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Flashcards in Obstetric Complications Deck (52)
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1

Define the different hypertensive disorders in pregnancy?

HTN
Chronic HTN
PIH
PET
Eclampsia
HELLP

HTN = raised BP defined by population (age, sex etc) – in pregnancy, >140/90

Chronic HTN = raised BP <20 weeks or with BP Tx

Pregnancy induced hypertension (PIH) or gestational hypertension (GH) = new hypertension >20 weeks gestation, no proteinuria

Pre-eclampsia (PET) = multisystem disorder characterised by hypertension >20 weeks gestation AND proteinuria (not 100% sensitive – not all fit these criteria)
o Proteinuria: >300mg (0.3g) protein / 24 hours (PCR > 30)

Eclampsia = seizure / convulsive episode caused by PET

HELLP syndrome = haemolysis, elevated liver enzymes + low platelets

2

Mild, moderate, severe HTN?

Mild 140-149 / 90 - 99
Mod 150-159 / 100-109
Severe 160 / 110

3

What is pre-eclampsia? (criteria)

How common is it?

>20 weeks gestation: pregnancy-induced HTN associated with proteinuria (>0.3g/24 hours). Oedema used to be 3rd in the classic triad, but now often not included as it is not specific.

Common: ~20% admissions, commonest cause of iatrogenic early delivery.

Mild PET may affect 6% of pregnancies
Severe in 1% (eclampsia in 1-2% of PET). Leading cause maternal mortality worldwide.

4

Symptoms of pre-eclampsia?

May be completely asymptomatic

Headache, visual disturbance, epigastric / RUQ pain, nausea / vomiting, rapidly progressive oedema, abdominal tenderness, disorientation/confusion, small for gestational age uterus, IUD, hyper-reflexia / clonus / involuntary movements

Features of SEVERE pre-eclampsia
• HTN typically >170/110mmHg + proteinuria
• Proteinuria dipstick ++/+++
• Headache
• Visual disturbance
• Papilloedema
• RUQ / Epigastric pain
• Hyperreflexia
• Platelet count <100*10⁶, abnormal liver enzymes or HELLP syndrome

5

Pathophysiology of pre-eclampsia?

Diffuse vascular endothelial dysfunction via release of angiogenic and angiolytic factors > widespread circulatory disturbances (to liver, kidneys, CVS, CNS, placenta etc). Failed differentiation of cytotrophoblastic cells during epithelial --> endothelial transformation. Three stages occur:

1. Abnormal placental perfusion: abnormal placentation and trophoblast invasion of the endometrium in which there is failure of vascular remodelling of the spiral arteries, therefore spiral arteries fail to become high capacitance, low-resistance vessels --> placental hypoxia and ischaemia

2. Maternal syndrome: placental ischaemia causes widespread endothelial dysfunction (poorly understood – possibly oxidative stress mechanisms / prostaglandin imbalance / NO compounds). Increased capillary permeability increases expression of cell adhesion molecules (CAM), increases pro-thrombotic factors and platelet aggregation, and causes vasoconstriction

3. Multisystem effects

6

What are the multisystem effects of pre-eclampsia? (go through each system)

o CNS: eclampsia (fits), hypertensive encephalopathy, IC haemorrhage, cerebral oedema, cortical blindness, CN palsies

o Renal: reduced GFR, proteinuria, increased serum uric acid (also in placental ischaemia), increased creatinine / K / urea, oligo / anuria, AKI (tubular / cortical necrosis)

o Liver: epigastric/RUQ pain, abnormal liver enzymes, hepatic capsule rupture, HELLP (haemolysis, elevated liver enzymes, low platelets) - emergency

o Haematology: decreased plasma volume (normally increased), haemo-contraction, thrombocytopenia, haemolysis, DIC

o CVS: pulmonary oedema (--> ARDS), PE, future hypertension, NB. CVS effects have high mortality

o Placental: IUGR, placental abruption, intrauterine death

7

What are the main maternal risks of having pre-eclampsia?

