High risk pregnancies Flashcards
Epidemiology and aetiology of diabetes in pregnancy
- 0.5-5% of pregnancies
- Women of south Asian and African-Caribbean origin at greater risk
- Obesity increases risk of type 2 and gestational diabetes
How can gestational diabetes be prevented?
- Preconception advice and optimisation of glycaemic control prior to pregnancy
- Weight loss
Pathogenesis of gestational diabetes
- Placental hormones e.g. human placental lactogen, cortisol and growth hormone promote insulin resistance
- Normally beta cells can compensate but this is impaired in pregnancy so hyperglycaemia occurs
- The rate of complications increases with increasing HbA1c levels
Complications of diabetes in pregnancy
Maternal:
- Hyperglycaemia, ketoacidosis, increasing insulin requirements or need to start insulin, hypoglycaemia, nephropathy, retinopathy, pre-eclampsia, increased risk of caesarean section
Foetal:
- insulin resistance, vomiting in early pregnancy, microvascular disease, often related to iatrogenic intervention
Babies born to mothers with high blood glucose have high basal levels of insulin to cope and are at risk of hypoglycaemia after birth. This results in hypoxia and erythropoiesis occurs which can cause polycythaemia and jaundice
The complications listed are those that occur in diabetics with poor control
Diagnosis of diabetes during pregnancy
Previous GD: offer 2-hour 75g OGTT ASAP after booking (whether 1st/2nd trimester) and further test at 24-28w if the results of first are normal
Screening for gestational diabetes at 24-28 weeks in women at risk done with oral glucose tolerance test
Women at risk:
- BMI >30
- Previous big baby
- FHx of diabetes
- Previous hx of gestational diabetes
Investigations: 🎶 5,6,7,8 🎶
- Oral GTT after woman has fasted overnight
- Serum glucose measured and the test is repeated after 2hrs following drinking a solution containing 75g glucose. Gestational diabetes diagnosed if blood glucose is >5.6mmol/L after fasting or >7.8mmol/L after 2hrs
- Threshold values are lower than for diabetes outside of pregnancy due to increase risk
Management of diabetes during pregnancy
Newly diagnosed - seen in clinic within 7 days
- High levels of folic acid protect against glucose induced foetal anomalies
- Lifestyle changes initially then if no changes started on metformin
- Medication: metformin or glibencamide are safe to use
Add insulin if metforminor glibencamide does not control DM
- Insulin: requirements increase during pregnancy peaking around 36 weeks. A sudden increase in insulin requirements indicates placental insufficiency so delivery is induced to prevent stillbirth
- Delivery: induced at 38 weeks to prevent risk of late stillbirth. Macrosomic babies delivered by c-section to reduce risk of shoulder dystocia
- Post natal: insulin requirements rapidly decrease so women with gestational diabetes immediately stop medication and those with pre-existing diabetes go back to normal regimen
Ideal blood glucose levels: 3.5-5.9mmol/L fasted and <7.8mmol/L 1hr after food
Measure blood glucose 4x day
Diagnosed > joint diabetes and antenatal clinic within 1 week
- glucose > 7: insulin
- glucose 6-6.9 + symptomatic (macrosomia/ polyhydramnios): insulin
- glucose 6-6.9 + asymptomatic: exercise > metformin > insulin
- delivery: good control + no macrosomia: 38+6; recued movements: surveillance.
- delivery: good control + macrosomic: induce at 36 weeks
- delivery: non-reactive CTG: C-section
Define gestational diabetes
Defined as glucose intolerance with onset or first recognition during pregnancy. However, changing definition to being diagnosed in 24-28w of gestation that is clearly not overt diabetes
Epidemiology of gestational diabetes
Ep: affects 1/20 pregnancies
87.5% have GDM, 7.5% have T1DM, 5% have T2DM
Hypertension in pregnancy
Common, classified according to blood pressure
- Mild = 140-149/90-99 mmHg
- Moderate = 150-159/100-109 mmHg
- Severe = >160/110 mmHg
Severe hypertension can cause placental abrupt ion, foetal growth restriction, cerebrovascular accident and maternal and foetal death.
Terms used to describe HTN in pregnancy with or without proteinuria
- Without proteinuria = gestational hypertension
- With proteinuria = pre-eclampsia
Outline types of HTN in pregnancy
Chronic HTN: onset <20 weeks gestation, foetal growth restriction, super-imposed pre-eclampsia, en organ disease, placental abruption, PTB
Gestational HTN: >20 weeks gestation, no significant proetinuria, cause unknown but may be due to abnormal placentation, low risk of maternal or foetal complications
Pre-eclampsia: significant proetinuria, >20 weeks gestation, due to abnormal placentation, failure of invasion of he spinal arteries by trophoblasts, maternal BP increases to compensate for increased vascular resistance, endothelial damage causes proteinuria, causes IUGR, prematurity, eclampsia, HELLP, disseminate intravascular coagulation, maternal and foetal death
What is pre-eclampsia?
Hypertension developing after 20 weeks gestation in association with significant proteinuria
What is eclampsia?
- Onset of generalised seizures in a woman with pre-eclampsia
- Only 1/3 of women with eclampsia have hypertension and proteinuria before their first eclamptic seizure
- Caused by a loss of cerebral auto regulation which leads to increased blood flow, vessel permeability and oedema
Epidemiology of pre-eclampsia
- 10-15% pregnancies affected by hypertension
- Eclampsia affects 1% of women with pre-eclampsia in UK, <1% of cases are fatal
- Higher incidence in low and middle income countries
Women at risk of hypertension in pregnancy
- Hx of hypertension in pregnancy
- Diabetes
- CKD
- Autoimmune disease
- First pregnancy or >10yrs between pregnancies
- 40+
- BMI >35
- Multiple pregnancy
What medication is recommended for women at risk of HTN in pregnancy?
