Obstetric Complications Flashcards

1
Q

Define the different hypertensive disorders in pregnancy?

HTN
Chronic HTN
PIH
PET
Eclampsia
HELLP
A

HTN = raised BP defined by population (age, sex etc) – in pregnancy, >140/90

Chronic HTN = raised BP <20 weeks or with BP Tx

Pregnancy induced hypertension (PIH) or gestational hypertension (GH) = new hypertension >20 weeks gestation, no proteinuria

Pre-eclampsia (PET) = multisystem disorder characterised by hypertension >20 weeks gestation AND proteinuria (not 100% sensitive – not all fit these criteria)
o Proteinuria: >300mg (0.3g) protein / 24 hours (PCR > 30)

Eclampsia = seizure / convulsive episode caused by PET

HELLP syndrome = haemolysis, elevated liver enzymes + low platelets

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2
Q

Mild, moderate, severe HTN?

A

Mild 140-149 / 90 - 99
Mod 150-159 / 100-109
Severe 160 / 110

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3
Q

What is pre-eclampsia? (criteria)

How common is it?

A

> 20 weeks gestation: pregnancy-induced HTN associated with proteinuria (>0.3g/24 hours). Oedema used to be 3rd in the classic triad, but now often not included as it is not specific.

Common: ~20% admissions, commonest cause of iatrogenic early delivery.

Mild PET may affect 6% of pregnancies
Severe in 1% (eclampsia in 1-2% of PET). Leading cause maternal mortality worldwide.

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4
Q

Symptoms of pre-eclampsia?

A

May be completely asymptomatic

Headache, visual disturbance, epigastric / RUQ pain, nausea / vomiting, rapidly progressive oedema, abdominal tenderness, disorientation/confusion, small for gestational age uterus, IUD, hyper-reflexia / clonus / involuntary movements

Features of SEVERE pre-eclampsia
• HTN typically >170/110mmHg + proteinuria 
• Proteinuria dipstick ++/+++
• Headache 
• Visual disturbance
• Papilloedema
• RUQ / Epigastric pain
• Hyperreflexia
• Platelet count <100*10⁶, abnormal liver enzymes or HELLP syndrome
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5
Q

Pathophysiology of pre-eclampsia?

A

Diffuse vascular endothelial dysfunction via release of angiogenic and angiolytic factors > widespread circulatory disturbances (to liver, kidneys, CVS, CNS, placenta etc). Failed differentiation of cytotrophoblastic cells during epithelial –> endothelial transformation. Three stages occur:

  1. Abnormal placental perfusion: abnormal placentation and trophoblast invasion of the endometrium in which there is failure of vascular remodelling of the spiral arteries, therefore spiral arteries fail to become high capacitance, low-resistance vessels –> placental hypoxia and ischaemia
  2. Maternal syndrome: placental ischaemia causes widespread endothelial dysfunction (poorly understood – possibly oxidative stress mechanisms / prostaglandin imbalance / NO compounds). Increased capillary permeability increases expression of cell adhesion molecules (CAM), increases pro-thrombotic factors and platelet aggregation, and causes vasoconstriction
  3. Multisystem effects
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6
Q

What are the multisystem effects of pre-eclampsia? (go through each system)

A

o CNS: eclampsia (fits), hypertensive encephalopathy, IC haemorrhage, cerebral oedema, cortical blindness, CN palsies

o Renal: reduced GFR, proteinuria, increased serum uric acid (also in placental ischaemia), increased creatinine / K / urea, oligo / anuria, AKI (tubular / cortical necrosis)

o Liver: epigastric/RUQ pain, abnormal liver enzymes, hepatic capsule rupture, HELLP (haemolysis, elevated liver enzymes, low platelets) - emergency

o Haematology: decreased plasma volume (normally increased), haemo-contraction, thrombocytopenia, haemolysis, DIC

o CVS: pulmonary oedema (–> ARDS), PE, future hypertension, NB. CVS effects have high mortality

o Placental: IUGR, placental abruption, intrauterine death

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7
Q

What are the main maternal risks of having pre-eclampsia?

A

(Now very safe in UK):
• Eclampsia (seizures)
• Haemorrhage: placental abruption, intra-abdominal, intra-cerebral
• Cardiac Failure
• Multi-organ failure
• Maternal death (<1 in million in UK but many deaths globally)
• Long-term: subsequent high BP & complications, CV disease (e.g. CVA, IHD)

HELLP & Placental Abruption: rarer complications of HTN especially PET - variable disease(s) often seen (e.g. ELLP)
• Abruption often causes / provokes PET
• Remember FATTY LIVER (acute fatty liver of pregnancy)

Intracranial haemorrhage is the most common cause of death in women who die from hypertensive disorders of pregnancy

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8
Q

In the UK, what are most common causes of direct maternal death?

