Small for gestational age, HT disease of pregnancy, Maternal medicine Flashcards

1
Q

What do we mean by small for gestational age?

A

● Estimated foetal weight less than the 10th centile.
○ Differs from intrauterine / foetal growth restriction (IUGR / FGR), which implies a
pathological restriction of full genetic growth potential (RCOG definition).
○ Severe SGA is defined at EFW less than 3rd centile.

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2
Q

How can we measure foetal size?

A

Surveillance of foetal size can be performed with the following measurements:
1. Symphyseal fundal height (measured regularly at routine antenatal appointments
from 24+0 onwards).
2. Foetal abdominal circumference.
3. Femur length.
4. Head circumference / biparietal diameter.
5. Liquor volume / amniotic fluid index (normal = 5-25cm)

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3
Q

What are the risk factors for small gestational age?

A

Maternal age >40
2. Smoker >11 cigarettes per day.
3. Maternal cocaine use in pregnancy.
4. Maternal daily vigorous exercise
5. Previous SGA baby
6. Previous stillbirth
7. Maternal SGA
8. Paternal SGA
9. Chronic hypertension
10. Diabetes with vascular disease
11. Renal impairment
12. Antiphospholipid syndrome
13. Nulliparity
14. Previous pre-eclampsia

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4
Q

What are the investigations that we do for small gestational age?

A

● Routine monitoring:
○ First Line: SFH measurement
○ SFH is plotted on a customised growth chart.
■ Adjusted to maternal height, weight, parity and ethnicity.
○ Second Line: USS scan (see Foetal Measurement).
● Any single major risk factor:
○ Serial (2 weekly) USS and umbilical artery Doppler from 26-28 weeks.
● Any single SFH <10th centile or slow / static growth:
○ Serial USS and umbilical artery Doppler.

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5
Q

What are some further investigations for SGA?

A
  • umbilical artery doppler
  • CMV and toxoplasmosis screening - indicated in severe SGA
  • MCA Doppler
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6
Q

Why do we use umbilical artery doppler for SGA?

A
  • Normal low-resistance placenta allows continuous positive flow from foetus to placenta
    throughout the cardiac cycle (i.e. in systole and diastole).
  • If end-diastolic flow is slowed / reversed, this suggests increased placental resistance, which
    implies placental compromise (for example due to pre-eclampsia) and is predictive of SGA.
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7
Q

Why use MCA doppler for SGA?

A
  • Measured in comparison to umbilical artery flow.
  • Hypoxic foetus diverts blood flow to the brain to spare cerebral function - this increases MCA
    diastolic flow in relation to UA diastolic flow.
  • MCA flow also increases in foetal anaemia.
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8
Q

How do we manage SGA?

A

● RCOG recommends umbilical artery Doppler as the primary surveillance tool for an
SGA foetus.
● Current guidelines state, in general:
○ An SGA foetus should be delivered by caesarean section before 37 weeks
gestation.

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9
Q

A woman is pregnant with her second baby - 20 weeks gestation – gush of fluid vaginally
Obstetrics think premature rupture of membranes
What do they do now?

A

Erythromycin for 10 days to reduce risk of chorioamnionitis

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10
Q

A woman is pregnant with her second baby - 20 weeks gestation – gush of fluid vaginally
Obstetrics think premature rupture of membranes
What about steroids?

A

Too early for that
About 50% chance of delivery in the next 7 days

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11
Q

When should we offer resuscitation?

A
  1. Assess gestational age
  2. Asess presence of non-modifiable risk factors
  3. Assess modifiable Risk Factors
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12
Q

How do we assess gestational age?

A

GA (weeks)
Extreme high risk: 22-23
High risk: 23-24
Moderate risk: 25-26

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13
Q

Non - modifiable RFs for resuscitation- what increases gestational age (Decreases GA risk is opposite of these)

A

Gestational week: Beginning of week
Fetal growth: fetal growth restriction
Fetal sex: Male
Plurality: Multiple

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14
Q

What are the modifiable risk factors for resuscitation which increase GA? Opposite for Decrease GA risk

A

Antenatal steroid: None
Setting for birth: Local Hospital

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15
Q

Monitored maternal temperature & foetal growth
Nothing happens
Now 22 weeks gestation – should we offer resuscitation?
At Jessop survival sub 23 weeks is 30% at best – if you make it to the neonatal unit.
What intervention now to improve outcome?

