Pre-eclampsia & Gestational diabetes Flashcards
Gestational diabetes (GDM)
Impaired glucose tolerance resulting in hyperglycaemia diagnosed in pregnancy – may be pre-existing or undiagnosed – significant risk of subsequent type II DM
Risk to fetus from GDM
Macrosomia and related birth complications
Neonatal hypoglycaemia and late pregnancy loss
Increased life time risk of obesity and diabetes
Epidemiology of GDM
Recurrent of GDM between pregnancies is about 60% – greater if they required insulin
South asian have an 7-11 fold risk and afrocaribbean 3x risk
50% risk of developing type II DM in the next 10yrs.
Risk factors for GDM
BMI over 30 Previous macrosomic baby (>4.5kg) or GDM FHx of diabetes Non-white (Nor africans but afro-caribbean) Advanced maternal age
Diagnosing GDM
Fasting of over 6.1mmol/L or >6.7mmol/L 2hrs after 75gs of glucose - higher cut-offs if capillary blood or plasma
Pathogenesis of GDM
Placental hormones including progesterone, cortisol, hPL, growth hormone and prolactin reduce insulin sensitivity
In healthy women this countered by increased insulin production – if this is not possible GDM develops
Cogenital malformations in GDM
Rare as GDM develops mainly in the 3rd trimester – unless there is pre-existing, uncontrolled diabetes leading to hyperglycaemia during organogenesis
Treatment of GDM
Women with GDM should be treated as it reduces the chance of complications –> can use diet, BM & fetal monitoring, oral hypoglycaemics and in 20% insulin
Labour in GDM
If well controlled may not need any special interventions but all should be offered elective birth after 38wks as this reduces the risk of shoulder dystocia and C-section
Aim to keep BM between 4-7mmol/L
Post natal care
Women with GDM should not require treatment after birth for the GDM –> monitoring should be continued until glucose returns to normal because of the risk of developing subsequent diabetes (6month then yearly diabetes checks after this)
Medication for GDM
Same as for DM (oral hypoglycaemic agents or insulin) but 80-90% of women are able to control it using diet and exercise
Target blood sugars for GDM
Before food – 3.4-5.9mmol/L
After Food – <7.8mmol/L
These measures are more closely associated with good outcomes than HbA1c
Fetal monitoring
Should be offered but there is little evidence this reduces the chance of stillbirth or macrosomia
Forms of Hypertension in Pregnancy
May be pre-existing chronic hypertension
Pregnancy induced hypertension (PIH) - Non-proteinuric PIH and pre-eclampsia
Pre-existing hypertension in pregnancy
Will develop before the 20th wk
If there is pre-existing proteinuria as well it is chronic renal disease
If there is new onset proteinuria then there is superimposed pre-eclampsia
Criteria for hypertension in pregnancy
Mild –>Diastolic 90–99, systolic 140–149
Moderate –> Diastolic 100–109 , systolic 150–159.
Severe –> Diastolic ≥ 110, systolic ≥ 160.
Criteria for proteinuria in pregnancy
> 300mg of protein/24hrs
OR
two properly collected samples over 4hrs apart with >2+s of protein
Albumin/creatinine ratio is a newer method which is very sensitive and specific
Pregnancy induced hypertension
Isolated Gestational hypertension or Proteinuria
Pre-eclampsia - gestational proteinuria hypertension
Eclampsia
A convulsive condition of malignant hypertension with proteinuria which can develop from pre-eclampsia
BUT only 50% of eclampsic women will have had previous hypertension and proteinuria
Maternal mortality from pre-eclampsia
Eclampsia occurs in 26.8/100,000 pregnancies
60,000 deaths per year worldwide –
1/4 admissions for monitoring are due to concerns over hypertension/proteinuria
Complications associated with pre-eclampsia
IUGR and placental abruption –> one of the commonest causes of iatrogenic preterm birth (15%) –25% of V. low birth weight infants – with associated adult health/IQ implications
Epidemiology of Pre-eclampsia
2-5% of antenatal cases will develop PE while PIH is about 3x higher (6-15%)
With one risk factor incidence increases to 15%
Risk factors for pre-eclampsia (5)
Likely genetic factors/FHx of pre-eclampsia
Link to paternal genetics - 2x risk if father has previously fathered an affected pregnancy
First pregnancy or young mothers
Increased exposure to spermatic antigens reduces risk
Underlying medical conditions increase risk
Pathogenesis of Pre-eclampsia
Likely genetic factor –> faulty interaction between trophoblast and decidua (failure of physiological vasodilation) –> decreased blood supply to placenta –> oxidative stress and release of inflammatory/endothelial activating factors –> widespread disease
