Obstretrics Flashcards

1
Q

What are common symptoms for pregnant women (antenally)?

A
  • Nausea
  • Heartburn
  • Constipation
  • SOB
  • Dizziness
  • Swelling
  • Backache
  • Abdominal discomfort
  • Headache
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2
Q

What kind of advice/education can you give women antenatally?

A
  • Provide information regarding the risks of smoking, alcohol and drug use during pregnancy
  • Provide support through smoking cessation programmes
  • Help with alcohol and drug problems may require specialist support (e.g. perinatal mental health teams)
  • Parentcraft education (e.g. NCT) is a form of formal group discussion allowing couples to discuss issues relating to pregnancy, labour, delivery and care of the newborn
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3
Q

What are the main risks of smoking in pregnant women?

A
  • FGR
  • Preterm labour
  • Placental abruption
  • Intrauterine foetal death
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4
Q

What antenatal care is done in the first trimester?

A
  • The first interaction with the health services is the booking visit
  • A midwife will take a detailed history, examine the woman and perform a series of routine investigations
  • If risk factors are identified, the woman may be referred to the hospital obstetric clinic or other specialist services
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5
Q

Describe height and weight assessment of the woman in antenatal care?

A
  • Height and weight should be recorded at the booking visit
  • If the BMI is > 35, it is recommended that the women is reviewed by an obstetric consultant or another healthcare professional that can provide advice on increased pregnancy risks
  • NOTE: there are differences in the recommended weight increase in pregnancy depending on the baseline BMI of the woman
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6
Q

What are some general pregnancy advice regarding food? (RCOG Guidelines)

A
  • Do NOT eat for two - maintain your normal portion size and try and avoid snacks
  • Eat fibre-rich foods such as oats, beans, lentils, grains, seeds, fruit and vegetables as well as whole grain bread, brown rice and pasta
  • Base your meals on starchy foods such as potatoes, bread, rice and pasta, choosing whole grain where possible
  • Restrict intake of fried food, drinks and confectionary high in added sugars, and other foods high in fat and sugar
  • Eat at least 5 portions of a variety of fruit and vegetables each day
  • Dieting in pregnancy is NOT recommended but controlling weight gain in pregnancy is advocated
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7
Q

What is some general exercise advice?

A
  • Aerobic and strength conditioning exercises in pregnancy are considered beneficial and safe
  • May help recovery following delivery, reduce back and pelvic pain during pregnancy and contribute to overall wellbeing
  • Avoid contact sports
  • Pelvic floor exercises during pregnancy may reduce the risk of urinary and faecal incontinence in the future
  • It is safe to resume exercise after delivery once the woman feels comfortable
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8
Q

Describe breastfeeding education

A
  • WHO recommends:
    • Initiation of breastfeeding within an hour of birth
    • Exclusive breastfeeding for the first 6 months
    • Continued breastfeeding beyond 6 months at least up to 2 years of age
  • Early education about breastfeeding is advocated to improve uptake and to engage women with breastfeeding services
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9
Q

What are the options for pregnancy care?

A
  • Home Birth
    • ADVANTAGES: familiar surroundings, no interruption of labour to go to hospital, no separation from family members, continuity of care
    • DISADVANTAGES: 45% of first-time mothers are transferred to hospital, poor perinatal outcome is twice as likely for home births, limited analgesic options
  • Midwifery Units or Birth Centres
    • ADVANTAGES: continuity of care, fewer interventions, convenient location
    • DISADVANTAGES: 40% of nulliparous women require transfer to a hospital birth centre, limited access to analgesic options
  • Hospital Birth Centre
    • ADVANTAGES: Midwives provide care during labour but doctors are available should the need arise
    • DISADVANTAGES: lack of continuity of care, greater likelihood of intervention
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10
Q

Describe Antenatal Urine Tests

A
  • An MSU should be sent for culture and sensitivity at the booking visit as a screening test
  • Urinalysis is performed every antenatal visit
  • Urine is screened for:
    • Protein - detect renal disease or pre-eclampsia
    • Persistent Glycosuria - pre-existing diabetes or gestational diabetes
    • Nitrites - detect UTIs
      • If nitrites are detected, an MSU is sent for MC&S to detect asymptomatic bacteriuria
      • Treatment will be initiated if a positive culture is found
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11
Q

What is asymptomatic bacteriuria associated with?

A
  • Increased risk of preterm delivery

- Increased risk of pyelonephritis during pregnancy

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12
Q

How does blood pressure change in pregnancy and what does BP measurement in first trimester enable?

A
  • Blood pressure falls a small amount in the first trimester
  • It will rise to pre-pregnancy levels by the end of the second trimester
  • Measurement of BP in the first trimester also allows identification of previously undiagnosed chronic hypertension
    • This allows early initiation of treatment (antihypertensives and aspirin)
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13
Q

What are the booking tests in pregnancy?

A
  • FBC: Haemoglobin, platelet count, mean cell volume
  • MSU: Asymptomatic bacteriuria
  • Blood group and antibody screen: Rhesus status and atypical antibodies
  • Haemoglobinopathy screening: Screening is based on Family Origin Questionnaire and blood test results
  • Infection screen: Hepatitis B, syphilis, HIV and rubella status
  • Dating scan and first trimester screening: Accurate pregnancy dating with provision of risk assessment for trisomy 21, 18, 13 and identification of major congenital anomalies
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14
Q

What is the purpose of FBC in booking bloods?
What is anaemia in pregnancy defined as?
What are additional investigations?

A
  • Allows identification of anaemia
  • NOTE: anaemia in pregnancy is defined as:
    • FIRST trimester < 110 g/L
    • SECOND and THIRD trimesters < 105 g/L
    • POSTPARTUM < 100 g/L
  • If anaemia is detected, MCV should be examined to identify the likely cause
  • Additional investigations include B12, folate or iron studies
  • f iron deficiency anaemia, a trial of oral iron should be considered (an increase in Hb at 2 weeks suggests positive response)
  • Women with a known haemoglobinopathy should have serum ferritin checked and offered oral supplements if ferritin < 30 mcg/L
  • FBC may show low platelets (may be due to ITP)
  • Gestational thrombocytopaenia rarely present in the first trimester
    • NOTE: it’s more common > 28 weeks
    • So, a low platelet count in the first trimester warrants further investigation
  • A baseline platelet count is also useful later in pregnancy if the patient is suspected of having developed pre-eclampsia or HELLP syndrome
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15
Q

Why is Blood Group requested in booking bloods?

A
  • Mainly to identify Rhesus D-negative women
  • These women should be informed about the risks of rhesus isoimmunisation and sensitisation from a RhD-positive baby
  • Anti-D immunoglobulin is administered (ideally < 72 hours) in cases of potential sensitising events (e.g. CVS, amniocentesis, trauma)
  • In pregnancies < 12 weeks, anti-D prophylaxis is only indicated if:
    • Ectopic pregnancy
    • Molar pregnancy
    • Therapeutic TOP
    • Uterine bleeding that is repeated, heavy or associated with abdominal pain
  • Minimum dose of anti-D = 250 IU
  • Women who are RhD-negative are offered prophylactic anti-D at 28 weeks
    • This can be done as a single large dose at 28 weeks
    • Or two doses at 28 and 34 weeks
  • RhD-negative mothers will receive anti-D postpartum once the baby has been confirmed as being RhD-positive on cord blood testing
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16
Q

How is gestational diabetes detected in booking bloods?

A
  • Women with previous GDM should be offered a glucose tolerance test or random blood glucose in the first trimester
  • This hopes to identify pre-existing diabetes that may have developed since the previous pregnancy
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17
Q

Describe thalassaemia

A
  • Autosomal recessive
  • Alpha chains are produced by FOUR genes, two on each chromosome 16
  • Severity of the disease depends on the number of alpha globin genes that are mutated
  • Beta chains are produced by TWO genes, one on each chromosome 11
  • Screening for thalassemia is offered to ALL pregnant women at the booking visit using the Family Origin Questionnaire (FOQ) and/or FBC results
  • Those deemed at high risk will be referred to a foetal medicine unit to discuss options for more invasive testing
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18
Q

Describe sickle cell screen

A
  • Carrier rate of sickle cell trait (HbAS) is 1 in 10 in Afro-Caribbean people
  • Carrier frequency of haemoglobin C trait is around 1 in 30
  • HbSS is the most serious form with patients suffering chronic haemolytic anaemia and acute sickle cell crises
  • People with HbSC have a milder features but are still at risk of sickle cell crises
  • Partners should also be tested if at high risk
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19
Q

Describe First Trimester Infection Screen

A
  • Rubella
    • The screening programme for rubella immunity has been stopped because the levels of rubella in the UK are so low thanks to MMR
    • If a woman is identified as not being immune, they should be advised to avoid contact with individuals known to be currently infected
    • They should be offered the MMR vaccination following delivery
  • Syphilis
    • In pregnancy, it can cause miscarriage or stillbirth
    • Women are routinely screened for syphilis
  • Hepatitis B
    • Routinely screened in pregnancy to reduce infant infection
    • Without preventative measures, 90% of babies born to women with hepatitis B will contract the virus
    • If a baby is born to a woman with active hepatitis B, the infant should receive:
    • Hepatitis B vaccine
    • One dose of hepatitis B immunoglobulin within 12 hours
    • This confers 95% protection
    • Additional doses of hepatitis B vaccine will be needed at 1 and 6 months
  • Hepatitis C
    • NOT routinely screened
    • May be offered to women at high risk (e.g. IVDU, HIV)
  • HIV
    • Interventions to minimise transmission include:
      • Initiation of ART by 24 weeks if naïve
      • Planned elective C-section if viral load > 400 copies/mL at 36 weeks
      • Exclusive formula feeding from birth
    • Women who decline initial screening should be offered screening again at 28 weeks
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20
Q

Describe Ultrasound for First Trimester Dating and Screening

A
  • First trimester ultrasound is important for:
    • Dating
    • Identification of multiple pregnancies
    • Screening for trisomies
    • Examination of the foetus for gross anomalies (e.g. anencephaly, cystic hygroma)
  • Best performed between 11+3 to 13+6 weeks
    • Crown-Rump Length (CRL) will be used to date the pregnancy during this phase
    • CRL will be expected to be 45-84 mm in this time
  • From 14-20 weeks, the head circumference is used to date the pregnancy
  • Beyond 20 weeks, genetic and environmental factors cause variability in foetal size so dating by ultrasound becomes progressively less accurate
  • First trimester screening involves:
    • Measurement of nuchal translucency (NT)
      • Median if CRL 45 mm = 1.2 mm
      • Median if CRL 84 mm = 1.9 mm
    • Measurement of maternal b-hCG and PAPP-A (pregnancy-associated plasma protein A)
      • Trisomy 21: High b-hCG, low PAPP-A
      • Maternal age
  • Using an algorithm taking into account the above three parameters, detects 90% of trisomy 21
  • The false-positive rate can be reduced by additionally examining the nasal bone, ductus venosus flow and tricuspid flow
  • Screening can also take place between 14-20 weeks using maternal biomarkers:
    • Alpha-fetoprotein
    • hCG
    • Unconjugated oestriol
    • Inhibin A
  • NOTE: newer techniques like non-invasive prenatal testing are coming to the forefront
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21
Q

What does NICE recommend for women at high risk of pre-eclampsia?

Which women are at high risk of pre-eclampsia?
What are moderate risk factors?

