Pre-eclampsia

- An overview

Fiona Lloyd Jones

Ashford & St Peter’s Hospitals

Introduction

• Remains a leading cause of maternal and

perinatal morbidity and mortality

• 19 deaths in CMACE 2011

• Complicates 2% - 6% of pregnancies

• Several risk factors identified

RISK FACTORS FOR DEVELOPING PRE-ECLAMPSIA

RISK FACTOR EXAMPLES

Socio-demographic factors Extremes of reproductive age

Socio-economic status

Ethnic group: Afro-Caribbean

Genetic Factors Mother or sister with pre-eclampsia

Partner previously fathered pregnancy

complicated by pre-eclampsia

Pregnancy Factors Multiple pregnancies

Primagravida

Previous pre-eclampsia

Personal Medical History Obesity

Chronic renal failure

Chronic hypertension

Diabetes mellitus

Thrombophilia

Collagen vascular diseases

• Complications common

• Treatment is delivery of fetus and placenta

• Subsequent pregnancies 10% recurrence and

20% in severe pre-eclampsia

• Long term effects - ↑ hypertension, IHD, CVA

• Definition

• Pathogenesis

• Pathophysiology

• Investigations

• Treatment

• Anaesthetic Issues

Definition

• Hypertension arising after 20 weeks gestation

with the involvement of one or more organ

systems with resolution by 3 months

postpartum

• Systolic ≥ 140mmHg and/or diastolic ≥

90mmHg

• Severe pre-eclampsia systolic ≥ 160mmHg

and/or diastolic ≥110mmHg

Pathogenesis

• Due to abnormal placentation

• Deficient trophoblastic invasion of spiral

arteries reduces placental perfusion

• Leads to generalised maternal endothelial

dysfunction in later pregnancy

• Leakage of protein and fluid from the

intravascular space

• Two theories for endothelial dysfunction

Endothelial Dysfunction 1 -

Release of circulating factors

• Placenta releases circulating factor(s)

• Vascular endothelial growth factor (VEGF),

TNF, lipid peroxides, syncitiotrophoblast

microfragments

• Likely to act in combination to disrupt normal

endothelial integrity

Endothelial Dysfunction 2 -

Oxidative stress

• Oxidative stress -> NO and superoxide ->

damage to cell membranes

• Markers of oxidative stress present in

endothelial cells 3% normal women but 73%

of women with pre-eclampsia

• Antioxidants Vits C and E given to women at

risk of pre-eclampsia reduced its incidence

compared with those given placebo

Pathophysiology

• What are the effects on the mother of

endothelial dysfunction?

Cardiovascular & Respiratory

• Women are relatively vasoconstricted and

hypovolaemic

• Exaggerated response to vaso-active drugs

• Low COP and leaky endothelium leads to

oedema – peripherally, airway mucosa and

pulmonary oedema

Haematological

• Platelet activation and consumption increased

• Thrombocytopaenia in 15%

• DIC in 7%

Renal

• Renal tubular function decreases early

• Monitored with serial urate

• Proteinuria caused by glomerular ischaemia

• Protein leak up to 5g/day

• Oliguria common – usually responds to fluid

optimisation

• Beware liberal use fluids -> pulmonary

oedema

Hepatic

• Abnormal liver function tests common

• Epigastric pain due to oedema and liver

capsule stretching or intrahepatic bleeds

• CMACE 2011 new onset pain = pre-eclampsia

• HELLP Haemolysis Elevated Liver enzymes Low

Platelets

Neurological

• Ischaemia due to vasospasm or oedema

• Headache, visual disturbance, hyperreflexia

• Seizures in eclampsia

Investigations

Renal

• Urinary protein

– >0.3g / 24hrs (mild / moderate)

– ≥5g/24 hrs or 3+ protein dipstick (severe)

• Urinary PCR >30 (mild / mod) or >50 (severe)