A

PET / eclampsia was 2nd biggest in 1985-7, 2012-14 dropped to 7th

  1. Thrombosis / thromboembolism
  2. Amniotic fluid embolism
  3. Haemorrhage
    4 / 5. Sepsis / early pregnancy deaths
    6/ 7. Anaesthesia / PET or eclampsia
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9
Q

What are the main fetal risks of having pre-eclampsia?

A
  • Prematurity (major cause of mostly iatrogenic early birth; 10% severe PET birth <34 weeks, 1 in 250 first pregnancy <34 weeks due to PET, 10% of all preterm births due to HTN disorders, 50% with severe PET give birth preterm)
  • IUGR (15-20% births with PET are <10th percentile)
  • Stillbirth (1 in 20 stillbirth without anomalies are associated with PET)
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10
Q

HIGH risk factors for pre-eclampsia?

A

o Hypertensive disease in previous pregnancy
o CKD
o Autoimmune disease (e.g. systemic lupus erythematosus, antiphospholipid syndrome)
o Type 1 or type 2 diabetes
o Chronic hypertension

If one of these factors - give aspirin

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11
Q

MODERATE risk factors for pre-eclampsia?

A
First pregnancy
Age ≥40 (doubles risk)
Pregnancy interval of >10 years
BMI ≥35 at first visit (doubles risk)
FHx pre-eclampsia (mother 20-25%, sibling up to 40%)
Multiple pregnancy

If 2 of these factors, aspirin is needed

Additional risk factors include: genetic abnormalities (triploidy), molar pregnancies.

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12
Q

Investigations for cases of PET?

A
o U+Es (raised creatinine, K⁺, urea), also serum uric acid (raised urate). 
o LFTs: abnormal liver enzymes
o FBC
o Coagulation screen
o USS (biometry / AFI / Doppler)
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13
Q

Aims of management for PET?

A

Protect mother from hypertensive complications (CVS, MI etc), long-term risks – does not prevent progression of PET.

Protect baby by improving condition at birth, steroids + ideal BP for growth, improved gestation (later vs earlier?).

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14
Q

What should be done for pre-eclampsia prior to a pregnancy?

A
Before pregnancy
o Assess risk + likelihood of pregnancy
o Weight reduction, stop smoking
o Review medications
o ACEI, ARB, diuretics, statins - stop and/or prepare to change
o Aspirin 75mg, start at 12 weeks (<20)
o Folate 400µg – start before pregnancy
o Discuss risks: worse BP, PET, SGA, prematurity + longer term outlooks
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15
Q

What should be done for pre-eclampsia during the pregnancy?

When to refer or admit?

A

Assess risk at booking + during 1st trimester. If BP rises 1st trimester, assess for other causes. Antenatal screening: BP, urine, maternal uterine artery doppler (MUAD).

When to refer: day case referral if any of the 3 major signs or concerning symptoms e.g. persistent headache.

Admission if: BP >170/110 (alone) or >140/90 + proteinuria, significant symptoms (e.g. headache, visual disturbance, RUQ pain), abnormal biochemistry, significant proteinuria (>300mg/day), need for antihypertensive treatment, signs of fetal compromise

Inpatient assessment: BP 4 hourly, daily urinalysis, fluid balance chart +/- collection for protein, regular bloods. Fetal surveillance: movements, CTG, USS, biometry, AFI, umbilical artery doppler

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16
Q

Main treatments for pre-eclampsia?

A

Aspirin 75mg OD (12 weeks -> birth)
• If 1 high or >1 moderate risk factor for PET

Consensus guidelines: treat BP >160/110 but many clinicians have lower threshold. Oral labetalol 1st line (NICE), nifedipine + hydralazine may also be used.

Severe Hypertension
• Stabilise then plan delivery (aim 140-150 / 80-100)
• Labetalol oral / IV
• Nifedipine oral
• Hydralazine IV (?preload)

Monitor effect (mother + baby): fluid balance (? catheter)
• Mg
• Anaesthetist + neonatalogist

Delivery = the only ‘cure’, must be stabilised beforehand

o Induction <34 weeks if severe HTN refractory to Tx or other complications necessitating delivery

o 34-36+6 weeks if mild-moderate HTN, depending on maternal and fetal condition, risk factors and services

o immediate induction (24-48 hours) if >37 weeks

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17
Q

How to look after patients with pre-eclampsia during labour / intrapartum?

A
• BP hourly or more frequently
• Control BP <150/100
• Care with fluids (80mls/hour): (plasma leaks out, lower intravascular circulating volume but adding more fluid > pulmonary oedema!!)
• Fluid balance (? Urine output)
• Monitor baby: continuous CTG
• Epidural for obstetric medications
must avoid excess fluids
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18
Q

Main management of HELLP syndrome?