(Now very safe in UK):
• Eclampsia (seizures)
• Haemorrhage: placental abruption, intra-abdominal, intra-cerebral
• Cardiac Failure
• Multi-organ failure
• Maternal death (<1 in million in UK but many deaths globally)
• Long-term: subsequent high BP & complications, CV disease (e.g. CVA, IHD)

HELLP & Placental Abruption: rarer complications of HTN especially PET - variable disease(s) often seen (e.g. ELLP)
• Abruption often causes / provokes PET
• Remember FATTY LIVER (acute fatty liver of pregnancy)

Intracranial haemorrhage is the most common cause of death in women who die from hypertensive disorders of pregnancy

8

In the UK, what are most common causes of direct maternal death?

PET / eclampsia was 2nd biggest in 1985-7, 2012-14 dropped to 7th

1. Thrombosis / thromboembolism
2. Amniotic fluid embolism
3. Haemorrhage
4 / 5. Sepsis / early pregnancy deaths
6/ 7. Anaesthesia / PET or eclampsia

9

What are the main fetal risks of having pre-eclampsia?

• Prematurity (major cause of mostly iatrogenic early birth; 10% severe PET birth <34 weeks, 1 in 250 first pregnancy <34 weeks due to PET, 10% of all preterm births due to HTN disorders, 50% with severe PET give birth preterm)
• IUGR (15-20% births with PET are <10th percentile)
• Stillbirth (1 in 20 stillbirth without anomalies are associated with PET)

10

HIGH risk factors for pre-eclampsia?

o Hypertensive disease in previous pregnancy
o CKD
o Autoimmune disease (e.g. systemic lupus erythematosus, antiphospholipid syndrome)
o Type 1 or type 2 diabetes
o Chronic hypertension

If one of these factors - give aspirin


11

MODERATE risk factors for pre-eclampsia?

First pregnancy
Age ≥40 (doubles risk)
Pregnancy interval of >10 years
BMI ≥35 at first visit (doubles risk)
FHx pre-eclampsia (mother 20-25%, sibling up to 40%)
Multiple pregnancy

If 2 of these factors, aspirin is needed

Additional risk factors include: genetic abnormalities (triploidy), molar pregnancies.

12

Investigations for cases of PET?

o U+Es (raised creatinine, K⁺, urea), also serum uric acid (raised urate).
o LFTs: abnormal liver enzymes
o FBC
o Coagulation screen
o USS (biometry / AFI / Doppler)

13

Aims of management for PET?

Protect mother from hypertensive complications (CVS, MI etc), long-term risks – does not prevent progression of PET.

Protect baby by improving condition at birth, steroids + ideal BP for growth, improved gestation (later vs earlier?).

14

What should be done for pre-eclampsia prior to a pregnancy?

Before pregnancy
o Assess risk + likelihood of pregnancy
o Weight reduction, stop smoking
o Review medications
o ACEI, ARB, diuretics, statins - stop and/or prepare to change
o Aspirin 75mg, start at 12 weeks (<20)
o Folate 400µg – start before pregnancy
o Discuss risks: worse BP, PET, SGA, prematurity + longer term outlooks

15

What should be done for pre-eclampsia during the pregnancy?

When to refer or admit?

Assess risk at booking + during 1st trimester. If BP rises 1st trimester, assess for other causes. Antenatal screening: BP, urine, maternal uterine artery doppler (MUAD).

When to refer: day case referral if any of the 3 major signs or concerning symptoms e.g. persistent headache.

Admission if: BP >170/110 (alone) or >140/90 + proteinuria, significant symptoms (e.g. headache, visual disturbance, RUQ pain), abnormal biochemistry, significant proteinuria (>300mg/day), need for antihypertensive treatment, signs of fetal compromise

Inpatient assessment: BP 4 hourly, daily urinalysis, fluid balance chart +/- collection for protein, regular bloods. Fetal surveillance: movements, CTG, USS, biometry, AFI, umbilical artery doppler

16

Main treatments for pre-eclampsia?

Aspirin 75mg OD (12 weeks -> birth)
• If 1 high or >1 moderate risk factor for PET

Consensus guidelines: treat BP >160/110 but many clinicians have lower threshold. Oral labetalol 1st line (NICE), nifedipine + hydralazine may also be used.