Aspirin is recommended from week 12
Inhibits the production of thromboxane A2 and reverses vasoconstriction that underlies hypertension and improves endothelial function
This reduces the risk of developing pre-eclampsia by 10%
Clinical features of pre-eclampsia
Hypertension usually asymptomatic so screening is vital
Symptoms and signs are related to increased vascular permeability and leakage of fluid into interstitial spaces: blurred vision, headaches, seizures, swollen face, epigastric pain, vomiting and others
Investigations for HTN in pregnancy
- Dipstick analysis to test for proteinuria
- Proteinuria in the context of new onset hypertension indicates pre-eclampsia
- Bloods: to identify end organ damage and HELLP syndrome
What is HELLP syndrome?
- Haemolysis
- Elevated liver enzymes
- Low platelets
Affects 15% of women with pre-eclampsia and has a 25% mortality rate. Mortality is related to liver rupture and cerebral oedema and haemorrhage
Other features of HELLP: renal function impaired, PT and APTT prolonged in the presence of disseminated intravascular coagulation
Clinical features of HELLP
RUQ pain
N&V
Headache
Malaise
- haemolysis (schistocytes, burr cells, polychromasia on smear are diagnostic),
- elevated liver enzymes (ALT > 70)
- low platelets (<100,000/microlitre).
Monitoring of HTN in pregnancy
- Chronic hypertension and mild - moderate gestational hypertension are managed in community. USS used to determine foetal growth and amniotic fluid volume at 28 & 32 weeks in cases of chronic hypertension.
- Severe hypertension and pre-eclampsia are monitored in hospital. Blood pressure checked 4x a day and bloods repeated every 3-4 days to detect HELLP syndrome
Timing of delivery in women with HTN
- Chronic and gestation hypertension have a good prognosis so delivery after 37 weeks
- Pre-eclampsia delivery after 34 weeks reduces risk of adverse events
Prognosis for foetus following eclamptic seizure
Foetal mortality 30% after eclamptic seizure
Medication used to treat eclamptic seizures?
Magnesium sulfate IV
Do not use diazepam, phenytoin or other anticonvulsants as an alternative to magnesium sulfate in women wit
Recommended blood pressure medication for women with pre-eclampsia
Labetolol 1st line
Nifedipine for those who cannot take abetolol
Methyldopa if the above are not suitable
Timing of birth in women with pre-eclampsia
Any adverse features such as
inability to control BP, maternals sats <90%, HELLP syndrome, neurological features, placental abruption, abnormal CTG or reversed end diastolic flow in the umbilical artery
Warrant planned early birth
Timing: <34 weeks continue surveillance unless delivery is absolutely necessary, 34-36 weeks is acceptable, 37 weeks+ initiate birth within 24-48hrs
What is obstetric cholestasis?
Liver disease unique to pregnancy, develops in third trimester, resolves after delivery
Slows or stops the normal flow of bile from the gallbladder causing jaundice
Pathogenesis of obstetric cholestasis
Increased oestrogen levels impair sulphation of bile acids and inhibit a bile acid export pump in hepatocytes.
This blocks excretion of bile salts and these are deposited in the skin which causes itching and damages hepatocytes.
This can also occur if women take the combined pill because it contains oestrogen
Clinical features of obstetric cholestasis
- Severe itching due to cholestasis, especially on palms and soles
- Skin excoriation due to scratching
- Dark urine
- Pale stools
- Jaundice
- Steatorrhoea
Diagnosis and investigations of obstetric cholestasis
Unexplained abnormalities in liver enzymes but other causes should be excluded
*symptoms can develop before LFTs are deranged so if symptoms are present, repeat bloods every 1-2 weeks
Investigations:
- LFTs: increased ALT and GGT, normal pregnancy adjusted ALP and bilirubin
- Bile acids: most specific test for obstetric cholestasis - raised
- Viral hepatitis screen to exclude othr causes
- Autoimmune hepatitis screen to exclude other causes
- Liver USS: exclude FLD and gallstones
- BP and urinalysis: exclude pre-eclampsia
What happens to ALP levels during pregnancy
Serum ALP levels are elevated in late pregnancy, usually in the third trimester. This increase is mainly due to the production of placental isoenzyme rather than elevation of hepatic isoenzyme
Levels in a pregnant woman can be as much as 2x the normal upper limit
What is acute fatty liver of pregnancy?
Acute fatty liver of pregnancy (AFLP) is a rare, potentially fatal complication that occurs in the third trimester or early postpartum period. Although the exact pathogenesis is unknown, this disease has been linked to an abnormality in fetal fatty acid metabolism
Often confused with HELLP
Causes hypoglycaemia, marked increase in serum iron acid conc. and coagulopathy
Managing obstetric cholestasis
Supportive, medication to relieve symptoms
Delivery of the baby is the only known cure
Medication:
- Topical emollients with menthol to block the action of histamine which is responsible for activating C fibres which transmit the sensation of itch
- Ursodeoxycholic acid 500mg 2-3x a day relieves itching and improves liver function by binding bile acids but not licensed for use in pregnancy
- If clotting abnormal: vitamin k
- Vitamin K given to babies when born to prevent haemorrhagic disease of the newborn
Delivery:
- Increased risk of meconium and foetal distress so women give birth in obstetric unit
- Delivery induced after 37 weeks because of the risk of stillbirth
Prognosis:
- Improves with delivery, can take time so repeat LFTs at least 10 days after delivery
- 90% risk of recurrence in future pregnancy
What is polyhydramnios?