A

HELLP syndrome usually managed in conjunction with PET (BP control, ultimately delivery, may require blood products where indicated, steroids for fetal development)
• Deliver if platelets <100 or ALT>80

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19
Q

Post-natal factors in pre-eclampsia? Management?

A

Post natal BP: may rise for first few days, often needs continued treatment- ET risk continuous for few days

  • Aim <140/90, reduce if <130/80
  • ACEI if hypertension for >2 weeks
  • Refer if BP still high at 6-8 weeks
  • Exclude persistent proteinuria (i.e. renal disease)
  • Lifestyle changes to continue
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20
Q

How to manage the following patients with pre-eclampsia

Mild 140-149 / 90-99
Mod 150-159 / 100-109
Severe 160/110

A

Mild: measure BP no more than 1/week, proteinuria at each visit using strip or urea/creat ratio, blood tests only as routine antenatal care

Mod: oral labetalol 1st line to keep systolic <150 and diastolic 80-100, BP at least 2/week, proteinuria at each visit, test kidney function, electrolytes, FBC, transaminases, bilirubin - do not carry out further blood tests if no proteinuria at subsequent visits

Severe; ADMIT until BP <159/109, labetalol first line as above, BP at least 4/day, daily proteinuria, blood tests at presentation then weekly: kidney, electrolytes, FBC, transaminases, bilirubin

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21
Q

Main antihypertensives for pregnancy?

A

Beta blockers (labetalol): good safety data, standard treatment, licence for use in pregnancy; uncertain risk for neonatal hypoglycaemia (babies are monitored if taken). a+b antagonist, 100mg BD starting dose - 600mg QDS. CI in asthma

Nifedipine MR & SR: good safety record, effective in pregnancy especially PET; start at modified release (MR) 10mg BD, max 40mg BD, side effects of headaches & tachycardia (may mimic impending eclampsia)

Methyldopa: centrally acting a-agonist, effective antihypertensive, extensive safety data, side-effects: hepatitis, pancreatitis, depression, haemolytic anaemia, bone marrow depression etc. Start at 250mgs BD / TDS and up to 3g (1g TDS?)

Hydralazine: vasodilator, 25mg TDS - 75mg QDS

All of the above safe in breast feeding.

Also: Prazosin (75mg)

22
Q

What is gestational diabetes? How does it occur?

A

GD = ‘Any hyperglycaemia with first onset of presentation during pregnancy’. Affects 2-4% of women.

Resistance to insulin = normal physiological response in pregnancy (induced by human placental lactogen i.e. human chorionic somatomammotophin: reduces insulin sensitivity and alters fat metabolism – releases fatty acids as alternate energy source for mother – allowing more glucose for the fetus).

Maternal blood glucose levels rise to provide for fetus, particularly in 3rd trimester. In some women: reduced ability of pancreas to produce enough insulin to overcome the insulin resistance –> gestational diabetes.

23
Q

Risk factors for GD?

A
o >35 years
o BMI >30
o Smoking
o Previous stillbirth
o Previous ‘large’ baby >4.5kg
o Previous episode gestational diabetes
o FHx TYPE 2 DIABETES (but not GD!)
o Asian, Middle East &amp; Black African ethnicity

40% of women with GD have no risk factors

24
Q

How does GD present?

A

Often asymptomatic and only discovered on screening (common diabetic symptoms of thirst, hunger, polyuria, tiredness are not particularly common, but are also seen in normal pregnancy in 3rd trimester)

25
Q

What are the risks of GD to the fetus?

A

Fetal Risks greatest when glycaemic control is poor around time of conception

o Macrosomia: store more fat than usual, defined as abdominal circumference >70 percentile

o Newborn hypoglycaemia (producing their own endogenous insulin during pregnancy to counteract hyperglycaemia of the mother: usually self-limiting but may require IV glucose)

o Type II diabetes later life + obesity in childhood

o Shoulder dystocia during delivery
o Jaundice
o Stillbirth
o To reduce risk: offer C-section 38-39 weeks (instead of 40). All should be offered C section or induction at 38 weeks, and if proven macrosomia: inform of the risks of vaginal birth

o 2x increased risk of congenital defects: congenital heart disease, respiratory distress syndrome, NTDs

  • Risks inversely related to level of control of the GD, and highest in type II, moderate in GD and lowest in type I
26
Q

What are the risks of GD to the mother?

A

o Increased risk of tears
o Increased risk of type II diabetes (50% will develop type II within 15 years, 50% of those requiring insulin will develop type II within 5 years)
o Increased risk of GD in subsequent births (30-85%); particularly if pregnancy occurs within 1 year

27
Q

What investigations are done for GD?

