IB WCS 19
HYPERTENSION & PREGNANCY
Dr KY Leung
O&G
Mon 09-09-02
HT IN PREGNANCY
- Incidence: 3-7%
- Leading cause of maternal mortality: eclampsia, CVA, pulmonary
- Perinatal mortality: preterm, SGA
- Pre-eclampsia (PET): pregnancy specific syndrome
- Heterogenous conditions:can be chronic HT/renal disease
CLASSIFICATION
A) Gestational HT/ proteinuria:
- Gestational HT
- Gestational proteinuria,
- Gestational proteinuric hypertension (PET)
B) Chronic hypertension/ renal disease:
- Chronic HT,
- Chronic renal disease,
- Chronic HT with superimposed pre-eclampsia
C) Unclassified:
- Presents > 20 weeks, or insufficient information
Incidence in HK (1994)
Total incidence: 2.9%
A) Gestational HT/ proteinuria
- Gestational HT (54.7%)
- Gestational proteinuria (2.3%)
- Gestational proteinuric hypertension (24.6%)
B) Chronic hypertension:
- Chronic HT (5.6%)
- Chronic HT with superimposed PET (1.9%)
C) Unclassified: 10%
Risks of PET
Maternal
- Eclampsia (0.5%)
- CVA
- Deranged renal and liver function
- Coagulopathy:DIC
- Pulmonary oedema
- Placental abruption
- HELLP (hemolysis, liver, low platelet)
Fetal
- IUGR
- Fetal hypoxia
- Fetal distress
- IUD
Pathophysiology of pre-eclampsia
- Decreased perfusion to virtually all organs
- Endothelial dysfunction: vasospasm, and microthrombi
- Reduced vasodilator prostacyclin, increased vasoconstrictive thromboxane
- Circulatory factors: lipid peroxides, cytokines, syncytotrophoblast microvillous membranes
- Reduced uteroplacental blood flow.
- Lack of endovascular invasion cytotrophoblastic invasion in maternal spiral arteries
- Immunological mediated, vascular disease, increased trophoblast
Predisposing factors
- Primigraivida
- Age
- Past obs: PET
- Pre-existing maternal diseases: DM, HT, renal disease, anticardiolipin antibody syndrome
- Obstetric conditions: multiple pregnancy, hydatiform mole, hydrops.
Diagnosis of pre-eclampsia
- Classical triad: HT, proteinuria, oedema.
- Classical : PET then eclampsia
- Asymptomatic if mild (regular A/N visit)
- Presentation is variable
- Atypical presentation: PET without preceding proteinuria; eclampsia without preceding features of PET
Hypertension
- BP>= 140/90mmHg for two consecutive readings 4 hrs apart with rest
- Or one reading of DBP >=110mmHg
- Some: increase of DBP by 15 or 25mmHg
- Sitting, appropriate cuff, heart level
- K4: muffling, not to zero, conventional, but less agreement
- K5: disappearance of sound , more identified and agreement, but may at or near zero, conventional Mx not base on K5
- Mercury sphygmomanometry: errors, white coat HT
- Automated: reduce errors, measures K5.
Proteinuria
- Dipstick, false positive and negative, MSU
- 24 hr urine protein>=300mg/day
- Heavy proteinuria >=1g/day
Oedema
- Common
- Oedema is now omitted from all definitions of PET ® but widespread severe oedema of sudden onset is of clinical importance.
Differentiation
If BP normal and no proteinuria before 20 wks,
(a) HT and proteinuria afterwards => PET;
(b) HT alone => gestational HT
HT + symptoms / abnormal liver / thrombocytopenia / hyperuricemaia / IUGR => PET
If HT/proteinuria develops before 20 wks => ? Chronic HT/ renal disease
Need to rule out secondary causes: renal (GN, polycystic kidneys), CVS (renal artery stenosis, COA), endocrine (DM, phaecochromocytoma), autoimmune (SLE)
Management
- The definitive treatment of pre-eclampsia is delivery( not just control of HT, a multi-system disorder)
- The timing is a balance between severity of pre-eclampsia and risk of prematurity
Mild non-proteinuric hypertension
- Day case reduces inpatient stay, convenient
- Monitoring of maternal and fetal well being: S/S, LRFT, urate, kick chart, +/- USG
- Progressive disorder
- Bed rest: no evidence to improve outcome
- AntiHT therapy: controversial
- Induction before 40 wks
Severe PET or imminent eclampsia
- Symptoms: headache, visual disturbance, epigastric or RUQ pain, nausea and vomiting
- Signs: BP>=160/110, proteinuria (3 or 4 + or >3g/d), gross and rapidly progressive oedema, brisk jerks or clonus, oliguria (<30ml/h)
- Lab: thrombocytopenia, impaired LFT, RFT, clotting profile
Treatment of severe PET
- Early delivery: Induction or C/S
- Conservative if extreme prematurity, improve neonatal outcome, close monitoring of maternal well being.
