs.
• Occurs most often when gonadotrophins are given in assisted reproduction.
• Symptoms.
o Diffuse lower abdominal pain.
o Nausea & vomiting
o Abdominal distension
o Dyspnoea.
o Cystic ovarian enlargement on palpation

o Presentation is normally.
o 3 – 7 days after HCG treatment if not conceived.
o 12 – 17 days after HCG treatment if pregnancy has resulted.
o High oestrodiol
o Many follicles stimulated.

• Incidence.
o Mild cases occur in 22 – 33% of treatment cycles.
o Severe cases occur in 0.5 – 2% of women having ovarian stimulation.
o Commoner in conception cycles.
o Women with PCOS are at particular risk.

• Complications.
o Ascites
o Reduced intravascular volume
o Pulmonary effusions
o Pericardial effusions.
o Rare.
o Thomboembolisms.
o Upper limbs
o Cerebral vessels.

• Prevention.
o Hyperstimulation is suspected if.
o Peak serum oestrodiol > 6000 pg/ml
 o > 30 follicles stimulated.
o Can be prevented from progressing by .
o Not administer HCG.
• Prevents stimulated follicles from ovulating.
• Effectively aborts treatment cycle.
• Embryos can be selectively cryopreserved for later transfer
o Discontinuing gonadotrophins, and waiting for oestrodiol to fall to
“safe” levels before giving HCG.

• Risk factors.
o Age < 35 years.
o Asthenic habitus
o Pregnancy
o Luteal phase HCG stimulation
o PCOS
o Serum oestrodiol > 4000 pg/ml
o Stimulation of > 35 follicles

• Management.
o Admit.
o Give adequate analgesia.
o Opiates may be necessary.
o Bloods.
o FBC
o U&E
o LFT
o Coagulation profile.
o CXR.
o If chest pathology suspected.
o ABGs.
o Tachyopnoea
o Dyspnoea
o Monitor urine output.
o Catheterise if oliguric.
o Ovarian size is a good indicator of severity.
o Unless eggs have be harvested.

o Severe hyperstimulation is diagnosed if.

o Haematocrit > 45%
o WCC > 15 x 109/L
o Massive ascites
o Oliguria
o Mild renal dysfunction
o Liver dysfunction
o If severe.
o Get IV access.
o Consider CVP monitoring.
o Consider fluid replacement.
• Eg. 500 ml albumin over 2 hours.
o Paracentesis of ascites can improve renal function.
 o Reduce risk of thromboembolism.
• TED stockings
• Encourage leg mobility
• Heparinize whilst an inpatient.

o Critical hyperstimulation is diagnosed if.

o Haematocrit > 55%
o WCC > 25 x 109/L
o Tense ascites
o Renal failure
o Thromboembolic phenomena.
o Acute respiratory distress syndrome.
o If critical.
o Refer to ITU.
o Symptomatic pleural effusions may need drainage.
o Reduce risk of thromboembolism.
• TED stockings
• Encourage leg mobility
• Heparinize whilst an inpatient.
o Meticulously control fluid balance.
• Maintain intake at 3L/24 hours.
• Alternate normal saline and dextrose saline.
o Beware hyponatraemia.
• Prognosis.
o Severity of effusions determines time to recovery.
o In non – menstruation cycles, with little ascites, effusion should resolve with
next menstruation.
o In conception cycles, effusions may persist for weeks.
o Effusions normally resolve.
o In exceptional cases, termination of pregnancy will be required.
o Deaths from the effusions are extremely rare.
• 1:500,000 stimulated cycles.

Menstruation.
• Puberty.
o Development of adult sexual characteristics.
o The normal sequence is.
o Growth spurt
• Finishes about 2 years after menses start with epiphysial
fusion.
o Development of breast buds
o Growth of pubic hair
o Growth of axillary hair
o Start of menstruation.
• Age of menarche.
o Normal from 10 ½ years onwards.
o May be earlier if short and overweight.
o Mean age of onset is about 13 years.
o Was falling.
o Now stabilised.
o Investigate if periods haven’t started by age 16.
• Menstrual cycle.
o Controlled by the hypothalamic – pituitary – ovarian axis.
o Pulses of gonadotrophin – releasing hormone (GRH) from the
hypothalamus.
o Stimulates pituitary to produce gonadotrophins.
• Follicular stimulating hormone (FSH)
• Leutenising hormone (LH)
o Gonadotrophins stimulate the ovaries to produce.
• Oestorgen
• Progesterone.
o Oestrogen and progesterone modulate the production of GRH, FH and
LH by positive and negative feedback.

o Day 1 of the cycle is the first day of menstruation.

o Cycle lengths vary greatly.
o Only 12% are actually 28 days.
o Cycles soon after menarche, and soon before the menopause, are often.
o Irregular
o Anovulatory.
o In the first 4 days of the cycle.
o FSH levels are high
o High FSH stimulates the development of a primary follicle in the ovary.

o The follicle produces oestrogen.

o Stimulates proliferation of
• Endometrium
o “Glandular phase”
• Cervical mucus.
o Makes cervix receptive to sperm.
o Is clear and stringy
 Looks like raw egg white.
o High salt content.
 Forms fern – like pattern if allowed to dry
on a slide.
o 14 days before ovulation.
o Oestrogen levels become high enough to stimulate a surge of LH.
o This stimulates ovulation.
o Having released the ovum, the primary follicle forms a corpus luteum.
o Starts to produce progesterone.
o Under progesterone, endometrial lining is prepared for implantation.
• Glands become convoluted.
o “Secretory phase”
• Cervical mucus becomes.
o Viscid
o Hostile to sperm
o No longer fern – like.
o If ovum is not fertilised.
o Corpus luteum breaks down.
 • Hormone levels fall.
o Causes spiral arteries constrict.
• Causes lining to slough.
• Seen as menstruation.

