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BIG QUIZ 2020 > HYPERTENSION/PET > Flashcards

HYPERTENSION/PET Flashcards

1
Q

Define hypertension in pregnancy ( SOMANZ)

A

Hypertension in pregnancy = BP > 140/90 over several hours
Severe hypertension = > 160/110
Severe hypertension requiring urgent treatment = >170 with or without >110

Gestational hypertension: new HT > 20/40, normalises within 3m

Chronic hypertension: BP > 140/90 < 20/40

  • essential: with no known cause
  • secondary: CKD, systemic disease with renal involvement ( DM, SLE), endocrine ( phaeo,, bushings, primary aldosteronism)

PET superimposed
- known CHT + develops systemic features

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2
Q

How do you diagnose PET?

A

SOMANZ
Hypertension + evidence of end organ dysfunction
RENAL
–> UPCR > 30 (unless pre-existing renal disease)
–> creat > 90
–> oliguria < 80mL/4hrs
–> increased urate common but non dx

HAEM

  • PLT < 100
  • haemolysis ( fragments, schistocytes, increased bill, LDH > 100, decreased haptoglobin ( protein that cleans free Hb from blood)
  • DIC

LIVER

  • raised transaminases
  • RUQ/epigastric pain

NEURO

  • eclampsia
  • hyper-reflexia + clonus
  • persistent new headache or visual change
  • stroke

LUNG
-pulm oedema

PLACENTAL
- IUGR ( if pre-existing HT, need evidence of placental disease for dx ie abnormal. dopplers, liquor)

IHSSP 
- creat > 90
- ALT/AST > 40
- PLT < 150 
(not hyper-reflexia)
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3
Q

What are some rare disorders that may present with features of PET/HELLP

A 
Acute fatty liver of pregnancy
HUS
TTP
Exacerbation of SLE
Phaeochromocytoma ( very labile BP, fasting free metanephrines, 24h urinary catecholamines)
  • if HELLP continues > 72h, consider TTP, APLS, HUS
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4
Q

When should you deliver women with PET?

A

< 23+6: TOP (maternal morbidity 65-71%, perinatal mortality >80%)

24-31+6: Likely PTB, consult tertiary

32-36+3: aim to prolong where possible

37+: stabilise BP and deliver

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5
Q

What is the rationale for delivery when PET onset < 34/40?

What is the rationale for delivery in HELLP?

A
  • PET < 34/40 - 25-41% will develop severe morbidity ( HELLP, abruption, pulmonary oedema, eclampsia)
  • HELLP: 6.3% incidence maternal death, increased risk of abruption
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6
Q

What is mild, moderate and severe HT?

When should you treat?

A

Mild: 140-160/90-100
Consider treatment
? treat: halves incidence of severe HT + assoc. consequences
? don’t treat: little maternal risk for mild HT for short duration, fatal perfusion depends on maternal BP, no clear effect of treatment on R/O NND, PTB, SGA, abruption

Mod: > 160/100
Treat ( risk of ICH, eclampsia)

Severe: >170/110
Treat urgently

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7
Q

Whats the dose, action, CI of methyldopa

A

250-750mg TDS
centrally acting
contraindicated in depression
SE: anticholinergic blurred vision, dry mouth/eyes, depression

Slow onset over 24h

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8
Q

What’s the dose, action, CI of labetalol

A

100-400mg TDS PO
20-80mg IV ( bolus over 2min, repeat q10min, max 80)
Infusion 20-160mg/hr)

b-blocker
mild alpha vasodilator

CI: asthma, lung disease

SEs: bronchospasm, bradycardia, headache, nausea, hypotension, fetal brady

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9
Q

Whats the dose, action, SEs of hydralazine?

A

25-50mg q8h PO
IV: 5mg- 10mg ( q20min, max 30)

Vasodilator

SE: flushing, headache, reflex tachycardia ( give b blocker)

  • rapidly inactivated by fluids containing glucose
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10
Q

What is the dose, action, CI and SEs of nifedipine

A

20-60mg slow release PO BD
10-20mg immediate release PO stat (q45min, max 40)

Ca++ channel blocker

CI: aortic stenosis

SEs: headache in first 24h, flushing, bradycardia, peripheral oedema, constipation

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11
Q

Whats the dose, action, SE of prazocin?

A

0.5-5mg q8h
a-blocker
SEs: orthostatic hypotension

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12
Q

How do you manage low PLT in PET?

A

abnormal < 100
spinal EDB concerns 50-100
Peripartum bleeding concerns only if < 50

Consider PLT infusion at CS
Give FFP if coagulopathy ( active bleeding, prolonged APTT
Give cryoprecipitate if fibrinogen low

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13
Q

How do you manage eclampsia?