• U & E – raised urea & creatinine >120mmol/l

• Urate >400 mmol/l

Hepatic

• LFT’s AST >70IU.l⁻¹ & LDH >600IU.l⁻¹

Haematological

• FBC - platelets <100x10⁹.l⁻¹

• Clotting - prolonged APTT and PT

Treatment of Hypertension

• Non –severe hypertension

• Oral labetolol (first line) or methyldopa

• Severe hypertension

• Nifedipine (oral 10mg)

• Labetolol (oral or intravenous 10-20mg bolus)

• Hydralazine (intravenous 5mg bolus)

• GTN infusion 5μg/min for pulmonary oedema

• Aim to reduce BP 10-20mmHg every 10-20 min

Treatment & Prevention of Seizures

• Magnesium sulphate is the mainstay

• Indicated in severe pre-eclampsia associated

with hyper-reflexia and eclamptic seizures

• Initial bolus 4g over 5 mins

• Maintenance 1-2g per hour for 24hrs

• Therapeutic levels 2-3 mmol/l

• Monitor reflexes and give 10% Calcium

gluconate 1g in overdose

Anaesthetic Issues

1. Neuroaxial blockade for labour

2. Anaesthesia for Caesarean Section

3. Postoperative analgesia

4. Intravenous fluid administration

5. Use of oxytocic agents

Neuroaxial Blockade for Labour

• Good for blood pressure control

• Safe if platelets > 100 x10⁹/l

• Check clotting first if below this level

• Do not pre-load with iv fluid before

establishing a low dose epidural

• Intravenous opiates can be used if an epidural

is contraindicated

Anaesthesia for Caesarean Section

• Neuroaxial anaesthesia is the preferred

technique

• Single shot spinal, CSE and epidural all used

• No evidence that one is better than another

• Hypotension requiring vasopressors is less

common

• Use small boluses of phenylephrine (50μg) or

low dose phenylephrine infusion

General Anaesthesia for LSCS

• May be indicated

• 2 problems

– Airway oedema leading to difficult intubation

– Ablating the hypertensive response to intubation

• Airway – have small endotracheal tubes

available and prepare for a difficult intubation

• Blunting the hypertensive response –

alfentanil, remifentanil, MgSO₄, lidocaine,

esmolol

• Avoid complications on emergence

• Avoid pulmonary oedema from fluid overload

• Give syntocinon infusions in smaller volumes

Post Eclamptic Fit

• Left lateral position and A, B, C

• Regional anaesthesia preferable in absence of

fetal compromise and stable mother

• Need a recent platelet count

• GA only if woman unstable and / or reduced

level of consciousness

Post-operative Analgesia

• Avoid NSAID’s

• Consider avoiding paracetamol in severe

HELLP syndrome

• Regional or TAP blocks are suitable – care with

epidural removal if thrombocytopaenia

• Opiates and tramadol are mainstay

Intravenous fluids

• Acute pulmonary oedema is a leading cause of

maternal death

• Fluid restriction usually practiced

• In severe pre-eclampsia limit to 80ml / hour

total intake (NICE guidance)

• Treating oliguria in the presence of normal

renal function not recommended

• Invasive monitoring may be required

Use of Oxytocic Agents

• Management of PPH in the presence of pre-

eclampsia is challenging

• Syntocinon is the drug of choice

• Beware large volume infusions and fluid

retention

• Avoid ergometrine – hypertensive crisis

• Carboprost and misoprostol can be used

• Invasive monitoring may be required

Summary

• Remains a leading cause of maternal and fetal

morbidity and mortality

• Abnormal placentation leads to a multisystem

disease process

• Anaesthetic management can be challenging

• Treatment is ultimately achieved by delivery

References

• A.T Dennis. Management of pre-eclampsia:

issues for anaesthetists

Anaesthesia 2012 67 1009-1020

• Hypertension in Pregnancy NICE Clinical

Guideline Modified January 2011

guidance.nice.org.uk/cg107

• Saving Mothers Lives Reviewing Maternal

deaths to make motherhood safer: 2006–2008

BJOG March 2011