• Menstruation.
o Loss of blood.
o Uterine epithelial slough.
o Lasts 2 – 7 days.
o Usually heaviest at the beginning.
o Normal loss is 20 – 80 ml.
o Median is 28 ml.
• Climacteric.
o Ovaries fail to develop follicles.
o Without hormonal feedback from the ovary, gonadotrophin levels rise.
o Periods cease.
o Normally occurs at about 50 years old.
• Postponing menstruation.
o Eg. When going on holiday.
o Two options.
o Norethisterone PO.
• Start 3 days before period is due.
• Continue until bleeding is acceptable.
o Take COCP continuously, without taking the normal break.

LH

FSH

Ovulation

Oestrogen

Progesterone

Proliferation Secretion
Menses Day 5 Day 14 Day 28 Menses

Abnormal menstruation.
• Primary amenorrhoea\.
o Failure to start menstruating.
o Investigated in.
o 16 or over
o 14 or over with no breast development.
o For normal menstruation to occur, a person must be.
o Structurally normal
• Are there secondary sexual characteristics?
• Are internal genitalia normal.

• If not, examine and perform karyotyping, which can detect.

o Turner’s syndrome
o Testicular feminization.
• Aim of treatment is to help patient.
o Look and feel normal.
o Function sexually
o Reproduce, if she wishes to.
o Functioning hypothalamic – pituitary – ovarian axis.
o Always consider possibility of pregnancy.
o May cause great anxiety.
o Often due to familial late puberty, and requires reassurance..

• Secondary amenorrhoea.
o When periods stop for >6 months, in a non – pregnant woman.
o Hypothalamic – pituitary – ovarian disorders are common causes.
o Menstrual hormones are easily disturbed.
• Emotion
• Exam stress
• Weight loss
• Excess prolactin.
o 30% have galactorrhoea.
• Other hormone imbalances.
• Severe systemic disease.
o Eg. Renal failure.
o Rare causes include.
• Pituitary tumour.
o Sheehan’s syndrome
• Pituitary necrosis.
o Hypothalamic – pituitary axis malfunction
• Mild
o Causes.
  Stress
 Moderate weight loss
o Sufficient activity to stimulate enough ovarian
oestrogen to produce endometrium.
 This will be shed after a progesterone
challenge.
• `eg. Norethisterone 5 mg TDS for 7
days.
o Timing is disordered, so cycles are not initiated.
o
• Severe.
o Normally due to severe weight loss.
o Serum levels of hormones will be low.
 FSH
 LH
 Oestrogen
• Management.
o Reassure.
o Advise on stress and diet management.
o Refer for psychiatric help if an eating disorder is
suspected.
o Use contraception, as ovulation may happen at any
time.
o If wanting fertility restored immediately, or the
reassurance of seeing a period, one can try:
 Mild: Clomifene
 Severe: GRH

o Ovarian and endometrial causes are rare.

o Ovarian.
• PCOS
• Tumours
• Ovarian failure.
o Premature menopause.
o Uterine.
• Pregnancy – related.
• Asherman’s syndrome.
o Uterine adhesions following D&C.
• Post – pill amenorrhoea.
o Generally oligomenorrhoea masked by regular
withdrawal bleeds.
o Investigations.
o Serum LH & testosterone.
• Raised in PCOS.
 o FSH.
• Very high in premature or normal menopause.
o Prolactin.
• If high, do MRI.
o 40% will have tumour.
• Raised in.
o Stress
o Prolactinoma
o Phenothiazides
o TFTs.
• Oligomenorrhoea in thyrotoxicosis
• Menorrhagia in hypothyroidism.
o Treatment.
o Depends on cause.
o Premature menopause can’t be cured.
• HRT to control oestrogen deficiency and protect against
osteoporosis.
• Pregnancy can be achieved with oocyte donation and in vitro
fertilisation.

Menorrhagia
• This is increased menstrual blood loss.
o Theoretically defined as > 80 ml/cycle.
o Blood loss rarely actually measured, so management is for those who’s blood
loss interferes with normal life.
• A woman may present because of:
o Increased volume of blood lost.
o Clots
o Floods
o Etc.
o Change in life.
o Change in job
o Depression
o Etc.
o Ask about both.
• Also consider.
o Hypothyroidism
o Anaemia.

• Causes.
o In girls and young women, most common causes are.
o Pregnancy
o Dysfunctional uterine bleeding.
o With increasing age, think about.
o IUCD
o Fibroids
o Endometriosis
o Adenomyositosis
o Pelvic infection
o Polyps
o Hypothyroidism
 o In post – menopausal women, the main worry is endometrial carcinoma.
o In any age group ask about generalised bleeding problems.
o Eg. Von Willebrand’s disease.
• Examination.
o Pelvic exam
o Abdominal exam.

o Looking for.
o Polyps
o Fibroids
o Endometriosis.
• Investigations.
o FBC
o TFTs
o Clotting studies.
o If pelvic pathology suspected, consider.
o US
o Laparoscopy
o If irregular bleeding, or suspected cancer, consider.
o US
o Endometrial sampling
o Hysteroscopy + directed biopsy
• Dysfunctional uterine bleeding (DUB).
o Defined as.
o Heavy and/ or irregular bleeding.
o Absence of recognizable pelvic pathology.
o Associated with anovulatory cycles.
o Common at extremes of reproductive age.
o May be ovulatory.
o Where there is an inadequate luteal phase.
o Diagnosis by exclusion with.
o PV exam is normal
o Organic pathology is ruled out.