A

ABC resus ( call for help from ALS team consultant, anaesthetics and OT, ensure patent airway, O2 my mask, IV access + bloods, continuous maternal obs)

Manage seizure: IV diazepam 2mg/min max 10mg

Prevent further seizures: MgS04: 4g loading ( in 100mL n. saline over 15min, 1-2g/hr maintenance

Control severe hypertension with IV agents ( hydralazine or labetalol)

Arrange delivery when stable- no role to continue pregnancy
CTG when mum stable

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14
Q

Describe antenatal USS/CTG monitoring in pregnancy hypertension (SOMANZ)

A

Chronic HT: early dating, growth/AFI/dopplers in third trimester, repeat as necessary

Gest. hypertension: USS growth/AFI/dopplers at time of dx and 3-4 weekly

PET: USS growth/AFI doppler at time of dx and 2-3 weekly

PET + IUGR: USS growth second weekly, AFI/dopplers on admission and weekly or more
CTG: twice weekly or more

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15
Q

What’s the rationale to give steroids? (as per SOMANZ)

A

< 34/40 reduces ICH, RDS, NEC, NND, NIC admission and resp support

Insufficient evidence < 34/40

Some evidence for CS 37-39/40

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16
Q

What’s the incidence of chronic hypertension in pregancy?

A

0.2-5%

17
Q

What’s the risk of perinatal death with pre-existing hypertension compared with normal pregancy?

A

3 fold increase ( highest risk > 39/40)

18
Q

What are ask factors for PET?

What are protective factors? (SOMANZ)

A 
RISK FACTORS 
Mum: 
Nulliparity
Multiple pregnancy
Age extremes (>40)
BP >130/80 < 20/40
Previous PET
IPI > 10 years
Overweight/obese
comorbidities- pre-existing diabetes, renal disease, autoimmune disease

Baby:
Multiple preg
GTD
Fetoplacental triploidy

PROTECTIVE FACTORS
Smoking
miscarriage with same partner in null
High fruit intake
>12 m to conceive

*FVL, prothrombin gene mutations not associated

19
Q

What’s the PET/hypertension in pregnancy recurrence risk ?

A

Previous gestational hypertension

  • GH 16-47%
  • PET 2-7%

Previous PET

  • GH 13-53%
  • PET 16%

Severe PET < 34/40
- PET 25%

Severe PET < 28/40
- 55%

Delivery due to pre-eclampsia in pre-ceding pregnancy (wk)	Recurrence risk (%)
20 – 28/40, 	40%
29 – 32/40, 	30%
33 – 36/40, 	20%
37+	10%
  • 10% overall risk of recurrence in 2nd pregnancy
  • 30% risk of recurrence if delivery necessitated <32/40
  • 40% risk of recurrence if delivery necessitated <28/40
20
Q

What’s the mechanism of aspirin in reducing pre-eclampsia?

A

Theory: PET secondary to imbalance of the prostaglandins, prostacyclin and thromboxane a2.

Prostacyclin = decreases vasoconstriction and decreased PLT aggregation

TXAa2 = increased vasoconstriction and increased PLT aggregation ( ie. is prothrombotic)

Aspirin inhibits TXAa2 production by by inhibiting COX, thereby increasing the proportion of prostacyclin

21
Q

What’s the mechanism of calcium and Vit D in preventing pre-eclampsia?

A

Ca2+ causes vascular constriction.

Vit D increases gastric absorption of calcium

Low serum calcium activates the parathyroid ( by PTH)
–> increased renal reabsorption of calcium
–> Ca2+ movement intracellularly in smooth muscle
= increased vasoconstriction

Giving calcium stops PTH release, therefore reducing intracellular calcium and smooth muscle contractility

22
Q

What’s the risk of PET for Mum long term?

Why?

A

Increased risk of ;
- subsequent hypertension and CV disease ( women with term PET who had no further pregnancies had 3.4 fold increase in cardiovascular death. Only 1.5% increase if had further pregnancies)

  • DVT
  • ESRD
  • T2DM
  • Hypohtyroidism
23
Q

What’s the recommended investigation, treatment goals, monitoring and delivery in chronic essential hypertension? ( SOMANZ and IHSSP)

A 
Investigations
PET bloods
\+/- haemolysis screen screen
Urinalysis 
USS
\+/- SLE ix
\+/- underlying renal disease KUB, BGL
\+/- fasting free plasma metanephrines or 24h urinary catecholamines to look for phaeo

Treatment goals
- management base on degree of hypertension .Consider management if BP mild 140-160/90-100
(SOMANZ) OR tight control 110- 140/85 (IHSSP):

Monitoring

  • Urinalysis each visit (IHSSP, SOMANZ)
  • Bloods 28 and 34/40 minimum (IHSSP) or if increase in BP or new proteinuria (SOMANZ)
  • USS 26/40 and 2-4 weekly thereafter
  • Delivery as per PET or by 39/40
24
Q

What’s the recommended treatment goals, monitoring and delivery in gestational hypertension? ( SOMANZ and IHSSP)

A

Treatment goals
- management base on degree of hypertension. Consider management if BP mild 140-160/90-100
(SOMANZ) OR tight control 110- 140/85 (IHSSP)

Monitoring

  • growth monitoring particularly if uric acid high ( IHSSP)
  • UA 1-2 x week, weekly PET bloods, USS growth/AFI/dopplers at time of dx and 3-4 weekly ( SOMANZ)

Delivery

  • as per PET indications ( SOMANZ)
  • by 39+6 if BP well controlled and baby normally grown ( IHSSP)
25
Q

How many women with GH will get PET?

