HYPERTENSIVE DISORDERS IN PREGNANCY

•	Types of hypertension in pregnancy.
•	Chronic hypertension. 
•	Pregnancy-induced hypertension.
•	Pre-eclampsia.
•	Management of PIH.
•	Management of Eclampsia.
•	Drugs used in management. 

Types of hypertension in pregnancy

1.	Blood pressure normally falls in pregnancy, with the lowest recordings at 14 – 20 weeks’ gestation, before rising towards pre-pregnancy values by term.

2.	Definition of hypertension:

a.	Blood pressure at or above 140 mmHg systolic and 90 mmHg diastolic.

b.	Rise of BP 30 mmHg systolic or 15 mmHg diastolic.

c.	Noted on 2 separate occasions 4 hours apart.

3.	Causes of hypertension in pregnancy:

a.	Pregnancy-induced hypertension (PIH).

b.	Chronic hypertension or pre-existing hypertension.

c.	Chronic hypertension with superimposed pre-eclampsia.

d.	Hypertension due to other causes, e.g. renal or collagen diseases, but detected for the first time in late pregnancy.

Chronic hypertension

1.	Definition: pre-existing hypertension or hypertension detected before 20 weeks.

2.	Secondary hypertension:

a.	Renal causes, e.g. chronic glomerulonephritis, immune nephropathies.

b.	Collagen vascular diseases, e.g. SLE.

c.	Endocrine disorders or tumors, e.g. thyrotoxicosis, phaechromocytoma.

d.	Coarctation of aorta.

e.	Hydatidiform mole.

3.	Physical examination:

a.	Pulse.

b.	General:

i.	thyroid enlargement.

ii.	fundoscopy to detect chronic hypertensive retinal changes.

c.	CVS examination.

d.	Abdominal and pelvic examination.

4.	Investigations:

a.	Blood chemistry: urea, uric acid, creatinine and electrolytes.

b.	Urine microscopy.

c.	24 hours’ urine: total protein and creatinine clearance.

d.	Thyroid function test.

e.	ECG.

5.	Pregnancy risks:

a.	Maternal risk: five-fold increase in the risk of developing superimposed PIH.

b.	Fetal risk: secondary to the development of superimposed PIH, when the perinatal mortality is doubled.

c.	Secondary hypertension: the maternal prognosis is that of the underlying condition.

d.	There is no evidence that pregnancy affects the long-term prognosis of a patient with hypertension. 

6.	Management:

a.	Admit for control of BP if hypertension is severe (160 / 110 mmHg or more) or symptomatic.

b.	Antihypertensives:

i.	drug of choice is alpha-methyldopa starting at 250mg t.i.d.

ii.	contraindicated: ACE inhibitors, diuretics and beta-blockers. 

c.	Low-dose aspirin at 50 to 100mg started 12 to 14 weeks into pregnancy may reduce the incidence of PIH.

d.	Monitor closely for development of superimposed PIH.

e.	For patients with uncomplicated chronic hypertension, fetal risks are negligible and they should aim to deliver at term. 

Pregnancy-induced hypertension

1.	Definition: 

a.	Development of hypertension after 20 weeks.

b.	Complicates 6 – 7% of all pregnancies.

2.	Classification of PIH:

a.	Non-proteinuric PIH.

b.	Proteinuric PIH or pre-eclampsia: a diastolic blood pressure exceeding 90 mmHg, on at least two occasions in the second half of pregnancy, where the blood pressure was previously normal, accompanied by significant proteinuria of > 300 mg/24h.

c.	Eclampsia: when the above picture is complicated by tonic-clonic seizures not caused by coincidental neurological disorders. 

3.	Degree of hypertension:

a.	Mild: 140/90 to 149/99 mmHg.

b.	Moderate: 150/100 to 159/109 mmHg.

c.	Severe: > 160/110 mmHg. 

Pre-eclampsia

1.	Risk factors for pre-eclampsia:

a.	Primigravida.

b.	Over 35 years old.

c.	Pre-existing chronic hypertension, renal disease, autoimmune disorders.

d.	Multiple pregnancy.

e.	Previous history of PIH.

f.	Diabetes mellitus. 

2.	Pathophysiology:

a.	Total or patchy failure of throphoblast invasion of the myometrial segments of the spiral arteries. 

b.	Associated with IUGR and abruptio placentae.

c.	A poorly perfused trophoblast may release a ‘factor X’ which enters the maternal circulation and damages the vascular bed.

d.	Vasospasm and endothelial cell dysfunction, with subsequent platelet activation and micro-aggregate formation account for many of the pathological features of pre-eclampsia.

e.	In the kidney, a highly characteristic lesion called glomeruloendotheliosis is seen: this consists of endothelial and mesangial cell swelling, basement membrane inclusions. 

f.	In the liver, subendothelial fibrin deposition is associated with elevation of liver enzymes with hemolysis and a low platelet count due to platelet consumption (HELLP syndrome).