A
  • 75 mg aspirin everyday from 12 weeks to delivery
  • Women at HIGH risk:
    • High BP during previous pregnancy
    • Chronic kidney disease
    • Autoimmune diseases such as SLE and antiphospholipid syndrome
    • DM
    • Chronic hypertension
  • Women with 2 or more moderate risk factors should also start aspirin
  • Women at moderate risk:
    • Primiparity
    • Advanced maternal age (> 40 years)
    • Pregnancy interval of more than 10 years
    • BMI > 35 at booking visit
    • Family history of pre-eclampsia
    • Multifoetal pregnancy
  • ALL women should be screened at every antenatal visit for pre-eclampsia by measurement of blood pressure and urinalysis for protein
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22
Q

Which type of women are at risk of preterm birth

A
  • Previous preterm birth
  • Previous late miscarriage
  • Multifoetal pregnancies
  • Cervical surgery (e.g. cone biopsy)
  • These women may be offered serial cervical length screening (with or without monitoring foetal fibronectin)
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23
Q

From when does NICE recommend that SFH measurements should be made at every appointment?

A
  • NICE recommend that SFH measurements should be performed at every antenatal appointment from 24 weeks
  • If there are concerns of slow or arrested foetal growth, an ultrasound scan should be performed
  • Typically, a dating scan is offered at the end of the first trimester and an anomaly scan at 20-22 weeks, but no further growth assessment unless clinically indicated
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24
Q

Describe vitamin D screening

A
  • NO routine screening
  • Those at risk (e.g. obesity, skin colour) may be given vitamin D supplementation (oral cholecalciferol or ergocalciferol)
  • NICE recommends that ALL pregnant and breastfeeding women should be advised to take 10 µg of vitamin D supplements daily
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25
Q

Describe the Anomaly scan in Second Trimester Care

A
  • Carried out at 20-22 weeks
  • Mainly assessed foetal anatomy
  • Conditions that may be identified:
    • Spina bifida
    • Major congenital anomalies
    • Diaphragmatic hernia
    • Renal agenesis
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26
Q

What are the criteria for diagnosis and risk factors for gestational diabetes mellitus (Second Trimester Care)?

A
  • Risk-based screening available in the UK
  • Criteria for diagnosis of GDM:
    • Fasting plasma glucose > 5.6 mmol/L
    • 2-hour plasma glucose > 7.8 mmol/L
  • Risk Factors
    • Previous GDM
    • Previous macrosomia
    • Raised BMI
    • First-degree relative with diabetes
    • Asian, black Caribbean or Middle-Eastern origin
  • If risk factors are present, the woman should be offered a 2-hour 75 g oral glucose tolerance test (OGTT) at 24-28 weeks
  • Women with a previous history of GDM should have an OGTT at 16-18 weeks and then a repeat should be performed at 24-28 weeks
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27
Q

What is the Barker Hypothesis?

A
  • There is an association between reduced foetal growth and increased susceptibility to several adult diseases (e.g. coronary heart disease, stroke and diabetes)
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28
Q

What are the two ways of measuring foetal growth?

A
  • Externally using a tape measure to assess uterine size from the superior edge of the pubic symphysis to the uterine fundus
  • Using ultrasound to measure specific parts of the foetus and calculating estimated foetal weight (EFW)
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29
Q

How is foetal size described?

A
  • In terms of its size for gestational age and is presented on centile charts (NOTE: these vary depending on the population)
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30
Q

What is SGA?

A
  • Small for Gestational Age
  • A foetus < 10th centile
  • Many SGA foetuses may be constitutionally small (they have reached their growth potential)
  • However, some SGA foetuses may have failed to reach their full growth potential - this is foetal growth restriction (FGR)
    • This is associated with significant increased risk of perinatal morbidity and mortality
    • Growth-restricted foetuses are at increased risk of intrauterine hypoxia/asphyxia
    • Therefore, they are more likely to be stillborn or have features of hypoxic ischaemia encephalopathy (HIE)
      • E.g. seizures, multi-organ failure
    • Other complications that they are at increased risk to in the neonatal period:
      • Hypoglycaemia
      • Hypothermia
      • Infection
      • Necrotising enterocolitis
    • Adult consequences: hypertension, cardiovascular disease and diabetes
  • IMPORTANT: not all growth-restricted foetuses will be SGA - some may have a birthweight that is within the normal range for gestation but they may still have failed to reach their full growth potential
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31
Q

What are determinants of foetal growth?

A
  • Foetal growth is dependent on adequate delivery to, and transfer of nutrients and oxygen across, the placenta
  • The placenta relies on appropriate maternal nutrition and placental perfusion
  • Foetal hormones that affect metabolic rate, growth of tissues and maturation of individual organs are also important (e.g. insulin-like growth factors (IGF) is important in coordinating a precise and orderly increase in growth through late gestation)
  • Insulin and thyroxine are required throughout late gestation
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32
Q

What does foetal hyperinsulinaemia lead to for the foetus?

A
  • Results in foetal macrosomia and excessive fat deposition
  • This can lead to complications such as:
    • Stillbirth
    • Shoulder dystocia
    • Neonatal hypoglycaemia
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33
Q

What are genetic influences (from the foetus itself) on foetal growth?

A
  • Chromosomal defects
    • (e.g. Patau syndrome (trisomy 13) and Edward’s syndrome (trisomy 18))
  • Sex
    • (Males have a higher birthweight)
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34
Q

What are foetal epigenetic influences of foetal growth?

A
  • These are modification of DNA which occur without any altering of the underlying sequence
  • Genomic imprinting is an epigenetic process that silences one parental allele
  • Evidence suggests that genes that are paternally expressed promote growth, whereas maternally expressed genes suppress growth
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35
Q

How does infection in foetus affect foetal growth?

A
  • Infections such as CMV, Toxoplasmosis and syphilis have been implicated in FGR
  • If a foetus is found to be very small on USS, it is common to test maternal blood for antibodies to these infections and compare it with the results at booking to check whether the mother may have seroconverted during pregnancy (i.e. acute infection)
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36
Q

What are maternal influences of foetal growth?

A
  • Maternal height
  • Pre-pregnancy weight
  • Age
  • Ethnicity
  • Increasing parity (associated with increased birthweight)
  • Teenage pregnancy (associated with FGR)
  • Smoking, alcohol and recreational drug use (LBW)
  • Cocaine (associated with spontaneous preterm birth, LBW and small head circumference)
    • Placental abruption is also associated with cigarette smoking and recreational drug use
  • Chronic maternal disease (usually those that affect placental function or result in maternal hypoxia)
    • E.g. hypertension, cystic fibrosis, cyanotic heart disease
    • Maternal thrombophilia
    • Hypertension can lead to placental infarction
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37
Q

What is placental insufficiency?
What are its causes?
What placental factors can affect foetal growth?

A
  • Placental insufficiency occurs when there is inadequate transfer of nutrients and oxygen across the placenta to the foetus
  • Causes include:
    • Poor maternal uterine artery blood flow
    • Thicker placental trophoblast barrier
    • Abnormal foetus villous development
  • Placental infarction
  • Acute premature separation (e.g. in placental abruption)
  • Antepartum haemorrhage
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38
Q

What four shunts ensure that oxygenated blood from the placenta is delivered to the foetal brain?

A
  • Umbilical circulation
  • Ductus venosus
  • Foramen ovale
  • Ductus arteriosus
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39
Q

What does umbilical circulation do?

A
  • Carries foetal blood to and from the placenta for gas and nutrient exchange
  • Umbilical arteries arise from the caudal end of the dorsal foetal aorta
  • They carry deoxygenated blood from the foetus to the placenta
  • The umbilical vein returns oxygenated blood from the placenta to the foetal liver
  • Usually there are:
    • 2 x foetal arteries
    • 1 x foetal vein
  • A small proportion of blood is used to oxygenate the liver, but most of it will bypass the liver via the ductus venosus and joins the IVC
  • Deoxygenated blood returning from the foetal head and lower body flows through the right side of the heart into the pulmonary artery
  • It will then bypass the lungs and enter directly into the descending aorta via the ductus arteriosus
  • This means that deoxygenated blood from the right ventricle will pass down the aorta and enter the umbilical arterial circulation to be returned to the placenta for oxygenation
  • Before birth, the ductus arteriosus remains patent due to the production of prostaglandin E2 and prostacyclin (local vasodilators)
  • Premature closure of the ductus arteriosus can be caused by COX inhibitors
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40
Q

What happens to the umbilical circulation at birth?

A
  • Cessation of umbilical blood flow causes cessation of flow into the ductus venosus
  • This leads to a fall in pressure in the right atrium
  • Which causes the closure of the foramen ovale
  • Ventilation of the lungs opens the pulmonary circulation, causing a rapid fall in pulmonary vascular resistance
  • This dramatically increases pulmonary circulation
  • Ductus arteriosus closes within a few days of birth
  • Sometimes, the transition from foetal to adult circulation is delayed, usually because the pulmonary vascular resistance fails to fall despite adequate breathing
  • This is called persistent foetal circulation and results in LEFT-to-RIGHT shunting of blood from the aorta through the ductus arteriosus into the lungs
  • The baby will be cyanosed and can suffer from life-threatening hypoxia
  • This delay in closure of the ductus arteriosus is most commonly seen in preterm infants (< 37 weeks)
  • It results in congestion of the pulmonary circulation and a reduction in blood flow to the GI tract and brain
    • It is also implicated in the pathogenesis of necrotising enterocolitis and intraventricular haemorrhage
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41
Q

Describe central nervous system development in a foetus

A
  • Neural development is one of the EARLIEST systems to start developing and one of the LAST to be completed
  • It begins as a simple neural plate that folds to form a groove then a tube (initially open at each end)
  • Failure of closure of these open ends leads to neural tube defects
  • Later development of the foetal brain involves elaborate folding of the neurocortex (mainly in the 2nd half of pregnancy)
  • There is a rapid increase in grey matter in the last trimester
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42
Q

Describe resipratory system development in a foetus

A
  • The lungs first appear as an outgrowth from the primitive foregut at about 3-4 weeks post-conception
  • By 4-7 weeks, epithelial tube branches and vascular connections are forming
  • By 20 weeks, the conductive airway tree and parallel vascular tree is well developed
  • By 26 weeks, type I and type II epithelial cells are beginning to differentiate
  • By 30 weeks, surfactant production has started
  • Up to delivery, dilatation of the airspaces, alveolar formation and maturation of surfactant continues
  • In utero the foetal lungs are full of fluid
  • At birth
    • Production of this fluid ceases
    • Fluid is absorbed
    • Adrenaline appears to play a major role in this process
    • The clearance of fluid and the onset of breathing leads to a fall in pulmonary pressure and a rise in pulmonary blood flow
    • A consequent increase in left atrial pressure causes closure of the foramen ovale
  • Surfactant prevents the collapse of small alveoli during expiration by lowering surface tension
  • The main phospholipid in surfactant is phosphatidylcholine (lecithin) which accounts for 80% of total phospholipid
  • Production of phosphatidylcholine is enhanced by:
    • Cortisol
    • Growth restriction
    • Prolonged rupture of membranes
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43
Q

In what condition is surfactant production delayed?

A
  • Maternal diabetes mellitus
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44
Q

What does inadequate surfactant in developing fetus lead to?

A
  • Poor lung expansion and poor gas exchange
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45
Q

What happens to infants that are born preterm before producing enough surfactant?

A
  • If infants are delivered preterm (before they produce enough surfactant) they will develop respiratory distress syndrome (RDS)
  • This usually presents within the first few hours of life with signs of respiratory distress (e.g. tachypnoea and cyanosis)
  • This occurs in 80% of infants born at 23-27 weeks
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46
Q

What are the acute complications of RDS?

A
  • Hypoxia/asphyxia
  • Intraventricular haemorrhage
  • Necrotising enterocolitis
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47
Q

How can incidence and severity of RDS be reduced?