• Management of menorrhagia
o Treat any underlying condition.
o For DUB.
o Treatment depends on age.
o Reassurance helps.
o Teenage menorrhagia normally settles as cycles stabilise and become
ovulatory.
o Refer if uterus is irregular or bulky
 o Uterus > 10 week size.

o Drugs.
o Antifibrinolytics.
• Eg. Tranexamic acid
• Take during bleeding, for up to 4 days..
• Contraindicated in thromboembolic disease.
o Tranexamic acid doesn’t increase clot risk in a
normal person.
o Antiprostaglandins.
• Eg. Mefenamic acid.
• Take during days of bleeding.
• Reduces bleeding by 29%
• Particularly helpful if dysmenorrhoea is also a problem.
• Contraindicated in peptic ulceration.
o Hormones.
• COCP.
o Effective.
o Contraindicated in smokers > 35 years old.
• Danazol.
o Effective
o Expensive
o Only use on specialist advice.
o Unreliably suppresses ovulation.
 Advise to use condoms as well.
 If pregnancy does occur, there will be
masculinisation of a female foetus.
• Progestogens.
o Cyclical low dose is not effective.
o Mirena coil.
 Good for those wanting to avoid pregnancy.
 Will reduce bleeding by up to 86% at 3
months.
• 97% reduction at 1 year.
 Effective in DUB.
 Consider as first line treatment for other
causes of menorrhagia.
 Also will reduce fibroid volume by 6 – 18
months.
 At 5 years, satisfaction levels are similar to
those for hysterectomy.
• Noethisterone.
o Useful in stopping heavy bleeding.

• Endometrial ablation/ hysterectomy.

o Consider in those who have completed their families.
o Endometrial resection removes a few millimetres of endometrium by.
o Roller ball
 o Laser therapy
o Microwave or balloon ablation.
• More effective if.
o Endometrium is thin.
o Pre – treatment with goserelin or leuproprelin.
 Better than progesterone or danzol.
• About 30 % become amenorrhoeic.
• A further 50% have reduced flow.
• Contraception still required.
• Give HRT.

• Primary Dysmenorrhoea
o Pain without organ pathology.
o Often starts with anovulatory cycles after menarche.
o Features.
o Crampy
o Ache in back or groin.
o Worse during first day or two.
o Excess prostaglandins cause uterine contraction.
o Causes ischemic pain.
o Management.
o NSAIDs.
• Give during menstruation
• Inhibit prostaglandins.
o Paracetamol.
o COCP.
• If pain with ovulatory cycles.
• Ovulation will be suppressed, which may help.
• Patients sometimes present complaining of dysmenorrhoea as
a covert way to get contraception.
o Smooth muscle antispasmodics.
• Unreliable results.
• Eg. Alverine
• Eg. Hyosine butylbromide.
o Surgical dilatation of the cervix was formerly used.
• Now no longer due to risk of making cervix incompetent.

• Secondary dysmenorrhoea.
o Menstrual pain associated with an underlying pathology.
o Adenomyosis
o Endometriosis
o Chronic sepsis.
• Eg. Chlamydia infection.
o Fibroids.
o Tends to appear later in life than primary dysmenorrhoea.
o More constant during period.
o Often associated with deep dyspareunia.
o Management.
o Treat the underlying cause.
o IUCDs generally increase severity of dysmenorrhoea.
• Mirena coils usually reduces severity
• Intermenstrual bleeding.
o May follow a midcycle fall in oestrogen production.
o Other causes include.
o Cervical polyps.
o Ectropion
o Carcinoma
o Cervicitis
o Vaginitis
o Hormonal contraception.
• Normally just spotting
o IUCD
o Pregnancy – related.
• Post coital bleeding.
o Causes.
o Cervical trauma
o Polyps
o Carcinoma
• Cervix
• Endometrium
• Vagina

• Invasive carcinoma found in 3.8% of those referred to

hospital.
o Cervicitis
o Vaginitis
o Smears may be normal, so refer all patients for colposcopy.

• Post – menopausal bleeding.

o Bleeding occurring > 1 year after last period.
o Is due to endometrial CA until proven otherwise.
o Other causes include.
o Vaginitis.
• Often atrophic.
o Foreign bodies.
• Eg. Pessaries.
o Carcinoma of cervix or vulva.
o Polyps.
• Endometrial
• Cervical.
o Oestrogen withdrawal.
• Hormone replacement therapy.
• Ovarian tumour
o Patient may confuse sources of bleeding.
• Vaginal
• Rectal
• Urethral.
Other gynae cancers.
• Cervical cancer.
o Aim to detect pre – invasive disease.
o 1600 a year die in the UK.
o Most of these have never been screened.
• This is now improving.

o Causes.
o Main cause is HPV, mainly.
• HPV 16
o Squamous CA
• HPV 18
o Adenocarcinoma
• HPV 33

• Vaccine is effective.
o Cost – effective if combined with screening program.
o Vaccine given intra – utero can cause CIN I – III to
regress.
o COCP.
• Can increase risk by 4 times in HPV +ve.
o High parity
o > 4 sexual partners.
o Partner with may other partners.
o Uncircumcised partner.
o Early first coitus
o HIV
o Other STDs
o Smoking.

o Screening.
o Cervical CA has pre – invasive stage of cervical intraepithelial
neoplasia (CIN).
o Papanicolaou smears collect cervical cells for microscopy for
dyskaryosis.
• Abnormalities that represent CIN.
o Degree of dyskaryosis reflects grade of CIN.
o Half of CIN I lesions return to normal.
o Most CIN III lesions progress to invasive cancer.
• May take 10 years.
• Can happen much faster in young women.
o In the UK.
• Screening starts at 25.
• Continues every 3 years until 49.
• Every 5 years from 50 – 64.
• Continue after 65 if any of the previous 3 smears were
abnormal.
 o Those most at risk are hardest to persuade to attend for smears.
• Older women
• Smokers
• Inner cities.
o 83% of the eligible population is regularly screened, hence the
reduction in mortality.
o In the UK we do 6 million smears per year.
o Cervical cancer deaths have fallen by 15% to < 1900/year.
o Incidence of CA cervix fell by 42% between 1988 – 97.
o Screening has reduced death rate by about 5000/year.