A

12 mg betamethasone, 24 hours apart, hopefully up to 24 hours before delivery

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16
Q

Monitored maternal temperature & foetal growth
Nothing happens
Now 22 weeks gestation
Given 12 mg betamethasone, 24 hours apart, hopefully up to 24 hours before delivery
Mother remains apyrexial
Foetal growth is faltering, down to second centile
Now 25 weeks gestation, estimated foetal weight 600 grams
What other assessments should they do?

A
  • Foetal blood flow – using Doppler
  • Absent end diastolic flow is a bad sign
  • Reversed end diastolic flow is even worse
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17
Q

Monitored maternal temperature & foetal growth
Nothing happens
Now 22 weeks gestation
Given 12 mg betamethasone, 24 hours apart, hopefully up to 24 hours before delivery
Mother remains apyrexial
Foetal growth is faltering, down to second centile
Now 25 weeks gestation, estimated foetal weight 600 grams
Still pregnant however, now 28 weeks, estimated foetal weight 650 grams
Reversed end diastolic flow.
High concern about foetal demise
What should we do now?

A

Another course of steroids – only last 1 to 4 weeks
Intravenous MgSO4 – as neuroprotection 30% reduction in risk of cerebral palsy if given within 24 hours of birth

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18
Q

What are the birth weight categories?

A

 1500g Very low birth weight
 1000g Extremely low birth weight
 750g Incredibly low birth weight

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19
Q

What are the different types of Hypertensive disease of pregnancy?

A

Pregnancy-induced hypertension, Pre-eclampsia, Eclampsia, HELLP syndrome

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20
Q

What is PIH?

A

PIH: new-onset hypertension, developing after 20 weeks gestation.

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21
Q

What is Pre- eclampsia?

A

new-onset hypertension associated with proteinuria or systemic
features*, developing after 20 weeks gestation.
spiral arteries of the placenta form abnormally, leading to a high vascular resistance in these vessels.

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22
Q

What is the presentation for PIH?

A

asymptomatic, headaches, blurred vision

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23
Q

What is the presentation for pre- eclampsia?

A
  • asymptomatic,
  • headaches,
  • upper abdominal pain,
  • blurred vision,
  • reduced foetal
    movements //
  • brisk reflexes,
  • systemic hypertension
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24
Q

Classic triad of pre-eclampsia

A

Hypertension
Proteinuria
Oedema

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25
Q

What is the pathophysiology of pre-eclampsia?

A

When the blastocyst implants on the endometrium, the outermost layer, called the syncytiotrophoblast, grows into the endometrium. It forms finger-like projections called chorionic villi. The chorionic villi contain fetal blood vessels.

Trophoblast invasion of the endometrium sends signals to the spiral arteries in that area of the endometrium, reducing their vascular resistance and making them more fragile. The blood flow to these arteries increases, and eventually they break down, leaving pools of blood called lacunae (lakes). Maternal blood flows from the uterine arteries, into these lacunae, and back out through the uterine veins. Lacunae form at around 20 weeks gestation.

When the process of forming lacunae is inadequate, the woman can develop pre-eclampsia. Pre-eclampsia is caused by high vascular resistance in the spiral arteries and poor perfusion of the placenta. This causes oxidative stress in the placenta, and the release of inflammatory chemicals into the systemic circulation, leading to systemic inflammation and impaired endothelial function in the blood vessels

SHORTEN PLEASE

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26
Q

What are the RFs for pre- eclampsia?

A

High-risk factors are:

Pre-existing hypertension
Previous hypertension in pregnancy
Existing autoimmune conditions (e.g. systemic lupus erythematosus)
Diabetes
Chronic kidney disease

Moderate-risk factors are:

Older than 40
BMI > 35
More than 10 years since previous pregnancy
Multiple pregnancy
First pregnancy
Family history of pre-eclampsia

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27
Q

Which women are offered aspirin from 12 weeks gestation for pre- eclampsia?

A

Women are offered aspirin from 12 weeks gestation until birth if they have one high-risk factor or more than one moderate-risk factors.

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28
Q

What are the symptoms of pre-eclampsia?