A
  • Administering steroids antenatally to mother at risk of preterm delivery
  • The steroids will cross the placenta and stimulate premature release of stored foetal pulmonary surfactant in the foetal alveoli
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48
Q

Describe foetal breathing movements

A
  • Several intermittent foetal breathing movements (FBM) occur in utero especially during REM sleep
  • These movements help maintain a high level of lung expansion that is essential for normal lung growth and maturation
  • During the apnoeic episodes in between FBM, active laryngeal constriction opposes lung recoil by preventing the escape of lung liquid via the trachea
  • Prolonged absence or impairment of FBM is likely to result in reduced mean lung expansion and can lead to hypoplasia of the lungs
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49
Q

What are causes of pulmonary hypoplasia?

A
  • Oligohydramnios
  • Decreased intrathoracic space (e.g. diaphragmatic hernia)
  • Chest wall deformities
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50
Q

Describe alimentary system development in a foetus

A
  • The primitive gut consists of the foregut, midgut and hindgut
  • It is suspended by a mesentery through which the blood supply, lymphatic and nerves reach the gut parenchyma
  • The foregut endoderm gives rise to:
    • Oesophagus
    • Stomach
    • Proximal half of duodenum
    • Liver
    • Pancreas
  • The midgut endoderm gives rise to:
    • Distal half of duodenum
    • Jejunum
    • Ileum
    • Caecum
    • Appendix
    • Ascending colon
    • Transverse colon
  • The hindgut endoderm gives rise to:
    • Descending colon
    • Sigmoid colon
    • Rectum
  • Between weeks 5-6, due to a rapidly enlarging liver and elongation of the intestines accompanied by a lack of space in the small abdomen, the midgut extrudes into the umbilical cord as a physiological hernia
  • Whilst herniated, the gut will undergo rotation and then re-enter the abdominal cavity by 12 weeks gestation
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51
Q

What does failure of the gut to re-enter the abdominal cavity results in?

A
  • Omphalocele (exomphalos)
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52
Q

What are other malformations in alimentary system development?

A
  • Failure of normal rotation (malrotation)
    • Malrotation can result in volvulus and bowel obstruction
  • Fistulae
    • MOST COMMON: tracheo-oesophageal fistula
    • Some children with tracheo-oesophageal fistula also have other congenital abnormalities (e.g. VACTERL)
  • Atresias
    • When a segment of bowel has a lumen that is NOT patent
    • Usually occur in the upper GI tract (e.g. oesophagus or duodenum)
    • The foetus continuously swallows amniotic fluid, so an obstruction that prevent passage of the amniotic fluid through the GI tract will cause polyhydramnios
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53
Q

After the physiological hernia, what happens next in alimentary system development?

A
  • Peristalsis in the intestines occurs from the 2nd trimester
  • The large bowel will be filled with meconium at term
  • Defecation in utero, and hence meconium in the amniotic fluid, is associated with:
    • Post-term pregnancies
    • Foetal hypoxia
  • Aspiration of meconium-stained liquor by the foetus at birth can cause meconium aspiration syndrome or RDS
  • In the last trimester, water content decreases and glycogen and fat stores increase about fivefold
    • As such, preterm infants have virtually no fat and have a reduced ability to withstand starvation
    • This can be compounded by poor sucking, uncoordinated swallowing mechanisms, delayed gastric emptying and poor absorption
    • Growth-restricted foetuses also have reduced glycogen stores
    • These infants are more prone to hypoglycaemia
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54
Q

Describe the liver, pancreas and gallbladder in alimentary system development

A
  • They derive from the foregut endoderm
  • The liver and biliary tree appear late in the 3rd week as the hepatic diverticulum (an outgrowth from the ventral wall of the distal foregut)
  • The larger portion of this diverticulum gives rise to the parenchymal cells (hepatocytes) and the hepatic ducts
  • The smaller portion becomes the gallbladder
  • By the 6th week, the foetal liver performs haematopoiesis
    • This will peak at 12-16 weeks and continue until 36 weeks
  • In utero the normal metabolic functions of the liver are performed by the placenta (e.g. unconjugated bilirubin from haemolysis in the foetus is transferred to the mother rather than being conjugated in the foetus)
  • The foetal liver is less able to conjugated bilirubin than the adult liver because of deficiencies of enzymes (e.g. UGT)
    • After birth, the loss of the placenta and this immature ability to conjugate bilirubin (particularly in premature infants) may results in transient unconjugated hyperbilirubinaemia (physiological jaundice)
  • Glycogen is stored in small quantities in the liver from the 1st trimester and peaks in the 3rd trimester
  • Growth-restricted and premature infants have deficient glycogen stores (therefore, they are prone to hypoglycaemia)
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55
Q

Describe kidney and urinary tract development

A
  • The permanent final form of the kidney (metanephric kidney) is preceded by the development and regression of two primitive forms: pronephros and mesonephros
  • Pronephros originates at about 3 weeks in a ridge that forms on either side of the midline in the embryo (nephrogenic ridge)
  • In this region, epithelial cells will arrange themselves in a series of tubules and join laterally with the pronephric duct
  • The pronephros is non-functional
  • Each pronephric duct will grow towards the tail of the embryo during which it will induce intermediate mesoderm in the thoracolumbar area to become mesonephric tubules
  • The prenephros will then degrade whilst the mesonephric (Wolffian) duct extends towards the most caudal end of the embryo, ultimately attaching to the cloaca
  • During the 5th week, the ureteric bud develops as an outpouching from the Wolffian duct
  • This bud grows into the intermediate mesoderm and branches to form the collecting duct system (ureter, pelvis, calyces and collecting ducts) of the kidney
  • It also induces the formation of the renal secretory system (glomeruli, convoluted tubules, loops of Henle)
  • Then, the lower portions of the nephric duct will migrate caudally and connect with the bladder, thereby forming the ureters
  • As the foetus develops, the torso elongates and the kidneys rotate and migrate upwards within the abdomen causing the length of the ureters to increase
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56
Q

What can failure of normal kidney migration lead to?

A
  • A pelvic kidney
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57
Q

What can abnormal development of the collecting duct system in kidneys lead to?

A
  • Duplications such as duplex kidneys
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58
Q

What is a posterior urethral valve?

A
  • An obstructing membrane in the posterior male urethra
  • SEVERE obstruction in utero can lead to hydronephrosis and renal interstitial fibrosis
  • Although the structures of the urinary system are in place by 32-36 weeks, the excretory and concentrating ability of the foetal kidneys is gradual and continues after birth
  • In preterm infants, this may result in abnormal water, glucose, sodium and acid-base homeostasis
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59
Q

What does renal agenesis lead to?

What does bilateral renal agenesis cause and what is this condition associated with?

A
  • oligohydramnios (because foetal urine forms much of the amniotic fluid)
  • Bilateral renal agenesis causes Potter’s syndrome which is associated with:
    • Widely-spaced eyes
    • Small jaw
    • Low set ears
    • Secondary oligohydramnios
    • Renal failure (and death)
    • Pulmonary hypoplasia (secondary to oligohydramnios)
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60
Q

How does the skin develop in a foetus?

A
  • The skin and its appendages develop from ectodermal and mesodermal germ layers
    • Epidermis = comes from the surface ectoderm
    • Dermis and Hypodermis = mesenchymal cells in the mesoderm
  • By 4 weeks gestation, a single-cell layer of ectoderm surrounds the embryo
  • At 6 weeks, the ectodermal layer differentiates into an outer periderm and an inner basal layer
    • The periderm will slough off as vernix
    • The basal layer produces the epidermis and the glands/nails/hair follicles
  • Eventually the epidermis becomes stratified and by 16-20 weeks, all layers of the epidermis are developed
  • Preterm babies have NO vernix and thin skin
    • This leads to increased insensible fluid loss
    • They also have poor thermal control due to having a large surface area to body weight ratio and little insulation
    • They also have immature vascular tone meaning that they can’t use peripheral vasoconstriction to limit heat loss
  • Hair follicles develop as hair buds at around 12-16 weeks
  • By 24 weeks, the hair follicles are producing lanugo hair
    • This is usually shed before birth
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61
Q

Describe blood and immune system development

A
  • RBCs and immune cells are derived from pluripotent haematopoietic cells which are first found
    • Initially, in the blood islands of the yolk sac
    • By 8 weeks, the yolk sac is replaced by the liver as the source of blood cells
    • By 20 weeks, all cells are produced by the bone marrow
  • T cell precursors transit to the thymus by 9 weeks gestation
  • The mature naïve and memory T cells will be found in the spleen and lymph nodes at 12-14 weeks
  • Circulating mature T cells are present from 16 weeks
  • In the second trimester there are more Tregs than at any other point in life because it is important in the induction of tolerance
  • B cells appear in the circulation by around 12 weeks
  • They will then undergo functional maturation in secondary lymphoid tissue
  • Much of the IgG in the foetus will be from the mother
  • The foetus produces small amounts of IgA and IgM
  • Detection of IgM or IgA in the newborn without IgG is suggestive of foetal infection
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62
Q

Describe haemoglobin development

A
  • Most haemoglobin is HbF (2 alpha + 2 gamma)
  • Adult haemoglobins are either:
    • HbA (2 alpha + 2 beta)
    • HbA2 (2 alpha + 2 delta)
  • Up to 28 weeks gestation, 90% of foetal Hb is HbF
  • From 28-34 weeks there is a switch to HbA
  • At term, the ratio of HbF to HbA is 80:20
  • By 6 months, only 1% is HbF
  • HbF has a higher affinity for oxygen
  • Infants also have a higher haemoglobin concentration which enhances transfer of oxygen across the placenta
  • Abnormal haemoglobin production results in thalassemia
    • This is a group of disorder characterised by reduced or absent production of the globin chains (e.g. beta-thalassemia is caused by reduced or absent production of beta-globin)
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63
Q

Describe endocrine system development

A
  • Major components of the hypothalamo-pituitary axis are in place by 12 weeks
  • Testosterone is produced in the first trimester, increasing to 17-21 weeks which mirrors the development of the male urogenital tract
  • Growth restricted foetuses exist in a state of relative hypothyroidism (may be a compensatory measure to decrease metabolic rate and oxygen consumption)
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64
Q

Describe foetal behavioural states

A
  • First activity is beating of the foetal heart
  • Foetal movements = 7-8 weeks
    • These will begin as discernible movements, and progress to startles, movements of arms and legs and breathing movements
  • By 12 weeks, yawning, sucking and swallowing can be seen
  • From this point onwards, no new behaviours are acquired but their patterns change
  • There are FOUR foetal behavioural states
    • 1F - quiescence (like non-REM sleep in a neonate)
    • 2F - frequent and periodic gross body movements with eye movements (like REM sleep)
    • 3F - no gross body movements but eye movements (like quiet wakefulness)
    • 4F - vigorous continual activity with eye movements (like active wakefulness)
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65
Q

Describe amniotic fluid in foetal development

A
  • By 12 weeks, the amnion comes into contact with the inner surface of the chorion and the two surfaces become adherent (but they never fuse)
  • The amnion and chorion do NOT contain vessels or nerves but they contain a significant quantity of phospholipids as well as enzymes involved in phospholipid hydrolysis
  • Choriodecidual function is thought to be important in the initiation of labour by the production of prostaglandins E2 and F2a
  • Amniotic fluid is initially secreted by the amnion
  • By the 10th week, it is mainly transudate of foetal serum via the skin and umbilical cord
  • From 16 weeks, the foetal skin becomes impermeable to water
  • The net increase in amniotic fluid thereafter is due to contributions through the kidneys and lung fluids
  • Removal of amniotic fluid is by foetal swallowing
  • Amniotic fluid contains growth factors and multipotent stem cells (although the function is uncertain)
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66
Q

What are the changes in amniotic fluid volume?