Grade Papanicolaou class Action Histology

I Normal Repeat in 3 0.1% CIN II –
years, unless III
clinically
suspicious
II Inflammatory Take swabs. 6% CIN II –
Treat infection III
Repeat in 6
months
Colposcopy
after 3
abnormal
Mild atypia Repeat in 4 20 – 37% CIN
months. II – III
Colposcopy
after 2
abnormal
III Mild dyskaryosis Colposcopy 50 – 75% CIN
II – III
Moderate dyskaryosis Colposcopy 80 – 90% CIN
II – III
IV Severe dyskaryosis Colposcopy 5% invasive
(Positive malignant cells)
V Invasion suspected Urgent 50% invasive
colposcopy
Abnormal glandular cells. Urgent Query
colposcopy adenocarcinom
a or
endometrial
CA.

o Third column shows the percentage of smears in each cytological class

that show more serious lesions on histology.
o With inflammatory smears.
• Take swabs
• Treat infection
 • 6% of inflammatory smears have serious underlying
pathology.
o Hence recommendation for colposcopy if
inflammation persists.

o Borderline nuclear abnormality (BNA).

o Implies doubt as to whether a change is neoplastic.
o Management.
• Re – smear at 3 – 6 months.
• Colposcopy.
o If 2 BNA smears with a static number of abnormal
cells.
o Part of the screening process, not urgent.
o Managing BNA as a routine matter over time reduces false negatives
and overtreatment.
o However.
• 2.4% of smears show mild dyskaryosis
• 2.2% of smears show BNA.
• Most of these will eventually need colposcopy, so there is an
argument that they should be given immediate colposcopy,
with directed biopsy.
o This approach costs $1 billion dollars in the USA.
o There have been no randomized control trials done to
investigate which approach is better.
o Having immediate colposcopy is likely to be very
anxiety provoking.

o Treatment of pre – invasive carcinoma.

o Examine cervix using 10x binocular colposcope.
• Abnormal epithelium has.
o Characteristic blood vessel staining.
o White staining with ethanoic acid.
• Take punch biopsies for histology.
• CIN is destroyed by.
o Cryotherapy.
o Laser ablation
o Cold coagulation
o Large loop excision of transformation zone (LLETZ).

o Give 90% cure rate with one treatment.

• Arrange annual follow up smears for the next 10 years.
• Core biopsy can be used as alternative to loop biopsy if.
o Squamocolumnar junction can be seen
o Small volume invasive carcinoma is found on
histology.
o Colposcopy doesn’t detect adenocarcinoma, as it lies in the
endocervical canal.
o Invasive disease.
o Most are squamous cancers.
o 15 – 30% are adenocarcinomas from endocervix.
• Risk factors are unknown.
• Especially affects women < 40 years.
o Spread is local and via lymphatics.

o Staging.
• Stage I: Confined to the cervix.
• Stage II: Spread locally to upper 2/3 vagina.
• Stage IIb: Spread to parametria.
• Stage IIIa: Spread to lower 1/3 vagina.
• Stage IIIb: Spread to pelvic wall.
• Stage IV Spread to bladder or rectum.
• Stage IVb: Distant metastases.
• Most tumours present as stage I or II.

o Diagnosis
• Overt cancer is rarely detected on smear.
• Classical sign is non – menstrual bleeding.
• Early tumour is.
o Firm
o Friable
o Bleeding on contact.

o Treatment.
• Stage Ia1.
o Microscopic lesions with invasion < 3 mm.
o Cervical conisation if wanting to retain fertility.
o Extrafascial hysterectomy if family complete.
• Stage Ia2 – Stage Ib1.
o Microscopic invasion, 3 – 5 mm deep and < 7 mm
width.
o Macroscopic tumour < 4 cm.
o Radical hysterectomy with pelvic lymphadectomy or
radiotherapy.
• Stage Ib and over.
o Chemoradiotherapy.
 o Use of chemotherapy in advanced and recurrent
disease is palliative.
o Main agent is cisplatin.
o Pelvic exenteration is sometimes used in stage Iva
disease.
o Radiotherapy causes vaginal stenosis.
 Encourage intercourse with lubricant within
2 months of treatment.
• 5 – year survival is.
o 80% at Stage I
o 60% at Stage II
• Follow up treatment with annual smears.
o No use after radical radiotherapy.
• Problems in terminal disease include.
o Pain
o Fistulae
o GI/ GU obstruction.
• Endomettrial cancer.
o Postmenopausal vaginal bleeding must be investigated as it may be due to
endometrial cancer.
o Endometrial CA is less common than CA cervix.
o Normally presents after menopause. Most tumours are adenocarcinoma
o Related to excessive exposure to oestrogen, unopposed by
progesterone.
o Marked geographical variation.
• North America: China ratio of 7:1

o Risk factors.
o Obesity
o Nulliparity
o Late menopause
o Diabetes
o Unopposed oestrogen therapy
o Functioning ovarian tumour
o Tamoxifen
o Pelvic irradiation
o Family history of cancer of.
• Breast
• Ovary
• Colon
o Polycystic ovaries.
o Presentation.
o Normally presents with post – menopausal bleeding.
• May start as:
o Scanty
o Occasional
o Associated with a watery discharge.
• Gradually becomes.
o Heavier
o More frequent
• 10 – 20% of post – menopausal bleeding is due to a genital
cancer.
 o Premenopausal women may have intermenstrual bleeding.
• 30% have only menorrhagia.

