Hypertension in Pregnancy Flashcards

1
Q

Baseline % risk of PET in a well woman with no RFs

A

2-3% low risk multips

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2
Q

Risk of PET with antiphosholipid syndrome

A

8x background risk. 2x9 = 18%

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3
Q

Risk of PET with nulliparous women

A

3-5%

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4
Q

List different classes of hypertension in pregnancy

A

Pre-existing hypertension (white coat, chronic, essential - when ruled out other causes)
Gestational hypertension
Pre-eclampsia

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5
Q

Causes of pre-existing hypertension

A

White coat
Essential - no other cause found
Other medical - renal (renal artery stenosis, glomerulonephritis, polycystic kidneys), cardiac (aortic co-arctation), endocrine (hyperparathyroidism, cushing’s, conn’s, phaeochromocytoma)

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6
Q

Investigations for other causes of hypertension (renal, cardiac, endocrine)

A

Renal - USS, creatinine U+Es, baseline PCR, urine for casts
Cardiac - echocardiogram, L and R arm BPs
Endocrine - hyperparathyroidism (parathyroid hormone, Ca, Phos), Cushing’s (cortisol - early morning/24h), Conn’s (renin/aldosterine ratio - affected by pregnancy however), Phaeo (plasma metanephrines)

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7
Q

Definition of hypertension

A

Systolic BP equal/greater than 140 and/or diastolic BP equal/greater than 90, on 2 or more occasions at least 4h apart …. OR one episode of severe hypertension = systolic equal/greater than 160 or diastolic equal/greater than 110

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8
Q

When should gestational HTN resolve by postpartum?

A

3 months - if elevated at this point then defined as chronic hypertension

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9
Q

Can a women be hypertensive with PET 6 weeks postpartum?

A

Yes

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10
Q

When should gestational HTN resolve by postpartum?

A

3 months - if elevated at this point then defined as chronic hypertension

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11
Q

Definition of PET

A

Gestational HTN: and evidence of end organ dysfunction - haematological Hb Plt DIC, biochemical Creat/LFTs/proteinuria/oliguria, neurological eclampsia/stroke, placental SGA/IUGR/abruption

Pre-existing HTN: and TWO other criteria of end-organ dysfunction

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12
Q

Visual/neurological symptoms of PET, and where in the brain does this affect?

A

Altered mental status, photopsia, persistent visual
scotomata, cortical blindness, retinal vasospasm

Occipital lobe

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13
Q

Pre-existing HTN risks

A

PET - 25%, 46% if severe HTN

Preterm delivery - 15% if no PET, 50% if PET

SGA - 27% if not PET, 48% if PET

CS - 44% if no PET, 70% if PET
Placental abruption

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14
Q

Gestational HTN - risk of PET if diagnosed at <30 weeks vs at 38 weeks

A

a) 40% vs b) 7%

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15
Q

Risk factors for PET

A
Age > 40 - 2 x
BMI > 30 - 2 x
Family history - 3 x
Primip - 2-3 x
Multiple pregnancy -32 x
Previous PET - 7 x
Long birth interval - 2-3 x if > 10 years

Pre-existing HTN , renal disease, diabetes, antiphospholipid syndrome
(10x), connective tissue disease, sickle cell disease

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16
Q

Rare presentations of PET <20 weeks include

A

Consider if hydatidiform mole, tripoloidy,

multiple pregnancy, severe renal disease or antiphospholipid syndrome

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17
Q

Timing of eclampsia (ante/intra/postpartum)

A

Antepartum (45%), intrapartum (20%), postpartum (35%).

Only 1/3 of women with eclampsia have a diagnosis of PET preceding eclapsia

40% of eclamptic fits are after delivery!

Note treat all pregnant women with seizures as though they have eclampsia, however remember it is not the most common cause of seizures

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18
Q

Other differentials for a seizure/possible eclamptic fit in a pregnant woman

A

Epilepsy, pseudoseizure, stroke, intracranial bleed (burst aneurysm, or post assault) intracranial mass, severe electrolyte disturbance (e.g. hyponatraemia)

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19
Q

Methyldopa - max dose, onset of action, side effects and contraindications

A

750mg QID (3g/day), 6h onset, drowsiness and low mood, contraindications depression/concurrent MAOI use/postpartum

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20
Q

Labetalol - max dose, onset/peak effect, side effects and contraindications

A

Varies - 300mg QID, 400mg QID, up to maximum of 2.4g/day - however recommend not to max out to prevent saturation of beta receptors.
Peak effect 2-4h.
SE bronchospasm. Beware in brittle asthma, Raynaud’s disease, phaeo

