S4: Complications of Pregnancy

Question 1

What are complications in pregnancy?

Answer 1

The majority of pregnancies are completely straightforward (no major problems) and low risk, this is because it is mostly young, fit and healthy women who are pregnant. However nearly all women experience minor troublesome symptoms to a degree, such as heartburn.
Some women feel a great sense of wellbeing, they feel wonderful. Another point is that a pregnant woman can also get other medical problems that normal people do e.g. an asthma attack or the flu.

Question 2

List minor symptoms of pregnancy

Answer 2

Tiredness, Nausea and vomiting, constipation, heartburn, breast tenderness, urinary frequency, backache, piles, headache, heat intolerance, scramble brain (airhead) and emotional liability.

Question 3

How to tell difference between a pregnancy symptom or abnormality?

Answer 3

If looking for abnormalities it depends on the degree of symptoms. It is difficult to spot pathology in pregnancy underneath all the common symptoms of pregnancy.
If a woman has a headache and is pregnant is it because she is pregnant or because she has meningitis?

Question 4

Describe first trimester complications

Answer 4

• Miscarriage is very common and at least 15% pregnancies miscarry. This is a real underestimate as miscarriages also occur to mothers who don’t know they are pregnant. Miscarriages often occur when the sperm and egg meet during non-disjunction which causes aneuploidies.
• Ectopic pregnancy occurs around 2% of pregnancies.
• Hyperemesis gravidarum is constantly excess vomiting, about 2-5% of women will have this. This women often need rehydration in a hospital.

Question 5

Describe

Second and Third Trimester complications

Answer 5

On the maternal side complications include:
- UTIs.
- Anaemia is common.
- Pre-eclampsia (4-5%).
- Gestational diabetes (5%, but varies).
- Antepartum haemorrhage (bleeding during pregnancy).
On the foetal side complications in this period include:
- Premature labour, this is delivering before you should, delivery before 37 weeks.
- Intrauterine growth restriction (IUGR) is when the unborn baby is not growing at the rate it should be in the womb, it is failure to reach its growth potential and its weight is under the 5th percentile, this is less than 2.5kg.
- Macrosomia is a weight over the 95th percentile for the baby, this is anything over 4.5kg e.g. Gestational diabetes. Babies are getting bigger but women pelvises are not.

Question 6

Describe urinary tract infections (UTI) in pregnancy

Answer 6

• Urinary tract infections are more common in pregnant women. Part of it is due to increased diagnosis as the pregnant woman comes into hospital regularly and gives urine samples.
• The key physiological reason why UTIs are more common in pregnant women is that the high progesterone leads to mass smooth muscle relaxation. This causes urinary stasis, making it more likely to get infected.
• There is also relative immune-suppression that occurs in pregnancy in order to prevent rejection/attacking the foetus.
• In a pregnant woman the symptoms of a UTI can be mild or absent.
• However it is really important that the mothers urine is tested at every visit along with blood pressure.
  because UTIs in pregnancy are associated with obstetric problems especially pre-term delivery (i.e. delivering early!).

Question 7

Describe anaemia in pregnancy

Answer 7

• In non-pregnant females Hb concentration is in the range of 12-16g/dl.
• In the pregnant female, despite there being more RBCs, the normal range is lower due to haemodilution due to increased body water. The circulating volume increases from 4.5l to 6l. This puts the normal Hb concentration of the pregnant woman at 10.5-13g/dl (reference changed due to physiological changes in pregnant body).
• Maximal dilution is seen at 28-30 weeks so if a pregnant women is going to have anaemia, it is likely to be in this period of time!
• If Hb in the pregnant woman is under 10.5g/dl this warrants investigation into the cause of it!

Question 8

What are the different causes of anaemia during pregnancy?

Answer 8

• Most commonly the cause is iron deficiency. Microcytic anaemia where mean cell volume is low.
• If it is vitamin B12 deficiency or folate deficiency then give them what they are deficient in.
• Sickle cell or thalassemia trait may also be the cause or a blood dyscrasisas e.g. leukaemias that needs to be managed. Look at Asian and African Caribbean population especially. This shows how anaemia can be due to abnormal cells rather than iron deficiency.