o Diagnosis.
o Postmenopausal bleeding is an early sign.
• Often leads woman to present to her GP.
o Endometrial CA can sometimes be seen on cervical smears.

o Investigations.
o Uterine US
• Can be suggestive
o Uterine sampling.
• Diagnostic
• Sample all areas of the uterus
• Send all material to histology
o Hysteroscopy.
• Enables visualisation of abnormal endometriaum to improve
accuracy of sampling.
• May be increased risk of disseminating cancerous cells
through Fallopian tubes to peritoneum.

o Pathology.
o Most start in the fundus.
o Tumours spreads slowly to the uterine muscle.
o Eventually it may invade.
• Cervix
• Peritoneum
• Vagina
o 5%
• Ovary
o 5%
• Pelvic lymph nodes
o 7%
o Endometrial sampling as an outpatient.
o Use in patients who have.
• Postmenopausal bleeding.
• Premenopausal irregular bleeding.
• Unexpected bleeding patterns in women on HRT.
o Good screening test as.
• Cheap
• Reliable
• Quick results without need for anaesthesia.
o Less useful in women with menorrhagia and regular cycles.
• Pathology is less common in this group.
o Not indicated if patient is < 35 years.
o If transvaginal US is used prior to the procedure for screening.
• Sample women with endometrium > 5 mm thick.

o Sample obtained by inserting side – opening plastic cannula with

central plunger that generates a vacuum.
 o As cannula is withdrawn and rotated, endometrial tissue from all parts
of the endometrium is drawn into it.
o Successful insertion possible in 90 – 99% of women.
• D&C possible in 99% of women.
• Abandon the procedure if.
o Impossible to enter the uterus.
o Patient being caused too much pain.
o Adequate samples will be acquired in 91% of patients.
• In 84% of those for whom postmenopausal bleeding was the
indication.
o Technique.
1. Bimanual examination to assess size and shape of uterus.
2. Bend cervical cannula to follow shape of uterus.
3. Insert device, watching centimetre scale on the side.
Observe any resistance on.
• Entering the internal os (3 – 4 cm)
• Tip reaching the fundus (6 cm if
postmenopausal, 8 cm if oestrogenised)
4. When tip is in fundus, cause vacuum by withdrawing
plunger until the stopper prevents further withdrawal.
5. Move cannula up and down in the uterus and rotate.
6. Repeat step 5.
7. Remove cannula and expel tissues into formalin, and send
for histology.
• Vabra vacuum aspiration.
o Samples more tissue.
o Greater cancer detection rate.
o More uncomfortable.
o Management.
• Reassure those who’s samples show.
o Normal endometrium
o Atrophied endometrium
o Insufficient sample for diagnosis.
• If those with postmenopausal bleeding rebleed.
o Refer for hysteroscopy
o Fibroids or polyps will be present in 20%
• Refer those with polyps or necrotic areas for hysteroscopy and
curettage.
• Refer those with atypical hyperplasia, or carcinoma, for
hysterectomy and bilateral salpingo – oophrectomy.
• If transvaginal US not already performed, do it in those for
whom endometrial sampling wasn’t possible due to narrow
cervix or pain.
o Normal if endometrial thickness < 5 mm.
o Refer for hysteroscopy and curettage if.
 Endometrium > 5 mm thick.
 Polyps seen.

o Staging.
o Stage I: Confined to body of the uterus.
o Stage II: Confined to body of uterus and cervix
o Stage III: Extension beyond uterus, but within pelvis.
 o Stage IV: Extension outside the pelvis.
Often to bladder or bowel

o Treatment.
o Stages I or II.
• Total hysterectomy + bilateral salpingo – oophrectomy
• Radiotherapy.
o If unfit for surgery.
• Post – operative vault irradiation reduces recurrence.
o Stage III – IV.
• Radiotherapy + High – dose progestogens.
o Eg. Medroxyprogesterone acetate.
o Causes fluid retention.
o Radiotherapy may be given.
• Pre – operatively.
o Caesium or radium rods inserted into uterus and
upper vagina
• Post – operatively.
o Externally.

o Survival.
o At 5 years, survival is
• Stage I: 72%
• Stage II: 56%
o Recurrent disease normally presents in first 2 – 3 years.
o Common sites for non – irradiated patients include.
• Lung
• Bone
• Inguinal lymph nodes
• Supraclavicular lymph nodes
• Vagina
• Liver
• Peritoneum
o In recurrent disease, try:
• Surgical extenteration
• Radiotherapy
• Medoxyprogesterone
• Use cytotoxics if disease is resistant to the above treatments.

Failure to conceive.
• 84% of young couples having regular intercourse conceive within one year.
o 92% conceive within 2 years.
• Offer investigation after a year, or earlier if:
 o Woman > 35 years
o Amenorrhoea
o Oligomenorrhoea
o Previous PID
o Undescended testes
o Previous cancer treatments which may have affected fertility.

• Arrange counselling throughout.

• Consider.
o Is she producing eggs?
o Anovulation causes 21% of infertility.
o Is he producing enough, healthy sperm?
o Male factors cause 24% of infertility.
o Are the egg and the sperm meeting?
o Tubal problems cause 14%
o Hostile mucus causes 3%
o Sexual dysfunction causes 6%
o Is the embryo implanting.
• Aim for intercourse 3 times a week thought cycle.