A
  • Increase in amniotic fluid volume
    • 10 weeks = 30 ml
    • 20 weeks = 300 ml
    • 30 weeks = 600 ml
    • 38 weeks = 1000 ml
  • IMPORTANT: from term, there is a rapid fall in amniotic fluid volume
    • 40 weeks = 800 ml
    • 42 weeks = 350 ml
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67
Q

What are the functions of amniotic fluid?

A
  • Protect the foetus from mechanical injury
  • Permit movement of the foetus while preventing limb contracture
  • Prevent adhesions between foetus and amnion
  • Permit foetal lung development in which there is two-way movement of fluid into the foetal bronchioles (absence of amniotic fluid in the second trimester is associated with pulmonary hypoplasia)
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68
Q

What are causes of oligohydramnios?

A
  • Renal agenesis
  • Cystic kidneys (PCKD)
  • FGR
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69
Q

What are the causes of polyhydramnios?

A
  • Congenital neuromuscular disorders
  • Anencephaly
  • Oesophageal/duodenal atresia (prevents swallowing of amniotic fluid)
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70
Q

What is transvaginal ultrasonography useful for?

A
  • It isuseful in early pregnancy, for examining the cervix later in pregnancy and for identifying the lower edge of the placenta
  • It is also useful in women who have a lot of adipose tissue
  • In general, after around 12 weeks, an abdominal transducer will be used
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71
Q

What is acoustic impedance?

A
  • Related to the density of tissues
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72
Q

How does doppler ultrasound work?

A
  • It allows assessment of the velocity of blood within the foetal and placental vessels (thus providing an indirect assessment of foetal and placental condition)
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73
Q

When can the gestational sac, yolk sac, embryo and beating of the heart be observed? (Early Pregnancy)

A
  • The gestational sac can be visualised from 4-5 weeks
  • The yolk sac can be visualised at about 5 weeks
  • The embryo can be observed and measured at 5-6 weeks
  • Beating of the heart can be seen at 6 weeks
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74
Q

How is transvaginal ultrasound important in early pregnancy?

A
  • It is important in early pregnancy to diagnose disorders of early pregnancy (e.g. incomplete or missed miscarriage, blighted ovum where no foetus is present and ectopic foetus)
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75
Q

What is a Blighted Ovum?

A
  • The gestational sac is present but it is empty because the foetus has not developed
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76
Q

What is the determination of Gestational Age and Assessment of Foetal Size and Growth?

A
  • Crown-Rump Length (CRL) is used up to 13 weeks + 6 days
  • Head Circumference is used from 14-20 weeks
  • Biparietal diameter and femur length can also be used to assess gestational age
  • The earlier the measurement is made, the more accurate the prediction
  • Later on in pregnancy, measuring foetal abdominal circumference and head circumference will help assess size and growth
  • In addition to AC and HC, BPD and FL can be combined in an equation to give a more accurate estimate of foetal weight than any of the parameters on their own
  • In foetuses at risk of growth restriction, serial measurements are plotted
  • This also helps differentiate between types of growth restriction (e.g. symmetrical vs asymmetrical)
  • Cessation of growth is suggestive of placental failure
  • Gestational age can no longer be accurately calculated by ultrasound after 20 weeks (because of a broad range in normal values)
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77
Q

What is chorionicity?

What are monochorionic twin pregnancies at higher risk of

A
  • It is important in determining the chorionicity (number of placentas) of the pregnancy
  • Monochorionic twin pregnancies (i.e. sharing a placenta) are at increased risk of pregnancy complications (e.g. twin-to-twin transfusion syndrome and higher rates of perinatal mortality)
  • Dichorionic twins have a thicker dividing membrane (formed of two layers of amnion and two layers of chorion) - this can be viewed on ultrasound
  • The best time to perform the ultrasound to determine chorionicity is 9-10 weeks
  • Ultrasound is also useful for confirming growth restriction, foetal anomaly and the presence of placenta praevia (more common in twins)
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78
Q

When can foetal structural abnormalities be diagnosed?

What are common examples of foetal abnormalities?

A
  • Major foetal structural abnormalities can be diagnosed by US at or before 20 weeks
  • Common examples
    • Spina bifida
    • Hydrocephalus
    • Skeletal abnormalities (e.g. achondroplasia)
    • Abdominal wall defects (e.g. gastroschisis)
    • Cleft lip/palate
    • Congenital cardiac abnormalities
  • These are usually detected at the 20-week anomaly scan
  • Factors affecting sensitivity of the scan include the woman’s BMI and position of the baby at the time of the scan
  • Repeat scans may be required if visualising certain structures is difficult
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79
Q

What is placenta praevia?

A
  • When a placenta is inserted into the lower segment of the uterus and can cause life-threatening haemorrhage in pregnancy
  • US scans are very useful in the localisation of the site of the placenta
  • US scans can identify the lower edge of the placenta (transvaginal is better than transabdominal)
  • About 15-20% of women will have a low-lying placenta at 20 weeks, but only 10% of this group will eventually develop placenta praevia
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80
Q

Describe Amniotic Fluid Assessment

A
  • US scans can be used to assess increased and decreased amniotic fluid volumes
  • The foetus swallows amniotic fluid, absorbs it in the GI tract and excretes urine into the amniotic sac
  • Congenital abnormalities that impair the ability of the foetus to swallow (e.g. oesophageal atresia, anencephaly) results in INCREASED amniotic fluid volume
  • Congenital abnormalities that cause a failure of urine production (e.g. renal agenesis, posterior urethral valves) will result in REDUCED amniotic fluid
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81
Q

What are the TWO ultrasound measurement approaches that give an indication of amniotic fluid volume?

A
  • Maximum vertical pool
  • Amniotic fluid index
  • Amniotic fluid volume is reduced in FGR, because of redistribution of foetal blood away from the kidneys to vital structures like the brain and heart (this leads to reduced renal perfusion and GFR)
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82
Q

Describe Assessment of Foetal Wellbeing

A
  • Evaluating foetal movements, tone and breathing can give an indication of foetal wellbeing
  • Doppler ultrasound can give an indication of placental function
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83
Q

How is cervical length measured?

A
  • Cervical length can be measured best using a transvaginal probe
  • 50% of women who deliver before 34 weeks have a short cervix at midtrimester
  • NICE recommends serial measurements of cervical length from 16 weeks in women with a history of spontaneous preterm birth or midtrimester loss
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84
Q

What other obstretric conditions are US scans useful for?

A
  • Confirmation of intrauterine death
  • Confirmation of foetal presentation in uncertain cases
  • Diagnosis of uterine and pelvic abnormalities during pregnancy (e.g. fibromyomata and ovarian cysts)
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85
Q

What is the Ultrasound schedule according to NICE?

A

NICE recommends that all pregnant women should be offered scans at:

  • 10-14 weeks
    • Mainly to determine gestational age, detect multiple pregnancy and determine nuchal translucency as part of screening for Down syndrome
  • 18-21 weeks
    • Primarily screens for structural anomalies
    • Give couples reproductive choice (e.g. termination of pregnancy)
86
Q

Describe Cardiotocography

A
  • A CTG is a continuous trace of the foetal heart rate that is used to assess foetal wellbeing
  • It is sometimes called electronic foetal monitoring (EFM)
  • It is performed whilst the pregnant woman is in the left lateral or semi-recumbent position
  • Two external transducers are placed on the mother’s abdomen, each attached with a belt
  • One transducer is a pressure-sensitive contraction tocodynometer (stretch gauge) which measures the pressure required to flatten a section of the abdominal wall
    • This correlates with the internal uterine pressure and indicates if there is any uterine activity (contractions)
  • The second transducer uses ultrasound and the Doppler effect to detect motion of the foetal heart
    • It allows continuous assessment of the foetal heart rate
  • Recordings are taken for 30 mins
  • The output from the CTG machine produces TWO lines
    • A tracing of the foetal heart rate
    • A tracing of uterine activity
87
Q

What are important CTG features?

A
  • Pathological events like hypoxia modify the signals to the foetal heart resulting in changes in the heart rate patterns
  • Features reported on a CTG
    • Baseline rate
    • Baseline variability
    • Accelerations
    • Decelerations
88
Q

What is a normal foetal heart rate?

What are causes of foetal tachycardia?

A
  • Normal foetal heart rate = 110-150 bpm
  • Foetal heart rate decreases with advancing gestational age
  • 160 bpm is considered the upper limit of normal
  • Baseline rate is determined over 5-10 mins
  • Causes of foetal tachycardia
    • Maternal or foetal infection
    • Acute foetal hypoxia
    • Foetal anaemia
    • Drug (e.g. ritodrine)
89
Q

Describe Baseline Variability

A
  • In normal physiological conditions, the interval between successive foetal heart beats varies
  • This is called short-term variability and is increases with gestational age
  • It is not visible on a standard CTG but can be measured by computer
  • There are also longer-term fluctuations in heart rate occurring 2-6 times per minute, known as baseline variability
  • Normal baseline variability is suggestive of a normal foetal autonomic system
  • Baseline variability is considered abnormal if it is < 10 bpm
  • Foetuses have 20-30 min deep sleep cycles so baseline variability may be normally reduced for this length of time (but should be preceded and followed by a normal CTG)
90
Q

What factors affect baseline variability?

A
  • Foetal sleep states and activity
  • Hypoxia
  • Foetal infection
  • Drugs (e.g. opioids)
91
Q

What are foetal heart rate accelerations?

A
  • These are increases in baseline foetal heart rate of at least 15 bpm lasting for at least 15 seconds
  • The presence of 2 or more accelerations on a 20-30 min antepartum foetal CTG defines a reactive trace and is indicative of a non-hypoxic foetus
92
Q

What are foetal heart rate decelerations?

A
  • These are transient reductions in foetal heart rate of at least 15 bpm, lasting more than 15 seconds
  • Causes
    • Foetal hypoxia
    • Umbilical cord compression
93
Q

What is a normal CTG?

A
  • Baseline heart rate of 110-150 bpm
  • Baseline variability exceeding 10 bpm
  • More than 1 acceleration in a 20-30 min tracing
94
Q

What is a biophysical profile?

A
  • A biophysical profile (BPP) takes into account FIVE acute foetal variables (of which 4 are shown on ultrasound):
    • Foetal breathing movements (FBMs)
    • Foetal gross body movement
    • Foetal tone
    • CTG
    • Amniotic fluid volume
  • A score of 2 (normal) or 0 (sub-optimal) is assigned to each of the variables giving the foetus a score between 0 and 10
  • A score of 8-10 is NORMAL
  • A score of 6 is borderline and requires a repeat to exclude a period of foetal sleep as a cause
  • There is insufficient evidence to support the use of BPP as a test of foetal wellbeing in high-risk pregnancies
95
Q

Describe Umbilical Artery Doppler Investigations

A
  • Waveforms from the umbilical artery provide information on placental resistance to blood flow, and hence an indicator of placental health
  • E.g. an infarcted placenta secondary to maternal hypertension will have increased blood flow
  • In cases of a diseased placenta, the placenta wont allow blood to flow freely through it, and therefore there will be a backlog of blood in the umbilical artery
  • In a diseased placenta, blood flow in the umbilical artery during diastole may be reduced, absent or reversed
  • Reversed end-diastolic flow means that, during diastole, blood is flowing away from the placenta back to the foetus
    • It is associated with foetal hypoxia and intrauterine death
  • In other words, low diastolic flow indicates high resistance
  • Indices such as pulsatility index or resistance index are useful as they calculate the variability of blood velocity in a vessel (high indices suggests high resistance to blood flow)
  • Normally, diastolic blood flow through the umbilical artery increases through gestation
96
Q

Describe Foetal Vessel Doppler Investigations

A
  • Falling oxygen levels in the foetus leads to redistribution of blood flow to the essential organs (e.g. brain, heart, adrenals)
  • This is often called cerebral redistribution
  • As hypoxia worsens, the pulsatility index in the middle cerebral artery will fall, indicating increasing diastolic flow
  • There will also be increased resistance in the foetal aorta (thus reducing blood flow to the rest of the body)
  • Absent diastolic flow in the foetal aorta is suggestive of foetal acidaemia
  • The most sensitive index of foetal acidaemia and impending heart failure is increasing pulsatility in the central veins supplying the heart (e.g. ductus venosus, inferior vena cava)
  • The ductus venosus flow reflect atrial pressure-volume changes
  • As FGR worsens, hypoxia and acidaemia affects cardiac function, leading to increased preload and afterload
  • This leads to reduce velocity in the ductus venosus A-wave which is suggestive of increasing end-diastolic pressure
  • A retrograde ductus venosus A-wave is suggestive of overt cardiac compromise and may require early delivery
  • The velocity of blood flow in the middle cerebral artery is an indicator of foetal anaemia
    • When the foetus is anaemic, the peak systolic velocity increases
    • This is useful in Rhesus isoimmunistion disease and twin-to-twin transfusion syndrome
97
Q

What can uterine artery dopplers be used for?