Severe Hypertension
• Stabilise then plan delivery (aim 140-150 / 80-100)
• Labetalol oral / IV
• Nifedipine oral
• Hydralazine IV (?preload)

Monitor effect (mother + baby): fluid balance (? catheter)
• Mg
• Anaesthetist + neonatalogist

Delivery = the only ‘cure’, must be stabilised beforehand

o Induction <34 weeks if severe HTN refractory to Tx or other complications necessitating delivery

o 34-36+6 weeks if mild-moderate HTN, depending on maternal and fetal condition, risk factors and services

o immediate induction (24-48 hours) if >37 weeks

17

How to look after patients with pre-eclampsia during labour / intrapartum?

• BP hourly or more frequently
• Control BP <150/100
• Care with fluids (80mls/hour): (plasma leaks out, lower intravascular circulating volume but adding more fluid > pulmonary oedema!!)
• Fluid balance (? Urine output)
• Monitor baby: continuous CTG
• Epidural for obstetric medications
must avoid excess fluids

18

Main management of HELLP syndrome?

HELLP syndrome usually managed in conjunction with PET (BP control, ultimately delivery, may require blood products where indicated, steroids for fetal development)
• Deliver if platelets <100 or ALT>80

19

Post-natal factors in pre-eclampsia? Management?

Post natal BP: may rise for first few days, often needs continued treatment- ET risk continuous for few days

• Aim <140/90, reduce if <130/80
• ACEI if hypertension for >2 weeks
• Refer if BP still high at 6-8 weeks
• Exclude persistent proteinuria (i.e. renal disease)
• Lifestyle changes to continue

20

How to manage the following patients with pre-eclampsia

Mild 140-149 / 90-99
Mod 150-159 / 100-109
Severe 160/110

Mild: measure BP no more than 1/week, proteinuria at each visit using strip or urea/creat ratio, blood tests only as routine antenatal care

Mod: oral labetalol 1st line to keep systolic <150 and diastolic 80-100, BP at least 2/week, proteinuria at each visit, test kidney function, electrolytes, FBC, transaminases, bilirubin - do not carry out further blood tests if no proteinuria at subsequent visits

Severe; ADMIT until BP <159/109, labetalol first line as above, BP at least 4/day, daily proteinuria, blood tests at presentation then weekly: kidney, electrolytes, FBC, transaminases, bilirubin

21

Main antihypertensives for pregnancy?

Beta blockers (labetalol): good safety data, standard treatment, licence for use in pregnancy; uncertain risk for neonatal hypoglycaemia (babies are monitored if taken). a+b antagonist, 100mg BD starting dose - 600mg QDS. CI in asthma

Nifedipine MR & SR: good safety record, effective in pregnancy especially PET; start at modified release (MR) 10mg BD, max 40mg BD, side effects of headaches & tachycardia (may mimic impending eclampsia)

Methyldopa: centrally acting a-agonist, effective antihypertensive, extensive safety data, side-effects: hepatitis, pancreatitis, depression, haemolytic anaemia, bone marrow depression etc. Start at 250mgs BD / TDS and up to 3g (1g TDS?)

Hydralazine: vasodilator, 25mg TDS - 75mg QDS

All of the above safe in breast feeding.

Also: Prazosin (75mg)

22

What is gestational diabetes? How does it occur?

GD = ‘Any hyperglycaemia with first onset of presentation during pregnancy’. Affects 2-4% of women.


Resistance to insulin = normal physiological response in pregnancy (induced by human placental lactogen i.e. human chorionic somatomammotophin: reduces insulin sensitivity and alters fat metabolism – releases fatty acids as alternate energy source for mother – allowing more glucose for the fetus).

Maternal blood glucose levels rise to provide for fetus, particularly in 3rd trimester. In some women: reduced ability of pancreas to produce enough insulin to overcome the insulin resistance --> gestational diabetes.

23

Risk factors for GD?

o >35 years
o BMI >30
o Smoking
o Previous stillbirth
o Previous ‘large’ baby >4.5kg
o Previous episode gestational diabetes
o FHx TYPE 2 DIABETES (but not GD!)
o Asian, Middle East & Black African ethnicity

40% of women with GD have no risk factors

24

How does GD present?