• Endometriosis is the cause in about 6%

• Cause is unexplained in 27% of couples.
o With unexplained infertility, 60 – 70% will achieve conception within 3 years.

• Initial management.
o See and involve both partners.
o Advise
o Both to stop smoking.
o Her to take folic acid daily while trying to conceive.
o If her BMI > 29, advise to lose weight.
o Ask her about.
o Menstrual history.
o Previous pregnancies
o Contraception used before
o History of pelvic infections
o Abdominal surgery
o Drugs
o Ask him about.
o Puberty
o Previous fatherhood
o Previous surgery.
• Hernias
• Orchidoplexy
• Bladder neck surgery
o Disease.
 • STDs
• Adult mumps
o Drugs
o Alcohol intake
o Job
• Is he home when ovulation occurs.
o Ask them both about.
• Technique, frequency and timing of intercourse.
o Non – consummation is a rare, but significant, problem.
• Feelings about infertility and parenthood.
• Previous tests.

• Examination.
o Check her
o General health
o Sexual development
o Abdomen
o Pelvis
o If sperm count is abnormal, check for abnormalities of
o Endocrine system
o Penis
o Varicocele
o Testes
o Confirm there are two normal testes.

• Tests for ovulation.

o If cycle is regular, ovulation is likely.
o Temperature rises midcycle.
• Charting it is difficult and may raise anxieties.

• Blood tests.
o Check rubella status.
• Immunize if not immune
o If anovulation suspected, check.
• Progesterone.
o 7 days before expected period.
o > 30 nmol/L indicates ovulation.
• FSH.
o > 10 U/L indicates poor response to ovarian stimulation.
o May indicate primary ovarian failure.
o FSH release is pulsatile, so dependant on exact stage of the
cycle.
 So can get false positives quite easily.
• LH.
o High value suggests PCOS.
• TFTs.
o If symptomatic of hypothyroidism.
 • Prolactin.
o Also check in galactorrhoea.
o If high, may be due to prolactinoma
 MRI brain and pituitary.

• Semen analysis.
o Volume.
• Should be > 2 ml
• Mean ahs fallen to a mean of 2.75 ml now, compared with 3.4 ml in the
1940s.
o Sperm count & morphology.
o Infection.
o Normal count.
• > 20 million sperm.
o Mean of 66 million/ml
o Mean in 1940s was 113 million/ml
o May be due to environmental factors, or more ejaculations.
• > 50% motile within 1 hour of ejaculate production.
• > 30% normal forms
• WBC < 1 x 106/ml
o Examine 2 specimens.
• Ideally 3 months apart so sperm cycle can complete.
• Sooner if severely deficient.
o Masturbate sample into a wide topped container, and transport fresh sample to
the lab.
• Avoid temperatures < 15 oC or > 38 oC
o Reduced counts require specialist referral.

• Options in subfertility.
o Donor insemination (DI).
• In some countries children have no rights to trace their fathers.
• In the UK, since 2006, there has been legislation to enable tracing of
fathers.
o Foetal egg child (FEC).
• Offspring from an egg taken from an aborted foetus.
o Intracytoplasmic sperm injection (ICSI)
• Sperm injected directly into an egg.
• If necessary, sperm can be needle harvested directly from the testis or
epidydimis.
• Increases risk of pre – eclampsia due to lack of exposure to partners
sperm.
o Intrauterine insemination (IUI).
 • Very common in the USA.
• Causes twins in 20%.
• Causes higher – order pregnancies in 10%
o Ooplastic transfer/ Nuclear transfer procedure (OT/NTP)
• Baby has two mothers.
• One, who is too old to conceive, provides a nucleus.
• One provides fresher cytoplasm and mitochondrial DNA for the ovum.
• Example of human germline modification.
o Illegal in the UK
o Legal in the USA.
o Purcutaneous epididymal sperm aspiration (PESA)
• Similar to MESA, but 22|G needles inserted into the epididymis.
• So scrotal exploration is not needed.
o Pregnancy by Human Cloning (PHC).
• Illegal in many countries.
• Concerns about premature aging.
• Achieved by Italian doctors in April 2002, to 8 weeks gestation.
o Pregnancy by ovarian transfer (POT).
• China leads the field in this area.
o Subzonal sperm injection (SUZI)
• Sperm injected directly into the egg
• Glossary.
o IVF – In vitro fertilisation.
o GIFT – Gamete intrafallopian transfer
o MESA – Microepididymal sperm aspiration for testis.
o TET – Tubal embryo transfer.
o TUFT – Transuterine fallopian transfer.
o ZIFT – Zygote intrafallopain transfer.

• Investigations
o Tests of tubal patency.
• Screen for Chlamydia.
• If damaged tubes are not expected, start with hysterosalpingogram or
hysterosalpingo – contrast ultrasound.

• Hysterosalpingogram.
o A contrast X – ray.
o |Demonstrates
 Uterine anatomy.
 Tubal ‘fill and split’
o Unpleasant and may require premedication.
 o False positives may occur with tubal spasm.
o Give broad – spectrum antibiotics for 5 days following to
prevent pelvic infection.
 Eg. Cefradine + Metronidazole.
• Laparoscopy.
o Begin with this if high probability of damaged tubes.
o Visualise pelvic organs.
o Inject methylene blue dye through the cervix.
o Proximal blockage of tubes will prevent tubes from filling
with dye.
o Distal blockage of tubes will prevent dye from spilling into
peritoneal cavity.