A
  • Predict at-risk pregnancies e.g. pre-eclampsia
  • Doppler ultrasound of the uterine arteries may show markers of increased resistance
  • High resistance patterns are associated with:
    • Pre-eclampsia
    • GFR
    • Placental abruption
  • These pregnancies will need close monitoring of foetal growth rate and the possible development of maternal hypertension
98
Q

What is the Cerebroplacental ratio?

A
  • This is the ratio of the pulsatility indices of the middle cerebral artery and the umbilical artery
  • Foetuses with an abnormal ratio that are appropriately grown for gestational age or have late-onset SGA (> 34 weeks) have a higher incidence of abnormal intrapartum CTG requiring emergency Caesarean section, lower cord pH and an increased rate of admission to NICU
  • In foetuses with early-onset SGA, an abnormal ratio is associated with an increased rate of adverse neonatal outcome and perinatal death
99
Q

What is US necessary for? (Procedures)

A
  • Amniocentesis, chorion villus sampling and cordocentesis

- It is also necessary for therapeutic procedures such as inserting foetal bladder shunts or chest drains

100
Q

What is pre-eclampsia often associated with in the foetus?

A
  • Foetal growth restriction
  • Women entering pregnancy with chronic hypertension have an increased risk to both the mother and the baby (e.g. pre-eclampsia and FGR)
101
Q

How do you classify the severity of hypertension?

A
  • MILD = 140-149 systolic, 90-99 diastolic
  • MODERATE = 150-159 systolic, 100-109 diastolic
  • SEVERE = > 160 systolic, > 110 diastolic
102
Q

What are the three conditions which pregnant women presenting with hypertension in pregnancy have?

A
  • Non-proteinuric pregnancy-induced hypertension
  • Pre-eclampsia
  • Chronic hypertension
103
Q

Describe non-proteinuric pregnancy-induced hypertension

A
  • Hypertension that arises for the first time in the second half of pregnancy in the absence of proteinuria
  • It is NOT associated with adverse pregnancy outcomes
  • Mild-to-moderate increases in blood pressure in this setting do NOT require treatment
  • IMPORTANT: 1/3 of women with gestational hypertension will develop pre-eclampsia
104
Q

What is chronic hypertension?
What are the different types of chronic hypertension?
What can chronic hypertension predispose to?
Why may chronic hypertension be masked in pregnancy?

A
  • Women who have confirmed hypertension in the first half of pregnancy are likely to have chronic hypertension
  • Most will have essential hypertension, but secondary causes should be excluded
  • Chronic hypertension can predispose to the development of pre-eclampsia
  • Even without pre-eclampsia, chronic hypertension is associated with increased maternal and foetal morbidity
  • IMPORTANT: the physiological fall in blood pressure that occurs in the first trimester due to peripheral vasodilation can mask chronic hypertension
105
Q

What is pre-eclampsia?

A
  • Hypertension of at least 140/90 mm Hg recorded on at least 2 separate occasions and at least 4 hours apart and in the presence of at least 300 mg protein in a 24-hr collection of urine, arising de novo after the 20th week of pregnancy in a previously normotensive woman and resolving completely by the 6th postpartum week
  • 2-3% of all pregnancies
106
Q

What are the risk factors of pre-eclampsia?

A
  • First pregnancy
  • Multiparous with a previous history of pre-eclampsia
  • 10 years or more since last baby
  • Age 40 years or more
  • BMI > 35
  • Family history of pre-eclampsia in mother or sister
  • Booking diastolic pressure of 80 mmHg or more
  • Booking proteinuria (of >= 1 + on more than one occasion or quantified at >= 0.3g/24 h
  • Multiple pregnancies
  • Certain underlying medical conditions
  • Antiphospholipid syndrome
  • Coarctation of the aorta
  • NOTE: the protective effect of first pregnancy is lost if a woman has a child with a new partner
107
Q

Why is trophoblast tissue associated with pre-eclampsia?

A
  • Pre-eclampsia can occur in pregnancies lacking a foetus (molar pregnancies) and in the absence of a uterus (abdominal pregnancies)
  • This suggests that the trophoblast tissue provides the stimulus for the disorder
108
Q

What is the two stage process of pre-eclampsia?

A

Stage 1
- Trophoblast invasion is patchy

  • Spiral arteries retain their muscular walls
  • This prevents the development of a high-flow, low-impedance uteroplacental circulation
  • This leads to uteroplacental ischaemia

Stage 2
- Uteroplacental ischaemia results in oxidative and inflammatory stress

  • Involvement of secondary mediators leads to endothelial dysfunction, vasospasm and activation of the coagulation system
  • Because the target cell of the disease process (vascular endothelial cell) is so ubiquitous, pre-eclampsia is a multisystem disorder
109
Q

Describe pre-eclamspia and the cardiovascular system

A
  • In normal pregnancy, peripheral vasodilation —> decreased total peripheral resistance despite an increase in plasma volume and HR
  • In pre-eclampsia: peripheral vasoconstriction –> hypertension
  • Increased BP and loss of endothelial cell integrity leads to increased vascular permeability —> oedema
110
Q

How does pre-eclampsia affect the renal system?

A
  • A lesion called glomeruloendotheliosis is seen (specific for pre-eclampsia)
  • Associated with impaired glomerular filtration and selective protein loss (albumin and transferrin) leading to proteinuria
  • This leads to a reduction in plasma oncotic pressure which exacerbated the oedema
111
Q

How does pre-eclampsia affect the haematological system?

A
  • Diffuse vascular damage in pre-eclampsia is associated with laying down of fibrin and the adherence of platelets
  • Pre-eclampsia is associated with increased fibrin deposition and a reduced platelet count
112
Q

How does pre-eclampsia affect the liver?

A
  • Subendothelial fibrin deposition is associated with elevation of liver enzymes
  • This can be associated with haemolysis and low platelet count
  • This is called HELLP Syndrome
    • Haemolysis
    • Elevated Liver enzymes
    • Low Platelets
  • HELLP syndrome is a particularly severe form of pre-eclampsia
  • It is associated with a high foetal loss rate
113
Q

What do women with HELLP syndrome present with?

A
  • Epigastric pain

- Nausea and vomiting

114
Q

What are the severe complications of HELLP syndrome

A
  • Acute renal failure
  • Placental abruption
  • Stillbirth
115
Q

How does pre-eclampsia affect the neurological system?

A
  • Presence of tonic-clonic convulsions
    • No other identifiable cause
  • Likely to be due to vasospasm and cerebral oedema
116
Q

What is the clinical presentation of pre-eclampsia?

A
  • Classic symptoms
    • Frontal headache
    • Visual disturbance
    • Epigastric pain
    • Vague ‘flu-like’ symptoms
  • Hypertension is usually the first sign
  • Rapidly progressive oedema of the face and hands may suggest pre-eclampsia
    • NOTE: dependent oedema of the feet is very common in pregnancy
  • Epigastric tenderness suggest liver involvement (worrying)
  • Neurological examination may show hyperreflexia and clonus in severe cases
  • Urine protein should be tested as part of the examination
117
Q

What is the management of pre-eclampsia?

A
  • There is NO CURE for pre-eclampsia other than to end the pregnancy by delivering the baby
  • This can be a major problem if pre-eclampsia occurs early in pregnancy (particularly < 34 weeks)
118
Q

What are the principles of pre-eclampsia management?

A
  • Early recognition of the symptomless syndrome
  • Awareness of the serious nature of the condition in its severest form
  • Adherence to agreed guidelines for admission to hospital, investigation and the use of antihypertensive and anticonvulsant therapy
  • Well-timed delivery to pre-empty serious maternal or foetal complications
  • Post-natal follow-up and counselling for future pregnancies
119
Q

What are the investigations for pre-eclampsia? (both in mother and foetus)

A
  • To monitor for MATERNAL complications
    • FBC (focus on falling platelet count and rising Hct)
    • Clotting studies (of platelet count is abnormal)
    • Serum renal profile
    • Serum liver profile
    • Frequent repeat proteinuria quantification
  • To monitor for FOETAL complications
    • Ultrasound assessment of:
      • Foetal size
      • Amniotic fluid volume
      • Maternal and foetal Doppler scan
    • Antenatal CTG
120
Q

What is the treatment of hypertension?

A
  • The most common cause of death in women who die of pre-eclampsia is cerebral bleeding secondary to uncontrolled SBP
  • Antihypertensive therapy aims to lower blood pressure to reduce the risk of a maternal CVA without compromising uterine blood flow
  • Labetalol (alpha-blocker) is the drug of choice in most guidelines
  • Nifedipine (CCB) has a rapid onset of action but can cause a severe headache which mimics worsening disease
  • In SEVERE cases, IV hydralazine or labetalol can be used
121
Q

What is the treatment and prevention of eclampsia?

A
  • IV magnesium sulphate is the drug of choice
  • Used prophylactically in women with severe pre-eclampsia
  • Loading IV dose of 4g over 5 - 15 mins then infusion of 1g/hour for 24 hours
  • After fit: infusion continued for 24h after last fit
122
Q

Describe screening and prevention of eclampsia

A
  • There is NO screening test for pre-eclampsia
  • Doppler ultrasound uterine artery waveform analysis has been investigated with varying success
  • This may be useful in screening women at risk of pre-eclampsia, but it is NOT useful in low-risk women
  • Preventive interventions include low-dose aspirin (75 mg daily) modestly reduces the risk of pre-eclampsia in high-risk women
123
Q

What is further management of pre-eclampsia?

A
  • Iatrogenic premature delivery is often required
  • If < 34 weeks, IM corticosteroids should be given to the mother
  • Delivery before term is usually by C-section
  • These patients are usually at HIGH RISK of thromboembolism and should be given prophylactic SC heparin and given anti-thromboembolic stockings
  • In spontaneous or induced labour (if clotting studies are normal), epidural anaesthesia is indicated as it helps control blood pressure
  • Ergometrine should be AVOIDED as it significantly increases blood pressure
  • Post-natally, blood pressure and proteinuria should resolve within 6 weeks
  • If it fails to resolve, consider chronic hypertension or renal disease
124
Q

What is the MANAGEMENT of pre-eclampsia (NICE Guidelines)?