Often asymptomatic and only discovered on screening (common diabetic symptoms of thirst, hunger, polyuria, tiredness are not particularly common, but are also seen in normal pregnancy in 3rd trimester)

25

What are the risks of GD to the fetus?

Fetal Risks greatest when glycaemic control is poor around time of conception

o Macrosomia: store more fat than usual, defined as abdominal circumference >70 percentile

o Newborn hypoglycaemia (producing their own endogenous insulin during pregnancy to counteract hyperglycaemia of the mother: usually self-limiting but may require IV glucose)

o Type II diabetes later life + obesity in childhood

o Shoulder dystocia during delivery
o Jaundice
o Stillbirth
o To reduce risk: offer C-section 38-39 weeks (instead of 40). All should be offered C section or induction at 38 weeks, and if proven macrosomia: inform of the risks of vaginal birth

o 2x increased risk of congenital defects: congenital heart disease, respiratory distress syndrome, NTDs

- Risks inversely related to level of control of the GD, and highest in type II, moderate in GD and lowest in type I

26

What are the risks of GD to the mother?

o Increased risk of tears
o Increased risk of type II diabetes (50% will develop type II within 15 years, 50% of those requiring insulin will develop type II within 5 years)
o Increased risk of GD in subsequent births (30-85%); particularly if pregnancy occurs within 1 year

27

What investigations are done for GD?

Screen of all women with a known risk factor at 24 + 28 weeks: fasting glucose or random glucose test; if +ve or suspicious, confirm with OGTT.

If previous GD, test may be done at 16-18 weeks (for early diagnosis).

o 2 hour 75g OGTT (day before test: eat, drink + exercise normally, then fast 8-14 hours overnight, following day test glucose then drink solution (usually 75g)

Normal: fasting <6, 1 hour <10, 2 hours <7.8

Impaired fasting glucose: fasting 6-7, 2 hour <7.8

Impaired glucose tolerance: fasting <7, 2 hour >7.8

Diabetes: fasting >7, 2 hour >11


Type A1: abnormal OGTT, but normal glucose levels during fasting and 2 hours after meals (usually controlled with diet & exercise)

Type A2: abnormal OGTT and high glucose during fasting and 2 hours after meals (may require pharmacological intervention)

28

What treatment is available for GD? (before labour)

Reduces risk of congenital defects but not of C-section or perinatal mortality

1. Glucose levels every 1-2 weeks during pregnancy

2. Diet + exercise: low impact e.g. walking/swimming/yoga / pilates esp. if BMI >27. Regular meals with controlled fat intake (low fat not recommended in pregnancy) - complex carbs taht reduce high peaks of glucose and digested slowly, consider restricting carb. intake at breakfast. Consider low GI foods (GI <55), monitor salt, 5 fruit/veg, oily fish lean meat and polyunsaturated fats. Sufficient in 80-90% of patients

3. If not controlled within 2 weeks consider METFORMIN (no other oral Tx suitable for pregnancy) +/- insulin (rapid acting e.g. aspart and lispro more effective than endogenous insulins in pregnancy). Recommend pumps to those not adequately controlled by MDIs, if insulin used in pregnancy, dose usually increased by 50%. Tx can usually be stopped after birth as resistance normalises, usually random glucose test (not OGTT) at 6 week checkup confirms treatment can be stopped.

29

What treatment is available for GD? (during labour)

Glucose during labour should be monitored every hour and kept between 4-7mmol/L (consider insulin + dextrose infusion in those with type I, or poorly controlled diabetes)- sliding scale insulin

30

Management of GD after birth?

Feeding of baby should be encouraged, to reduce risks of hypoglycaemia

Tx can usually be stopped after birth as resistance normalises, usually random glucose test (not OGTT) at 6 week checkup confirms treatment can be stopped.

Glibenclamide + metformin are safe to use while breastfeeding, other oral agents should be avoided

Some patients then go for regular type II diabetes screening (?annual)