2 source(s) cited.
# Diagnosis, classification and risk stratification of hypertensive disorders in pregnancy LO id: `3A.WOMENS.OBS_HTN.DIAGNOSIS` | importance: core ## Classify hypertensive disorders of pregnancy: chronic/pre-existing hypertension, gestational (pregnancy-induced) hypertension, and pre-eclampsia - Three categories: pre-existing (chronic) hypertension, pregnancy-induced hypertension (PIH), and pre-eclampsia (PET) [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p007] - Women with pre-existing hypertensive disease are automatically classified high-risk for **superimposed** pre-eclampsia [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p006, hypertension-in-pregnancy-lecture-transcript-d4784c#p013] - Pre-eclampsia is a disease of placentation with signs of end-organ damage; very rare before 20 weeks, most commonly onsets late third trimester, and mostly resolves soon after delivery [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p009] - Most women are diagnosed with hypertensive disease of pregnancy in the third trimester, though second-trimester onset marks the early severe cases [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p002, hypertension-in-pregnancy-lecture-transcript-d4784c#p012] ## Diagnostic blood pressure thresholds and the role of proteinuria in distinguishing pre-eclampsia from gestational hypertension - Pre-eclampsia: hypertension **with** proteinuria; pregnancy-induced hypertension: hypertension **without** proteinuria — proteinuria signals kidney involvement/end-organ damage, which is the key severity differentiator [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p007, hypertension-in-pregnancy-lecture-transcript-d4784c#p013] - The lecturer states the diagnostic BP threshold discussed in this session as >135/85, reflecting a tightened target discussed alongside the CHIPS trial (see the Management note, mgmt.antenatal-drugs) — note this is presented in the same breath as the *treatment target* shift from 140/90; the slides separately state a >140/90 cutoff for pre-existing/PIH classification, so treat the exact numeric cutoff as something to confirm against current national guidance rather than a single fixed figure from this source alone [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p007, hypertension-in-pregnancy-lecture-transcript-d4784c#p013] - Booking-visit BP and urine dipstick are the first-line screen that feeds into this classification [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p005] ## High-risk and moderate-risk factors for pre-eclampsia and their use in aspirin-prophylaxis decisions - High-risk factors: previous hypertensive disease in pregnancy, chronic kidney disease, some autoimmune/inflammatory disorders, pre-existing diabetes, chronic hypertension [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p008] - Moderate-risk factors: nulliparity, age >40, pregnancy interval >10 years, BMI >35, first-degree relative with pre-eclampsia [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p008] - One high-risk factor, or two moderate-risk factors, triggers aspirin prophylaxis under the NICE risk-factor approach [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p013] - An alternative to the risk-factor checklist is an individualised algorithmic risk score (referenced in this session as the "Tommy's"/fetal medicine foundation algorithm), combining maternal history, mean arterial pressure, and uterine artery Doppler; it stratifies into low/moderate/high risk and determines aspirin allocation and scan frequency (low risk: no extra scans unless otherwise indicated; moderate: two scans; high: later, more frequent scanning plus aspirin) [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p010, hypertension-in-pregnancy-lecture-transcript-d4784c#p011, hypertension-in-pregnancy-lecture-slides-5cf2f7#p006] ## Diagnostic/monitoring adjuncts: uterine artery Doppler, placental growth factor (PlGF) testing, growth scans - Uterine artery Doppler measures blood-flow velocity/resistance in the uterine artery; an abnormal Doppler at 20–24 weeks is defined by a pulsatility index above the 95th percentile and/or the presence of an early diastolic notch [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p007, hypertension-in-pregnancy-lecture-transcript-d4784c#p009] - In normal pregnancy, spiral artery remodelling causes the diastolic notch to disappear and end-diastolic flow to rise; in abnormal placentation (pre-eclampsia/FGR) this remodelling is inadequate and the notch/high-resistance pattern persists [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p008] - Placental growth factor (PlGF) testing (evaluated in the PARROT trial) reduced median time-to-diagnosis (4.1 vs. 2 days) in suspected pre-eclampsia and reduced severe adverse outcomes (5% vs. 4%) in a multicentre RCT [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p013, hypertension-in-pregnancy-lecture-transcript-d4784c#p020] - PlGF testing is presented as most useful where diagnosis is otherwise difficult — e.g. patients with pre-existing renal disease who already have baseline proteinuria, making pre-eclampsia hard to distinguish from their underlying condition — rather than as a universal screen, partly on cost grounds [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p021] ## Pathophysiology: placentation, spiral artery remodelling, systemic vascular resistance changes in normal vs. hypertensive pregnancy - Normal pregnancy: vasodilation driven by mediators including nitric oxide and progesterone; reduced systemic vascular resistance; increased plasma volume via augmented renin-angiotensin-aldosterone activity; increased stroke volume and heart rate [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p003, hypertension-in-pregnancy-lecture-transcript-d4784c#p001] - This produces a high-flow, low-resistance circulation that maximises maternal blood flow to the placental villi at the maternal-fetal interface [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p004] - Basic BP physiology: arterial BP = peripheral vascular resistance × cardiac output (heart rate × stroke volume); systolic = peak during cardiac contraction, diastolic = trough during cardiac relaxation [source: hypertension-in-pregnancy-lecture-slides-5cf2f7#p002] - In normal placentation, extravillous cytotrophoblast cells invade the decidua and myometrium, remodelling the spiral arteries into dilated, low-resistance vessels; in pre-eclampsia/FGR this trophoblastic invasion is inadequate, spiral arteries remain high-resistance, and this drives abnormal Doppler findings [source: hypertension-in-pregnancy-lecture-transcript-d4784c#p008]