Hypertenson in Pregnancy / Eclampsia
Classification
Chronic hypertension: HTN that pre-existed pregnancy / diagnosed <20/40 / persists >6/52 PP; may be new end organ damage
Transient hypertension of pregnancy: no proteinuria / adverse effects; resolves within 2-4/52 PP
Gestational hypertension: HTN of onset >20/40 with no other features of pre-eclampsia; resolves within 3/12 PP; 25% develop pre-eclampsia
Pre-eclampsia:
1) BP:
>140/90 on 2 occasions 4-6hrs apart
or >160/110 on one occasion
or incr from baseline >20 SBP / >10 DBP (?no longer used)
2) Proteinuria: >300mg/24hrs, 1+ on dipstick
3) Other end organ damage (at least one of): rapid onset generalised oedema
renal
hepatic
CNS
haem
fetal growth retardation
APO
Mild:
Mod:
Severe:
Epidemiology
Pathophysiology
Risk Factors
Complications
Assessment
Investigation
Management
BP
DBP <100
or incr 30/15 from baseline
DBP >100, SBP <160
DBP >110, SBP >160
Urine
Minimal / absent proteinuria
2+ proteinuira
Severe proteinuria (>5g/24hrs, or 2-4+)
oligura <500ml/24hrs, Cr >0.09
incr transaminases, RUQ pain
hyperreflexia + clonus, headache, visual
scotoma, seizures (usually self-terminating
but recurrent), not FND
decr plt, DIC, haemolysis
Sx
Oedema
Oedema
End organ dysfunction (as above)
.
.
.
.
HTN: occurs in 10% pregnancies; >50% if due to pre-eclampsia
Pre-eclampsia: 5-7% of pregnancies; rare <20/40 (may be seen this early if has hydatiform mole), 10% <34/40, usually occurs in last few weeks, can
occur up to 7/7 PP; 30% will recur in next pregnancy, incr maternal risk of HTN in later life; fetal + maternal mortality 2%
Eclampsia: incidence 1:2000 pregnancies; ICH is most common cause of maternal mortality; fetal mortality up to 30%
Normal = 10-15mmHg decr BP up to 18/40  BP return to pre-pregnancy values at 20/40
Pre-eclampsia: dysfunction of uteroplacental bed (incr vascular resistance in placental bed, abnormal responsiveness of spiral arteries to
vasocontrictors)  systemic vasospasm, ischaemia, thrombosis  maternal organ damage (ischaemia and thrombosis), placental insufficiency, fetal
compromise; incr levels of ADMA (inhibitor of NOS, impairs endothelium-dependent vasoD); state of fluid overload; proteinuria due to incr cap perm
(not necessarily renal damage); DBP rises more than SBP
Primigravida (incidence 5-10%), PMH/FH of same, more babies, hydatiform mole, multigravida with new partner, obesity, renal disease, HTN, DM,
autoimmune disease, thrombophilia, <20yrs
Intracerebral haemorrhage
Symptoms: headache, visual disturbance, hyperreflexia, V, epiG pain, weight gain (>2kg/wk), generalised oedema (esp feet, hands, face), pregnant
woman with RUQ pain has pre-eclampsia until proven otherwise; should resolve with lowering of BP
Examination: BP, oedema, vol status (depletion), clonus, hyperreflexia, RUQ pain / tenderness (liver haematoma, capsule rupture)
Bloods: U+E: decr CrCl more sensitive than incr Cr
LFT: decr protein, incr AST then ALT, incr bil if haemolysis, incr LDH
Coag: incr INR/APTT, decr fibringogen (DIC) (features of DIC)
FBC: haemolysis, decr Hct, decr plt (assoc with incr maternal morbidity)
Incr urate: hallmark of severe pre-eclampsia (due to decr tubular excretion, incr production by ischaemic tissue; serial levels
monitor disease progression)
Urine: proteinuria (not useful in monitoring disease progress ; pre-eclampsia until proven otherwise), casts, cells
CTG:
CT: do if: prolonged coma, persistent neuro changes, seizure / altered LOC, refractory seizures, <20/40, >48hrs post-partum
CXR: ARDS
ECG: evidence of myocardial dysfunction
Delivery is only cure (give oxytocin in 3rd stage; avoid ergometrine / syntometrine)
Indications for immediate delivery: eclampsia, pre-eclampsia >37/40, inability to control BP, abnormal CTG, placental abruption, deteriorating LFT /
renal function, progressive decr plt
Aim to prevent seizures and tissue ischaemia; prevent with good antenatal care
Anti-hypertensives: trt SBP >170, DBP >110
aim SBP <160 (or reduction by 20-30)
DBP <110 (or reduction by 10-15)
MAP <125 to prevent CVA
greater reductions in BP may cause fetal ischaemia
1MgSO4: consider if brisk reflexes / clonus / headache / visual changes; measure levels Q6h; monitor for hyporeflexia and monitor Ca, Mg (>5 =
toxic), RR, LOC; often given during labour and delivery, for 24hrs PP; lowers BPs as well as controlling seizures; 40mmol over 15mins (if seizing, rpt
20mmol Q15min to max 60mmol)  10-30mmol/hr INF; CaGlu is antidote for OD; monitor Mg levels Q4hrly and for SE’s
1) Hydralazine: 5-10mg IV / IM over 5-10min  rpt Q20min  5-60mg/hr infusion; consider other drug if no effect after 20mg; give IVF to prevent
tachycardia
2) Labetalol: 100mg PO BD  max 400mg PO BD
10 - 20mg IV  double to 40, then 80mg IV Q10min to max 220mg  1-2mg/hr infusion
Less hypotension and tachycardia than hydralazine
3) Nifedipine: 10mg PO  rpt Q30min  then PO Q4hrly
30mg PO OD of long-acting  titrate to max 120mg/day
3) Methyldopa: 250mg PO Q6hrly  titrate up to control BP to max 3g/day
4) Nitroprusside: 0.25-5mcg/kg/min infusion; don’t use if <30min to delivery; risk of cyanide toxicity (unlikely if given <4mcg/kg/min or infusion
duration <30mins)
Low dose aspirin: small-mod benefits
Conservative: minimise auditory and visual stimulation, bed rest, salt restriction, position in L lateral position, continuous CTG, IDC
Steroids: if <34/40; betamethasone 11.4mg Q24hr X2
IVF: be cautious as APO and cerebral oedema; give 500ml bolus if oliguria / vol depletion  maintenace with 1-2ml/kg/hr crystalloids; use FFP to
correct coag abnormalities
Following delivery, trt will be needed for up to 10/7
Notes from: Dunn, Cameron, TinTin