• Management.
o Treatment depends on the cause.

o Azoospermia.
• Is no specific treatment.
• Low sperm count may be improved by avoiding.
o Tobacco
o Alcohol.
o Tight trousers
• Will the couple consider donor insemination?
o Check ovulating.
o Investigate if tubal damage suspected. give three cycles of
intrauterine insemination post – ovulation.
o If unsuccessful, further investigate for tubal damage.
o Attempt 3 more cycles of IUI.
o If still unsuccessful, offer other treatments.
o Problems of sperm deposition.
• Eg. Erectile dysfunction.
• Can be circumvented by using artificial insemination with the partner’s
sperm.
o Hyperprolacaemia.
• Remove the cause if one is found.
o Pituitary tumour
o Macro – adenoma
o Drugs.
• If no cause found, give bromocriptine.
o Titrate dose up until prolactin levels are normal.

o Anovulation.
• Classified by the WHO as:
o Class I: Hypothalamic – pituitary failure.
 Will respond to pulsed gonadotrophins or leutenising
hormones.
o Class II: Hypothalamic – pituitary dysfunction.
 Usually due to PCOS.
 Follicle development is stimulated with clomifene.
 • Side effects.
o Flushes
 In 10% of patients.
o Visual disturbances.
 In 1.5% of patients.
o Abdominal pain.
 In 5.5% of patients.
• Warn about risk of.
o Multiple pregnancies
o Ovarian cancer.
• Monitor response with.
o Luteal phase progesterone
o US in at least 1 cycle.
• If clomifene doesn’t stimulate follicles, try
gonadotrophins.
• If still unsuccessful after 6 moths of
clomifene treatment, offer clomifene
assisted IUI.
o Class III: Ovarian failure.
 Give IVF with donor eggs.
o Tubal problems.
• May respond to surgery.
o Results are poor.
• Proximal blocks may respond to.
o Tubal catheterisation
o Hysteroscopic cannulation.
o Intrauterine adhesions.
• Hysteroscopic adhesiolysis.
o Endometriosis.
• Treat as per normal.

• Assisted fertilization.
o Screen couple for
• HIV
• Hepatitis B & C
o Women with hydrosalpinges should have salpingectomy prior to IVF.
 • Increases chance of live birth.
o Assess psychological stability.
• Some non – UK clinics are happy to give IVF to single women > 65
years old.
o Chance of live birth per treatment cycle is age dependant.
• 20% if < 35 years.
• 15% if 36 – 38 years.
• 10% if 39 years
• 6% if > 40 years.
o In vitro fertilisation.
• Ovaries are stimulated with gonadotrophins.
o Risk of hyperstimulation.
• Ova are collected by transvaginal aspiration, under transvaginal US
guidance..
• Ova are fertilised, and 2 are returned to the uterus under US guidance..
• Can be done as an outpatient procedure.

• Possibility of adoption should not be forgotten.

• Offer counselling or a self – help group to those who remain childless.

Male infertility
• Spermatogenesis occurs in the seminiferous tubules.
• Undifferentiated diploid germ cells (spermatogonia) multiply and are transformed into
haploid spermatozoa.
o Takes 74 days.
o FSH and LH are both important for initiation of spermatogenesis at puberty.
• LH stimulates Leydig cells to produce testosterone.
• LH and testosterone stimulate Sertoli cells to produce substances
essential for metabolic support of germ cells and spermatogenesis.
• Spermatogenesis.
o Spermatozoon has a dense oval head.
• Containing haploid chromosome component.
o The head is capped by a acrosome granule.
• Containing enzymes essential for fertilization.
o The sperm is propelled by a motile tail.
o Seminal fluid forms about 90% of ejaculate.
• Is alkaline to buffer acidic vaginal conditions.
o Only about 200 sperm reach the middle third of the fallopian tubes when
fertilisation normally occurs.

• Male infertility.
o Male factors are the cause of infertility in about 24% of infertile couples.
o In reality, most are subfertile rather than infertile.
o Only a small number of men have an identifiable cause.
o The most common causes are.
• Asthenozoospermia/ tetratozoospermia 17%
o Sperm motility is reduced due to structural problems with the
tails.
o Tetratozoospermia indicates an excess of abnormal forms.
• Varicocele 17%
o Controversial, as varicocele is found in 15% of all men, most
of whom have normal fertility.
• Idiopathic oligo/azoospermia. 16%
o Small testes
o High FSH
• Genital tract infection 4%
o Gonococci
o Chlamydia
o Gram – ve enterococci

o Cause adnexal infection.

 Painful ejaculation
 Urethral discharge
 Hamatospermia
 Dysuria
 Tender epididymis
 Tender, boggy prostate.
o Confirm with.
 Semen culture.
 Urethral swab
 Detection of > 106 perioxidase +ve polymorphs/ml
semen
o Treatment has not been shown to restore fertility.
• Congenital. 2%
o Cryptorchidsm
o Chromosome disorders.
 Klinefelter’s syndrome accounts for 50%
o Optimise fertility by fixing undescended testes in the scrotum
by age 2 year.
• Obstructive azoospermia 1.8%
o Suggested by:
 Azoospermia
 `Normal sized testes
 Normal or high FSH
o May follow.
 Infection
 Vasectomy
 Congenital.
• Eg. Cystic fibrosis.
o May be amenable to surgery.
 Eg. Epididymovasostomy
 To bypass epididymal obstruction.
 • Sperm autoimmunity. 1.6%
o Risk factors for autoimmunity.
 Vasectomy
 Testis injury
 Genital tract obstruction
 Family history of autoimmunity.
o Most are
 On sperm membrane
 In seminal fluid.
o May also occur in women.
• Systemic. 1.3%
o Iatrogenic
o Drugs.
 Eg. cannabis
• Coital disorders 1%
• Gonadotrophin deficiency 0.6%
o Only cause of testicular failure which is consistently treatable
by hormone replacement.