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21
Q

Nifedipine - max dose, onset/peak effect, side effects and contraindications

A

30mg BD. Long acting onset 3-4h, short acting 30-45 min.
SE - headache
Contraindications/cautions - worsening pre-existing headaches, short acting can cause large drops in BP - recommend to be on CTG

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22
Q

Prazosin - max dose, onset/peak effect, side effects and contraindications

A

4th line - consult with obs med. Start at 0.5mg daily/nocte. Can cause abrupt drop in BP esp postural, sx dizziness

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23
Q

IV labetalol - dose, onset of action, repeat dosing

A

Labetalol - 20mg IV as a bolus over 2 min, 5 min maximal onset of action

Repeat 15 mins. If still > 160/110,
given 40mg IV
Repeat in 15 mins. If still > 160/110, give 80mg IV over 2 mins.

Max 300mg.

Infusion 20-160mg/hr.

Give in ED/HDU/MCA setting, not on ward. Consider arterial line

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24
Q

IV hydralazine - dose, onset of action, repeat dosing

A

5-10mg IV bolus over 3-10min, onset of action 20 min. Repeat every 20 mins if BP remains >160/110. Max 30mg

Give in ED/HDU/MCA setting, not on ward. Consider arterial line

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25
Q

Why are ACE-i contraindicated in pregnancy

A

Second and third trimester - oligohydramnios, renal failure, bony malformations

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26
Q

Is an eclamptic fit an indication for immediate delivery?

A

NO
Stabilise the mother (MgSO4, transfer to MCCA/HDU, antihypertensives, bloods)
Stabilise the baby (steroids if preterm, MgSO4 if <30 weeks)
Discuss with the Obstetric and Obs Med SMOs re: timing of delivery
Remember to consider other differentials for seizure

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27
Q

MgSO4 dosage

A

Loading: 4g IV over 20 mins
Then infusion 1g/hr (0.5mg/hr in AKI/CKD) for 24h after delivery or after the last seizure, whichever is later. If undelivered or stable after 24h, SMO review if there is still potential for delivery

If recurrent seizure given another 2g loading

28
Q

MgSO4 monitoring and antidote

A

Hourly: UO, BP, HR, reflexes
If signs of toxicity: low RR, reduced/absent reflexes, N+V/flushing - send off Mg levels

MgSO4 can cause reduced variability on CTG as well

Antidote: calcium gluconate 10% - 1g/10mL). Give 10 mL over 10 minutes

29
Q

MgSO4 risk reduction of cerebral palsy for the fetus if <30 weeks

A

Reduces risk of cerebral

palsy by 31% - RR 0.69.

30
Q

PET <24 weeks - risks of maternal and fetal morbidity/mortality

A

Discuss TOP

Maternal morbidity 70%, perinatal mortality 80%

31
Q

PET <34 weeks, rates of serious morbidity

A

25-40% of those managed expectantly will develop severe morbidity
(HELLP, abruption, pulmonary oedema, eclampsia)

32
Q

HYPITAT II study - multi centre, unblinded, randomised trial comparing
immediate delivery vs expectant management with non severe
hypertensive disorders 34-37 weeks gestation

A

Immediate delivery - reduced incidence of composite maternal
morbidity (thromboembolic disease, pulmonary oedema,
eclampsia, HELLP syndrome, placental abruption, or maternal
death) RR 0.36 but significant increase in neonatal RDS therefore
aim for expectant management

Follow up study - poorer neurodevelopment outcomes in those
with immediate delivery at 2 years but not at 5 years.

33
Q

Should you deliver if a woman has severe PET <36 weeks? Y/N

A

Yes if maternal deterioration/fetal deterioration, i.e. risks>benefits for expectant management

34
Q

Hypertension in absence of PET - timing of delivery

A

aim for delivery > 37 weeks, consider

up to 39 weeks if mild and well controlled

35
Q

What do you consider giving if fibrinogen levels are low

A

Cryoprecipitate

36
Q

Thrombocytopenia in PET - at what level is the risk of PPH increased for delivery?

A

Not until <50. However anaesthetics would not put in an epidural if <80

Consider platelet transfusion at
time of CS or in case of PPH, haematoma, wound bleeding etc

37
Q

Why is regional anaesthesia (if possible) more preferable to GA for severe PET?