A

15%

26
Q

What’s the recommended treatment goals, monitoring and delivery in PET ? ( SOMANZ and IHSSP)

A

Treatment goals
- 110-140/85 ( cease or reduce if diastolic < 80) IHSSP

Monitoring

  • growth monitoring particularly if uric acid high ( IHSSP)
  • UA 1-2 x week,
  • weekly PET bloods,
  • USS growth at time of dx and 2 weekly from 24/40 if IUGR or 26/40 normally grown ( IHSSP)
  • AFI/dopplers weekly or more if increased UA resistance (IHSSP)

Delivery (IHSSP)
- no later than 34/40 if absent EDF
- 30/40 if reversed EDF < 30/40 ( + admit, 3 x weekly AFI/dopplers, daily CTG)
- CS if REDF, AEDF or very preterm
- immediately if severe HT > 3 agents, worsening PLT/LFTs, euro symptoms, REDF, pulm oedema, non- reassuring petal status
(not proteinuria)

intra/post partum ( IHSSP)

  • MgS04 severe HT, severe HA, per persistent/repeat visual change,
  • Fluid restrict 60-80mL.hr
  • BP 4-6 hourly for 3 days
  • avoid NSAID
  • Repeat abn. PET bloods
  • Taper meds after 3-6 days
  • RV with GP in one week. 3m RV to ensure resolved
  • IX for ongoing symptoms
27
Q

What tests can determine which women would benefit from 150mg aspirin to prevent preterm PET? ( IHSSP)

A
  1. No set of tests reliably predict women who will get PET
  2. A combination of markers can be used;
    - UA dopplers
    - angiogenic factors ( best for early onset but only comprises 10% of HTN)
    esp sFLT1 ( placental hypoxia releases into circ. These mop up VEGF and PlGF (these factors cause angiogenesis) –> antiangiogenesis

(^ ASPRE trial for prevention PTB used these 2 factors to predict and prevent PTB with aspirin 150mg nocte)

  • PAPPA, homocysteine, uric acid PP13, lepton, urinary albumin, calcium) BUT NOT WIDELY ESTABLISHED
28
Q

IHSSP recommends aspirin 150-150mg (and calcium 1.2-3.5g/day if intake low) daily for women with which major/minor x 2 risk factors ?

A

Major

  • Prior PET
  • Chronic HT
  • pre existing TIIDM
  • BMI > 30
  • APLS
  • ART

Minor x 2

  • AMA
  • fam hx PET
  • short duration of sexual relationship
  • primiparity
  • primipaternity
  • connective tissue disorder ( no assoc. with thrombophilias, FVL may be a RF)
  • Use below <160/40 ideally but definitely < 20/40
29
Q

What’s the PIERS model ( clinical predictor ) that IHSSP recommends be used for women first admitted with PET?

A

Predicts likelihood of composite severe maternal adverse outcomes using information gathered infers 48h of admission

a. GA
b. Chest pain
c. O2 sat
d. PLT count
e. Creat
f. ALT

30
Q

What’s the pathophysiology of PET

A

Poorly understood
Primarily placental disorder ( resolved when placenta delivered)

Theories

  1. Abnormal placental endovascular invasion
    Phase 1: impaired trophoblastic invasion into spiral arterioles 20/40
    = poorly perfused placenta +

Phase 2: placenta has inflammation response and releases factors into maternal circulation –> endothelial dysfunction

  1. widespread endothelial dysfunction. Predominance of vasoconstrictive substances ( endothelia, TXAa2) over vasodilators ( prostacyclin).
    = Increased vasc. permeability –> oedema
    = Injury –> increased fibronectin–> increased PLT agg –> depressed ATIII levels –>HELLP, coagulopathy
    =Cerebral vasospasm –> oedema, disruption of BBB
    = Glomerular endotheliosis (structural changes in glomerulus)
    - Swelling of endothelial cells, subendothelial fibrinoid deposition, mesangial cell interposition–> reduced GFR-> renal insufficiency
  2. imbalanced maternal conc. angiogenic v antiangiogenic factors