o Examination.
• Look at body form and secondary sexual characteristics.
• Gynaecomastia?
• Normal testicular volume is 15 – 35 ml.
o Measure and compare with Prader orchidometer.
• Rectal examination may reveal prostatitis.
o Investigations.
• Semen analysis.
• Plasma FSH.
o Distinguishes primary and secondary testicular failure.
• Serum Testosterone & LH
o Indicated if androgen deficiency suspected.
• Agglutination tests.
o Detect antibodies.
o Treatment.
• Intracytoplastic sperm injection, directly into the egg, is the main
treatment for most male infertility.
• Source of sperm in obstructive azoospermia is.
o Epididymis
o Testis.
• Even if problem is non – obstructive, sperm can be retrieved from these
sites in 50%.
Unwanted pregnancy
• Under UK law.
o Nobody MUST have an abortion
o Nobody MUST perform an abortion.
• Worldwide 30% of pregnancies are terminated.
• In the UK, 1/3 of women will have had a termination by the time they are 45.
o 197,500 ToP per year in Great Britain.
• Legal constraints.
o Controlled by:
• Abortion Act 1967.
o Amended in 2002
• Human Fertilization and Embryology Act 1990
o Termination is allowed on grounds of:
• A Risk to mother’s life if pregnancy continues.
• B Termination necessary to prevent grave injury to physical or
mental health of mother.
• C Continuing pregnancy risks injury to physical or mental health
of woman, greater than risks if terminated, and foetus < 24
weeks.
• D Continuing pregnancy risks injury to physical or mental health
of mother’s existing children, greater than risks if terminated
and foetus < 24 weeks.
• E Substantial risk of child being severely handicapped due to
being born with physical or mental abnormalities.

• Two doctors must sign Certificate A.

• If aged < 16, try to get consent from the patient to inform her parents or
other adult.
o If mother is a ward of the courts, then the Court MUST
approve termination.
• Breakdown of reasons for termination.
o 94% under section C
o 4% under section D.

o < 1% performed after 20 weeks.

 Normally following
• Discovery of abnormalities on
amniocentesis
• Young or perimenopausal women who have
hidden or not detected pregnancy earlier.
• Terminations after 24 weeks can only be performed in NHS hospitals.
• Before Termination.
o Termination is a major decision, with lifelong consequences.
• Make sure that the woman is well counselled so she reaches the
decision that she will regret the least.
o Is she definitely pregnant?
o Is ToP what she really wants?
o Why?
o Has she considered the alternatives?
o What does her partner think?
• Ideally give her time to consider her decision.
• Do scan or vaginal exam to confirm dates if she chooses ToP.
o Screen for Chlamydia.
• 25% get post – op salpingitis if untreated.
o Take bloods.
• Hb
• Blood group
• Rhesus status.
o If Rh –ve, needs anti – D prophylaxis regardless of gestation
of method of termination
• If relevant.
o HIV
o Hepatitis B & C
o Haemoglobinopathies.
o Give antibiotic prophylaxis.
• Reduces post – op infection rate from 10% to 6%.
• Metronidazole at time of op.
• Azithromycin later that day.
• Methods.
o Medical abortion.
• Antioestrogen to dis – implant the foetus.
o Eg. Mifepristone.
• Followed by prostaglandin to complete abortion.
o Eg. Gemeprost
o Eg. Misoprostol

o Misoprostol can be used orally as well as vaginally, and is

much cheaper than gemeprost.
o Very effective early on.
 98% when < 7 weeks with misoprostol.
 95% when 7 – 9 weeks with misoprostol.
 Gemeprostol is more effective than misoprostol at 7 –
9 weeks.
• For early abortions, arrange follow up and scan to confirm complete
abortion at 2 weeks.
o Unless complete abortion seen on day of procedure.
• 5% will require surgical evacuation.

o Suction termination.
• Used from 7 – 15 weeks.
• Cervical priming is required if.
o Woman < 18 years old.
o Gestation > 10 weeks.
• Local anaesthesia is safer than general.
o Rarely used in the UK.
• Medical termination is preferable when < 7 weeks.
o Gestation sac may be missed with early gestations.
• Mortality is 1:100,000
• Risk of infection is similarly low.

o Dilatation and evacuation.

• Used at 15 – 18 weeks.
• Requires a skilled user of surgical forceps.
• Real time US reduces risk of uterine perforation.
• Mortality increases with increased gestation.

o Late term terminations.

• If termination is to occur beyond 21 weeks and 6 days, it will require
delivery of a dead foetus.
• May be achieved with use of intracardiac potassium chloride.
 o Can give anaesthetic and/or muscle relaxant before hand to
abolish foetal movements.
• Confirm asystole with US.
• If born after 24 weeks, the dead foetus is a stillbirth and will need to be
registered as such.
• If there are any signs of life, a death certificate will need to be issued.

• Complications.
o Failure to abort.
• Medical ToP 1 – 14:1000
• Surgical ToP 2.3:1000
o Haemorrhage.
• 1:1000
o Uterine perforation.
• 1:1000
o Uterine rupture.
• 1:1000
• Increased if
o Mid – trimester
o Presence of previous uterine scar.
o Cervical trauma.
• 1:100
o Subsequent miscarriage or preterm labour.
• Small risk.

• Follow up.
o Give Anti – D if needed.
o Arrange contraception.
• Can begin COCP that day.
o Arrange follow up appointment in 2 weeks.
• Psychological support.
• Confirm complete abortion.