3.	Organ-specific changes associated with pre-eclampsia:

System	Changes	
Cardiovascular	•	Generalized vasospasm.
•	Increased peripheral resistance.
•	Reduce central venous / pulmonary wedge pressures.	
Haematological	•	Platelet activation and depletion.
•	Coagulopathy.
•	Decreased plasma volume.
•	Increased blood viscosity.	
Renal	•	Proteinuria.
•	Decreased GFR.
•	Decreased urate excretion.	
Hepatic	•	Periportal necrosis.
•	Subcapsular haematoma.	
Central nervous	•	Cerebral edema.
•	Cerebral haemorrhages. 	

4.	Maternal complications:

Complications	Signs	
Cerebral haemorrhage	•	Altered level of consciousness.
•	Irritability.
•	Localizing signs, altered response to stimuli and reflexes.	
Ocular	•	Visual disturbances.
•	Blindness.
•	Retinal haemorrhage / detachment.	
CVS	•	Hypertensive cardiac failure.
•	Cardiomyopathy.
•	Coronary insufficiency.	
Pulmonary	•	Pulmonary edema.
•	Pneumonia.
•	Pleural effusion.	
Hepatic	•	Liver enlargement.
•	Haematoma, rupture.
•	Jaundice.	
Renal	•	Oliguria.
•	Haematuria.
•	Renal failure.	
Coagulopathy	•	DIVC.
•	Haemorrhage. 	

5.	Fetal complications:

a.	Chronic hypoxia: IUGR.

b.	Acute hypoxia: fetal distress and death. 

Management of PIH

1.	Principles of management:

a.	Admit.

b.	Assess severity.

c.	Control BP.

d.	Monitor mother to detect worsening of disease.

e.	Monitor fetus for growth and hypoxia.

f.	Deliver after 37 weeks or earlier. 

2.	Immediate action:

a.	Transfer to labor ward.

b.	Immediate review and BP monitoring by resident. 

c.	Obtain IV access.

d.	Urinary catheter, check urine for protein. 

3.	Initial clinical assessment:

a.	Elevation of blood pressure.

b.	Fluid retention: non-dependent edema / rapid weight gain.

c.	Brisk reflexes.

d.	Ankle clonus: more than 3 beats.

e.	Signs and symptoms of eclampsia.

4.	Investigations:

a.	24 hours urine output.

b.	24 hours urine protein (UTP).

c.	FBC: platelets and haematocrit.

d.	Serum urea, creatinine, uric acid.

e.	Creatinine clearance (CCT).

f.	Liver panel.

g.	Coagulopathy screen: PT / PTT. 

5.	Acute BP control:

a.	Labetalol infusion 20 mg/h or bolus regime up to 220 mg.

b.	Hydralazine 20 mg in 100 ml N/S at 10dpm or bolus dose of 2.5 mg IV in N/S.

c.	Aim to achieve BP 140 – 15- / 90 – 100 within 30 minutes from starting treatment.

d.	When BP is stable and oral antihypertensive has been commenced, infusion may be tailed off by 4ml/hr every 20 min.

6.	Chronic BP control:

a.	Methyl-dopa 250 – 500 mg tds/qds; takes 6 – 12 hours to act.

b.	Alternatives: nifedipine labetalol.

7.	Maternal monitoring:

a.	PE chart:

i.	4 hourly observation for signs and symptoms of PE.

ii.	BP chart and pulse rate.

iii.	urine output: < 30 ml/hr may indicate either hypovolaemia or renal compromise.

iv.	reflexes and clonus.

b.	Weekly / twice weekly investigations:

i.	24 hrs urine UTP / CCT.

ii.	FBC.

iii.	Renal panel and uric acid.

iv.	Liver panel and clotting screen. 

8.	Fetal monitoring:

a.	Growth:

i.	clinical: symphysis fundal height weekly.

ii.	3 weekly ultrasound.

b.	Acute hypoxia:

i.	clinical: daily FM chart, liquor volume.

ii.	CTG.

iii.	AFI. 

iv.	umbilical artery Doppler velocimetry.

v.	biophysical profile.

9.	Aim to deliver after 37 weeks unless:

a.	Maternal condition worsens:

i.	impending eclampsia / eclampsia.

ii.	uncontrolled BP.

iii.	 platelets < 100.

iv.	oliguria.

v.	deranged liver function.

b.	Fetal condition worsens:

i.	low AFI.

ii.	abnormal CTG.

iii.	fetal growth ceases.

