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Women's Health > Complications in Pregnancy > Flashcards

Complications in Pregnancy Flashcards

1
Q

What are some high risk factors for pre-eclampsia?

A
  • Hypertensive disease during a previous pregnancy
  • CKD
  • Autoimmune disease such as SLE or antiphospholipid syndrome
  • T1 or T2DM
  • Chronic HTN
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2
Q

What are some moderate risk factors for pre-eclampsia?

A
  • First pregnancy
  • > /= 40yrs
  • Pregnancy interval of >10yrs
  • BMI of 35kg/m^2 or more at first visit
  • FH of pre-eclampsia or previous pre-eclampsia
  • Multi-foetal pregnancy
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3
Q

What does NICE recommend to reduce the risk of pre-eclampsia?

A

Recommend commencing aspirin 75mg to reduce the risk of developing pre-eclampsia.

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4
Q

What is the difference between pregnancy-induced hypertension and pre-eclampsia?

A
  • Pregnancy-induced hypertension = hypertension >20 wks, without proteinuria
  • Pre-eclampsia = hypertension >20 wks with proteinuria (PCR > 30)
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5
Q

What is the significance of anaemia in pregnancy?

A
  • Hb concentration <110g/l in 1st trimester + <105g/l in 2nd and 3rd trimesters and <100g/l postpartum
  • Iron deficiency with/without anaemia, is associated with maternal fatigue and potentially, poorer QoL and increased risk of postpartum depression
  • Maternal anaemia increases the risk of PPH, perinatal/neonatal mortality, LBW and pre-term birth
  • Need to be commenced on iron replacement therapy
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6
Q

What are the symptoms of pre-eclampsia?

A
  • Severe headache
  • Problems with vision, such as blurring or flashing before the eyes
  • Severe pain just below the ribs - epigastric region
  • Vomiting
  • Sudden swelling of face, hands or feet
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7
Q

What questions do you want to ask when suspecting pre-eclampsia?

A
  • Headache - SOCRATES
  • Any epigastric pain?
  • Visual disturbances?
  • Examination: inspect abdomen, measure symphysis fundal height. Palpate for presentation, lie and auscultation of foetal heart
  • Tests: BP, urine dip (protein and glucose)
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8
Q

What are uterine stimulants?

A
  • Endothelin
  • Ergometrine
  • Prostin
  • Misoprostol
  • Oxytocin
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9
Q

What are uterine relaxants?

A
  • Nifedipine
  • Relaxin
  • Terbutaline
  • Magnesium
  • Nitric oxide
  • Atosiban
  • Indomethacin
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10
Q

What is the normal plasma volume in pregnancy?

A

Maternal plasma volume increases by ~50% above the non-pregnant value by the late 2nd trimester. Red cell mass only increases by 25-30%, resulting in a fall in Hb concentration (physiological anaemia in pregnancy).

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11
Q

What is the normal platelet volume in pregnancy?

A

Up to 10% of healthy pregnant women have a count below the non-pregnant reference range of 150-400x10^9/L at term (gestational thrombocytopenia). The count rarely falls below 100x10^9/L and there is no increase in bleeding risk.

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12
Q

What are the normal coagulation factors values in pregnancy?

A

Many coagulation factors, include plasma fibrinogen and Factor VIIIc, are increased in normal pregnancy and the anticoagulant factor protein is reduced. This contributes to the increased risk of thrombotic complications in pregnancy.

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13
Q

What is the pattern of BP in pregnancy?

A
  • 1st trimester: ~120/70
  • 2nd trimester: BP falls
  • 3rd trimester: increases and returns to pre-pregnancy levels
  • PIH has a similar trend but ends with a higher BP
  • Pre-eclampsia starts with a higher BP, doesn’t have a marked dip and ends at a much higher BP
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14
Q

How is pre-eclampsia diagnosed?

A
  • Incidence 3-5%
  • > 140/90 on 2 occasions 4hrs apart
  • Proteinuria >300mg/24hrs or >30mg/mmol on spot test protein creatinine ratio
  • Spectrum of disease - majority get mild disease later in pregnancy
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15
Q

What investigations can be done for pre-eclampsia?