A

Screen of all women with a known risk factor at 24 + 28 weeks: fasting glucose or random glucose test; if +ve or suspicious, confirm with OGTT.

If previous GD, test may be done at 16-18 weeks (for early diagnosis).

o 2 hour 75g OGTT (day before test: eat, drink + exercise normally, then fast 8-14 hours overnight, following day test glucose then drink solution (usually 75g)

Normal: fasting <6, 1 hour <10, 2 hours <7.8

Impaired fasting glucose: fasting 6-7, 2 hour <7.8

Impaired glucose tolerance: fasting <7, 2 hour >7.8

Diabetes: fasting >7, 2 hour >11

Type A1: abnormal OGTT, but normal glucose levels during fasting and 2 hours after meals (usually controlled with diet & exercise)

Type A2: abnormal OGTT and high glucose during fasting and 2 hours after meals (may require pharmacological intervention)

28
Q

What treatment is available for GD? (before labour)

A

Reduces risk of congenital defects but not of C-section or perinatal mortality

  1. Glucose levels every 1-2 weeks during pregnancy
  2. Diet + exercise: low impact e.g. walking/swimming/yoga / pilates esp. if BMI >27. Regular meals with controlled fat intake (low fat not recommended in pregnancy) - complex carbs taht reduce high peaks of glucose and digested slowly, consider restricting carb. intake at breakfast. Consider low GI foods (GI <55), monitor salt, 5 fruit/veg, oily fish lean meat and polyunsaturated fats. Sufficient in 80-90% of patients
  3. If not controlled within 2 weeks consider METFORMIN (no other oral Tx suitable for pregnancy) +/- insulin (rapid acting e.g. aspart and lispro more effective than endogenous insulins in pregnancy). Recommend pumps to those not adequately controlled by MDIs, if insulin used in pregnancy, dose usually increased by 50%. Tx can usually be stopped after birth as resistance normalises, usually random glucose test (not OGTT) at 6 week checkup confirms treatment can be stopped.
29
Q

What treatment is available for GD? (during labour)

A

Glucose during labour should be monitored every hour and kept between 4-7mmol/L (consider insulin + dextrose infusion in those with type I, or poorly controlled diabetes)- sliding scale insulin

30
Q

Management of GD after birth?

A

Feeding of baby should be encouraged, to reduce risks of hypoglycaemia

Tx can usually be stopped after birth as resistance normalises, usually random glucose test (not OGTT) at 6 week checkup confirms treatment can be stopped.

Glibenclamide + metformin are safe to use while breastfeeding, other oral agents should be avoided

Some patients then go for regular type II diabetes screening (?annual)

31
Q

What is PPROM?

How common, what complications?

A

Preterm prelabour rupture of membranes (PPROM):

2% of pregnancies but around 40% of preterm deliveries.

Complications: fetal prematurity, infection, pulmonary hypoplasia, maternal: chorioamnionitis.

32
Q

Ix / Tx of PPROM?

A

Sterile speculum examination, but digital examination avoided due to infection risk. Nitrazine sticks, which detect pH change, are also sometimes used. USS may also be useful to show oligohydramnios.

Management: admit, regular obs to ensure chorioamnionitis not developing

  • oral erythromycin for 10 days
  • antenatal corticosteroids (dexamethasone) to reduce the risk of RDS, delivery considered at 34 weeks gestation (balance between increased risk of maternal chorioamnionitis and decreased risk of respiratory distress syndrome).
33
Q

What is chorioamnionitis?

How common / risks?

A

Potentially life-threatening condition to mother + fetus (can affect ~5% of all pregnancies).

Usually due to ascending bacterial infection of the amniotic fluids / membranes / placenta.

Major risk factor: preterm premature rupture of membranes exposes uterus to pathogens (however, can still occur when membranes are intact, particularly with genital mycoplasma). Associated with prolonged labour. Risk also increases with each vaginal examination performed in the last month of pregnancy, including during labour.

Can be a risk factor for premature birth, periventricular leukomalacia & cerebral palsy.

34
Q

Diagnosis of chorioamnionitis?

A

o Maternal leucocytosis, tachycardia, pyrexia
o Fetal tachycardia
o Uterine tenderness
o Foul odour of amniotic fluid

Exclusion of maternal URTI or UTI.

35
Q

Tx of chorioamnionitis?

A

Prompt delivery (via C-section if necessary) + IV Abx

Standard = ampicillin 2g IV every 6 hours + gentamicin 1.5mg/kg every 8 hours.

36
Q

What is SGA, LBW and IUGR?

How common?