Management of Eclampsia

1.	Principles of management:

a.	Airway.

b.	Control fits.

c.	Control BP.

d.	Assessment of mother and fetus.

e.	Planned delivery.

f.	Post-delivery management.

2.	Immediate management:

a.	Airway:

i.	remove dentures.

ii.	insert airway tubes, soft mouth gag to prevent tongue getting bitten.

iii.	lateral postion, head low and tilted to one side, neck extended.

b.	Breathing:

i.	suction of secretions.

ii.	oxygen by mask.

c.	Circulation:

i.	obtain IV access x 2 large born cannulae.

ii.	bloods: FBC, DIVC, renal panel, LFT, GXM.

3.	Control and prevention of fits:

a.	Indications for IV MgSO4:

i.	eclamptic fits / post-eclamptic seizures.

ii.	proteinuric hypertension with pre-ictal symptoms and signs.

b.	Loading dose: 2 ampoules of MgSO4 (10ml) in 100ml N/S run in rapidly.

c.	Maintenance dose: 5 ampoules of MgSO4 (25ml) in 100ml N/S run at 10mls/hr over 12.5 hours.

d.	If conversions recur, give 1 ampoule IV MgSO4 in 100ml N/S run rapidly.

e.	If convulsions recur third time, consider diazepam 10mg IV or Thiopentone 50mg IV.

4.	Control of BP:

a.	20 mg hydralazine in 100ml N/S start at 10dpm for 10 min.

b.	Consider bolus dose of 2.5mg IV if BP is persistently high at 30 min.

c.	Nifedipine should be avoided while patient is on IV MgSO4 because it may have a synergistic hypotensive effect. 

5.	Monitoring:

a.	Mother:

i.	pulse and BP.

ii.	pulse oximetry.

iii.	intake-output.

iv.	urine albumin on dipstick.

v.	level of consciousness.

b.	Fetus:

i.	gestation age.

ii.	CTG.

iii.	liquor volume.

iv.	other complications: IUGR, abruptio, multiple pregnancy. 

6.	Planned delivery:

a.	Induction of labor:

i.	ARM and IV syntocinon if there are no contraindications and vaginal delivery is anticipated in a short period.

ii.	epidural used.

iii.	IV syntocinon in 3rd stage (not ergot).

b.	Emergency LSCS if:

i.	vaginal delivery is not possible.

ii.	progress is slow during labor.

iii.	maternal or fetal condition worsens.

7.	Post-delivery management:

a.	Monitor in LW while patient on IV MgSO4.

b.	Continue close attention to BP and fluid balance:

i.	strict fluid balance, indwelling catheter.

ii.	dextrose saline at 85mls/hr.

c.	Daily blood tests.

d.	Once condition stabilized: consider oral hypertensives.

e.	If condition deteriorates: consider transfer to ICU. 

Drugs used in management

1.	Methyldopa:

a.	Taken up into central and peripheral adrenergic nerve terminals and converted to a false transmitter alpha-methylnoradrenaline. 
  
c.	Alpha-methylnoradrenaline stimulates alpha2-receptors in the hindbrain nuclei to suppress sympathetic discharge resulting in a fall in blood pressure. 
  
d.	Adverse effects: drowsiness, sedation, headache, nightmares, depression, involuntary movements, nausea, flatulence, constipation, haemolytic anaemia, leukopenia, thrombocytopenia and hepatitis. 

2.	Labetalol:

a.	A racemic mixture of beta and alpha-blocker.

b.	Can cause postural hypotension.

c.	Contraindicated in:

i.	asthmatics.

ii.	2nd or 3rd degree heart block.

iii.	bradycardia.

3.	Hydralazine:

a.	Side effects: SLE-like syndrome, arthralgia, myalgia, fever and skin rash.

b.	Contraindicated in:

i.	rheumatic heart disease.

ii.	mitral valve disease.

iii.	tachycardia.

4.	Magnesium sulphate:

a.	Narrow therapeutic window of 2 – 4 mmol/L.

b.	Serum levels should be checked in:

i.	oliguric patients on continuous infusion.

ii.	absent patellar reflexes.

iii.	respiratory depression. 

c.	Signs of toxicity:

i.	absent knee jerks.

ii.	arrhythmias and fatigue.

iii.	respiratory depression.

iv.	cardiac arrest.

d.	Management:

i.	intubate and ventilate promptly.

ii.	give 1 ampoule of IV Ca gluconate over 3 min.

iii.	continue ventilation till normal spontaneous respiration is resumed.