A
  • Refer to table above
  • Manage pregnancy in women with pre-eclampsia conservatively until 34 weeks
  • Set maternal and foetal thresholds for elective birth before 34 weeks
  • Write a plan for foetal monitoring during birth
  • Offer birth to women with pre-eclampsia before 34 weeks after a course of corticosteroids if:
    • Severe hypertension develops which is refractory to treatment
    • Maternal or foetal indications as specified in the management plan
  • Recommend birth in women with severe hypertension after 34 weeks when blood pressure is under control and a course of corticosteroids has been completed
  • Offer birth to women with mild or moderate hypertension at 34-37 weeks depending on foetal and maternal condition
  • Recommend birth within 24-48 hours for women with pre-eclampsia and mild-moderate hypertension after 37 weeks
  • Anticonvulsants
    • Give IV magnesium sulphate if:
      • In critical care setting with severe hypertension or previous eclamptic fit
      • Severe hypertension and proteinuria
      • Symptoms (e.g. severe headache, visual disturbance, epigastric pain, liver tenderness)
    • Loading dose of 4 g should be given IV over 5 mins followed by an infusion of 1 g/hour for 24 hours
125
Q

What is Chronic Hypertension mainly due to?

A
  • Essential hypertension is responsible for 90% of cases

- Renal causes are responsible for 80% of cases of secondary hypertension

126
Q

What are the causes of chronic hypertension?

A
  • Idiopathic
  • Essential hypertension
  • Vascular disorders
  • Renal artery stenosis
  • Coarctation of the aorta
  • Renal disease
  • Polycystic disease
127
Q

What are the risks of pre-existing hypertension in pregnancy?

A
  • Pre-eclampsia
  • Abruption
  • Heart failure
  • Intracerebral haemorrhage
128
Q

What is the management of chronic hypertension?

A
  • Mild cases (< 150/100 mm Hg)- don’t treate
    • Should be monitored to detect BP changes or pre-eclampsia features
    • Monitor for FGR by serial ultrasounds
  • Antihypertensive medication pre-pregnancy can usually be stopped for the first half of pregnancy as there is a physiological reduction in BP
  • ACE inhibitors, ARBs and atenolol should be discontinued (may cause teratogenicity and negative effects on foetal growth)
  • If blood pressure is consistently > 150/100 mm Hg, offerantihypertensive medication
    • Preferred agents include:
      • Labetalol
      • Nifedipine
      • Methyldopa
    • Treatment to maintain BP < 160/80-100 mm Hg
  • Delivery is usually offered around 39 weeks
  • After delivery, maternal blood pressure often decreases but tends to increase again on the 3rd or 4th day postpartum
  • Consider which drugs are safe with breastfeeding
129
Q

What is foetal growth restriction?

A
  • failure of a foetus to achieve its genetic growth potential
  • This usually results in a baby that is small for gestational age (SGA) meaning that they are below the 10th centile for its gestation
  • IMPORTANT
    • Most SGA foetuses are constitutionally small
    • FGR suggests that there is a pathological process leading to restricted growth
130
Q

What are the causes of FGR?

A
  • Reduced foetal growth potential
    • Aneuploidies
    • Single gene defects (e.g. Seckel’s syndrome)
    • Structural abnormalities (e.g. renal agenesis)
    • Intrauterine infections (e.g. CMV, toxoplasmosis)
  • Reduced foetal growth support
    • Maternal factors
      • Undernutrition (e.g. poverty)
      • Maternal hypoxia (e.g. living at altitude, cyanotic heart disease)
      • Drugs (e.g. alcohol, cigarettes, cocaine)
        • Smoking increases the amount of carboxyhaemoglobin in the maternal circulation thereby reducing the amount of oxygen available to the foetus
  • Placental factors
    • Reduced uteroplacental perfusion (e.g. inadequate trophoblast invasion, sickle cell disease, multiple gestation)
    • Reduced fetoplacental perfusion (e.g. single umbilical artery, twin-to-twin transfusion syndrome)
131
Q

What is the pathophysiology of FGR?

A
  • FGR is often classified as symmetrical or asymmetrical
  • Symmetrical
    • Directly impair foetal growth (e.g. chromosomal disorders and foetal infections)
  • Asymmetrical
    • Ureteroplacental insufficiency –> decreased oxygen to the foetus and reduced carbon dioxide removal
    • When the foetus is hypoxic, more of the well-oxygenated blood from the umbilical vein will go via the ductus venosus, meaning that the liver will receive little oxygenated blood
    • This results in an asymmetrical foetus with relative brain sparing and reduced abdominal girth and skin thickness
    • Vasoconstriction in the foetal kidneys results in impaired urine production and oligohydramnios
  • Chronic foetal hypoxia in FGR can lead to foetal acidaemia (both respiratory and metabolic) which can lead to intrauterine death if prolonged
132
Q

What is the management of FGR?

A
  • Detection of SGA consists of TWO elements:
    • Accurate assessment of gestational age
    • Recognition of foetal smallness
  • Early measurement of foetal CRL (< 13+6 weeks) or head circumference (13+6-20 weeks) is the method of choice for confirming gestational age
  • The most precise way of assessing foetal growth is by ultrasound biometry (biparietal diameter, head circumference, abdominal circumference and femur length) serially at set intervals (usually 4 weeks)
    • Serial measurements tend to only be performed for at-risk pregnancies
  • Once SGA is diagnosed, the next step is to clarify whether the foetus is constitutionally small or whether it is FGR
  • There are no widely accepted treatments for FGR due to uteroplacental insufficiency (but smoking, alcohol and drugs should be stopped)
  • Low-dose aspirin may have some role in preventing FGR in high-risk pregnancies but has no effect once it has been established
133
Q

What are the risk factors for FGR?

A
  • Multiple pregnancies
  • History of FGR in previous pregnancy
  • Current heavy smokers
  • Current drug users
  • Women with underlying medical disorders
    • Hypertension
    • Diabetes
    • Cyanotic heart disease
    • Antiphospholipid syndrome
  • Pregnancies where symphysis-fundal height is less than expected
134
Q

What is the prognosis of FGR?

A
  • For survivors of FGR due to uteroplacental insufficiency, prognosis is good and most infants show catch-up growth after delivery
  • There is an association between FGR and adult-onset hypertension and diabetes
135
Q

What are symptoms of pre-eclampsia?

A
  • Severe headache
  • Visual disturbance (e.g. burring, flashing)
  • Severe pain just below the ribs
  • Vomiting
  • Sudden swelling of the face, hands or feet
136
Q

What are NICE guidelines for management for pregnancy with chronic hypertension at the timing of birth and for the assessment of proteinuria?

A

Timing of Birth
- If there’s chronic hypertension and BP < 160/110 mm Hg do NOT offer delivery before 37 weeks

  • Offer birth if refractory severe chronic hypertension (after corticosteroids if needed)
  • Monitor blood pressure in women with chronic hypertension who have given birth and consider changing antihypertensive medication

Assessment of Proteinuria
- Use an automated reagent-strip reading device or a spot urinary protein: creatinine ratio

  • If a result of 1+ or more is obtained, use spot urinary protein: creatinine ratio or 24-hour urine collection to quantify proteinuria
  • Diagnose significant proteinuria if the urinary protein: creatinine ratio is > 30 mg/mmol or a validated 24-hour urine collection shows > 300 mg protein
137
Q

Describe postnatal investigation, monitoring and treatment for gestational hypertension

A
  • In women with gestational hypertension who have given birth, measure blood pressure:
    • Daily for the first 2 days
    • At least once between days 3 and 5
    • As indicated if antihypertensive treatment changes after birth
  • In women with gestational hypertension who have given birth:
    • Continue use of antenatal antihypertensive treatment
    • Consider reducing antihypertensive treatment if their blood pressure falls < 140/90 mm Hg
    • Reduce antihypertensive treatment if their blood pressure falls < 130/80 mm Hg
  • Consider reducing antihypertensive treatment if the blood pressure falls
  • If the woman was taking methyldopa during pregnancy, stop within 2 days
  • Write a care plan for women with gestational hypertension who have given birth and are being transferred to community care
  • Offer women who have had gestational hypertension and remain on antihypertensive treatment 2 weeks after transfer to community care, a medical review
138
Q

Describe postnatal investigation, monitoring and treatment for pre-eclampsia

A
  • Monitor blood pressure:
    • At least 4/day if inpatient
    • At least once between day 3 to 5
    • On alternate days until abnormal BP becomes normal on days 3-5
  • Pre-eclampsia woman not on antihypertensives, start treatment if BP > 150/100 mm Hg
  • Ask about severe headache and epigastric pain every time BP is measured
  • Pre-eclampsia woman who have taken antihypertensive treatment and given birth:
    • Continue antenatal hypertensives
    • Consider reducing antihypertensive if BP < 140/90 mm Hg
    • Reduce antihypertensive treatment if BP < 130/80 mm Hg
  • If a woman has taken methyldopa for her pre-eclampsia, stop within 2 days of birth
  • Offer transfer to community care if all the following have been met:
    • No symptoms of pre-eclampsia
    • Blood pressure < 149/99 mm Hg
    • Blood test results are stable or improving
  • Write a care plan including frequency of blood pressure monitoring, thresholds for reducing/stopping treatment, indications for referral and self-monitoring of symptoms
  • Offer women who have pre-eclampsia and are still on antihypertensive treatment 2 weeks after transfer to community care a medical review
139
Q

Which foetal monitoring should be done in chronic hypertension?

A
  • Ultrasound foetal growth
  • Amniotic fluid volume assessment
  • Umbilical artery Doppler velocimetry
  • Between 28-30 weeks and 32-34 weeks
  • Only do CTG if activity is abnormal
140
Q

Describe foetal monitoring in mild or moderate gestational hypertension

A
  • Carry out ultrasound foetal growth, amniotic fluid volume assessment and umbilical artery Doppler velocimetry if diagnosis is confirmed at < 34 weeks
  • Only do CTG if activity is abnormal
141
Q

Describe foetal monitoring in Severe gestational hypertension or pre-eclampsia

A
  • Do CTG at time of diagnosis
    • If normal, do not repeat more than weekly
    • Repeat CTG if:
      • Woman report change in foetal movement
      • Vaginal bleeding
      • Abdominal pain
      • Deterioration in maternal condition
  • If conservative management planned, carry out:
    • Ultrasound foetal growth and amniotic fluid volume assessment
    • Umbilical artery Doppler velocimetry
142
Q

What foetal monitoring in Women at high risk of pre-eclampsia should be done and when?

When would you repeat this foetal monitoring?

A
  • Carry out ultrasound foetal growth, amniotic fluid volume assessment and umbilical artery Doppler velocimetry starting at 28-30 weeks
  • Repeat 4 weeks later in women with:
    • Severe pre-eclampsia
    • Pre-eclampsia that needed birth before 34 weeks
    • Pre-eclampsia with an SGA baby
    • Intrauterine death
    • Placental abruption
143
Q

Describe Blood pressure intrapartum care

A
  • During labour, measure blood pressure:
    • Hourly if mild/moderate hypertension
    • Continually if severe hypertension
  • Continue to use antenatal antihypertensive treatment during labour
  • Do NOT routinely limit the duration of the second stage of labour:
    • In women with mild/moderate hypertension
    • If blood pressure is controlled within target ranges in women with severe hypertension
  • Recommend operative birth in the second stage of labour in women with severe hypertension whose hypertension has not responded to initial treatment
144
Q

What is the Medical management of severe hypertension or severe pre-eclampsia in a critical care setting?