Question 9

Describe diagnosis and management of anaemia in pregnancy

Answer 9

• At the 12 weeks booking, the mothers Hb concentration will be checked, it will be checked when maximally diluted at 28 weeks and then checked again at 36 weeks (so mother has decent haemoglobin level at the time of birth in case of bleeding out during it to build up Hb reserves). This is because if the mother is anaemic at 12, 28 or 36 weeks you can do something about it! However after 36 weeks, the mother is going to deliver soon, if the mother is anaemic and bleeds a lot then this puts the mother in danger.
• So when the [Hb] is checked, if anaemic the cause must be investigated and treated. E.g. if under 10.5 give ferrous sulphate if low Fe.
• If [Hb] is under 7 or they are displaying symptoms of anaemia, then transfuse blood.

Question 10

Difference pre-existing diabetes in pregnancy and gestational diabetes

Answer 10

• True gestational diabetics are not diabetic before pregnancy. Once they become pregnant, the pregnancy causes them to become diabetic. If you recognise the diabetes after 20 weeks then it is gestational.
• Some mothers will have pre-existing insulin dependent diabetes mellitus/non-insulin dependent diabetes mellitus would have already been diagnosed prior to pregnancy. As they are young women it will generally be insulin dependent diabetes (type1) and they will know about it! If you recognise the diabetes before 20 weeks, then it was pre-existing i.e. was diabetic before the pregnancy.
• Remember that diabetes is a spectrum.

Question 11

Why does gestational diabetes (GDM) occur?

Answer 11

All the steroids being released such as HPL, cortisol, E2 and glucagon from the placenta cause insulin resistance and this is physiological. It is an adaptation because it allows the foetus to access more sugars at the placenta.
Most women will remain insulin resistant and not tip over to diabetes (when beta cells start producing insufficient insulin or body stops responding), the ones who do tend to be at risk e.g. obese, older mothers.

Question 12

Why is a diabetic pregnancy high risk/high risk obstetrics?

Answer 12

• Increased perinatal morbidity and mortality.
• Increased maternal morbidity.
• Small increase in maternal mortality.

Question 13

What is the risk population for GDM?

Answer 13

GDM (gestational diabetes) only usually occurs in women who are already susceptible, like the obese (32% of our population), having a family history of DM, having had GDM in the past, a previous baby who was obese 4.5kg, PCOS and being older!

Question 14

When do we screen for gestational diabetes?

Answer 14

• Because GDM is bad for the pregnancy, we screen high-risk groups at booking and then screen everyone at 28 weeks.
• Because the insulin resistance is progressive, it will be worse at 34 weeks than at 28 which will be worse than at 20.
• However if we diagnose it late there isn’t much time to do anything about it. We use the OGTT as the screening tool.
• Too early at 20 weeks, some women with GDM will be missed.

Question 15

Describe link between mother with pre-existing insulin/noninsulin dependent diabetes mellitus (IDDM/NIDDM) and congenital malformation

Answer 15

• Women who have pre-existing DM are strongly advised NOT to just get pregnant without consulting with a physician first.This is because hyperglycemia at conception can be very toxic for the foetus and increases the risk of sacral agenesis (sacrum doesn’t form), CHD, skeletal malformation or neural tube defects.
• The background risk in the population of a baby having a congenital malformation is 2-3%.
  Women with DM who periconceptually have an:
• HbA1c of 5-8% have a 4-5% risk of a child with congenital malformation.
• HbA1c of 8-10% have a 9% risk of a child with congenital malformation.
• HbA1c of >10% have a 25% risk of having a child with congenital malformation (these women would have bad control of diabetes).
• To combat this risk of malformation in women with pre-existing IDDM, they must be told when young that when they want to get pregnant they should see the doctor 6 months in advance in order to get sugars sorted before conception. I.e. counselling pre-pregnancy.
• This increased risk is NOT present for mothers with true GDM because they were not diabetic at conception.