Excess amniotic fluid
Affects 1% of pregnancies
Classification: according to single deepest pool depth
- Mild: 8-11cm
- Moderate polyhydramnios: 12-15cm
- Severe: >16cm
What causes polyhydramnios?
Mixture of maternal and foetal factors
Maternal
- Gestational diabetes
- Cardiac failure
- Haemolytic disease of the newborn
- Placental chorioangioma
- 80% unexplained
Foetal
- TORCH infections
- Oesophageal/ duodenal atresia
- Diaphragmatic hernia
- Anencephaly
- Twin to twin transfusion syndrone
- Chromosomal abnormalities
- Skeletal dysplasia
Clinical features of polyhydramnios
- Higher than expected symphysis fundal height
- Maternal abdo skin is stretched and shiny
- Tense uterus
- Difficult to palpate parts of the foetus
- Splinting of diaphragm by enlarged uterus causes SOB
Investigations into polyhydramnios
- USS to measure amniotic fluid pool depth
- Amniocentesis offered if generic anomaly suspected
- Maternal blood checked for evidence of TORCH infection
- Oral GTT to screen for diabetes
Management and prognosis of polyhydramnios
Management:
- Mild and asymptomatic cases managed expectantly - no intervention
- Medication: indometacin decreases volume of fluid by reducing urine production by the foetal kidneys but it causes premature closure of DA
- Surgery: amniocentesis but procedure carries risk of miscarriage and fluid builds up again
Prognosis:
- Risks of increased uterine stretch:
- Preterm labour
- Abruption
- Rupture of the membranes
- Post partum haemorrhage
- Unstable foetal lie
What is oligohydramnios?
Reduced amniotic fluid, <500ml at 32-36w
Causes of oligohydramnios
Foetal: urethral obstruction, bilateral renal agenesis, ARPKD, chromosomal abnormalities, multiple pregnancies
Maternal: late term, PROM, pre-eclampsia, placental insufficiency
What is Potter’s sequence?
Describes the typical physical appearance caused by pressure in utero due to oligohydramnios. It can occur in conditions such as infantile polycystic kidney disease, renal hypoplasia, and obstructive uropathy
Urine is not produced >> oligohydramnios >> baby is squashed in utero and does not develop properly
Investigations into oligohydramnios
Abnormal size for dates, ultrasound, Amniotic fluid index (<5cm)
What are the most common causes of perinatal infection?
TORCH organisms
Toxoplasmosis
Other: syphilis, varicella-zoster, parvovirus
Rubella
Cytomegalovirus
Herpes
Discuss perinatal toxoplasmosis infection
- Infection with toxoplasma gondii is asymptomatic in the mother in most cases but can present as flu with lymphadenopathy
- Infections can cause miscarriage especially if within the first 10 weeks of pregnancy
- Can cause hydrocephalus and intellectual disability in the foetus, cerebral calcification, chorioretinitis which can cause blindness later in life
Discuss perinatal infection with varicella-zoster
- Presents in the mother with fever, malaise and a maculopapular rash (chickenpox)
- No increased risk of miscarriage
- Can cause foetal varicella syndrome which presents with scarring in dermatomal distribution, eye defects, microcephaly, cortical atrophy, learning disability, bladder and bowel sphincter dysfunction
- Mortality rate of 30% in babies
Discuss perinatal parvovirus infection
- Asymptomatic in the mother in 20-30% of cases, otherwise presents with a non vesicular (slapped cheek) facial rash, malaise, sore throat, mild fever, arthropathy, anaemia and anaplastic crisis
- No increased risk of congenital abnormalities
- Hydrous fetalis (accumulation of fluid in two or more foetal compartments) is a complication of foetal anaemia and cardiac failure
Which virus causes slapped cheek sydrome?
Parvovirus 19
Discuss perinatal rubella infection
- Presents in mother with malaise, fever, conjunctivitis, coryzal symptoms, macular rash, arthropathy, post auricular lymphadenopathy
- Foetal complications: miscarriage, stillbirth, growth restriction, deafness, microcephaly, cataracts, cardiac defects
Discuss perinatal CMV infection
- Most cases asymptomatic in mother but can cause flu like symptoms and lymphadenopathy
- Foetal complications: hepatosplenomegaly, thrombocytopenia, intracranial calcification, hearing loss, chorioretinitis, microcephaly and learning disability, growth restriction and stillbirth
- Of the 5-15% of infected babies symptomatic at birth, 30% die and 80% have serious consequences. 10-15% of asymptomatic babies will develop auditory, visual or neurological defects
Discuss perinatal herpes infection
- Mother: painful genital ulcers, encephalitis, hepatitis and skin lesions if disseminated herpes
- No increased risk of miscarriage
- Morbidity <2% with antivirals
- 70% of cases there is disseminated disease with or without CNS involvement
Herpes can be contracted as the baby passes through birth canal causing baby to be irritable, blisters over body, difficulty breathing, jaundice and easy bleeding
Can be fatal if not treated with antivirals
Investigations for perinatal infection
- HIV+ women have viral load and CD4 levels checked once a trimester
- Women with hep C or B have viral load assessed early in pregnancy
- Positive immunoglobulin M antibodies to a TORCH organisms are diagnostic of a recent infection and increasing IgG confirms acute disease
- Amniocentesis and viral detection by PCR or culture confirm foetal infection
- Serial USS scans to screen for complications of infection
Management of perinatal infections
Aim is to reduce transmission
Termination offered to women with TORCH infections depending on the organism, gestation when infection occurred and presence of foetal abnormalities
Medication:
- HIV: women continue antiretrovirals throughout pregnancy. Cabergoline is used to suppress lactation. Some retrovirals cause gestational diabetes
- Hepatitis: antivirals used in third trimester for women with hep B and high viral load. No safe treatment for hep C in pregnancy
-
Toxoplasmosis: spiramycin given prophylactically to reduce risk of parasite transmission, doesn’t reduce risk of foetal anomalies. If foetus is infected, pyrimethamine and spiramycin are given to reduce severity.