Clinical Features of Pre-eclampsia
Hypertension and proteinuria developing after 20wks
Multisystem disorder –> risk of progressing to eclampsia and death due to convulsions, cerebral haemorrhage and respiratory distress
Management of Pre-eclampsia
Survalience, early delivery and prophylaxis are mainstays of treatment
Doppler artery waveform
Cheap and easy – if reduced or reversed end diastolic flow it is a sign of future PE – the later it is performed the greater the predictive strength – at 20wks abnormal waveform indicates 6 times increased risk
Angiotensin II test
measure response of BP to infusion of Angiotensin II – poor predictor and costly
Prophylaxis in PE
Low-dose aspirin has a 10% reduction in pre-eclampsia and associated complications and is recommended for high risk women
Calcium supplementation has also been investigated with promising results
Treatment of Eclamptic fits
Magnesium sulphate (up to 8gs) is 1st line, 2nd is diazepam (10mg) -- usually will self limit unless of brain pathology is present (bleed) MgSO4 reduces chance of further fits and need for ventilation/ITC admission
Magnesium sulphate
1st line anticonvulsant/prophylaxis –> 2g loading dose with 1-2g/hr infusion –> renally excreted so care must be taken in oligouria
Membrane stabilizer vasodilator which reduces ischemia
Time of onset of hypertension in pregnancy
Occuring after 37wks rarely results in morbidity
Before 20wks is likely pre-existing HTN but must still be monitored
Before 28wks is a bad signs and 50% will go on to develop pre-eclampsia
Clinical Signs of eclampsia
Nausea, vomiting, headaches, visual disturbance may precede convulsions - 1/3 are post-partum (can be 3-4days)
Also abdominal pain, liver failure, HELLP syndrome, pulmonary edema, and oliguria.
HELLP syndrome
Haemolysis, Elevated Liver enzymes and Low platelets
A complication of Pre-eclampsia which usually occurs in the 3rd trimester and 8% after birth
Will present with malaise (90%), nausea/vomiting (50%) and epigastric/upper right quadrant pain (90%)
30% will have neurological symptoms and 20% DIC
There must be some hypertension
Treatment of HELLP syndrome
The only definite treatment is delivery but antihypertensives and transfusion may be needed as well
The usefulness of MgSO4 is debated but may help to prevent the development of eclampsia
Management of hypertension
Mild –> monitor BP and urine multiple times/day
Moderate –>monitor and give oral labetalol (aim Oral/IV labetalol or IV hydralazine
Timing of birth in pre-eclampsia
Only in severe refractory hypertension consider birth before 34wks – attempt to complete steroid maturation)
34-37wks – necessary if severe but controlled hypertension and offer if mild/moderate and appropriate facilities are available
Aftre 37wks – recommend with 24-48hrs if mild/moderate hypertension
Obstetric Cholestasis
Whole body pruritis (palms and soles) which presents 30-32 wks gestation –> linked to mass effect of gravid uterus and cholestatic effects of oestrogens – > Usually have mildly elevated transaminases (AST, ALT) but these can be normal with only raised bile salts or GGT – may have dark urine, pale stools etc
Epidemiology of OC
0.7% prevalence in the uk - higher in south america, indian and Scandinavian women
1/3 of suffers have a positive family history
Risks of OC
PPH due to low Vit k due to malabsorption
preterm labour, MEC stained liquor, fetal distress and fetal death
Risk of fetal death correlates with bile salt levels and increases with gestational age
Management of OC
antihistamines and emollients for the itching –> ursodeoxycholic acid (UDCA) has been shown to improve itching and liver function but impact on fetal risk is unclear
Fetal surveillance and early delivery are the only measures –> usually aiming for delivery by 37/38 wks but the evidence is conflicted
Use of syntometrine IM in HTN
Contraindicated. Oxytocin alone is preferred
How many pregnant women are diabetic?
2-5% – 60-65% are gestational. 40% pre-existing.
Risk of congential abnormalities if mother is poorly controlled diabetic?
If HbA1c is over 10% the risk of congenital abnormalities is 25%, women in this situation should use contraception until better control is reached.
If there is very poorly controlled diabetes and/or evidence of complications how do you treat?
If complications (macrosomnia) then start on insulin straight away.