- Steroid: dexamethasone to promote fetal lung maturity.
- Control of BP: decrease risk of cerebral hemorrhage (>= 160/110 mmHg), but avoid sudden lowering of BP=> fetal distress. Keep DBP between 90 and 100
- Antihypertensive therapy- IV hydrallazine or oral therapy (methyldopa)
- Prophylactic anticonvulsant is controversial. Choice: Magnesium sulphate
Delivery: High risk
- Epidural> GA, pain relief, exclude coagulopathy
- CFHM, BP, proteinuria, jerks, convulsion
- Avoid prolong labour
- Low threshold of C/S
- Postpartum: convulsion, pulmonary oedema
- At least 24 hrs after delivery or last fit
- Appropriate fluid management, diuretics
Eclampsia
- Occurrence of convulsion in pregnancy unless known epilepsy or cause.
- Can occur up to 10 days
- 1.8% mortality
- Tonic-clonic type followed by coma
Mx of eclampsia
- Acute: prevention of injury and aspiration
- Control of convulsion and prevent recurrence +/- control of HT
- Stabilisation of woman
- Expeditious delivery
Anticonvulsants
- Collaborative trial:magnesium sulphate is superior to diazepam
- However, low therapeutic-toxic range
- Toxicity: respiratory depression and cardiac arrest
- Monitor: patellar reflex, urine output( >30ml/h), respiratory rate (>12/min), +/- magnesium level(4-8mg/dl)
PN Counselling
- Recurrence of PET: 1 in 10, 1 in 4 (if eclampsia)
- Long term risk of CVD if recurrent PE or HT in pueperium.
- If BP normal, no contraindication to OC'
Prevention of PE
- Low dose aspirin increases prostacyclin to thromboxane ratio. A RCT (CLASP)*- not for routine prophylaxis,may be beneficial for high risk cases with previous adverse fetal outcome
- Calcium supplementation: no value
- Fish oil reduces formation of thromboxane: no reduction in PET.
Chronic hypertension and renal disease
- Prognosis depends on superimposed PET(17%), renal function (nephropathy), and progression of underlying disorder(e.g. SLE)
- Are antihypertensive agents (she has been taking) safe in pregnancy?
- BP may fall slightly in second trimester
Superimposed PET
- Sudden raised BP
- Increased or development of proteinuria
- Progressive increasing urate level
- IUGR
- Features of multi-system disorders
Antihypertensive therapy
- Reduces the rsik of severe HT but not risk of superimposed PE.
- Consider if BP>=150/100 mmHg
- Methyldopa: central action, widely use, safe in pregnancy, well tolerated, S.E: dizziness, postural hypotension, nightmare, depression, abnormal LFT
- Labetolol: combined alpha and beta blocker, vasodilatation, effective and safe in pregnancy
- Hydrallazine: vasodilator, increase HR and CO, tachyphylaxis
- Nifedipine: new, calcium channel blocker, appears safe, SE: headache, tachycardia.
- No short term effects on breastfeeding infants: Methyldopa, hydralazine, calcium channel blockers
- Avoid
propanolol (IUGR, neonatal depression), ACE inhibitors (fetal death, neonatal renal failure)
Summary
- Maternal and perinatal mortality
- PET is a multi-system disorder
- PET is progressive
- Early detection
- Approach to HT: establishment of diagnosis, differentiate between different causes, and assessment of severity of HT
- Definitive treatment is delivery
SUMMARY: RISKS & Mx
- Eclampsia: anticonvulsant (MgSO4)
- CVA: antihypertensive:IV hydrallazine; oral methyldopa
- Abnormal LRFT, coagulopathy, HELLP: delivery
- Placental abruption: delivery
- Pulmonary oedema: fluid restriction, diuretics
- IUGR/ hypoxia: foetal monitoring/ delivery