- *pyrimethamine is teratogenic so not used in first trimester. It also antagonises folate so supplements are needed to prevent folate deficiency
- Parvovirus: no drug treatment available, intrauterine infusions to treat foetal anaemia
- Rubella: no drug treatment available, cochlear implants and cardiac surgery may be needed after birth
- CMV: antivirals given to babies with congenital infection to reduce risk of hearing loss
- Herpes: primary disease treated with aciclovir and given from 36 weeks to reduce need for c-section
Do all women with HIV have to have c-section?
No
HIV: viral load <50 RNA copies/mL at 36 weeks means woman can have vaginal delivery otherwise c-section. If load >1000 IV zidovudine is given
Woman has a primary herpes infection in 3rd trimester - how is delivery managed
Indication for c-section
Breastfeeding with perinatal infections
- HIV: avoid in high income countries
- Hep B and C: encouraged
- TORCH: all ok apart from CMV but even in CMV transmission is rare
What vaccinations are given to babies born to mothers with neonatal infection
- Babies born to mothers with hep B receive the first dose of the vaccine and a dose of hep B immunoglobulin within 12hrs birth
- Further doses of hep B vaccine given at 1 and 6mo
- No vaccinations against TORCH
Why do babies infected with parvovirus suffer with anaemia?
Parvovirus suppresses EPO
Treatment of perinatal parvovirus infection
No treatment
Pregnant woman has come into contact with varicella zoster virus - what is done?
VZV IgG antibodies:– if not immune (IgG negative give VZIG ASAP - effective up to 10d after exposure
Acyclocir within 24h of rash
Most common TORCH infection?
CMV - affects 1/100
What % of pregnant women in the UK have a BMI >30?
20%
What are the risks of maternal obesity?
To mother:
- Gestational diabetes
- Gestational HTN and pre-eclampsia
- Difficulty with epidurals
- Wound infection
- PPH
- VTE
To foetus:
- Miscarriage
- Foetal anomalies: neural tube defects, cardiac defects, omphalocele
- Stillbirth
- Prematurity
- Shoulder dystocia
- Childhood obesity
What advice, regarding weight, is given to obese pregnant women?
Advised to maintain weight neutral pregnancy meaning they don’t lose or gain weight but light exercise and diet modification is recommended
Pregnant woman is obese, what investigations are done?
- USS to screen for abnormalities, assess growth
- Blood pressure and urinalysis for pre-eclampsia
- Organ GTT for gestational diabetes
Management of delivery in obese women
- BMI >35 - babies delivered in obstetric led centres
- BMI >40 - heparin injections for at least 1 week after delivery
What is the most common neurological condition in pregnant women?
Epilepsy
Affects 0.5% women of childbearing age
Investigations for epilepsy in pregnancy
First seizure - measure blood pressure and urinalysis for proteinuria
- first seizure in pregnancy is eclampsia until proven otherwise
Bloods to check platelets, renal and liver function, coagulation tests, glucose levels and calcium concentration, drug screen to check for other causes of seizure
CT or MRI head to exclude mass lesions or haemorrhage
EEG if epilepsy suspected
Management of epilepsy in pregnancy
- Balance between teratogenic risk of drugs and worsening seizure control
- Medication: many are teratogens and cause neural tube defects, cleft lip and palate, cardiac defects
- Sodium valproate has the highest rate of genetic abnormalities, twice that of other anti-epileptics
- Carmabazepine and lamotrigene have a 2-2.5% incidence of malformations
- Generally drugs should be continued because risk of seizure is higher than risk to foetus but women on sodium valproate are encouraged to switch to a different drug before pregnancy. If sodium valproate is the only drug that works, the dose is split over the day
- All anti-epileptics have the potential to cause foetal anticonvulsant syndrome
Women prescribed liver enzyme inducing drugs such as carbamazepine are given what from 36 weeks?
Vitamin K from 36 weeks to reduce risk of vitamin K dependant clotting deficiency
What is advised, regarding delivery, in women with epilepsy?
No indication for c-section but seizures can be triggered by pain, anxiety and lack of sleep so early epidural may be beneficial
Epidemiology of maternal cardiac disease
- Increasing as more women with congenital cardiac disease are surviving into adulthood
- In high income countries 80% of cardiac disease in pregnancy is congenital
- Outside of Europe and North America rheumatic heart disease is the most common cause of cardiovascular disease
Causes of maternal cardiac disease
- Rising incidence of obesity leading to cardiovascular disease
- Peripartum cardiomyopathy is a dilated cardiomyopathy, cause unknown, causes loss of cardiac function. Unique to pregnancy and presents between the last month of pregnancy and 6 months after birth
Why might cardiac disease become apparent during pregnancy?