A

Headache
Visual disturbance or blurriness
Nausea and vomiting
Upper abdominal or epigastric pain (this is due to liver swelling)
Oedema
Reduced urine output
Brisk reflexes

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29
Q

What are the initial investigations for PIH and Pre- eclampsia?

A

○ blood pressure measurement (140/90mmHg, +30/+15 in pre-existing
hypertension)
○ urinalysis (protein 2+ on dipstick, >30mg/mmol protein-creatinine ratio)
○ sFLT : PlGF ratio (>85 is diagnostic)

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30
Q

What are some further investigations for for PIH and Pre- eclampsia?

A

○ Bloods: FBC, U+E, LFT twice-weekly
○ Ultrasound scan: to assess foetal growth and AFI, 2-weekly
○ Umbilical Artery Doppler velocimetry: assess placental perfusion, 2-weekly
○ Cardiotocography: upon diagnosis, + if RFM, PV bleed, abdo pain, deterioration
○ Auscultation of foetal heart: offer at every appointment

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31
Q

How do we make a diagnosis for pre-eclampsia?

A

The NICE guidelines (2019) advise a diagnosis can be made with a:

Systolic blood pressure above 140 mmHg
Diastolic blood pressure above 90 mmHg
PLUS any of:

Proteinuria (1+ or more on urine dipstick)
Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)
Placental dysfunction (e.g. fetal growth restriction or abnormal Doppler studies)

Proteinuria can be quantified using:

Urine protein:creatinine ratio (above 30mg/mmol is significant)
Urine albumin:creatinine ratio (above 8mg/mmol is significant)

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32
Q

What is placental growth factor?

A

The NICE guidelines (2019) recommend the use of placental growth factor (PlGF) testing on one occasion during pregnancy in women suspected of having pre-eclampsia. Placental growth factor is a protein released by the placenta that functions to stimulate the development of new blood vessels. In pre-eclampsia, the levels of PlGF are low. NICE recommends using PlGF between 20 and 35 weeks gestation to rule-out pre-eclampsia.

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33
Q

What is the management for gestational HT without proteinuria?

A
  • Treating to aim for a blood pressure below 135/85 mmHg
  • Admission for women with a blood pressure above 160/110 mmHg
  • Urine dipstick testing at least weekly
  • Monitoring of blood tests weekly (full blood count, liver enzymes and renal profile)
  • Monitoring fetal growth by serial growth scans
    PlGF testing on one occasion
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34
Q

What is the management for PIH and pre-eclampsia?

A

Prevention: 75mg aspirin OD from 12/40 onwards.
● First Line: labetalol (beta-blocker)
● Second Line: nifedipine
● Third Line: methyldopa
● Plus: consider early delivery at 37 weeks
● Intravenous hydralazine may be used as an antihypertensive in critical care in severe pre-eclampsia or eclampsia
● IV magnesium sulphate is given during labour and in the 24 hours afterwards to prevent seizures
● Fluid restriction is used during labour in severe pre-eclampsia or eclampsia, to avoid fluid overload

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35
Q

What is given to women having a premature birth?

A
  • Corticosteroids should be given to women having a premature birth to help mature the fetal lungs.
  • Blood pressure is monitored closely after delivery. Blood pressure will return to normal over time once the placenta is removed.

For medical treatment, NICE recommend after delivery switching to one or a combination of:

  • Enalapril (first-line)
  • Nifedipine or amlodipine (first-line in black African or Caribbean patients)
  • Labetolol or atenolol (third-line)
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36
Q

What are one of the main complications of pre- eclampsia?

A

Eclampsia: Tonic-clonic seizures in presence of pre-eclampsia

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37
Q

How do we manage Eclampsia?

A

intravenous magnesium sulphate, emergency delivery via
LSCS.

38
Q

What is HELLP syndrome?

A

syndrome of Haemolysis, Elevated Liver enzymes, Low Platelets.

39
Q

Investigations for HELLP?

A

○ blood pressure measurement (140/90mmHg, +30/+15 in pre-existing
hypertension)
○ urinalysis (protein 2+ on dipstick, >30mg/mmol protein-creatinine ratio)
○ sFLT : PlGF ratio (>85 is diagnostic)

40
Q

What is the management for HELLP syndrome?