A

SGA = born with birth weight <10th centile
• SGA birth = estimated fetal weight (EFW) or abdominal circumference (AC) <10th centile.
• Severe SGA = EFW or AC <3rd centile.

Low birth weight = infant with birth weight <2500g

FGR not synonymous with SGA: implies pathological restriction of genetic growth potential. Some (not all) growth restricted foetuses / infants are SGA .

FGR is more likely in severe SGA infants, and FGR may show signs of fetal compromise (abnormal Doppler studies, reduced liqor volume).

~10% pregnancies are SGA, 1/3 of these IUGR (3% pregnancies)

37
Q

Causes of SGA (small fetus)?

A
Constitutionally small (50-70% of SGA foetuses)
o Fetal size appropriate for maternal size &amp; ethnicity

Non-placental mediated growth restriction
o Structural or chromosomal anomaly
o Inborn errors of metabolism
o Fetal infection

Placenta mediated growth restriction
o Maternal factors: low pre-pregnancy weight, malnutrition, substance abuse, smoking/alcohol
o Medical conditions: pre-eclampsia, autoimmune disease (anti-phospholipid), thrombophilias, renal disease, diabetes and essential hypertension, severe anaemia

Multiple pregnancy

38
Q

What risks are associated with an SGA fetus?

A

Structurally normal SGA foetuses are at increased risk of perinatal mortality and morbidity, but most adverse outcomes are concentrated in the growth restricted group.

Studies shown that neonates defined as SGA by population-based birthweight centiles but not customised centiles are not at increased risk of perinatal morbidity or mortality.

39
Q

How is SGA / IUGR diagnosed and managed?

A

Diagnosis: USS of fetal AC or EFW.

Management: timely delivery
CTG, Doppler, USS to assess biophysical activity but there is controversy about which test or combination of tests should be used to time delivery.

Booking Assessment

If ≥3 minor risk factors: reassess at 20 weeks

If low PAPP-A (<0.4) or fetal echogenic bowel (major risk factors) refer to major risk factor pathway. If still 3 minor risk factors: uterine artery doppler at 20-24 weeks.

Abnormal (pulsatility index [PI] >95th centile and/or notching) : serial assessment of fetal size + umbilical artery Doppler from 26-28 weeks (every 14 days if normal umbilical Doppler, but more frequently if severely SGA).

Normal: assess fetal size and umbilical artery Doppler in 3rd trimester -> if severe pregnancy induced HTN, PET, unexplained APH or abruption then initiate serial assessment of fetal size and umbilical artery Doppler

If ≥1 major risk factor: consider aspirin at <16 weeks if risk factors for pre-eclampsia. Reassess at 20 weeks: PAPP-A (<0.4) or fetal echogenic bowel = major risk factors.

Serial assessment of fetal size and umbilical artery Doppler from 26-28 weeks.

Note: all women should have SFH measurements from 24 weeks as part of antenatal care. If single measure <10th centile or serial measurements showing slow/static growth > refer for USS. Women who are unsuitable for monitoring of growth by SFH measurements should have serial assessments & umbilical artery doppler from 26-28 weeks.

40
Q

What are minor risk factors for IUGR?

A
  • ≥ 35
  • IVF singleton
  • Nulliparity
  • BMI <20
  • BMI 25-34.9
  • Smoking 1-10/day
  • Low fruit intake pre-pregnancy
  • Previous pre-eclampsia
  • Pregnancy interval <6 months
  • Pregnancy interval ≥60 months
41
Q

What are major risk factors for IUGR?

A
  • > 40 years
  • > 11 cigarettes/day
  • Paternal SGA
  • Cocaine
  • Daily vigorous exercise
  • Previous SGA baby
  • Previous stillbirth
  • Maternal SGA
  • Chronic HTN
  • Diabetes with vascular disease
  • Renal impairment
  • Antiphospholipid syndrome
  • Heavy bleeding similar to menses
  • PAPP-A <0.4MoM
42
Q

What is fetal haemolytic disease?

A

HDFN = haemolytic disease of the fetus and newborn (i.e. Rhesus disease).

Alloimmune condition in fetus where maternal IgG passes through placenta: bind to antigens on fetal RBCs > haemolysis. IgG crosses placenta, IgM does not.

  • ABO
  • Anti-RhD (Rhesus disease: prophylactic RhD immunoglobulin given)
  • Anti-RhE
  • Anti-Rhc
  • Anti-Rhe
  • Anti-RhC
  • Multiantigen combinations
  • anti-Kell

Ranges from mild to very severe.