Increased strain on the heart
Circulating volume inceases so heart is working overtime
Investigating cardiac disease in pregnancy
Maternal:
ECG: palpitations or arrhythmias
Echo: ventricular and valve function
Exercise testing: Functional capacity and heart failure
Foetal:
- Cardiac USS: detect congenital heart disease
- Genetic testing: to identify abnormalities associated with congenital heart disease e.g. Down’s
- Serial assessment of foetal growth from 28 weeks: detect placental dysfunction and foetal compromise (increased risk if mother has cardiac disease)
Management of heart disease in pregnancy
Extent of intervention depends on extent of cardiac function
Medication: aspirin used prophylactically in women with coronary artery disease
Women with metallic heart valves take warfarin outside of pregnancy but it is a teratogenic so it is avoided. Heparin is safe but thrombosis more likely
Delivery:
- Takes place in obstetric led departments
- Vaginal delivery preferred
Prognosis of heart disease in pregnancy
Outcome is good if woman has left to right shunt and minimal symptoms but those with stenotic valves and reduces ventricular function do less well
Pulmonary hypertension is a contraindication to pregnancy because the maternal mortality rate is 30-50%
What is haemolytic disease of the newborn?
- Severe form of anaemia caused by incompatibility between maternal and foetal blood.
- Caused by passage of maternal RBC across the placenta to foetus.
- The antibodies are created in response to previous exposure to incompatible blood
Most commonly the rhesus group of antigens but also ABO and Kell and Duffy antigens
Epidemiology of haemolytic disease of the newborn
- Atypical antibodies are detected in 1.2% of pregnancies but only 0.4% are clinically relevant
- Severe haemolytic disease of the newborn affects 7-8 per 100,000 pregnancies
Pathophysiology of haemolytic disease of the newborn
IgM antibodies are produced when cells of the maternal immune system are exposed to a foreign antigen on foetal RBCs
This doesn’t affect the current pregnancy because the mothers immune system is exposed to a small amount of antigen but the immune system is sensitised for subsequent pregnancies.
This results in immune mediated haemolysis in the foetus which results in haemolytic disease of the newborn
- Most commonly caused by rhesus antibodies which are produced when a rhesus negative woman becomes pregnant by a rhesus positive father and the foetus is rhesus positive
- The rhesus incompatibility between the mother and the foetus causes immune sensitisation in the mother in the first pregnancy and destruction of foetal RBCs in future pregnancies - IgG antibodies cross the placenta and mediate this
Clinical features of haemolytic disease of the newborn
- Anaemia
- Increased erythropoiesis and hepatosplenomegaly
- Jaundice arising from hyperbilirubinaemia
- Oedema and polyhydramnios as a consequence of high output heart failure
- In severe cases foetal death can occur
Diagnosis of haemolytic disease of the newborn
- Blood group screening to detect atypical antibodies if offered at the first booking visit and 28 weeks
- Women with clinically significant antibodies are referred
Investigation for haemolytic disease of the newborn
- Antibody titres are used to guide management
- Significantly high antibodies warrants foetal genotype being determined
- To detect anaemia in at-risk pregnancies Doppler USS is used weekly to measure blood velocity in middle cerebral artery of foetus
- An anaemia foetus tries to maintain oxygen delivery by increasing cardiac output
- Blood viscosity of the foetus is also reduced because of decreased RBCs
- The combination of an increased CO and decreased viscosity results in high blood flow velocity in the middle cerebral artery
- If the velocity is >1.5x the median for gestation a sample of foetal blood is taken from the umbilical cord or hepatic vein to determine Hb concentration
Management and prognosis of haemolytic disease of the newborn
Management:
- Depends on gestation and degree of foetal compromise
- Delivery: brought forward when the risk of the foetus remaining in the womb > risk of prematurity - usually at 37-38 weeks
- Intrauterine transfusion: can be carried out weekly to treat significant anaemia but not used after 35 weeks as delivery more appropriate at that time
Prognosis:
- 50% of affected babies have normal Hb
- 25% have moderate disease requiring transfusion
- 25% have severe disease
- Survival is 84-90%
- <40% survival if cardiac failure is not reversed in utero
What risks are associated with multiple pregnancy?
- Increased risk of most pregnancy related complications such as pre-eclampsia, growth restriction and pre-term birth
- Twin-twin transfusion syndrome if a single placenta is shared
Epidemiology of multiple pregnancy
- Multiple births = 1-2% of all but proportion is increasing due to fertility treatments
- 1 in 80 naturally conceived pregnancies produce twins and 1 in 6400 produce triplets
Discuss chronionicity and amnionicity
Refers to whether a multiple pregnacy shares amniotic sac and foetal part of placenta (chorion)
- Chorionicity - can be dichorionic or monochorionic - refers to whether the foetuses have one or two placenta between them
- The chorionicity and amnionicity of monozygotic twins is determined by the time at which the zygote splits, or cleaves. If the cleavage occurs by day 3, you will have two separate blastocysts, and therefore, two sites of implantation, resulting in dichorionic-diamniotic (di-di) twins
- This can be determined using USS before 14 weeks gestation
How is chorionicity diagnosed?