A

Prevention: 75mg aspirin OD from 12/40 onwards.
● First Line: labetalol (beta-blocker)
● Second Line: nifedipine
● Third Line: methyldopa
● Plus: consider early delivery at 37 weeks
● Expedite delivery

41
Q

What is the diagnostic criteria for severe pre-eclampisa requiring urgent hospital admission

A
  1. Systolic BP > 160mmHg
  2. Severe headaches, visual scotomata, N+V, Oliguria, epigastric pain, pulmonary oedema
  3. Rising creatinine, elevated liver enzymes, thrombocytopenia
42
Q

Pathophysiology of pre- eclampsia?

A
  1. Defective remodelling of maternal spinal arteries - inadequate oxygenation of trophoblastic tissue > oxidative stress
    1a. Stressted trophopblast releases pro-inflamm cytokines + sFLT into maternal circulation
    1b. Pro-inflamm cytokines distrupt maternal endothelium - leads to systemic inflamm response and reduced blood flow to maternal organs
    1c. HT due to impaired renal blood flow and reduced eGFR a s well as elevated sFLT
    1d. Proteinuria arises from glomerular changes of basement membrane and podocytes
  2. Defective remodelling results in placental hypoperfusion - inadequate nutrient deliver to foetus causing IUGR
  3. Systemic features arise from maternal endothelial dysfunction and resulting vasodilation - leads to hypovolemic shock
    3a. Seizures thought to be due to cerebral vasospasm
43
Q

What is obstetric cholestasis? (Definition)

A

● Obstetric condition causing increased serum bile acids and hepatic dysfunction.

44
Q

What is the pathophysiology for obstetric cholestasis?

A

○ Oestrogen inhibits hepatic bile acid receptors in genetically susceptible women,
leading to impaired bile acid homeostasis.
● Leads to deposition of bile salts in various tissues including skin and placenta.
● Skin deposition leads to pruritus (itching).
● Placental deposition causes raised foetal bile acid levels - this can cause acute foetal
deterioration - thought to be either foetal arrhythmia / cardiomyopathy or placental
vasoconstriction

45
Q

What are the S + S of obstetric cholestasis/ presentation?

A

● Pruritus (sparing hands and face).
● Excoriations (scratch marks).

46
Q

What are the investigations for obstetric cholestasis?

A

● Serum bile acids (raised above 19 micromol/L)
● Liver function tests

47
Q

What is the management for obstetric cholestasis?

A

● First Line: emollient plus antihistamine
● Second Line: ursodeoxycholic acid
● Plus: consider expedited delivery
○ Dependent on serum bile acid concentration
○ For example: delivery at 35-36 weeks for women with peak bile acid
concentration >100 micromol/L due to increased stillbirth risk.

48
Q

What is the definition of Gestational Diabetes mellitus?

A

● Chronic hyperglycemia and insulin resistance due to pregnancy

49
Q

What are the risk factors for gestational diabetes?

A
  • Previous gestational diabetes
  • Previous macrosomic baby (≥ 4.5kg)
  • BMI > 30
  • Ethnic origin (black Caribbean, Middle Eastern and South Asian)
  • Family history of diabetes (first-degree relative)
  • PCOS
  • Maternal age >40
50
Q

What should anyone with RFs for with gestational diabetes do?

A

Anyone with risk factors should be screened with an oral glucose tolerance test at 24 – 28 weeks gestation. Women with previous gestational diabetes also have an OGTT soon after the booking clinic

51
Q

Screening and diagnosis of GDM in pregnancy?

A

Oral Glucose Tolerance Test (OGTT) at 24-28 weeks in women with risk factors

Women with previous GDM also have an early OGTT at 13-14 weeks

Fasting blood glucose and 2-hour blood glucose following 75g OGTT:
Fasting ≥ 5.6
2 hour ≥ 7.8

52
Q

Other indications to screen for GDM in pregnancy?

A
  • Large for gestational age fetus > 90th centile
  • Glycosuria of +2 or +1 or more than more occasion
  • Increased fluid (polyhydramnios)
53
Q

What is the aetiology/ pathophysiology of gestational diabetes?