Question 16

Describe the pathophysiology of maternal hyperglycaemia to foetus

Answer 16

• The mother being hyperglycaemia causes the foetus to be hyperglycaemic as the glucose passes into foetal circulation at the placenta.
• Normally, the foetus will not produce insulin as mother is controlling the blood sugar (both have normal). However, when the mothers glucose is high, it causes the foetus to have high plasma glucose and the foetus responds to this by making lots of insulin. This causes increased storage of sugars in the foetus making it fat and heavy (big around shoulder, head and trunk), this is macrosomia and will make the foetus have hyper-isulinaemia. This can make it very difficult to deliver the baby during birth a the shoulders can get stuck.
• Hyperglycaemia appears to inhibit surfactant production, this increases risk of respiratory distress on delivery.
• Another problem is neonatal hypoglycemia, this occurs as once the baby is born the cord is clamped and this cuts off the glucose supply, however the foetus is still full of high insulin that quickly stores the glucose resulting in low plasma glucose.
• The placenta also doesn’t work properly due to the hyperglycaemia and this results in the baby being slightly hypoxic, so it responds by making lots of RBCs and this is polycythaemia. However once delivered, there is an abundance of oxygen, so the excess RBCs are broken down resulting in jaundiced due to bilirubin excess.
• Hyperglycaemia also causes glycosuria due to the high glucose in the filtrate pulling water out of the interstitium. This happens in the foetus, foetal glycosuria.
  It pees a lot resulting in a high amount of amniotic fluid, this is polyhydramnios. Polyhydramnios is uncomfortable for the mother and increases risk of premature delivery due to rupture of the amniotic sac, also can overstretch the uterus muscle which is needed the stop bleeding during pregnancy.

Question 17

Describe maternal problems with maternal hyperglycaemia in pregnancy

Answer 17

• Increased infection especially UTI.
• Hypo-G (tighter regime).
• Deterioration in nephropathy (reversible).
• Two fold risk of progression of retinopathy.
• If GDM = 50% lifetime risk of NIDDM.

Question 18

Describe management of DM in pregnancy

Answer 18

• First and foremost will be pre-pregnancy counselling in women who have known DM, this allows time to achieve normoglycaemia and this is the most important thing.
• To achieve normal blood sugar levels (fasting of less than 5mmol/l and 1hr post-prandial of less than 7-7.5mmol/l. If the mother has normal blood sugar none of those bad consequences will happen.
• To achieve this we will try control diet and possibly give insulin (if metformin doesn’t work as desired). This will require obstetrician plus a diabetologist.
  Metformin is being increasingly used, to help control maternal sugar levels.
• During the pregnancy ultrasounds will be done to detect possible congential abnormalities as well as assess foetal growth.

Question 19

What is pre-eclampsia (PET)?

Answer 19

PET is a significant rise in BP or a BP over 140/90 at over 20 weeks on two separate occasions at least four hours apart, PLUS significant proteinuria. This is abnormal as usually BP goes down during pregnancy due to vessels dilating.
- If there is a significant change from the BP at booking to a anytime before 20 weeks (a significant change counts as increase in 30 or more systolic, or increase in 20 or more diastolic) then it is not PET rather it is classified as something else.

Question 20

Is oedema normal in pregnancy?

Answer 20

Oedema is a normal finding, it is seen in up to 80% of women. Therefore it is only significant if it is severe or in an unusual site e.g. Facia or sacral.

Question 21

Describe the different classifications of HBP during pregnancy

Answer 21

• Preexisting hypertension: If at booking (before 20 weeks) the hypertension is recognised but no proteinuria, then the woman already had hypertension.
• Hypertension due to renal disease: If before 12 weeks they have hypertension and proteinuria they had renal disease.
• Pregnancy induced hypertension (PIH): Over 20 weeks we find it is over 140/90 but there is no protein in urine, the woman is hypertensive and this has been induced by the pregnancy (PIH -pregnancy induced hypertension).
• Pre-ecalpsia.
• The reason we categorise it like this, is that PET is the most significant as is dangerous. However any of the others can turn into PET if managed improperly.