USS
Dichorionic = 2 placentas (in twin pregnancy) - accounts for 80%
Monochorionic = 1 shared placenta - 20% and higher risk
Investigations during multiple pregnancies
- Combined test is used to screen for Down’s syndrome in twin pregnancies whereas nuchal thickness and maternal age are use in triplet pregnancies - both performed <14 weeks
- Serum screening for downs is used if the nuchal thickness can’t be measured
- It’s difficult to measure foetal growth in multiple pregnancy so serial ultrasound is used from 24 weeks - a size discordance of >25% is clinically significant
- Monitoring is more frequent in early stages of monochorionic pregnancies because of twin-twin transfusion syndrome so fortnightly USS are carried out from 16-24 weeks
Management of multiple pregnancies
Management:
- Managed in obstetric led units
- Monoamniotic and triplet pregnancies are referred to tertiary foetal medicine units
Delivery:
- Preterm delivery is common
- 60% twins arrive before 35 weeks and 75% of triplets
- To reduce risk of late stillbirth delivery is induced at 36 weeks
- Labour is induced for twin pregnancies when the first twin presents cephalically regardless of how the other one is presenting
- Monochorionic monoamniotic twins are the exception - they should be delivered at 32 weeks by c-section to reduce risk of cord entanglement
Incidence of multiple pregnancy
Twine 15:1000
Triplets 1:5000
Quads 1: 360 000
1 in 34 children in the UK are a twin or triplet
Cause of multiple pregnancy
- Prev. mutliple pregnancy
- Family hx
- Increasing parity
- Increasing maternal age
- Assisted reproduction
Risks to foetus in multiple pregnancy
IUGR
PTB
Cerebral palsy
Disability
Miscarriage
When does embryonic split occur in dichorionic, dizygotic twins?
Early on - at the morula stage before implantation has occurred and the the two separate blastocysts implant
When does the split occur in monochorionic diamniotic twins?
3-8 days after fertilisation
Single placenta but 2 amniotic sacs
When does the split occur in monochorionic monoamniotic twins?
8-13 days after fertilisation
Same amniotic sac, same placenta
Absence of lambda sign on USS in mutliple pregnancy indicates what?
Monochorionicity
When is delivery offered in multiple pregnancy?
37-38 weeks
What are the maternal risks of multiple pregnancy?
HG
Anaemia
Pre-eclampsia (5x risk)
Gestational DM
Antepartum and PPH
Polyhydramnios
Placenta praevia
Operative delivery
What is twin to twin transfusion syndrome?
Caused by shared circulation in monochronionic twins
Affects 8-25% of monochorionic pregnancies
80% mortality of not treated
Caused by abberant vascular anastomosies in the placenta which redistibute foetal blood from one to the other but not in the opposite direction
One twin receives too much blood and the other too little
Monitoring and treatment of twin to twin transfusion syndrome
MC twins monitored by USS every 2 weeks from 16-24 weeks
Then monitored every 3 weeks until delivery
Treatment:
- Laser ablation of placental anastamoses
- Selective foetice if the condtion is not retractable
Consequence of twin to twin transfusion syndrome
Donor: hypovolaemia, anaemia, oligohydramnios, IUGR
Recipient: hypervolaemia, polycythaemia, large bladder, polyhydramnios, cardiac overload and failure, foetal hydrop
Recipient twin is at greater risk than donor
Discuss delivery in mutliple pregnancy
Second twin is at higher risk of perinatal mortality
Usually induced at 38 weeks although many deliver before then
Foetal distress is more common so CTG is carried out - esp. after first baby has been born due to risk of foetal hypoxia in the second
Increased risk of uterine atony so oxytocin and syntometrine infusion recommended
Antenatal management of diabetes
Pre pregnancy: counselling - achievement of optimal control
Screening for retinopathy, nephropathy, heart defects
5mg folic acid due to increased risk of NTD
Antenatal: monitor glucose 4x daily, monthly HbA1c measurements (normal = <39mmol or 5.7%), dietician review
Anomaly scan: those with DM are at 5-10x increased risk of foetal anomalies depending on control
When is DM screened for in pregnancy?
24-28 weeks for those at risk: obese, previous macrosomia, FHx DM
Unless hx of GD in which case screening ASAP (@booking visit)
5678 rule
<5.6mmol/L when fasted, <7.8mmol/L after OGTT
Threshold values are lower than DM outside of pregnancy due to the risk of DM during pregnancy
Timing of delivery in mothers with DM
Some advise IOL at 38-39 weeks
Vaginal delivery preferred, CTG advised
Consider elective CS if EFW >4.5kg
Shoulder dystocia is more common in DM regardless of EFW
Sliding scale used during labour - insulin rate depends on blood glucose
What is the blood glucose range aimed for in the post partum period?
4-9mmol/L
*50% of those with GD develop T2DM over the next 25yrs
Normal BP changes during pregnancy
BP decreases until 24 weeks due to decreased systemic vascular resistance
BP increases after 24 weeks due to increased stroke volume
BP decreases again after delivery but may peak again 3-4 days PP
What is considered HTN in pregnancy?
>140/90 OR an increase of >30/>15 compared to booking visit
BP should be measured sitting or supine with a left sided tilt because the uterus can compress the IVC and give a falsely low BP reading
How can development of pre-eclampsia be predicted?
- 7x increased risk if PMHx in previous pregnancy
- Low PAPP = increased risk of pre-eclampsia
- USS uterine artery dopplers at 11-13 weeks or 22-24 weeks are predictive of early onset/ severe pre-eclampsia
Are most cases of pre-eclampsia symptomatic?
No - most are asymptomatic
Headache types associated with pre-eclampsia
Frontal headache associated with flashing lights
Oedema of which part of the body is associated with pre-eclampsia?