A
  • BP monitoring
  • Quantify proteinuria to confirm diagnosis
  • Maternal - U+Es, LFTs, urate, FBC with platelets and Hb
  • Foetal (associated with FGR) - USS for growth and markers of placental function
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16
Q

What is the management of pre-eclampsia?

A
  • ONLY cure is delivery of the placenta - induction of labour or caesarean section
  • Balance risks and benefits - woman needs to be in hospital for monitoring
  • Spectrum of disease - chronic vs rapidly fulminating
  • Gestation - very premature vs later in pregnancy
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17
Q

What is the treatment for pre-eclampsia?

A
  • Blood pressure - keep <160 systolic, labetalol, nifedipine (labetalol 1st line but give nifedipine if they have asthma), hydralazine (vasodilator)
  • Fluid balance - fluid restrict due to risk of pulmonary oedema
  • Prevention of fits (eclampsia) - magnesium sulfate infusion
  • Management of HELLP (Haemolysis, Elevated Liver Enzymes, Low Platelets) is supportive - blood transfusion (treat low platelets and RBCs), treat BP and give magnesium
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18
Q

What are signs of magnesium toxicity?

A
  • Loss of tendon reflexes (due to neuromuscular blockade)
  • Respiratory depression
  • Cardiac arrest
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19
Q

What is the management for pregnancy induced hypertension?

A
  • Much less severe but can develop into pre-eclampsia (25% risk)
  • Increased surveillance and monitoring - regular screening BP and urine for protein
  • Treat BP - nifedipine and labetalol
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20
Q

What is Small for Gestational Age (SGA)?

A

Foetus born with birth weight below 10th centile (ideally from customised growth chart as more sensitive for detecting small babies at higher risk of morbidity and mortality). Not all SGA babies are FGR - 50-70% are constitutionally small.

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21
Q

What is Foetal Growth Restriction (FGA)?

A

Failure of foetus to reach its pre-determined growth potential due to pathology. FGR is only used for babies where there is evidence (on growth charts) that growth has faltered (i.e. poor growth velocity, crossing of centiles).
SGA babies = increased risk of morbidity and mortality but FGR increases perinatal mortality dramatically

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22
Q

What is the difference between symmetrical and asymmetrical FGR?

A
  • Symmetrical FGR: head and abdomen size are equally small, may be due to an insult in early pregnancy; chromosomal/congenital issue, intrauterine infections, substance abuse
  • Asymmetrical FGR: foetus responds to inadequate nutrition by redirecting blood flow to head/brain and heart > abdominal fat stores are reduced (brain sparing). This is usually due to insult later in pregnancy e.g. PET, essential HTN, maternal smoking.
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23
Q

What are minor risk factors for FGR?

A
  • Maternal age >35yrs
  • IVF pregnancy
  • Nulliparity
  • BMI <20 or 25-34.9
  • Smoker 1-10pd
  • Previous PET
  • Pregnancy interval <6m or >60m
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24
Q

What are major risk factors for FGR?

A
  • Maternal age >40
  • Smoker >11pd
  • Paternal or maternal SGA
  • Cocaine use
  • Previous SGA or stillbirth
  • Chronic HTN
  • Diabetes with vascular disease
  • Renal impairment
  • APS
  • Heavy BPV
  • Low PAPP-A
  • Foetal echogenic bowel
25
Q

What is the management for FGR based on the number of risk factors in the pregnancy?

A

Minor:
- If >/= 3 risk factors: Uterine Artery Doppler at 20wk scan - if normal then single scan in 3rd trimester, abnormal then serial scans from 28 weeks
Major:
- If one of more RF, serial scanning from 28 weeks
- If patient unsuitable for monitoring of growth by SFH measurements (BMI >35 or fibroids) for serial scans from 28 weeks

26
Q

What is the aetiology of FGR?

A

Gas exchange and nutrient delivery to foetus is impaired due to:
- Impaired maternal oxygen carrying (heart disease, smoking haemoglobinopathies e.g. sickle cell, thalassaemia)
- Impaired oxygen delivery (due to maternal vascular disease e.g. HTN, diabetes, autoimmune disease)
- Placental damage (smoking, thrombophilia, PET, autoimmune diseases e.g. SLE or antiphospholipid syndrome)
Intrinsic problems within the foetus
- Chromosomal or congenital abnormalities
- Intrauterine infections e.g. congenital rubella, CMV, parovirus

27
Q

What are the short term implications of FGR for the foetus?

