Hypertension And PET Flashcards
What is the primary change in the circulation during pregnancy?
Vasodilation
Fall in the systemic vascular resistance
When is the nadir of BP in pregnancy?
22-24/40
What should be taken as the diastolic reading?
Phase V (Disappearance)rather than phase IV (muffling) or Korotkoff sounds
How should BP be taken in pregnancy?
Sitting or lying on side with 30 degree tilt
If taken supine, it will be falsely low due to decreased venous return
If you use a normal size cuff to measure BP on a larger women, what error will occur?
Over-estimate of BP
What is the prevalence of Gest HTN?
10-15%
What is the prevalence of PET?
3-5%
What is the commonest cause of iatrogenic prematurity?
PET
What are secondary causes of hypertension?
How do you investigate for them?
Renal artery stenosis - listening for renal bruits, USS
Underlying renal disease - urinalysis, ? Proteinuria, haematuria, serum Creat
Aortic coarctation - radiofemoral delay, CT
Conn’s - hypokalaemia
Cushing’s
Phaechromocytoma - urinary catecholamines
Hyper parathyroid is - serum Ca
What are women with pre-existing HTN at risk of in pregnancy?
PET (25%)
PTB (28%)
LBW (17%)
How does PET affect the kidney?
Decreased GFR Proteinuria Rise in serum creat Rise in rate Oliguria
What is the cause of hyperuricaemia in PET?
Placental ischaemia
Accelerating trophoblast turnover and production of purines (substrate for xanthine oxidase)
What is the cause of hyponatraemia in PET?
What is the treatment?
Fluid overload
With an element of SIADH?
Rx: fluid restriction
What are crises / complications in pre-eclampsia?
HELLP Pulmonary oedema Renal failure Hepatic rupture DIC Placental abruption Cerebral haemorrhage Cortical blindness (linked to PRES) Transient LV dysfunction
What are the two stages in the pathogenesis of PET?
- Abnormal placentation
- spiral arteries do not undergo normal vascular remodelling, failing to become high capacitance, low resistance vessels
- invading placenta unable to optimise its blood supply
- uteroplacental ischaemia - Maternal response
- metabolic disturbance
- exaggerates inflammatory response
- higher levels of pro-inflammatory cytokines associated with endothelial dysfunction, which leads to platelet activation and vasoconstriction
- cause widespread micro vascular damage and dysfunction
What is the role of VEGF and TCF-beta1 in a normal pregnancy?
Maintain endothelial health
By interacting with endogenous endothelial receptors
What factors are secreted by the placenta in excess in PET?
Soluble Flt1 (sFlt1) and soluble endoglin (sEng)
- anti-angiogenic factors
- antagonise VEGF and TGF-B1 (transforming growth factor) signalling, and PIGF (placental growth factor)
- therefore producing systemic endothelial dysfunction
sFlt1 and sEng and increased and PIGF is decreased in the maternal circulation weeks before the onset of PET
What is notching in the uterine artery at 20-24/40 predictive of?
PET
FGR
Placental abruption
When is there a risk of cerebral auto regulation in PET?
MAP > 150
Mother at risk of cerebral haemorrhage
How do you calculate MAP?
D + 1/3 (S-D)
Women with PET should be encouraged to use what in labour?
Regional analgesia / anaesthesia
How should postpartum oliguria in PET be managed?
Safer to err not he side of volume depletion and mild AKI than to treat immediate postpartum oliguria with aggressive volume replacement and risk pulmonary oedema
What are the risks for future health, in women who have had PET?
Hypertension (3-4x)
IHD (2x)
Cerebrovascular disease
What is the risk of recurrent PET?
15%
Increases with earlier gestation
Perinatal mortality rises with DBP > ______
90mmHg
What proportion of Gest HTN progresses to PET?
25%
More so when HTN presents <32/40
Aspirin to prevent PET
What is the NNT
(Cochrane 2019)
Reduces risk of PET by 18%
NNT = 61
Benefit most marked at doses >75mg and when commenced <20 weeks
Also reduces:
- risk of SGA babies
- preterm birth <37 weeks
- fetal and neonatal death
BUT
- slightly more women lost >500mL
- tends to more higher risk of abruption, but wide CI
THUS overall deemed safe and benefit outweighs risk
With HELLP, what is the maternal mortality rate of expectant management?
6.3%
SOMANZ
What was the conclusion of the CHIPS study?
The development of severe HTN (independent of PET) increases the risk of
- stroke
OTHER adverse perinatal and maternal outcomes including
- serious maternal complications
Antihypertensive therapy to normal maternal BP: tight BP control arm aimed for DBP <85
What were the findings of the Cochrane Review looking at Calcium supplementation to prevent HTN / PET?
2018
Calcium supplementation
Less likely to
- Die
- Have serious problems related to PET
For a women who has had previous PET, what is the RR of recurrent PET?
7
What was the conclusion of the PHOENIX Trial?
Late preterm PET 34-36+6/40
- Randomised to immediate delivery or expectant management
Planned delivery reduces maternal morbidity and severe HTN compared with expectant management
With MORE neonatal unit admissions related to prematurity but no indicators of greater neonatal morbidity.
This trade-off should be discussed with women with later preterm PET to allow shared decision making on timing of delivery
What were the findings of the CLASP trial 1994?
Why may its findings differ from other studies?
- Multicentre RCT
- Included women from 12-32 weeks gestation if risk factors for PET OR developing signs and symptoms of PET
- Treatment = 60mg aspirin
Findings:
- Risk reduction proteinic PET by 12% but not statistically significant
WHY??
- Low dose of aspirin - cochrane 2019 suggests benefit more clear when >75mg used, unclear benefit at doses <75mg
- Including later gestations - cochrane 2019 suggests significant benefit if commenced prior to 20 weeks, vs unclear benefit if commenced after 20 weeks gestation