A

● In normal pregnancy, local and placental hormones stimulate peripheral insulin
resistance - the purpose of this is to spare glucose for delivery to the developing foetus.
● This is accompanied by lipolysis and gluconeogenesis, further increasing free fatty acid
and glucose levels.
● Hypertrophy and hyperplasia of pancreatic beta-cells occurs to protect maternal glucose
homeostasis.
● Failure of this protective mechanism due to beta-cell dysfunction, in combination with
insulin resistance, leads to GDM.

54
Q

What are maternal complications of gestational diabetes?

A

○ Pre-eclampsia
○ Chronic type 2 diabetes (60%)
○ Increased risk of cardiovascular disease

55
Q

What are the foetal complications of gestational diabetes?

A

○ Macrosomia, leading to shoulder dystocia
○ Neonatal hypoglycaemia (due to dependence on maternal hyperglycaemia
raising endogenous foetal insulin).
○ Childhood obesity (2x background risk).
○ Increased risk of metabolic syndrome and associated complications in later life
○ Large for dates fetus

56
Q

What are the risk factors for gestational diabetes?

A

● BMI > 30
● Previous macrosomia
● Previous GDM
● Family history of diabetes mellitus
● Ethnicity with high prevalence of diabetes
Previous gestational diabetes
Previous macrosomic baby (≥ 4.5kg)
BMI > 30
Ethnic origin (black Caribbean, Middle Eastern and South Asian)
Family history of diabetes (first-degree relative)

57
Q

How do we perform an Oral Glucose Tolerance Test?

A

An OGTT should be performed in the morning after a fast (they can drink plain water). The patient drinks a 75g glucose drink at the start of the test. The blood sugar level is measured before the sugar drink (fasting) and then at 2 hours.

Normal results are:

Fasting: < 5.6 mmol/l
At 2 hours: < 7.8 mmol/l
Results higher than these values are used to diagnose gestational diabetes.

58
Q

How do we diagnose women with gestational diabetes?

A

● Women with any one of the above risk factors should be screened for GDM at 24-28
weeks.
● Women with glycosuria detected at a routine antenatal appointment should be
screened at any time in their pregnancy.
● First Line: oral glucose tolerance test (OGTT)
○ Fasting blood glucose, followed by 75g carbohydrate drink, with a second blood
glucose test 2 hours later.

59
Q

Diagnostic criteria for gestational diabetes

A

● Diagnostic Criteria: 5678
○ Fasting plasma glucose > 5.6mmol/L or
○ 2 hour glucose > 7.8mmol/L

60
Q

What is the management for gestational diabetes?

A

● First Line: 2 week trial of diet, exercise and self-monitoring glucose levels
● Second Line: if not successful, metformin
● If FPG >7.0: start insulin immediately.
● Plus: extra growth scans at 28, 32, 36 weeks.

61
Q

What is the NICE management guidelines for gestational diabetes?

A
  • Fasting glucose less than 7 mmol/l: trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin
  • Fasting glucose above 7 mmol/l: start insulin ± metformin
  • Fasting glucose above 6 mmol/l plus macrosomia (or other complications): start insulin ± metformin
  • Glibenclamide (a sulfonylurea) is suggested as an option for women who decline insulin or cannot tolerate metformin.
62
Q

What does metformin do?

A

Metformin – acts on the liver to lower glucose production, decreases intestinal absorption of glucose and enhances insulin sensitivity

63
Q

What do women who need to monitor their blood sugar levels targets should be according to NICE?

A

Fasting: 5.3 mmol/l
1 hour post-meal: 7.8 mmol/l
2 hours post-meal: 6.4 mmol/l
Avoiding levels of 4 mmol/l or below

64
Q

What should women with pre-existing diabetes do when pregnant or before becoming pregnant?

A

They should take 5mg folic acid from preconception until 12 weeks gestation.

65
Q

Maternal risks of pre-existing diabetes?