A
  • IV magnesium sulphate
  • Consider IV magnesium sulphate for women with severe pre-eclampsia in a critical care setting if birth is planned within 24 hours
  • Dosing of magnesium sulphate
    • Loading IV dose of 4 g over 5 mins, followed by an infusion of 1 g/hour for 24 hours
    • Recurrent seizures should be treated with a further dose of 2-4 g over 5 mins
  • Treat women with severe hypertension in a critical care setting during pregnancy or after birth immediately with one of the following:
    • Labetalol (oral or IV)
    • Hydralazine (IV)
    • Nifedipine (oral)
  • Monitor response to treatment:
    • To ensure blood pressure falls
    • To identify adverse effects
    • To modify treatment according to response
  • Use corticosteroids (betamethasone) if delivery is likely < 36 weeks
    • NOTE: do NOT use corticosteroids in HELLP syndrome
145
Q

What are features of severe pre-eclampsia?

A
  • Severe hypertension and proteinuria
  • Mild or moderate hypertension with one or more of the following:
    • Severe headache
    • Visual disturbance
    • Severe pain just below the ribs
    • Papilloedema
    • Signs of clonus
    • Liver tenderness
    • HELLP syndrome
    • Platelet count falling below 100 x 109/L
    • Abnormal liver enzymes
146
Q

Describe breastfeeding in women with severe pre-eclampsia

A
  • Avoid diuretics if breastfeeding or expressing milk
  • NOT recommended when breastfeeding:
    • ARBs
    • ACE inhibitors (except enalapril and captopril)
    • Amlodipine
  • Drugs that are ok: labetalol, nifedipine, enalapril, captopril, atenolol, metoprolol
147
Q

How does gestational hypertension and pre-eclampsia blood pressure in the future?

A
  • Gestational hypertension and pre-eclampsia increase the risk of the mother developing hypertension later on
  • Increased relative risk of kidney disease but the absolute risk is small if no proteinuria or hypertension at the 6-8 week review
  • If a woman had gestational hypertension their risk in future pregnancies of:
    • Gestational hypertension = 16-47%
    • Pre-eclampsia = 2-7%
  • If a woman had pre-eclampsia their risk in future pregnancies of:
    • Gestational hypertension = 13-53%
    • Pre-eclampsia = 16% (higher if they had severe pre-eclampsia, HELLP syndrome etc.)
148
Q

What is the Puerperium?

A
  • 6-week period following completion of the 3rd stage of labour
149
Q

What is Uterine involution?

A
  • Involution is the process by which the post-partum uterus (1 kg) returns to its pre-pregnancy stage (< 100 g)
  • The fundus goes from lying 12 cm above the pubic symphysis to becoming no longer palpable above the symphysis
  • Involution occurs due to autolysis (muscle cells diminish in size due to enzymatic degradation of cytoplasm)
  • This makes no difference to number of muscle cells
  • Excess protein is absorbed and excreted in the urine
  • Autolysis is accelerated by the release of oxytocin in women who are breastfeeding
  • A delay of involution with no other symptoms is NOT concerning
150
Q

What are signs of delayed involution?

A
  • Artefact
  • Full bladder
  • Loaded rectum
  • Retained products of conception (or clots)
  • Uterine infection
  • Fibroids
  • Broad ligament haematoma
151
Q

What genital tract changes occur during the Puerperium?

A
  • After delivery, the cervix can accommodate 2 fingers
  • After 1 week, it will barely accommodate 1 finger
  • After 2 weeks, the internal os should be closed
  • NOTE: the external os can remain open permanently, giving a ‘funnel-shape’ to the parous cervix
  • Assessing the postpartum cervix is important to diagnose retained products of conception
152
Q

What is lochia?

A
  • This is blood-stained uterine discharge comprising of blood and necrotic decidua
  • Only the top layer of decidua is sloughed off
153
Q

What are the three types of lochia?

A
  • Lochia Rubra - red coloured during the first few days after delivery (gradually changes to pink)
  • Lochia Serosa - becomes serous by the 2nd week
  • Lochia Alba - scanty yellow-white discharge lasting for 1 month
154
Q

Describe perineal tear after normal birth

A
  • 80% complain of pain for the first 3 days after delivery
  • 25% complain of pain at 10 days after delivery
  • Local cooling and topical anaesthetics (e.g. 5% lignocaine) provide short-term symptomatic relief
  • Regular paracetamol can offer effective analgesia
  • Diclofenac may also be added
  • Avoid codeine (causes constipation in mothers and may cause drowsiness in breastfed babies)
  • The perineum should be kept clean using tap water only and sanitary pads should be changed frequently
  • Safetynet about signs of infection (e.g. swelling, discharge, redness, fever)
  • Swabs for culture should be taken if infection is suspected and antibiotics should be started
  • Collections of pus should be drained
  • Spontaneous opening of repaired perineal tears and episiotomies is usually due to infection
  • Surgery can only be performed if there is no infection present
155
Q

Describe bladder function after normal birth

A
  • Voiding difficulty and overdistension of the bladder are not uncommon
  • Especially if regional anaesthesia has been used (bladder may take up to 8 hours to regain normal sensation after epidural anaesthesia)
  • During this time, around 1 L of urine may be produced
  • This can damage the detrusor, leading to a hypocontractile bladder
  • This can lead to overflow incontinence
  • NOTE: a distended bladder may cause an increase in the height of the fundus
156
Q

Why else can mothers experience increased post-partum urine production?

A
  • Fluid loading before epidural analgesia
  • Antidiuretic effect of high concentrations of oxytocin
  • Increased postpartum diuresis
  • Increased fluid intake by breastfeeding mothers
  • NOTE: therefore, fluid balance can be difficult to monitor
157
Q

What are causes of dysuria in mothers who have just given birth?

A
  • periurethral oedema
  • Prolapsed haemorrhoids
  • Anal fissures
  • Abdominal wound haematoma
  • Stool impaction o the rectum
158
Q

When is the best time to assess bladder function postpartum?

A
  • A formal assessment of bladder function is best made 6 hours postnatally (at least 300 mL of urine should have been passed)
  • If, after another attempt, little or no urine has been passed - a small intermittent catheter should be inserted
    • This should drain < 150 mL
    • If > 1 L is drained, an indwelling catheter is left for 48 hours to allow periurethral swelling to settle
    • To minimise the risk of overdistension in women who have had spinal anaesthesia, a urinary catheter is left in the bladder for at least 12 hours until the woman is mobile
159
Q

Why should incontinence be investigated (especially in early puerperium)?

A
  • Urinary stress incontinence is RARELY a problem in the early puerperium
  • So, any incontinence should be investigated to exclude:
    • Vesicovaginal fistula
    • Urethrovaginal fistula
    • Uterovaginal fistula
160
Q

Describe bowel function in puerperium

A
  • Constipation is a COMMON problem in early puerperium
  • Factors contributing to this include:
    • Interruption of a normal diet
    • Intrapartum dehydration
    • Opiate use
  • Advise adequate fluid intake and increase in fibre intake
  • Constipation may also be due to fear of evacuation due to pain from a sutured perineum, prolapsed haemorrhoids or anal fissures
  • Avoidance of constipation is very important in women with 3rd or 4th degree perineal tears
  • These women should receive lactulose and ispaghula husk (Fybogel) or methylcellulose immediately after the repair, for a period of 2 weeks
  • Consider a fistula as a cause of anal incontinence in the postpartum period (around 50% of small fistulae will close spontaneously over 6 weeks)
161
Q

How do pelvic floor exercises affect bowel function in puerperium?

A
  • Although widely believed, there is no solid evidence suggesting that antenatal pelvic floor exercises prevent incontinence or prolapse
  • Women are usually taught postnatal exercises to cultivate a feeling of pelvic floor awareness
162
Q

Describe recovery from Caesarean Section

A
  • C-section has a lower risk of pelvic floor problems but has a HIGHER RISK of:
    • Infection
    • Anaemia
    • Thromboembolism
  • A sterile dressing is placed in theatre but will be removed after 24 hours
  • The wound should be cleaned and dried daily with tap water
  • ALL C-section women to have their Hb measured postop (ideally at day 2-3)
  • Asymptomatic women with mild-moderate anaemia (Hb > 7 g/dL) can be treated with iron tablets
  • Those with more SEVERE anaemia, are likely to need a blood transfusion
  • Early mobilisation and good hydration is important in prevention of VTE
  • 1-6 weeks of LMWH for those with multiple risk factors
  • After the first few days, women should slowly increase their activity levels aided by oral analgesia as required
163
Q

Describe postnatal visits

A
  • A midwife normally visits the mother and child 1-2 times in the first 10 days
  • More frequent visits may be required in high-risk women or if an abnormality is detected
  • At east visit, women should be asked specifically about their recovery
  • Women should be provided with information about danger signs and given emotional support
  • Anti-D immunoglobulin should be given to ALL RhD-negative mothers of RhD-positive babies
  • The only routine test to perform at each postnatal visit in the first week is maternal blood pressure
164
Q

Apart from maternal blood pressure, what other tests should be done at postnatal visits if necessary?

A
  • Signs of infection –> temperature, pulse and signs of uterine involution
  • PPH –> pulse, blood pressure, signs of uterine involution
  • Antenatal anaemia, complicated deliveries or PPH –> Hb should be checked on days 1-3 and iron offered if anaemic
  • Women with Hb < 7 g/dL should be offered a transfusion
165
Q

What should women be asked 2 weeks postnatally?

A
  • Asked about baby blues
166
Q

What exam happens 6 weeks postnatally?

A
  • A formal postnatal exam by the GP
    • Assessment of woman’s mental and physical health and the progress of the baby
    • Direct questions should be asked about urinary, bowel and sexual function
    • Weight, urine analysis and blood pressure are checked
167
Q

How is pre-eclampsia managed in puerperium?

A
  • Nearly 50% of all eclamptic fits happen postnatally
  • It is also the highest risk time for fluid overload
  • Those with severe pre-eclampsia should be managed for the first 24 hours in an HDU until their BP is controlled and they achieve good diuresis
  • Those with mild or moderate pre-eclampsia are managed on a postnatal ward until stable
  • They should continue antenatally prescribed antihypertensives with the aim of keeping BP < 150/100 mm Hg
    • Labetalol and slow-release nifedipine are good options
    • Usually needed for 1-2 weeks postnatally
    • A BP should be measured at home every 2 days and the dosage should be halved when BP < 140/90 mm Hg
  • Those still on antihypertensives at 6 weeks should be referred to specialists
168
Q

What is secondary post-partum haemorrhage?

A
  • DEFINITION: fresh bleeding from the genital tract between 24 hours and 6 weeks after delivery
  • MOST COMMON time for secondary PPH is between days 7-14
169
Q

What are the causes of secondary post-partum haemorrhage?

A
  • Endometritis - lower abdominal pain and a tender uterus with a closed internal os
  • Retained products of conception - crampy lower abdominal pain, a uterus larger than appropriate, open internal os and a history of a prolonged 3rd stage of labour
  • Both may have signs and symptoms of infection (e.g. fever, pungent lochia, uterine tenderness)
170
Q

If post-partum bleeding is heavy, what may mothers need?

A
  • IV fluids or blood
  • Strong oxytocics (e.g. ergometrine)
  • Uterine evacuation
  • Antibiotics (if placental tissue is found)
  • NOTE: If there is NO clear diagnosis of PPH, expectant management with empirical antibiotics is usually used
171
Q

Apart from endometritis and retained products of conception, what other causes of secondary PPH are there?

A
  • Hormonal contraception
  • Bleeding disorders (e.g. von Willebrand disease)
  • Choriocarcinoma (RARE)
172
Q

What is obstetric palsy?

A
  • AKA traumatic neuritis

- Motor and/or sensory neuropathy in lower limbs following delivery

173
Q

What are presenting features of obstetric palsy?

A
  • Sciatic pain
  • Foot-drop
  • Paraesthesia
  • Hypoaesthesia
  • Muscle wasting
174
Q

What is obstetric palsy caused by?