Complications include:
• Kernicterus
• Hepatoslenomegaly
• Haemolytic anaemia + liver damage (do NOT treat with iron)
• Late onset anaemia (do NOT treat with iron)
• Cerebral palsy
• Neutropaenia
• Thrombocytopaenia
43
Q

Pathophysiology of fetal haemolytic disease?

How is it diagnosed?

A
  1. Fetal-maternal haemorrhage (fetal RBCs move across placenta due to termination, ectopic pregnancy, childbirth, ruptures in placenta / trauma, medical procedures breaching uterine wall). If subsequent pregnancies have similar incompatibility – antibodies cross placenta and bind RBCs.
  2. Previous therapeutic blood transfusion
  3. Type O mother with Type A/B fetus (~15% pregnancies, of which ~3% develop haemolytic disease)

Diagnosis
• Newborn: biochemistry for jaundice, reticulocytes, erythroblasts, direct Coomb’s test
• Mother: indirect Coomb’s test
• Father: erythrocyte antigen status

44
Q

What are congenital intrauterine infections?

A

Transmitted during pregnancy (transplacentally) or during delivery (peripartum).

Toxoplasmosis
Others
• Syphilis
• Varicella-zoster virus (VZV)
• Parvovirus B19
• Listeriosis
Rubella
Cytomegalovirus (CMV)
Herpes simplex virus (HSV)
45
Q

What is toxoplasmosis and what does congenital toxoplasmosis cause?

A

Toxoplasma gondii = protozoa. Prevented by avoiding raw, undercooked and cured meats, frequent handwashing (particularly after gardening / soil), avoid cat litter.

1st trimester: increased risk of premature birth + miscarriage.

Classic triad:
• Chorioretinitis (form of posterior uveitis)
• Diffuse intracranial calcifications
• Signs of hydrocephalus e.g. enlarged head circumference

Also non-specific features of TORCH infection: seizures, jaundice, fever, thrombocytopenia, hepatosplenomegaly, lymphadenopathy, pneumonitis, purpuric rash.

2nd / 3rd trimester: subclinical or mild toxoplasmosis

Complications: epilepsy, intellectual disability, visual disabilities (chorioretinitis  increased risk of retinal lesions extends into adult years – cataracts, glaucoma)

Four Cs: Cerebral calcifications, chorioretinitis, hydroCephalus, Convulsions

46
Q

How is congential toxoplasmosis diagnosed and treated?

A

o Fetus: PCR (amniotic fluid DNA)
o Newborn: CT/MRI for intracranial calcifications/hydrocephalus/ring-enhancing lesions, specific IgM antibodies, PCR (CSF / serum DNA), ophthalmological evaluation

Treatment: mother: immediate treatment with spiramycin, fetal (confirmed or highly suspected): switch to pyrimethamine, sulfadiazine + folinic acid

Newborn: pyrimethamine, sulfadiazine + folinic acid

47
Q

What is congenital syphilis?

What are the two types?

How is it diagnosed?

How is it treated?

A

Treponema palladium: transplacental transmission from infected mother. Prevention: maternal screening in early pregnancy, nationally notifiable condition.

Early congenital syphilis (onset >2 years) and late congenital syphilis (onset >2 years)

Diagnosis: newborn & pregnant women
• Initial test: RPR or VDRL (serum)
• Confirmatory test: darkfield microscopy or PCR of lesions / body fluids

Diagnosis: fetus: repeated USS – placentomegaly, hepatomegaly, ascites & hydrops fetalis

Treatment: IV penicillin G for both pregnant women & newborns.

48
Q

What are the features of early congenital syphilis?

A
  • Hepatomegaly + jaundice
  • Rhinorrhoea with white or bloody nasal discharge (snuffles)
  • Maculopapular rash on palms & soles
  • Skeletal abnormalities (e.g. metaphyseal dystrophy, periostitis)
  • Generalised lymphadenopathy (non-tender)
49
Q

What are the features of late congenital syphilis?

A
  • Facial features: saddle nose, frontal bossing, short maxilla
  • Dental: Hutchinson teeth (notched, widely spaced teeth) & mulberry molars (poorly developed 1st molars)
  • Eyes + ears: interstitial keratitis, sensorineural hearing loss, other abnormalities
  • Skin: rhagades (perioral fissures), gummas
  • Skeletal : ‘saber shins’ (anterior bowing of tibia), painless arthritis in knees & other joints
  • Neurological: cranial nerve defects, intellectual disability, hydrocephalus

Hutchinson’s triad: interstitial keratitis, sensorineural hearing loss, Hutchinson teeth

50
Q

What is congenital / newborn listeriosis?

What can it cause?

A

Listeria monocytogenes, prevented by avoiding soft cheeses, food & water safety – nationally notifiable condition. Vertical transmission during pregnancy or delivery.

