Complications of Pregnancy Flashcards
The majority of pregnancies are completely straightforward and low risk. Nearly all women experience minor troublesome symptoms to some degree. What do minor symptoms include?
- tiredness / nausea + vom / constipation / heartburn / breast tenderness / frequency / backache / piles / headache / heat intolerance / scramble-brain / emotional lability
- abnormality depends on degree of symptoms
- difficulty is spotting the pathology - “needle in a hay stack”
What are common complications in the first trimester?
- miscarriage (15% all pregnancies)
- ectopic pregnancy (0.5-2%)
- hyperemesis gravidarum (2-5%)
What are common complications in the second and third trimesters for the mother?
- UTI
- anaemia (common)
- pre-eclampsia (4-5%)
- gestational diabetes (variable - 5%)
- antepartum haemorrhage
What are common complications in the second and third trimesters for the foetus?
- premature labour (delivery <37 completed weeks)
- intrauterine growth restriction (IUGR) - failure to reach growth potential or <2500g at term
- macrosomia (>4500g at term)
Describe and explain the risk of UTI in pregnant women
- increased throughout pregnancy compared to non-preg women
- relative urinary stasis - mass effect + progesterone leading to sm muscle relaxation (rel hydro-ureters/nephrosis)
- immuno-suppression
- symptoms can be mild or absent
- UTIs associated w obstetric problems esp pre-term delivery
- TEST urine EVERY visit!!!!
What is the normal range for Hb in females (non-pregnant and pregnant)?
- non-pregnant females: Hb 12-16 g/dl
- pregnant range: Hb 10.5-13 g/dl
Why is the normal haemoglobin range in pregnant women lower?
- circulating volume increases from 4.5L -> 6L
- increased plasma volume > inc red cell volume
- there is physiological dilution of Hb concentration (not physiological anaemia of pregnancy!)
- maximal dilution occurs at 28-30weeks
When should anaemia be investigated for in pregnant women?
- when Hb <10.5g/dl
- common causes: Fe deficiency
- sickle cell or thalassaemia trait
- Vit B12 + folate deficiency
- blood dyscrasias eg. leukaemias etc.
How do you manage anaemia in pregnancy?
- check Hb at booking / 28 / 36 weeks
- investigate for cause of anaemia eg. serum ferritin / B12 / folate / electrophoresis
- treat underlying cause if Hb <10.5 eg. ferrous sulphate
- transfuse if Hb <7 or symptomatic
What is gestational diabetes?
- diabetes mellitus diagnosed or recognised for first time >20/40 gestation
- (true GDM + pre-existing DM)
How is pre-existing IDDM/NIDDM different to gestational diabetes?
Pre-existing - already diagnosed pre-preg or recognised <20/40
Why is diabetic pregnancy associated with high risk obstetrics?
- increased perinatal morbidity + mortality
- increased maternal morbidity
- small increase maternal mortality
Why does gestational diabetes happen?
- pregnancy
- increased HPL, cortisol, E2, glucagon (placental)
- leads to insulin resistance
- there is increased ability to provide carbohydrate to feto-placental unit
GDM only usually occurs in already susceptible women such as..?
- obese
- family history of DM
- previous GDM
- previous baby >4.5kg
- polycystic ovary syndrome
- older
Who/when should be screened for GDM?
Screen/test high-risk groups at booking + screen everyone at 28/40
What is the difference between IDDM and NIDDM?
- insulin dependent DM - insulin deficiency - TYPE 1
- non-insulin dependent DM - insulin resistance - TYPE 2
What is the link between pre-existing diabetes mellitus and risk of congenital malformation?
- 2-3%
- periconceptual:
- HbA1c 5-8% – 4-5% inc risk
- HbA1c 8-10% – 9% inc risk
- HbA1c >10% – 25% inc risk!!
typical congenital malformations: can lead to sacral agenesis, CHD, skeletal/NTD
What is the only way to alter the increased risk of malformation in pregnant women with pre-existing IDDM?
- PRE-pregnancy counselling
- not a problem for true GDM (not diabetic at conception)
- insulin requirements x2 by term
What is the pathophysiology following maternal hyperglycaemia?
- glucose is transferred from mother to baby by facilitated diffusion
- baby isn’t diabetic so will attempt to lower glucose by increasing insulin
- this leads to variety of things (eg. macrosomia)
- neonatal hypoglycaemia - baby has higher insulin levels at birth whereas glucose drops, so too much insulin!
- fetal glycosuria will lead to polyhydramnios - bc of osmotic diuresis, there is poly-hydramnios - baby is peeing a lot as there is glucose in urine
As a result of a pre-existing diabetic mother, there is inhibition surfactant in the fetus. What will inhibiton surfactant lead to?
Respiratory distress syndrome
What can macrosomia and hyperplacentation lead to?
- prolonged labour
- operative delivery
- shoulder dystocia
- pre-eclampsia
- anterpartum haemorrhage
- postpartum haemorrhage
Polycythaemia can lead to jaundice. What can polyhydramnios lead to?
- malpresentation
- cord prolapse
- postpartum haemorrhage
What are other maternal risks (for those who have pre-existing DM)?
- increased infections esp UTIs
- hypo-glycaemia (tighter regime) - type 1 usually
- deterioration in nephropathy (reversible)
- two fold risk of progression of retinopathy
- if GDM = 50% lifetime risk of NIDDM
What are the principles of management for diabetic mothers?
- pre-pregnancy counselling for known DM
- achieve normoglycaemia (fasting <5.0mmol/l, 1hr postprandial < 7-7.5 mmol/l)
- diet +/- insulin (obstetrician PLUS diabetologist)
- metformin - increasingly used for type 2 mothers
- ultrasound - to detect congenital abnormalities, to assess fetal growth/polyhydramnios
- screen for pre-eclampsia
- timing of delivery - risk of intra-uterine demise vs resp distress