A
  • Premature birth - necrotising enterocolitis, HIE + sequelae, CLD, NICU stay
  • Low Apgar’s (need for medical attention when born) - any score <7 needs medical attention
  • Hypoglycaemia/hypocalcaemia
  • Hypothermia
  • Polycythaemia + hyperbilirubinaemia
28
Q

What are the long term implications of FGR for the foetus?

A
  • Learning difficulties
  • Short stature
  • Failure to thrive
  • Cerebral palsy
  • HTN
  • T2DM
  • Heart disease
29
Q

What is the screening and diagnosis process for FGR?

A
  • All women will be screened for risk factors at booking
  • If risk factors present - need extra monitoring throughout pregnancy
  • If no risk factors - they are screened with SFH throughout pregnancy at each antenatal visit
  • If SFH measures below 10th centile or there is reduced velocity/static growth - referred for growth scan
30
Q

How is USS biometry used for measuring baby?

A
  • Abdominal circumference (AC), head circumference (HC) + femur length (FL) are combined using the Hadlock calculation to give estimated fetal weight (EFW).
  • Serially plotted on customised growth chart
  • Looked at in conjunction with liquor volume (LV) + umbilical artery doppler (measures resistance in artery - therefore in placenta) > in healthy baby there should be no resistance
31
Q

How is umbilical artery flow interpreted?

A
  • Characteristic saw-tooth appearance of arterial flow in one direction and continuous umbilical venous blood flow in the other
  • If, like in FGR, there is abnormal placental function there will be resistance in the umbilical artery. This results in decreased end-diastolic flow, gets worse until no forward flow in diastole > absent end-diastolic flow
  • Resistance becomes so great it reverses blood flow in artery > reverse end-diastolic flow > fetal acidosis and distress > likely imminent delivery
32
Q

How is early onset (<32 wks) FGR managed?

A
  • May suggest possibility of congenital infection or chromosomal abnormality
  • Detailed USS should be performed to exclude structural abnormalities
  • If chromosomal abnormality is suspected they should be offered amniocentesis
  • Steroids (for lung maturity)
  • Intensive monitoring - if doppler shows reverse end-diastolic flow then needs to be repeated everyday and delivery considered
33
Q

How is late onset (>32 wks) FGR managed?

A
  • Surveillance
  • Delivery if evidence of foetal compromise
  • Steroids if <36wks - if considering caesarean then steroids up to 39 wks
34
Q

How can you try and prevent FGR?

A
  • Smoking cessation
  • Aspirin for women at risk of PET
  • Appropriate screening
35
Q

What is the APGAR scoring system?

A
  • APGAR used to determine health of newborn baby
  • Take APGAR score 1 min after birth to give clues as to problem
  • Take at 5 mins also (if score >7, suggests normal, if score <3, suggests neuro damage e.g. cerebral palsy)
  • Can take score thereafter whenever needed to measure progress
36
Q

What are the values for the APGAR scoring system?

A
  1. Appearance - blue/pale, Pulse - absent, Grimace - absent facial expressions, Activity - absent movement, Respiration - absent
  2. A - acrocyanosis (half blue/half pink), P - <100, G - feeble/weak cry, A - some flexion, R - weak
  3. A - pink, P - >100, G - strong cry, A - full movement, R -strong
37
Q

What is the management for different APGAR scores?

A
  • <3 immediate critical care/NICU
  • 4-6 needs care, does not necessarily mean prominent neurological damage, take sequential readings for APGAR at 15/30 mins
38
Q

What pharmacological agents are used for management of PPH?

A
  • Syntocinon
  • Syntometrine
  • Ergometrine
  • Misoprostol
  • Carboprost
  • Transexamic acid
39
Q

What are uterine fibroids?

A
  • Reported incidence of fibroid varies from 5.4-77%, depending on the method of diagnosis used (gold standard is histological evidence)
  • They are oestrogen dependent and may increase in size in pregnancy. This increase in size leads to large for dates pregnancies.
  • They may be complicated by red degeneration when the blood supply to the fibroid is compromised leading to pain and uterine tenderness
  • Treatment is bed rest and analgesia
  • Other complications: malpresentation dependent on position of fibroid, obstructed labour, need for caesarean section, intrapartum and postpartum haemorrhage
40
Q

What is the breech presentation?

