Complications in Pregnancy

Question 1

What are some of the minor symptoms during pregnancy?

What are the common complications that occur during the 1ST TRIMESTER?

Answer 1

• Fatigue, N+V, Constipation, Heartburn, Breast tenderness, Urinary frequency, Headache, Backache, Emotional liability
• • Miscarriage (15% of pregnancies)
  • Ectopic pregnancy (0.5-2%)
  • Hyperemesis Gravidarum (1-2%)

Question 2

What are the common Maternal complications that occur during the 2ND + 3RD TRIMESTER?

Why is UTI common during pregnancy?

What are the common Foetal complications that occur during the 2ND + 3RD TRIMESTER? What does each mean?

Answer 2

- • UTI
• Anaemia (Common)
• Gestational Diabetes (5%)
• Pre-eclampsia (4-5%)
• Antepartum Haemorrhage

• Due to Urinary stasis (Mass effect and relaxation due to Progesterone) and Immunosuppression; TEST URINE EVERY VISIT
• • Premature Labour - Delivery before 37 weeks
  • Intrauterine Growth Restriction (IUGR) - Failure to reach growth potential or <2.5kg at term
  • Macrosomia - >4.5kg at term

Question 3

ANAEMIA (Very common):
How does the Hb range differ between non-pregnant and pregnant women?

How does the blood change during pregnancy?

What is it commonly caused by?

When are Hb levels checked?

How is it treated?

Answer 3

• • 12-16g/dL (Non-pregnant)
  • 10.5-13g/dL (Pregnant)
• Normal increase in Plasma volume, RBC mass, and Haemodilution (lower Hb concentration)
• Iron deficiency, Sickle cell/Thalassaemia, Vitamin B12/Folate deficiency, Blood disorders
• At Booking, Week 28, and Week 36
• • If Hb <10.5g/dL, give Ferrous sulphate
  • If Hb <7mg/dL or Symptomatic, give Transfusion

Question 4

GESTATIONAL DIABETES/GDM (5%):
What is it?

What is it associated with?

How does it occur?

In who is it more likely to occur?

When is it screened/tested for?

Answer 4

• True GDM diagnosed for the first time after 20 weeks, otherwise is Pre-existing T1/2 Diabetes
• Increased risk of Perinatal and Maternal morbidity and mortality
• Placental steroids (hPL, Cortisol, Oestradiol, Glucagon) lead to Insulin resistance, which increases glucose for placental transfer
• Obese, Family Hx, Medical Hx, Previous history of Macrosomia (baby >4.5kg), Polycystic Ovary Syndrome (PCOS), Older age
• • Screen high-risk groups at Booking
  • Screen everyone at 28 weeks

Question 5

PRE-EXISTING DIABETES MELLITUS:
What is an increased HbA1c at conception linked to?

What does Foetal hyperglycaemia lead to?
→ How do some of these affect delivery and the baby?

How is it managed?

Answer 5

• Linked to Congenital malformations - Sacral agenesis, Skeletal and NTDs, CHD
• • Glycosuria → Polyhydramnios
  • Hyperinsulinaemia and B-cell Hyperplasia → Macrosomia, Neonatal Hypoglycaemia, Polycythaemia, and Inhibition of pulmonary surfactant production
• • Polyhydramnios = Malpresentation, Cord prolapse, Post-partum Haemorrhage
  • Macrosomia = Prolonged labour, Post-partum Haemorrhage, Pre-eclampsia, Shoulder dystocia, C-section
  • Inhibition of surfactant production = RDS
  • Polycythaemia = Jaundice
• • Pre-pregnancy counselling to achieve normal glucose levels - Diet +/- Insulin/Metformin
  • USS - Detect congenital abnormalities and assess Foetal growth/Polyhydramnios
  • Timing of delivery - Evaluating risk between Intrauterine death and RDS, as well as between Macrosomia, Shoulder dystocia and C-section
  • Screening for Pre-eclampsia

Question 6

Pre-eclampsia (PET):
How is it diagnosed?

What change in BP is seen from Booking?

How does it relate to TPR? What causes this? What’s the normal change in TPR?

What occurs in the development of this condition?

What are the consequences of PET on the Mother?

What are the consequences of PET on the Foetus?

Answer 6

• HTN after 20 weeks gestation on 2 separate occasions at least 4 hours apart PLUS significant PROTEINURIA
  o Includes Oedema only if severe or in an unusual site e.g. Fingers, Face, Sacral
• > 30 Systolic/>20 Diastolic
• PET occurs due to an ↑TPR secondary to SYSTEMIC VASOSPASM
  o ↓TPR due to normal Vasodilation by placental steroids
• • Disorder of Placentation - Failure of 2nd wave of Trophoblastic invasion
  • Systemic Vasospasm
  • Systemic Microangiopathy - Endothelial Dysfunction leads to Microthrombosis and Infarction of end-organs
  • Increased Capillary permeability
• • Vasospasm → HTN → (Hypertensive) Encephalopathy → Eclampsia and Cerebral Haemorrhage
  • Microvascular damage → End-organ disease and Increased vascular permeability → Pulmonary oedema and Acute RDS
  • Glomerular dysfunction → Proteinuria → Oedema → Renal failure
• • Reduced placental transfer → Hypoxia, Malnourishment and Placental abruption
  • Reduced foetal renal perfusion → Oligohydramnios