A

Severe HTN usually accompanies intubation - can cause MI, cerebral
haemorrhage, pulmonary oedema

HOWEVER - GA may be indicated if severe fetal compromise, pulmonary
oedema, maternal haemodynamic instability, coagulopathy, severe
thrombocytopenia, post eclamptic seizure if persistent
neurological deficit

38
Q

What analgesia drug should you withold/use with caution in women with severe PET/those who have had eclampsia?

A

TRAMADOL - lowers seizure threshold

39
Q

Diazepam dose with eclampsia if prolonged? While MgSO4 being prepared?

A

Consider IV diazepam 2mg/min to max of 10mg

PR for status epilepticus - 10mg PR

40
Q

Risk of recurrent seizure despite MgS04?

A

10-15%, also control BP - threshold is lower for further seizures after eclampsia

41
Q

Why does BP spike on day 3-6 postpartum?

A

Previously normotensive women can become transiently hypertensive due
to vasomotor instability as non pregnancy vasoregulation is re-established.

42
Q

Pathophysiology - effect of low dose aspirin in preventing PET

A

Inhibits platelet cycle-oxygensase and TXA2 synthesis, reducing
platelet aggregation and dilating blood vessels. Anti-inflammatory
effect may also be useful

43
Q

LDA timing of starting and stopping

A

12-16 weeks ideally, up to 20 weeks. 100mg nocte. 1x trial suggesting increased risk of abruption/mc if taking <12 weeks however not backed up by other studies

Stop at 36/40 - studies have not shown benefit at term (effective at preventing preterm PET), also increases bleeding risk if labours

44
Q

Calcium supplementation - indications and dosage

A

1g elemental Ca daily. Supplement if low levels of dietary calcium - 2-3 servings a day. Until delivery

Calcium carbonate 1.25g (500mg elemental ca) = 2 tab a day

45
Q

Renal patients - aim for BP readings of?

A

130/80

46
Q

PET - yearly check ups with GP for what?

A

CVD assessment, BP, weight, discuss lifestyle changes e.g. wt loss, smoking cessation. 5 yearly bloods - HbA1c, lipids

47
Q

How does calcium supplementation help to prevent PET?

A

reducing PTH and renin release, reducing intracellular calcium in
vascular smooth muscle, reducing smooth muscle contractility and
vasoconstriction

48
Q

Is low vitamin D a risk factor for PET? Dosage?

A

Yes. Only check levels in those at risk of deficiency (eg Hijab wearing) -
don’t retest once commenced treatment.

Rx - cholecalciferol 1.25mg monthly for mild-mod deficiency. If severe 1.25mg for 10 days then once monthly

49
Q

Relative risk of developing PET pre-existing conditions: Andrea Patted A Rather Cute Happy Dandy Elephant

A
Antiphospholipid syndrome/SLE = 9
Prev PET = 7
ART = 4
Renal disease = 4
Chronic HTN = 3.6
prev HELLP = 3.7
Diabetes = 3.5
Ethnicity = 3 african, 2.5 indian
50
Q

Risk ratio: future risks with next pregnancy of 1) Gest HTN
2) PET
3) Chronic HTN
Does the risk change depending on whether you had gest HTN or PET this preg?

A

Gest HTN in future preg
- OR 3 if gest HTN this preg; 6 if PET this preg

PET future preg
- OR 7 whether gest HTN or PET this preg

Chronic HTN outside preg
- OR 3

51
Q

Contraindications to MgSO4

A

Hepatic failure, myasthenia gravis, severe renal failure, cardiac ischemia, heart block and pulmonary edema

52
Q

Magpie trial: purpose, type of trial, number of participants, location, years

A

To find out if women with PET and their babies benefited from MgSO4
Randomised double blinded RCT - 10,141 women in 33 countries, 1998-2001

53
Q

MAGPIE eligibility, exclusions

A

Eligibility: all women with PET, uncertainty about whether or not to give MgSO4, antepartum or within 24h of delivery

Excluded: MgSO4 hypersensitivity, liver and renal failure, myasthenia gravis

54
Q

MAGPIE primary outcomes results

A

Primary maternal: decreased risk of eclampsia RR 0.58 - 0.8% in Mg group vs 1.9% in placebo group. NNT=91.
Effect consistent regardless of gestations, severity of PET, previous anti-convulsant use, ante/postnatal, parity

Primary fetal: no change in rates of perinatal death (incl. at discharge)