Question 22

Describe normal physiology of BP in pregnancy. Why does it go wrong in PET?

Answer 22

• BP = CO x TPR. In a normal pregnancy, CO increases by 40% due to increased plasma volume. However TPR is reduced massively due to progesterone causing widespread vasodilatation and thus BP decreases. This helps accommodate the large placental flow. Remember high volume low pressure.
• In PET, the vasodilatation fails to occur and instead TPR actually increases due to vasoconstriction/vasospasm. This occurs systemically. The problem is a placental one. As the trophoblast invades, the normal dilatation of the vessels doesn’t occur due to abnormal trophoblastic invasion.
• In a normal pregnancy, the maternal BP will take a steep decline in the first trimester, it comes up in the second trimester and by the third trimester it is back up to normal.
  In mothers who will get PET, they have a blunted response in the first trimester (small if any decline) then they overshoot and by the third trimester it is very apparent.

Question 23

Describe the causes of PET

Answer 23

It is a disorder of placentation, this is certain. It is failure of the second wave of trophoblastic invasion at around week 15-16. The overriding big pathology that causes the problems is the systemic vasospasm.
But as well as this we have:
- Vessel abnormalities, there is increased capillary permeability causing movement of fluid into the interstitial space (EC space).
- There are small vessel abnormalities (microangiopathy), there is increased endothelial cell wall activation of platelets and coagulation factors resulting in micro-thrombosis this can cause infarction of the end-organs.
- Because of this, PET is a multi-system disorder and can affect any organ of the body because this is happening in any systemic microvessels. However it particularly affects the kidneys, liver, CNS, coagulation system and placenta.
Theories:
- Immunological : abnormal maternal immune reaction to trophoblast.
- Vasospastic substances : NO, TNF, free radicals, altered RAA sensitivity.
- Mineral/vitamin deficiencies: selenium, vitamin C.

Question 24

Describe effect of PET to mother

Answer 24

• The high BP can cause bleeding in cerebral circulation (Intercranial haemorrhage. This is because HBP above a certain level makes the vessels lose autoregulation of BP (myogenic response). This can cause fits and headaches.
• Damages nephron and can cause renal failure due to pseudopodia are falling apart.
• Damages liver, causing abnormal liver function. Liver makes more albumin due to excess excretion in urine, however it is not enough and serum albumin still decreases. Oncotic pressure is lost and even more fluid is lost through leaky vessels. The leaky vessels mean fluid can leak out in the brain and in the lungs and other organs. This is dangerous if doctors prescribe too much IV fluids.
• Proteinuria can lead to lower albumin in blood = low oncotic pressure = more fluid loss from vessels.
• As endothelium gets activated, platelets get used and thus there is tendency to bleed. Clotting factors also used up on the endothelium and this causes small clots around the body (DIC, disseminated intravascular coagulopathy). This is dangerous as women can bleed out during birth.

Question 25

Describe effect of PET to foetus

Answer 25

• The placenta isn’t working properly so the baby is under-perfused and hypoxic!
  In response to this the baby sends blood to its vital organs such as the brain, it uses up its glycogen stores and this makes the baby skinny. Thus growth has suffered. This appears as asymmetrical IUGR (abdomen skinny, head is normal sized).
• There can also be placental abruption this is where the placenta separates from the wall of the uterus.
• As underperfused, the foetus will have less renal blood flow, will urinate less, therefore there will be less amniotic fluid = oligohydramnios.

Question 26

Management of PET

Answer 26

If pre-eclampsia occurs at 36 weeks, they may as well deliver. If it occurs at 27 weeks, the baby is too premature, the clinician will try prolong the pregnancy by giving anti-BP medication in order to stave of the symptoms for some time. However the nature of pre-eclampsia is that it will get worse until the baby is delivered. Thus whether to deliver or not at a time is a balance of decision making.