Intra-uterine transmission: increased risk of premature birth and miscarriage
• Early-onset syndrome: granulomatosis infantispectica
• Severe systemic infection: disseminated abscesses, which may develop in any organ system.
• Most common findings: respiratory distress syndrome & skin lesions
• May be associated with signs of meningitis

Transmission during birth or postnatally (contact with mother or environment
• Late-onset syndrome (5 days > 3 weeks after birth): listeria meningitis / encephalitis

51
Q

How is listeria diagnosed and treated?

A

Diagnosis: blood or CSF cultures (pleocytosis)
Treatment: IV ampicillin & gentamicin (both pregnant and newborns)

52
Q

What is congenital / perinatal varicella?

A

Varicella-zoster virus (VZV) seroprevalence ~95%, most mothers already have immunity, rare in newborns.

Transmission vertical during pregnancy or delivery, or postnatally from infected adults. Prevention: immunisation of seronegative women before pregnancy, VZIG in pregnant women without immunity within 10 days of exposure. Nationally notifiable condition.

Congenital varicella syndrome (onset during 1st & 2nd trimester)
• Hypertrophic scars (cicatrical skin lesions)
• Limb defects (e.g. hypoplasia)
• Ocular defects (e.g. chorioretinitis, cataracts, micropthalmus)
• CNS defects e.g. cortical atrophy, seizures, intelectual disability
• ~30% mortality rate

Neonatal varicela
• Mild infection (maternal exanthem > 5 days before birth)
• Severe infection (maternal exanthem <5 days before birth): haemorrhageic exanthem, encephalitis, pneumonia, or congenital varicella syndrome

Diagnosis
• Newborn & pregnant women: usually clinical based on appearance of skin lesions (DFA / PCR of fluid collected from blisters or CSF, serology)
• Fetus: PCR for VZV DNA (fetal blood, amniotic fluid) and USS to detect abnormalities

Treatment
• Pregnant women or newborns with severe infection: acyclovir
• Post-exposure prophylaxis in newborns if mother displays symptoms <5 days before delivery  IgG antibodies (varicella-zoster immunoglobulin or VZIG)
• Breastfeeding encouraged for possible protective effect of antibodies

Congenital Parvovirus B19

~5% incidence of acute parvovirus B19 infection in pregnancy: especially high in daycare workers and primary school teachers. Transmission: transplacental transmission from infected mother. Prevention = hand hygiene.

  • Severe anaemia & possibility of fetal hydrops
  • Fetal demise & miscarriage or stillbirth in up to 10% of cases (risk is highest in the 1st or 2nd trimester).
  • Most intrauterine infections do not results in fetal developmental; defects.

Diagnosis: seronegative pregnant woman: serologic assays for IgG and IgM against parvovirus B19
• Positive IgG & negative IgM: maternal immunity (reassurance)
• Negative IgG & negative IgM: no immunity (counselling)
• Positive IgG & IgM: acute infection (refer to specialist)
• Negative IgG & positive IgM: very recent infection (refer to specialist) or false positive (repeat testing)

Fetus: PCR (amniotic fluid or blood), in suspected hydrops fetalis: Doppler USS of fetal vessels

Treatment: intrauterine blood transfusion in cases of severe fetal anaemia

Congenital Rubella
Rubella virus: rare due to vaccination. Immunisation of seronegative women before pregnancy. Nationally notifiable condition: suspected congenital rubella syndrome reported.

Risk of congenital rubella syndrome
• 1st trimester (period of organogenesis): especially from 1-11 weeks gestation: 90% risk
• Infection between 16-20 weeks  very low risk <1%
• Infection >20 weeks – no documented cases of congenital rubella syndrome

Miscarriage, preterm birth & fetal growth restriction (especially if 1st trimester infection)

Congenital rubella syndrome = antenatal manifestation of intrauterine rubella (triad)
• Cataracts (later in life other eye problems may manifest e.g. glaucoma, salt & pepper retinopathy)
• Cochlear defect: bilateral sensorineural hearing loss
• Cardiac defect: most common defects are patent ductus arteriosus & pulmonary artery stenosis

Additional non-specific features
• Early: hepatosplenomegaly, jaundice, haemolytic anaemia, thrombocytopenia, petechiae & purpura (blueberry muffin rash), transient meningitis and/or encephalitis, pneumonia.
• Late: CNS defects (microcephaly, intellectual disability, panencephalitis), skeletal abnormalities, endocrine disorders (e.g. diabetes, thyroid dysfunction), vascular disease, immune defects

Diagnosis
• Newborn & pregnant women: PCR for rubella RNA (throat swab, CSF), serology (IgM antibodies, IgG in abnormally high or persistent concentrations), viral culture (nasopharynx, blood)
• Fetus: IgM serology (chorionic villi, amniotic fluid), PCR for rubella RNA (chorionic villi, amniotic fluid)

