Hypertension in Pregnancy / Eclampsia and Pre-Eclampsia
Chronic hypertension: HTN that pre-existed pregnancy / diagnosed <20/40 / persists >6/52 post-partum;
may be new end organ damage
Transient hypertension of pregnancy: no proteinuria / adverse effects; resolves within 2-4/52 postpartum
Gestational hypertension: HTN of onset >20/40 with no other features of pre-eclampsia; resolves within
3/12 post-partum; 25% develop pre-eclampsia
Classification
Pre-eclampsia: 1) BP
>140/90 on 2 occasions 4-6hrs apart
or
>160/110 on one occasion
or
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
(oligura <500ml/24hrs, Cr >0.09); hepatic ( transaminases, RUQ pain); CNS
(hyperreflexia + clonus, headache, visual scotoma, seizures (usually self-terminating
but recurrent), not FND); haematological ( platelets, DIC, haemolysis); fetal
growth retardation; acute pulmonary oedema
Mild
Moderate
Severe
DBP <100 or  30/15 from baseline
DBP >100, SBP <160
DBP >110, SBO >160
Minimal / absent proteinuira
Oedema
2+ proteinuira
Oedema
Severe proteinuria
End organ dysfunction
(>5g/24 hrs or 2-4+)
Epidemiology
Hypertension: 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 post-partum; 30% will recur in next
pregnancy,  maternal risk of HTN in later life; fetal + maternal mortality 2%
Eclampsia: incidence 1:2000 pregnancies; intracerebral haemorrhage is most common cause of maternal
mortality; fetal mortality up to 30%
Pathophysiology
Normal = 10-15mmHg  BP up to 18/40  BP return to pre-pregnancy values at 20/40
Pre-eclampsia: dysfunction of uteroplacental bed ( 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; levels
of ADMA (inhibitor of NOS, impairs endothelium-dependent vasodilation); state of fluid overload;
proteinuria due to  capillary permeability (not necessarily renal damage); DBP rises more than SBP
Pathophysiology
Primigravida (incidence 5-10%), PMH/FH of same, more babies, hydatiform mole, multigravida with new
partner, obesity, renal disease, HTN, diabetes, autoimmune disease, thrombophilia, <20yrs
Complications
Assessment
Investigation
Intracerebal haemorrhage
Symptoms: headache, visual disturbance, hyperreflexia, vomiting, epigastric pain, weight gain (>2kg/wk),
generalised oedema (especially feet, hands, face), pregnant woman with RUQ pain has pre-eclampsia
until proven otherwise; should resolve with lowering of BP
Examination: BP, oedema, volume status (depletion), clonus, hyperreflexia, RUQ pain / tenderness (liver
haematoma, capsule rupture)
Bloods: U+E ( CrCl more sensitive than  Cr); LFT ( protein,  AST then ALT,  bilirubin if
haemolysis,  LDH); Coag ( INR/APTT, decr fibringogen (DIC) ; FBC (haemolysis,  Hct,  platelets
(associated with  maternal morbidity)
 urate: hallmark of severe pre-eclampsia (due to  tubular excretion,  production by ischaemic t
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 neurological 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  platelets
Aim to prevent seizures and tissue ischaemia; prevent with good antenatal care; Following delivery,
treatment will be needed for up to 10/7
Anti-hypertensives: treat if
aim
SBP >170, DBP >110
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
MgSO4: consider if brisk reflexes / clonus / headache / visual changes; measure levels Q6h; monitor for
hyporeflexia and monitor calcium, Mg (>5 = toxic), respiratory rate, LOC; often given during labour and
delivery, for 24hrs post-partum; lowers BPs as well as controlling seizures
40mmol over 15mins (if seizing, rpt 20mmol Q15min to max 60mmol)  10-30mmol/hr infusion
CaGlu is antidote for overdose; monitor Mg levels Q4hrly and for side effects
Hydralazine: 5-10mg IV / IM over 5-10min  rpt Q20min  5-60mg/hr infusion
Consider other drug if no effect after 20mg; give IV fluids to prevent tachycardia
Management
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
Nifedipine: 10mg PO  rpt Q30min  then PO Q4hrly
30mg PO OD of long-acting  titrate to max 120mg/day
Methyldopa: 250mg PO Q6hrly  titrate up to control BP to max 3g/day
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 left lateral
position, continuous CTG, IDC
Steroids: if <34/40; betamethasone 11.4mg Q24hr X2
IV fluids: be cautious as acute pulmonary and cerebral oedema; give 500ml bolus if oliguria / volume
depletion  maintenace with 1-2ml/kg/hr crystalloids; use FFP to correct coagulation abnormalities