55
Q

MAGPIE secondary outcomes

A
  • Serious maternal morbidity – resp depression or arrest, liver/renal failure, cerebral haemorrhage, coagulopathy
  • MgSO4 toxicity or side effects – need for calcium gluconate, SE’s
  • Neonatal morbidity/mortality – apgars, intubation, abnormal USS, convulsions, SCBU admission.
  • Labour and delivery complications – length of IOL, CS, retained placenta, transfusion, gestation
  • Use of healthcare resources – days of stay, ICU admit, ventilation, dialysis
56
Q

MAGPIE secondary outcomes results

A

Increased Side Effects reported from Mg group (25% v 5% - Blinding maybe influenced by degree of side effects)

IV Mg may be more effected than IM, however not randomised and was at the discretion of the treating team, interpret with care

No clear differences between maternal morbidity or composite outcomes, but the trend in decreased maternal mortality favoured MgSO4 group.
- No differences in use of healthcare resources, pregnancy outcomes/labour/delivery except lower risk of abruption in MgSO4 group.

  • No evidence to support MgSO4 as tocolytic or antihypertensive, no evidence that hypotension occurred in women with Mgs04 and nifedipine.
  • Most maternal deaths were from organ dysfunction as a consequence of severe PET rather than eclampsia. ??suggesting MgSO4 may have more widespread systemic benefits
57
Q

MAGPIE summary

A

MgSO4 reduces the risk of eclampsia, and may also reduce the risk of maternal death from pre-eclampsia. At the dosage used in this trial there are no significant harmful effects on the mother or child, although 25% of women experience side-effects.

58
Q

HYPITAT 1 - type of study, year, countries, aim of study

A

Multicentre open-label RCT
Published 2009
Whether IOL vs expectant management for gestational HTN or mild PET reduces severe maternal morbidity - evidence for this was scarce

59
Q

HYPITAT I

- Inclusion criteria

A

INCLUSION
36-41 weeks gestation
Singleton fetus
Cephalic presentation
Gestational HTN with DBP >/= 95 on two occasions at least 6 hours apart
PET with DBP >/= 90 on two occasions at least 6 hours apart with proteinuria

60
Q

HYPITAT I - Exclusion criteria

A

Severe hypertension

  • BP >/= 170/110
  • Severe PET with protein >5g/24 hour (PCR 500)
  • HELLP
  • oliguria
  • Pulmonary oedema
  • Cyanosis
  • IV antihypertensives

Maternal medical

  • Pre-existing HTN on meds
  • Previous caesarean section
  • DM on insulin
  • Renal failure, heart disease
  • HIV

Fetal

  • Congenital abnormality
  • Suspected IUGR
  • Abnormal CTG
61
Q

HYPITAT intervention - randomised to IOL or expectant management

A

756 women in the Netherlands

IOL:
Start within 24 hours (If BS > 6 – ARM, if BS41 weeks.

62
Q

HYPITAT I - primary outcomes

A

Composite measure of poor maternal outcomes

  • death
  • morbidity
    • eclampsia
    • HELLP
    • pulmonary oedema
    • VTE
    • abruption
  • progression to severe disease
    • BP >/=170/110
    • proteinuria >5g
  • major PPH (>1,000ml)
63
Q

HYPITAT I - primary outcomes results

A

Primary maternal composite RR 0.79 in induction group, NNT 8. Mainly by preventing progression to severe disease

Progression to severe disease: 23% intervention group, 36% expectant groups RR 0.64

Significantly less antihypertensive use in IOL group

Beneficial effect of IOL not present at < 37 weeks (however unreliable as low numbers, not powered to detect significant differences)

No difference in PPH

64
Q

HYPITAT I - secondary outcomes and results

A

Method of delivery
Neonatal morbidity and mortality

CS rates lower in intervention group, but not significant

No difference in instrumental deliveries

No difference in composite neonatal outcomes. Significantly lower birthweight in IOL group (understandable as earlier gestation)

65
Q

HYPITAT - final conclusion

A

Induction of labour recommended for women with gestational hypertension and mild PET at term (>37 weeks) to reduce poor maternal outcome, with no increase in caesarean section rate or neonatal outcomes.

66
Q

HYPITAT I - limitations

A
  • Does not follow WHO criteria for gest HTN or PET
  • Cross contamination of groups - 50% in expectant management were induced and 30% of these were for maternal request
  • Progression to severe disease was only single measurement of high BP resulting in broad criteria for primary outcome
  • Not powered to determine individual maternal outcomes (e.g eclampsia)
  • No long term follow up
  • Not clear benefit on neonatal or maternal mortality or morbidity as outcomes measures not associated with worse health outcomes really.