Obs - hypertensive disorders Flashcards
How does blood pressure change in pregnancy and why?
reduces slightly in 2nd trimester: 30/15mmhg (or 15-20)
because of reduced SVR - systemic vascular resistance
how does protein excretion change in pregnancy?
increases but <0.3g/24h
what point in pregnancy do you see PREGNANCY INDUCED hypertensive disorders arise?
after 20 weeks - so well into 2nd trimester
this means if BP high before then, it was not induced by pregnancy -> Chronic HTN
what is the origin / aetiology of pre-eclampsia?
‘not completely understood’
placental in origin
Stage 1 (development): incomplete trophoblast invasion
reduction in flow of blood in Spiral artery and Uteroplacental circulation
Stage 2 (manifestation):
Ischaemic placenta +
Exaggerated inflammatory response ->
Endothelial cell damage (virchow’s -> clotting) ->
increased vessel permeability (proteinuria + oedema) ->
vasoconstriction (HTN, Eclampsia, Liver damage)
define pre-eclampsia
Pre-eclampsia is a disorder of pregnancy characterized by hypertension (>140/90) & proteinuria (>0.3g/24h)
list risk factors for pre-eclampsia?
nulliparity
previous pre-eclampsia
family hx pre-eclampsia
older mothers
chronic HTN
DM
Kidney disease
Twin pregnancy
what are the types of pre-eclampsia
Mild : 140/90 - 149/99
Moderate: 150/100 - 159/109
Severe - >160/110
how may pre-eclampsia present?
Asymptomatic
Headache, drowsiness, nausea and vomiting
visual disturbances
epigastric pain
what examination would you conduct for pre-eclapmsia?
Bedside:
BP - may not be high
Urine dip - protein (exclude infection with MC&S)
Fundoscopy - disc oedema
Neuro exam - reflex, eye movement
Abdo exam - epigastric tenderness (dic, liver failure, hellp)
Others:
24 hour urine collection
Protein:creatinine ratio >30
complications of pre-eclampsia?
Maternal:
- Eclampsia - grand mal seizures
- > death due to brain vessel spasm + hypoxia
- > placental abruption
- Renal failure
- Pulmonary oedema
- HELLP syndrome (which has complications eg: DIC, abruption, renal failure)
- DIC
- Liver failure
more sever if earlier onset
Fetal:
IUGR, Stillbirth, Preterm delivery
If closer to term, less effect on growth. all gestatoins have equal risk abruption.
what is drug of choice in prophylaxis and treatment of eclampsia
magnesium sulphate - MgSO4
how would pulmonary oedema be managed?
furosemide and oxygen
list some fetal complications of pre-eclampsia? depending on date acquire?
IUGR - main problem if PET <34 wks
causing need for Preterm birth
Placental abruption
if PET around term:
Stillbirth
Placental abruption
what ivx would tell you some1 with pre-eclampsia is deteriorating?
fall in platelets - hellp
Low Hb - haemolysis (low haptoglobin too - haematocrit may be low or normal)
increased ALT - hellp, liver damge
increased LDH - haemolysis, liver damage
increased uric acid - very key feature!
how would you then monitor a baby?
US - fetal growth and weight
CTG
Umbilical artery doppler - key to outline prognosis
how is PET mitigated?
All pregnant women have regular BP and urinalysis checks - come to the DAU
Aspirin 75mg before 16 weeks in at risk women
uterine artery doppler 23 weeks (not routine)
where are PET patients managed? what is regular monitoring?
- Mild AND moderate -> OUTpatient care
Assess DAU
-> No proteinuria and mild/moderate htn are managed as outpatients and BP/urinalysis checked twice (▪ Mild: 1/week – Moderate: 2/week)
weekly, with USS every 2-4 weeks
2. Admission criteria in suspected PET A -> Symptoms B -> Proteinuria 2+ ore more on dipsticks, or >0.3g/24h collection C -> Diastolic BP >160/110mmHg D -> Suspected fetal compromise
Admission is necessary with severe htn and where there is proteinuria
-> New proteinuria of 2+ should be admitted with or without HTN
Severe: manage in specialist unit with neonatal facilities
how is PET managed? aim BP?
think this includes GHTN? review
Antihypertensives are given if BP reaches 150/100mmHg
Mod:
Labetalol
Severe:
1st - Oral Nifedipine
2nd - IV labetalol (usually contraindicated in severe)
+ IV MgSO4 - prevent eclampsia
+ Steroids
aim BP: 140/90
what is the mechanism of MgSO4?
what sx does toxicity cause?
mechanism - increases cerebral perfusion
toxicity - respiratory depression, hypotension
when do we deliver in pregnancy related HTN diseases?
Gestation htn - IOL 40wks
Mild PET - ‘deliver’ 37wks
Mod PET - deliver 34-36wks
Sev PET - deliver 34-36wks - more urgent, soon as steroids completed and BP stabilised
if sev with complications / fetal distress - deliver any gestation
delivery <34 wks - c-section
delivery >34 wks - IOL
when does PET resolve?
within 24 hours post delivery
BP reach highest level 5days post birth
BUT may get worse!
what does postnatal care of PET involve?
monitor closely -
bloods
urine output
BP - give labetalol. need long-term monitoring at GP
refer to renal clinic if persisting
How does pre-existing hypertension present in pregnancy?
BP is already or rises above 140/90 before 20 weeks
may increase more in late pregnancy
may notice clinical signs of the cause: eg renal bruit, radiofemoral delay
proteinuria at booking - if kidney disease
what are the causes of pre-existing hypertension in pregnancy?
Primary - essential HTN - Most common
Secondary - obesity, kidney disease (eg CKD),
- rare; phaeo, cushings, aortic coarctation - heart disease