A
  • Miscarriage
  • Three- to fourfold increased risk of pre-eclampsia. Increased if hypertension and/or renal disease
  • Infection – urinary tract, respiratory, endometrial and wound
  • Increased caesarean section rate
66
Q

Fetal risks of pre-existing diabetes

A

Congenital abnormalities - neural tube defects, skeletal abnormalities, congenital heart disease. Level of risk related to glycaemic control at time of conception and correlates with HbA1c

Perinatal and neonatal mortality – can be increased 5- 10-fold and relate to glycaemic control and HbA1c

Intrauterine fetal death

Fetal macrosomia – insulin is an anabolic, growth promoting hormone
- Can occur in women with good control, however more common with poor control
- Shoulder dystocia

Preterm birth
- Iatrogenic
- Idiopathic, can be related to polyhydramnios

Neonatal hypoglycaemia

Respiratory distress syndrome

67
Q

What should women with existing type 1 and type 2 diabetes aim for with insulin levels?

A

Same target levels as with gestational diabetes
Women with type 2 diabetes are managed using metformin and insulin, and other oral diabetic medications should be stopped.

68
Q

When should retinopathy screening be performed?

A

hould be performed shortly after booking and at 28 weeks gestation. This involves referral to an ophthalmologist to check for diabetic retinopathy. Diabetes carries a risk of rapid progression of retinopathy, and interventions may be required.

69
Q

What does NICE advise for a planned delivery for women with pre-existing diabetes?

A

advise a planned delivery between 37 and 38 + 6 weeks for women with pre-existing diabetes. (Women with gestational diabetes can give birth up to 40 + 6).

70
Q

When is a sliding-scale insulin regime considered?

A

during labour for women with type 1 diabetes. A dextrose and insulin infusion is titrated to blood sugar levels, according to the local protocol. This is also considered for women with poorly controlled blood sugars with gestational or type 2 diabetes

71
Q

Postnatal diabetes

A

Diabetes improves immediately after birth. Women with gestational diabetes can stop their diabetic medications immediately after birth. They need follow up to test their fasting glucose after at least six weeks.

72
Q

What is the management of postnatal GDM?

A
  • Stop medication
  • Healthy lifestyle advice
  • HbA1c at 13 weeks with GP
  • 39-47mmol/L – at high risk of diabetes
  • ≥ 48mmol/L diagnostic of type 2 diabetes
  • Annual HbA1c
73
Q

What should women with existing diabetes do?

A

Women with existing diabetes should lower their insulin doses and be wary of hypoglycaemia in the postnatal period. The insulin sensitivity will increase after birth and with breastfeeding.

74
Q

What are babies of mothers with diabetes at risk of?

A

Neonatal hypoglycaemia
Polycythaemia (raised haemoglobin)
Jaundice (raised bilirubin)
Congenital heart disease
Cardiomyopathy

75
Q

What do babies need for diabetes?

A

Babies need close monitoring for neonatal hypoglycaemia, with regular blood glucose checks and frequent feeds. The aim is to maintain their blood sugar above 2 mmol/l, and if it falls below this, they may need IV dextrose of nasogastric feeding.

76
Q

What are the physiological changes in glucose metabolism in pregnancy? 1

A

Pregnancy is a state of physiological insulin resistance and relative glucose intolerance

Glucose handling is altered in pregnancy
Fasting levels are decreased
Serum levels following a meal/glucose load are increased compared to non pregnant state

In second and third trimesters insulin resistance increases

77
Q

What are the physiological changes in glucose metabolism in pregnancy? 2

A

Glucose tolerance decreases with increasing gestation after the first trimester
Largely due to anti-insulin hormones secreted by the placenta in normal pregnancy (human placental lactogen, glucagon and cortisol)

Normal women show an approx. doubling of insulin production from the end of the first trimester to the third trimester

78
Q

What are the effect of the physiological changes of the physiological changes of glucose metabolism?

A

Likely to underlie the increased insulin requirements of women with existing diabetes
Lead to the development of abnormal glucose tolerance in gestational diabetes - where there is insufficient insulin secretion to compensate for the insulin resistance

79
Q

What are the types of diabetes in pregnancy?

A

Pre-existing:
Type 1
Type 2
Cystic fibrosis related
Maturity onset diabetes of the young (MODY) – rare

80
Q

What is the importance of identifying GDM?

A

Women with GDM have a higher chance of fetal macrosomia and adverse pregnancy outcome than control population without GDM – modifiable with intervention

Women with GDM have a greatly increased risk (40-60%) of developing type 2 diabetes within 10-15 years

A small proportion (1 in 1000) or women identified as having GDM will have diabetes pre-dating the pregnancy (type 1 and 2 and rarely MODY)

81
Q

What are the risks of GDM?