A
  • Caused by proximal nerve damage as the lumbosacral plexus and nerve tracks are stretched and compressed by the foetal head
  • Almost always associated with prolonged or obstructed labour
  • It is now RARE, thanks to modern labour management
  • If obstetric paralysis occurs after normal labour, consider epidural complications and herniation of the lumbosacral discs
175
Q

What is symphysis pubis diastasis?

A
  • This is spontaneous separation of the symphysis pubis

- Associated with forceps delivery, rapid second stage of labour or severe abduction of the thighs during delivery

176
Q

What are the presenting features of symphysis pubis diastasis?

A
  • Symphyseal pain aggravated by weight-bearing and walking
  • Waddling gait
  • Pubic tenderness
  • Palpable interpubic gap
177
Q

What is the management of symphysis pubis diastasis?

A
  • bed rest, anti-inflammatory agents, physiotherapy and pelvic corset
178
Q

Describe thromboembolism in puerperium

A
  • Those at risk should be given prophylactic heparin injections
  • If DVT or PE are suspected, full anticoagulant therapy should be initiated
  • Lower limb compression ultrasound and/or lung scan should be carried out within 24-48 hours
179
Q

What is puerperal pyrexia?

A
  • Temperature > 38 degrees on any 2 of the first 10 days postpartum, exclusive of the first 24 hours
  • Mildly elevated temperature is not uncommon in the first 24 hours
  • However, if this is associated with tachycardia, it warrants investigation
  • If a women develops a fever after C-section, it is much more likely to be infection
  • Common sites of puerperal pyrexia: chest, throat, breasts, urinary tract, pelvic organs, Caesarean scar, perineal wounds
180
Q

Describe chest complications in puerperium

A
  • Most likely to appear within the first 24 hours (particularly after general anaesthesia)
  • Atelectasis may be associated with a fever and can be prevented with early and regular chest physiotherapy
  • Aspiration pneumonia (Mendelson’s syndrome) must be suspected if there is a spiking temperature associated with wheezing, dyspnoea or evidence of hypoxia following general anaesthetic
181
Q

What is puerperal sepsis?

A
  • Genital tract infection following delivery
182
Q

What is the aetiology of puerperal sepsis?

A
  • Mixed flora of low virulence normally colonises the vagina
  • Puerperal infection is usually polymicrobial and involve contaminants from the bowel
  • Placental separation exposes a large raw area (like an open wound)
  • Vaginal delivery is almost inevitably going to cause some lacerations in the genital tract
183
Q

What organisms are commonly associated with puerperal genital infection?

A

Aerobes

  • Gram-positive
    • beta haemolytic streptococcus, groups A, B, D
    • Staphylococcus epidermidis and S. aureus
  • Gram negative
    • Escherichia coli
    • Haemophilus influenzae
    • Klebsiella pneumoniae
    • Psuedomonas aeruginosa

Anaerobes
- Peptococcus sp

  • Chlamydia trachomatis
184
Q

How do you prevent puerperal infection?

A
  • Increased awareness of hygiene
  • Good surgical approach
  • Use of aseptic techniques
  • C-section patients should receive prophylactic antibiotics
    • A single intraoperative dose of antibiotics (co-amoxiclav or cephalosporin with metronidazole) is given before the skin incision
185
Q

How does puerperal infection spread?

A
  • Ascending infection from the lower genital tract or primary infection of the placental site may spread via the Fallopian tubes to the ovaries (causing salpingo-oophoritis and pelvic peritonitis)
    • This could progress to generalised peritonitis and the development of a pelvic abscess
  • Infection may spread directly into the myometrium and parametrium
    • Causes endometritis and parametritis (aka pelvic cellulitis)
    • Pelvic peritonitis and abscess may occur
  • Infection may spread from distant sites via the lymphatics and blood vessels
    • This can cause septic thrombophlebitis, pulmonary infections or generalised septicaemia and endotoxic shock
186
Q

What are symptoms of puerperal infection?

A
  • Malaise, headache, fever, rigors
  • Abdominal discomfort
  • Vomiting and diarrhoea
  • Offensive lochia
  • Secondary PPH
187
Q

What are signs of puerperal infection?

A
  • Pyrexia and tachycardia
  • Uterus - boggy, tender and larger
  • Infected wounds
  • Peritonism
  • Paralytic ileus
  • Indurated adnexae (paramtritis)
  • Bogginess in pelvis (abscess)
188
Q

What is the management of puerperal infection?

A
  • Mild to moderate infections can be treated with broad-spectrum antibiotics (e.g. co-amoxiclav or cephalosporin + metronidazole)
  • In SEVERE infections, the release of vasoactive mediators can lead to septic or endotoxic shock
    • Immediate high-dose, broad-spectrum antibiotics and IV fluid resuscitation should be given in an HDU
189
Q

Where can necrotising fasciitis arise from?
Which organism is usually identified?
What are signs?
What is its management?

A
  • Necrotising fasciitis is rare but can arise from perineal tears, episiotomis and C-section wounds
    • Clostridium perfringens is usually identified
    • General signs of infection will be accompanied by extensive necrosis, crepitus and inflammation
    • Wide debridement of necrotic tissue under GA is absolutely essential to avoid mortality
190
Q

Describe puerperal psychiatric disorders

A
  • The risk of bipolar disorders and severe depressive illness are greatly increased postpartum
  • Women with previous mental health problems are at particular risk of recurrence during the antepartum and postpartum period
  • Changes in hormone levels are likely to contribute (e.g. progesterone)
  • NOTE: depression may be a manifestation of postpartum hypothyroidism
191
Q

What are the Pinks?

A
  • First 24-48 hours

- Elevated mood, a feeling of excitement, overactivity and difficulty sleeping

192
Q

What are the Blues?

A
  • Up to 80% experience postnatal blues in the first 2 weeks after delivery
  • Features: fatigue, short temper, difficulty sleeping, depressed mood and tearfulness
  • Spontaneous resolution in most cases
193
Q

What are abnormal features NOT consistent with baby blues?

A
  • Panic attacks
  • Episodes of low mood for a prolonged duration (> 2 weeks)
  • Low self-esteem
  • Guilt or hopelessness
  • Thoughts of self-harm or suicide
  • Mood changes that disrupt normal social functioning
  • Biological symptoms (e.g. poor appetite)
  • Change in affect
194
Q

What are screening questions for mental health problems during or after pregnancy? (at booking, and in the postnatal period (at least twice))

A
  • During the past month, have you often felt down, depressed or hopeless?
  • During the past month, have you often been bothered by having little interest or pleasure in doing things?
  • Are these feelings something you need or want help with?
195
Q

Describe Postpartum (non-psychotic) Depressive Illness

A
  • 10-15% will suffer some form of depression in the first year after delivery
  • Without treatment, most women recover spontaneously within 3-6 months (but 1 in 10 will remain depressed at 1 year)
  • Women with a history of severe depression are at higher risk
  • The Edinburgh Postnatal Depression Scale is a screening technique
  • ALL women should be asked about their mood at least twice in the postpartum period (ideally at 6 weeks and 3-4 months)
  • Women at HIGH RISK should be under close surveillance by the specialist community psychiatric nurse
196
Q

How long does post-partum depressive illness occur for?

A
  • Usually presents around 6 weeks with a gradual onset

- Therefore, 6-week postnatal check is ideal to pick this up

197
Q

What are symptoms of severe postnatal depressive disorder?

A
  • Early-morning wakening
  • Poor appetite
  • Diurnal mood variation (worse in the morning)
  • Low energy and libido
  • Loss of enjoyment
  • Lack of interest
  • Impaired concentration
  • Tearfulness
  • Feelings of guilt and failure
  • Anxiety
  • Thoughts of self-harm/suicide
  • Thoughts of harm to the baby
198
Q

What are risk factors for Postnatal Depressive Illness?

A
  • Past history of psychiatric illness
  • Depression during pregnancy
  • Obstetric factors (e.g. C-section, neonatal loss)
  • Social isolation and deprivation
  • Poor relationships
  • Recent adverse life events (e.g. bereavement)
  • Severe postnatal blues
199
Q

What are complications of Postnatal Depressive Illness?

A
  • Physical morbidity
  • Suicide
  • Damaged social attachment to infant
  • Disrupted emotional development of infant
  • Social/cognitive effects on child
  • Marital breakdown
  • Future mental health problems
200
Q

What is the management of severe postnatal affective disorders?

A
  • Remedy of social factors
  • Non-directive counselling
  • Interpersonal psychotherapy
  • CBT
  • Drug therapy
    • Usually TCAs and SSRIs
  • Encouragement to join a local postnatal group may prevent social isolation and limit depression
201
Q

What is Puerperal Psychosis?

A
  • MOST COMMONLY presents on the 5th day postpartum
  • In general, presents within 4 weeks
  • Abrupt onset
202
Q

What are the risk factors of puerperal psychosis?

A
  • Previous history of puerperal psychosis
  • Previous history of severe non-postpartum depressive illness
  • Family history of bipolar disorder/affective psychosis
203
Q

What are symptoms of puerperal psychosis?

A
  • Restless agitation
  • Insomnia
  • Perplexity/confusion
  • Fear/suspicion
  • Delusions/hallucinations
  • Failure to eat and drink
  • Thoughts of self-harm
  • Depressive symptoms (guilt, hopelessness)
  • Loss of insight
204
Q

What is the management of puerperal psychosis?

A
  • Refer urgently to psychiatry
  • Usually require admission (preferably to a mother-and-baby unit)
  • Acute pharmacotherapy with neuroleptics (e.g. chlorpromazine, haloperidol)
  • Treatment of mania with lithium carbonate
  • Electroconvulsive therapy
  • Antidepressants as 2nd line (takes 10-14 days to work)
205
Q

What is the prognosis of puerperal psychosis?

A
  • Recover usually occurs over 4-6 weeks but treatment with antidepressants will be needed for at least 6 months
  • Risk of recurrence in future pregnancy is 1 in 2
    • Women with previous puerperal psychosis should be considered for prophylactic lithium
206
Q

What is colostrum?

A
  • Yellowish fluid secreted by the breast that can be expressed as early as the 16th week of pregnancy (replaced by milk during the second postpartum day)
  • Colostrum has an important role in protection against infection
207
Q

What are the major constituents of breast milk?

A
  • Lactose
  • Protein (lactalbumin, lactoglobulin and caseinogen)
  • Fat
  • Water
  • All vitamins except vitamin K
208
Q

What do prolactin and oxytocin do in breastfeeding?

A
  • Prolactin stimulates milk synthesis and is essential for lactation
  • Oxytocin causes contractions of the myoepithelial cells lying longitudinally along the lactiferous ducts causing expulsion of milk
209
Q

What is the rooting reflex?

A
  • When the skin around the baby’s mouth is touched, the mouth begins to gape
  • Babies should be fed on demand and left on the breast until feeding finishes spontaneously
210
Q

What are the advantages in breastfeeding?

A
  • Readily available at the right temperature and ideal nutritional value
  • Cheaper than formula feed
  • Has a contraceptive effect associated with amenorrhoea
  • Reduced necrotising enterocolitis risk in preterm babies
  • Reduced childhood infective illness (especially gastroenteritis)
  • Reduced atopic illness (e.g. eczema, asthma)
  • Reduced juvenile diabetes
  • Reduced childhood cancer (especially lymphoma)
  • Reduced premenopausal breast cancer
  • NOTE: HIV is transmitted in breastmilk, however, mothers in resource-limited settings are advised to take antiretrovirals and exclusively breastfeed as the risk of childhood mortality is higher if not breastfeeding
211
Q

How can lactation suppression occur?

A
  • Fluid restriction

- Tight bra