Treatment: intrauterine infection <16 weeks = counselling for termination(?), >16 weeks reassure. Congenital rubella syndrome: supportive care (based on individual disease manifestations) and surveillance (including monitoring for late-term complications)

Triad congenital rubella syndrome: Cataracts, Cochlear defect, Cardiac abnormality

Congenital CMV
Cytomegalovirus = member of the herpesvirus family. ~1% live births in US. Transplacental transmission from infected mother or newborn transmission during birth or postnatal transmission via breastmilk. Prevention = frequent handwashing (especially after changing / bodily secretions of children, avoidance of food sharing / kissing small children).

  • 90% with subclinical infection (~10% of these develop at least some late complications, especially hearing loss).
  • 10% symptomatic at birth (~70-80% of these develop late complications)

Fetal Infection
• Increased risk fetal demise
• Intrauterine growth restriction
• Oligohydramnios or polyhydramnios, placental abnormalities
• USS signs: periventricular calcifications, hyperechogenic foci (bowel, liver & ascites), hydrops

Complications of Fetal & newborn infection
• CNS: abnormalities on brain imaging in 70% symptomatic infants (e.g. periventricular calcifications), hydrocephalus, intraventricular haemorrhage, microcephaly
• Sensorineural hearing loss: ~30%
• Chorioretinitis ~10%
• Non-specific findings (similar to other TORCH infections): petechiae & purpura (blueberry muffin rash), hepatosplenomegaly and jaundice, small for gestational age (SGA), seizures, lethargy, poor suck, haemolytic anaemia, thrombocytopenia, pneumonia
• Late complications: hearing loss, vision impairment, psychomotor retardation, intellectual disability & dental abnormalities

Diagnosis: newborn or pregnant women: IgM antibodies (blood), viral culture or PCR for CMV DNA (urine, saliva). Fetus: viral culture or PCR (amniotic fluid), IgM antibodies (blood)

Treatment
• If detected <12 weeks, consider termination. If 12-20 weeks, prenatal diagnosis required (usually RT-PCR of amniotic fluid). If >20 weeks, no action required.
• Fetus: intrauterine blood & platelet transfusions for severe anaemia & thrombocytopenia
• Pregnant women: no treatment recommended: ganciclovir etc. have potential teratogenic effects & known toxicity profile.
• Newborns, supportive therapy (fluid & electrolyte imbalances, anaemia and thrombocytopenia, seizures, secondary infections etc.)

Note: congenital toxoplasmosis may develop similar symptoms to congenital CMV infection

Herpes Simplex in Newborn

Primarily herpes simplex virus 2 (HSV-2), in rare cases, HSV-1. Primary HSV infection in genital tract of mother leads to perinatal transmission at birth: ~30% transmission rate if the mother has not yet undergone seroconversion at the time of delivery. Intrauterine infection is rare. Prevention: if history of HSV lesions known, antiviral therapy (acyclovir) beginning at 36 weeks of gestation. C-section in women with active genital lesions or prodromal symptoms (e.g. burning, pain).

Intrauterine infection (~5% cases):
• Fetal demise, preterm birth, very low birth weight
• Microcephaly, hydrocephalus & other CNS defects
• Microphthalmia: eye damage & chorioretinitis
• Vesicular skin lesions

Perinatal (85% of cases) and postnatal transmission (10% cases)
• Skin, eye & mouth disease (~45%): vesicular skin lesions, keratoconjunctivitis  cataracts & chorioretinitis, vesicular lesions of the oropharynx
• CNS disease (~30%): meningoencephalitis (e.g. fever or low temperature, lethargy, irritability, poor feeding, seizures, bulging fontanelle), possibly vesicular skin lesions
• Disseminated disease (~25%): similar findings to sepsis with involvement of organs (e.g. liver, lungs, CNS, heart, adrenals, bone marrow & blood, kidneys, GI tract), vesicular skin lesions, which may appear late in the disease course

Diagnosis: newborn & pregnant women typically clinical diagnosis, standard: viral culture from skin lesions, conjunctiva or oro/nasopharynx, rectum, alternative: PCR (CSF, blood)

Treatment
• Neonates & pregnant women: IV acyclovir or valaciclovir
• Neonates: supportive therapy, fluid & electrolyte imbalances, SIRS & septic shock, seizures, secondary infections etc.

  • Consider HSV in infants up to 6 weeks of age with vesicular skin lesions, symptoms of meningitis / encephalitis or persistent fever & negative cultures. High index of suspicion is warranted in neonatal HSV. Skin, eye & mouth disease has good prognosis if detected and treated early.