5.Immunological factors
• Evidence: prior exposure to paternal/fetal antigens appears to protect against preeclampsia (higher rates in nulliparous, long inter-pregnancy interval, use of barrier contraception, new partner)

  1. Genetic predisposition
    • Evidence: P0 women with a family history of preeclampsia have a 2-5x higher risk
    • Both maternal and paternal contributions to fetal genes may have a role
    • Candidate genes
    - Genes for sFlt-2 and Flt-1 on chromosome 13; trisomy 13 → higher risk of pre-eclampsia
    - Locus at 12q → ? linked to HELLP; alterations in non-coding RNA at 12q23 – regulates a large set of genes that may be important for extravillous trophoblast migration
  2. Increased sensitivity to antiogensin II
31
Q

LANDMARK TRIAL

Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks gestation (HYPITAT): a multicentre, open label randomised controlled trial,
Koopmans 2009

What was the aim, method, primary and secondary outcomes, result and criticism?

A

Aim: To determine if IOL in women with PIH or Mild PET reduced severe maternal morbidity
Study: Multi-centre RCT 750 women 36-41 weeks
Interventions
– IOL Vs Expectant
Primary: Composite of poor maternal outcome. Mortality + sequele of PET
Secondary: MOD and neonatal
Results ITT analysis
– Reduced maternal morbidity, NNT 8 – 31 vs 44%, RR 0.7, 13/1000 fewer outcomes
– Reduced CS (not statistically different). No difference in neonatal outcomes
– Results more pronounced with unfavorable cervix
Criticism
– Neonatal outcome was only for short term. Worsening PET defined by single BP not two 6 hours apart
CONCLUSION: IOL SHOULD BE ADVISED FOR WOMEN WITH GEST HTN OR MILD PET > 37 WEEKS GESTATION

? what is mild defined by

32
Q

CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group, Redman 1994

What was the aim, method, primary and secondary outcomes, result and criticism?

A

Aim: To assess the safety effect of low dose aspirin on fetal and neonatal morbidity in pts at high risk of PET and IUGR
Study: Multi centre (213) RCT 9300 women, 12-32 weeks,

Interventions
– Low dose Aspirin 60mg or placebo for
– Prophylaxis (74%) / treatment (12%) PET
– Prophylaxis (12%) / treatment (3%) IUGR

Primary: Proteinuric PET, Duration of pregnancy, Birth weight/IUGR FDIU/SB.
Results
– No-sig reduction in PET by 12%. Significant trend toward reduced proteinuric PET with more preterm delivery
– Reduced in preterm delivery 22 vs 19 2.5 /1000 women
– No increased harm – bleeding, for maternal/placental/fetal
Criticism
– PET defined as 1+ proteinuria, started after 12 weeks, small numbers in each group
- Aspirin dose too low (60mg vs. 100-150mg)
- Aspirin not started early 2nd trimester (<16 weeks) – started 12-32 weeks which may be too late (60% AT 12-20 weeks, 27% at 20-28 weeks, 11% >28 weeks!)
Some women receiving treatment already had symptoms/signs PET/IUGR so started too late

CONCLUSION: LOW DOSE ASPIRIN USE MAY PREVENT EARLY ONSET PET IN WOMEN AT RISK OF SEVERE PET WITH PTB. FINDINGS DOE NOT SUPPORT PROPHYLACTIC OR THERAPEUTIC USE FOR ALL WOMAN AT RISK OFIUGR/PET

33
Q

Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The MAGPIE Trial: a randomised placebo-controlled trial, Duley et al 2002

What was the aim, method, primary and secondary outcomes, result and criticism?

A

Aim: To determine if MgSO4 prevents eclampsia
Study: RCT Multicentre (33 countries) 10 000 antenatal women or < 24 hrs postpartum, BP >140/90 + 1+ proteinuria,
Interventions
– MgSO4 vs placebo
Primary: Eclampsia
Results ITT analysis
– MgSO4 58% lower risk of eclampsia, 11/ 1000 fewer, NNT 63 with severe PET, or 109 for mild PET
– Maternal mortality lower for MgSO4 RR 0.55 (non sig)
– Reduced riks of placental abruption RR 0.67
– Greater SE profile in Mg group
Criticism
– No threshold established for treatment – clinical unsure for benefit
– Clinical applicability – high NNT in lower PNM countries
–
CONCLUSION: MgS04 HALVES THE RISK OF ECLAMPSIA AND PROBABLY REDUCED RISK FO MORTALTIY

34
Q

Why are ACEi contraindicated in pregnancy ?

A

Early exposure may lead to cardiovascular and CNS malformations

Later exposure leads crosses placenta –> interference with renal fetal haemodynamics ( fall in GFR can cause decreased fetal urine production

Can also lead to limb contracture, craniofacial changes, pulmonary hypoplasia

BIG QUIZ 2020 (3 decks)

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