Face
What are the signs of pre-eclampsia?
HTN: >140/90
>0.3g proteinuria/ 24hrs
Hyperreflexia
IUGR
Management of pre-eclampsia
Cure = delivery of placenta
Oupatient monitoring is suitable if BP <160/110, no or low proteinuria and asymptomatic
Mild-moderate pre-eclampsia: <160/110 with significant proteinuria and no complications
Admission advised when proteinuria occurs:
- 4x BP measurement daily
- 24hr urine collection for protein
- 2x weekly doppler
- 2x monthly USS
If BP >160/110 - start labetolol
Management of severe pre-eclampsia
BP >160/110 and presence of significant proteinuria (>1g/ 24hrs or 2++ on urine dip)
- Involve senior midwives and obstetricians
Indications for immediate delivery:
- Worsening thrombocytopenia, worsening liver or renal function
- Severe maternal symptoms e.g. RUQ pain and derranged LFTs
- HELLP
- Eclampsia
- Foetal distress
Medication choices in pre-eclampsia
Labetolol = first line
Nifedipine if labetolol not tolerated
Methyldopa = 3rd line
If expediting delivery and <34 weeks: give steroids
What is used to treat and prevent eclamptic seizures?
Magnesium sulfate
⚠️ Can cause resp. depression - this is counteracted by calcium gluconate
Treatment is continued for 24hrs after delivery or 24hrs after last seizure
If seizures continue, give diazepam
What are the signs of magnesium sulfate toxicity?
Confusion, loss of reflexes, resp. depression and hypotension
What % of women with pre-eclampsia are affected by HELLP?
15%
25% mortality rate due to liver rupture, cerebral oedema and haemorrhage
How does pre-eclampsia cause HELLP?
HTN causes endothelial dysfunction and vasoconstriction
Vasoconstriction leads to Na+ retention and this causes vasospasm
Vasospasm reduces blood flow to liver causing injury, elevated liver enzymes and RUQ pain which is essentially hepatic angina
Low platelet levels due to endothelial injury which causes clot formation which consumes platelets
3 key symptoms of HELLP
- Epigastric or RUQ pain: liver hypoxia
- N&V
- Tea coloured urine: haemolysis
Woman presents with itching, dark urine and pale stools
On examination there are excoriation marks but no rash
Diagnosis?
Obstetric cholestasis
Typically causes itchy palms
1/3 have a FHx of obstetric cholestasis
Diagnosis of exlusion when bloods show abnormal LFTs, raised bile acids in the absence of any other cause of hepatic dysfunction
What are the blood results in obstetric cholestasis?
Bile acids: raised = most specific
LFTs: ALT raised, GGT raised
PTT increased because there is reduced fat absorption therefore less vitamin K available to make clotting factors
Liver USS needed to exclude gallstones and acute fatty liver of pregnancy
What are the risks of having obstetric cholestasis?
Vitamin K deficiency - PPH
PTB
Stillbirth
Increased risk of meconium stained liqour
Is obstetric cholestasis common?
Faily - affects 0.5-1% pregnancies
What is given to women with obstetric cholestasis?
Water soluble vitamin K
Topical menthol emollients
Ursodeoxycholic acid
90% risk of recurrence in future pregnancies
How is polyhydramnios categorised?
Single deepest amniotic pool depth
Mild: 8-11cm
Moderate: 12-15cm
Severe: >16cm
Classical appearance of an woman with polyhydramnios
Higher than expected SFH
Maternal skin stretched and shiny
Tense uterus
Difficult to palpate foetus
SOB due to enlarged uterus
Management of polyhydarmnios depending on severity
Mild/ aysmptomatic: no intervention
Indometacin: decreases fluid volume by reducing fluid made by foetal kidneys but cases premature DA closure
Amniocentesis
Volume of fluid classified at oligohydramnios?
<500mL at 32-36 weeks
Amniotic fluid index <5cm
How does rubella cause congenital defects?
Virus disrupts mitosis and retards cellular division which causes vascular damage in baby
Major malformations occur during organogenesis and severity decreases as gestation increases
Defects: sensorineural deafness, cardiac anomalies, cataracts, glaucoma, microcephaly
Can rubella vaccine be given during pregnancy
No
Risk of rubella associated defects based on gesation
<13 weeks: almost all infection, TOP offered
13-16 weeks: main issue is deafness, can be diagnosed by foetal blood sampling
>16 weeks: rarely causes defects, reassure
What are Kolpiks spots?
White spots in mouth - pathognomonic for measles
Does maternal measles infection cause congenital defects?
No but associated with foetal loss and PTB
How can anaemia be tested for in a foetus?
Peak systolic velocity in MCA via USS
- The greater the velocity the greater the chance of anaemia
What is CMV?
Common herpes virus transmitted through bodily fluids
Rates of congenital CMV infection following maternal infection
40% foetuses will be infected
90% normal at birth: 20% go on to develop minor sequelae
10% symptomatic at birth: 33% die, 67% have long term problems
Woman is in contact with someone with chicken pox - what is done?
Check if good hx of having chicken pox, if not then test VZV IgG antibodies
- If antibodies detected within 10 days of contact, reassure
- If antibodies not detected, give VZ immunoglobulin within 10 days of exposure
Foetal risks of VZV infection
If mother exposed <20 weeks 1-2% risk of foetal varicella syndrome - consider TOP
If exposed >20 weeks not associated with congenital abnormality
If exposed in 2nd or 3rd trimester: 1-2% risk of shingles in infancy
Exposed within 4 weeks of delivery 20% develop neonatal varicella syndrome which is fatal in 20% - give VZIG ASAP
How is VSV exposure in pregnancy managed?