A

Baby isn’t orientated properly in the stomach - ~25% of pregnancies at 28 weeks are breech, but only 3% near term.

  • Frank breech - most common, hips flexed and knees fully extended (bum first)
  • Footling breech - one/both feet come first (rare but high perinatal morbidity
  • Cord prolapse is more common in breech presentations
41
Q

What are risk factors for breech presentation?

A
  • Placenta praevia
  • Polyhydramnios/oligohydramnios
  • Foetal abnormality
  • Prematurity
42
Q

What is the management for a breech presentation?

A
  • Wait until 36 weeks, if at 36wks baby still breech then do external cephalic conversion (ECV) (works around 60% of the time) - involves doctor manually moving baby by pressing on stomach.
  • Do at 36wks in nulliparous women and 37 wks for multiparous
  • SE: small risk that ECV can induce labour > will probably need urgent C-section
43
Q

What are absolute contraindications to ECV?

A
  • Woman needs C-section
  • Antepartum haemorrhage in last 7 days
  • Abnormal CTG
  • Major uterine issue
  • Ruptured membranes
  • Multiple pregnancy
44
Q

What are the indications for induction of labour?

A
  • Prolonged pregnancy e.g. >12 days after estimated delivery date
  • Pre-labour premature rupture of membranes - where labour doesn’t start
  • Diabetic mother >38wks
  • Rhesus incompatibility
45
Q

What is a membrane sweep?

A

Doctor sweeps finger around cervix during internal exam > separates membranes of amniotic sac from cervix. This separation releases prostaglandins > triggers labour. If labour doesn’t start after a membrane sweep, induction of labour will be offered

46
Q

What are methods of inducing labour?

A
  • Intravaginal prostaglandins
  • Breaking of water
  • Oxytocin
47
Q

What is antepartum haemorrhage?

A

Bleeding after 24 weeks

48
Q

What are major causes of bleeding in 1st trimester of pregnancy?

A
  • Spontaneous abortion
  • Ectopic pregnancy
  • Hydatidiform mole
49
Q

What are major causes of bleeding in 2nd trimester of pregnancy?

A
  • Spontaneous abortion
  • Hydatidiform mole
  • Placental abruption
50
Q

What are major causes of bleeding in 3rd trimester of pregnancy?

A
  • Bloody show
  • Placental abruption
  • Placenta praevia
  • Vasa praevia
51
Q

What is a threatened miscarriage?

A

Painless vaginal bleeding, typically around 6-9 weeks

52
Q

What is a missed (delayed) miscarriage?

A

Light vaginal bleeding and symptoms of pregnancy disappear

53
Q

What is an inevitable miscarriage?

A

Complete or incomplete depending on whether all fetal and placental tissues have been expelled

54
Q

What is a complete and incomplete miscarriage?

A
  • Complete: little bleeding

- Incomplete: heavy bleeding and crampy, lower abdominal pain

55
Q

How does an ectopic pregnancy present?

A

Typically hx of 6-8 weeks amenorrhoea with lower abdo pain (usually unilateral) initially and vaginal bleeding later. Shoulder tip pain and cervical excitation may be present.

56
Q

How does hydatidiform mole present?

A

Typically bleeding in 1st or early 2nd trimester associated with exaggerated symptoms of pregnancy e.g. hyperemesis. The uterus may be large for dates and serum hCG is very high.

57
Q

How does placental abruption present?

A

Constant lower abdominal pain and woman may be more shocked than is expected by visible blood loss. Tender, tense uterus with normal lie and presentation. Foetal heart may be distressed.

58
Q

How does placenta praevia present?

A
  • Vaginal bleeding, no pain. Non-tender uterus but lie and presentation may be abnormal.
  • Vaginal exam should not be performed in primary care for suspected antepartum haemorrhage - women with placenta praevia may haemorrhage
59
Q

How does vasa praevia present?

A

Rupture of membranes followed immediately by vaginal bleeding. Fetal bradycardia is classically seen.

Women's Health (19 decks)

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