A

Fetal macrosomia (estimated or birthweight > 4kg)
Shoulder dystocia and birth related trauma (fetal and maternal)
Perinatal mortality – in utero fetal death and neonatal death
Neonatal hypoglycaemia

82
Q

What is the obstetric management of GDM?

A

Monitoring for pre-eclampsia with regular BP and urine checks

Regular fetal growth scans (usually 28, 32 and 36 weeks) – to assess fetal size, growth velocity and enable delivery planning

Timing of delivery – induction of labour or planned caesarean section
For uncomplicated GDM – delivery by 40+6
For complicated GDM – 37 – 38+6

Intrapartum care
Fetal monitoring
Hourly monitoring of blood glucose
May need variable rate insulin infusion to maintain blood glucose

83
Q

What are complications of diabetes?

A

Infections – candida, Staph skin infections
Macrovascular arterial disease – coronary artery disease, cerebrovascular disease, peripheral vascular disease
Microvascular disease - retinopathy, nephropathy, neuropathy
Reduced life expectancy due to accelerated arterial disease (stroke, myocardial infarction)

84
Q

Effects of pregnancy on diabetes

A

Increased insulin dose requirement, particularly in the third trimester. Often women with type 2 diabetes start insulin in pregnancy

Women with diabetic nephropathy may have deterioration of renal function and worsening degree of proteinuria

Risk of progression or development of retinopathy. Due to rapid improvement in glycaemic control and increased retinal blood flow

Hypoglycaemia with relative hypo unawareness

Diabetic ketoacidosis – risk in hyperemesis, infection and steroid therapy

85
Q

Features of diabetic ketoacidosis

A

Hyperglycaemia (capillary blood glucose >11mmol/l)
Acidosis (venous pH <7.3 and/or venous bicarbonate <15)
Ketonaemia or ketonuria (capillary ketones >3 mmol/l or urine ketones more than 2+)

86
Q

Predisposing factors of DKA

A

infection, vomiting, poor control/non-compliance, beta sympathomimetic drugs and antenatal corticosteroids

Emergency that demands prompt and vigorous treatment to reduce the maternal and fetal morbidity and mortality

87
Q

Obstetric management of GDM

A

Folic acid 5mg ideally from preconception (or as early as possible) until 14 weeks

Early dating and viability scan

Dating and nuchal translucency scan and detailed anomaly scan

Aspirin 150mg once daily from 12 weeks until delivery – to reduce risk of pre-eclampsia

Ultrasound scans for fetal growth at 28, 32 and 36 weeks

88
Q

Obstetric management - timing of birth in GDM

A

1 or type 2 diabetes and no other complications between 37 weeks and 38 weeks plus 6 days of pregnancy
Induced labour
Caesarean section

Sometimes need to consider birth < 37 weeks in women who have maternal or fetal complications.

89
Q

Intrapartum care of GDM

A

Woman with type 2 diabetes and some type 2 diabetics will need variable rate insulin infusion from onset of labour

Variable rate infusion commenced if 2 blood glucose levels >7

Hourly blood glucose monitoring

Aim for blood glucose 4-7mmol/L

90
Q

Care of neonates in GDM

A

Women with diabetes should feed their babies as soon as possible after birth (within 30 minutes) – reduce hypoglycaemia

Blood glucose testing routinely at 2 to 4 hours after birth in babies of women with diabetes

Minimum 24-hour hospital stay

91
Q

Postnatal care of GDM

A

Postpartum, insulin requirements rapidly return to pre-pregnancy levels

Clear plan to reduce insulin doses / or stop if indicated

Dose adjustment in breastfeeding women – increased energy expenditure

Tight glycaemic control not as important in postpartum period

Contraception discussion and plan

Counselling about importance of planned pregnancy and pre-pregnancy counselling

92
Q

Pre - pregnancy counselling features

A

Women with diabetes should ideally be seen for specialist pre-pregnancy counselling

Importance of good glycaemic control, aim HbA1c ≤ 48mmol/L. Women with an HbA1c level above 86 mmol/mol (10%) should be advised against pregnancy

Pre-pregnancy folic acid 5mg (reduce risk of neural tube defects)

Optimisation of diabetic control

Assessment and modification of any diabetic complications