If <20 weeks and not immune give VZIG ASAP within 10 days exposure
If >20 weeks and not immune then VZIG or aciclovir given 7-14 days after exposure (not given immediately)
Which type of herpes simplex is a problem in pregnancy?
HSV2
Neonatal risk of herpes infection
Transmission if mother has 1st degree infection during vaginal delivery
Neonatal herpes occurs during first 2 weeks - 25% confined to eyes and mouth, 75% widely disseminated and 70% die
Management: aciclovir may decrease severity and duration of primary attack if given <5 days within symptom onset
- Deliver via CS
Gold standard test for herpes?
Culture of vesicle fluid
Foetal risks of toxoplasmosis infection
Spontaneous miscarriage is common if infected in 1st trimester
If exposed <12 weeks, 17% infected and 75% chance of congenital abnormality
Management of toxoplasmosis in pregnancy
Spiramycin @ diagnosis may decrease risk of foetal infection
If foetus has infection confirmed - combination anti-toxoplasmosis therapy given: leukovarin, pyrimethamine (teratogen, do not give in 1st trimester), sulphadiazine
Pyrimethamine - antifolate so give supplement
Recommendation for future pregnancies following toxoplasmosis infection
Avoid until maternal IgM cleared - can take 12 months
Babies born to mothers with acute or chronic hep B infection shoudl recieve what within 24hrs of birth?
Hep B IgG and vaccination
Up to 95% effective in preventing neonatal HBV infection
Can hep B be transmitted via breastmilk?
No
What is group B strep?
Streptococcus agalactiae
20% women carry it vaginally
Asymptomatic
Management of maternal group B strep infection
Not routinely screened for
Women who’ve had GBS in previous pregnancy have 50% risk of recurrence - offer antibiotic prophylaxis or testing in late pregnancy then give antibiotics if positive
Swabs done at 35-37 weeks or 3-5 weeks before anticipated delivery
Discuss GBS infection in neonates
Early onset: <4 days from delivery
- 20% mortality, presents within pneumonia, sepsis of unknown origin, meningitis
Late onset: >7 days from delivery
- not associated with maternal GBS carriage, 20% mortality, 50% have neuro deficits e.g. cortical blindness, deafness
Discuss syphillis infection in pregnancy
Treponema pallidum spirochaete bacterium - causes syphilis - can cross placenta
Can cause PTB, stillbirth and congenital syphilis
- 8th nerve deafness
- Saddle nose
- Sabre shins
Management: penicillin
Epidemiology of HIV in pregnant women in UK
1/700 women giving birth are HIV+
HIV+ women have viral load and CD4 levels checked once/ trimester
Continue anti-retrovirals during pregnancy
Cabergoline to suppress lactation
If viral load <50 then can deliver vaginally
Vaccination during pregnancy
Live attenuated vaccines are contraindicated e.g. MMR, rubella, polio
Passive immunisation via specific immunoglobulin is safe e.g. VZIG
Vaccinations for travel on case by case basis
Women with a BMI of 40 are given which medication for 7 days PP?
Heparin
What is post partum thyroiditis?
Autoimmune condition causing destructive thyroiditis
Presents PP as immunity returns to normal following a period of suppresion during pregnancy
Pre-formed T4 is released = initial hyperthyroid state
Hypothyroidism develops as T4 is used up
Most recover spontaneously
If hyperthyroid state needs treatment b-blockers are used
Risk of hypothyroidism to foetus
Miscarriage, brain damage, GD
Management: contnue thyroxine - often dose is increased in pregnancy due to higher requirement
Risk of hyperthyroidism in pregnancy
IUGR, PTB, miscarriage
Management: propythiouracil in 1st trimester
Can use carbimazole but lowest dose
Radioactive iodine is contraindicated
Discuss haemolytic disease of the newborn
Severe form of anaemia cuased by incompatability between maternal and foetal blood - caused by passage of maternal RBCs across the placenta to the foetus
- Most commonly Rh group
Epidemiology: abnormal antibodies are detected in 1-2% pregnancies, 0.4% are clinically relevant
Severe HDN affects 7-8 per 100,000 pregnancies
Aetiology:
- IgM antibodies produced when cells of the maternal immune system are exposed to a foreign antigen on foetal RBCs
- Sensitisation occurs during 1st pregnancy and this causes immune mediated haemolysis in the newborn
Prevention:
- Anti-D given to Rh negative women during pregnancy to mop up any foetal RBCs in the mother’s circulation before she becomes sensitised
Clinical features:
- Anaemia
- Increased erythropoesis
- Hepatosplenomegaly
- Oedema and polyhydramnios
- Jaundice
- If severe: foetal death
Investigation:
To detect anaemia in foetus
- Anaemic foetus will increase HR to maintain o2 delivery, blood is less viscious because fewer RBCs
- This causes higher velocity blood flow in MCA detected via doppler
- If 1.5x median for gestationa. sample of foetal blood is taken from umbilical cord or hepatic vein to test Hb conc.
Management:
- Depends on gestation
- Delivery usually expedited to 37-38 weeks
- Intrauterine transfusion can be carried out weekly to treat significant anaemia but not used beyond 35 weeks as delivery more apt
Prognosis
- 50% have normal Hb
- 25% moderate disease and need tranfusion
25% severe disease: survival 84-90%
