33.

PRE-ECLAMPSIA
Preeclampsia is defined as the new onset of hypertension (SBP ≥ 140 mmHg, DBP ≥ 90 mmHg, or
both), at or after 20 weeks' gestation accompanied by one or more of the following features:
uteroplacental dysfunction (foetal growth restriction, abnormal umbilical artery doppler waveform or
stillbirth), acute kidney injury (oliguria, proteinuria), liver involvement (elevated hepatic enzymes,
with or without right upper quadrant or epigastric pain), neurological complications (seizures, severe
headaches, visual changes: scotomata and scintillations, stroke, altered mental state), pulmonary
oedema, cardiac failure and haematological complications (thrombocytopenia, haemolysis, DIC).
(Although proteinuria was previously considered  as an essential feature of pre-eclampsia, it is no
longer a prerequisite for diagnosis). HELLP syndrome is a subtype of severe preeclampsia
characterized by haemolysis (H), elevated liver enzymes (EL), and low platelet count (LP).
Preeclampsia affects 2 to 5% of all pregnancies. Strong predictors for developing preeclampsia
include previous preeclampsia, chronic HT, chronic kidney disease, maternal BMI > 30,
pregestational diabetes, and SLE. Moderate predictors include nulliparity, multiple pregnancy, and
maternal age > 40. The precise pathophysiology is incompletely understood. Preeclampsia usually
resolves within 48 hours of delivery but maternal end-organ complications may still worsen in the
postpartum period, particularly during the first 3 days.

Management of Pre-eclampsia

The definitive treatment of preeclampsia is delivery of the placenta. The decision to initiate delivery
should be guided by gestational age and maternal and foetal status. Although delaying delivery may
be  preferable for foetal maturation, the length of time for expectant management is unclear because
the mother is at increased risk of complications. The Preeclampsia Integrated Estimate of Risk
(PIERS) outcome prediction models, miniPIERS, and fullPIERS, have been developed to guide the
care of women from 20 weeks gestation. 
https://pre-empt.obgyn.ubc.ca/evidence/fullpiers. 
Delivery for pre-eclampsia at any gestational age is recommended when there is one or more of the
following conditions: eclampsia, severe hypertension that does not respond to treatment, abnormal
neurological features such as severe intractable headache, repeated visual changes, pulmonary
oedema, progressive thrombocytopenia, abnormal and rising serum creatinine, abruption with
evidence of maternal or foetal compromise, or  a nonreassuring foetal status. The mode of delivery is
determined by several factors that include gestational age, foetal condition, and other concurrent
obstetrics factors such as previous caesarean section. The mother’s condition must be stabilised so
that anaesthesia can be performed safely. This will involve controlling blood pressure, ensuring
adequate intravascular volume, prevention of eclampsia and early evaluation focusing on the airway
and coagulation abnormalities. Patients with preeclampsia are at risk for airway oedema and difficulty
with airway management which may worsen during labour. Epidural analgesia  is useful for blood
pressure control during labour.
.

Hypertension

The main aim of controlling maternal BP is the prevention of intracerebral haemorrhage and stroke,
with blood pressure targets of less than 160/110 mmHg, but also avoiding hypotension to maintain
uteroplacental perfusion. Vasopressors should be administered in small doses. 
The initial antihypertensive therapy is labetalol 100 - 400 mg every 8 hours. Alternatives are 
nifedipine 30 or 60 mg slow release every 12 hours or methyldopa 250 - 750 mg every 8 hours.
Second- and third-line agents include hydralazine and prazosin.
Hypertensive emergencies can be treated with intravenous labetalol (20 mg i.v. over 2 minutes, with
repeated doses every 10 minutes of 40 mg, then 80 mg to a maximum cumulative dose of 300 mg),
hydralazine (initial dose of hydralazine 5–10 mg i.v. over 2 minutes followed by a further 5 - 10 mg
i.v. every 20 minutes to a maximum of 30 mg) and immediate-release oral nifedipine (10 mg,
followed by a further 20 mg every 30 minutes to a maximum of 50 mg). 
Blood pressure monitoring and a gradual withdrawal of antihypertensive therapy may be required for
up to 3 months postnatally.
 
Fluid Resuscitation

Fluid management in the setting of preeclampsia is difficult as various  pathophysiologic processes

may lead to decreased urine output, however excessive intravenous volumes  risk causing pulmonary
oedema. Accurate assessment of fluid input/output is essential. In general intravenous fluid
administration should be less than 80 mL/h. Persistent oliguria (<80 mL/ four hours) requires medical
assessment. Oliguria that does not respond to a modest fluid bolus (e.g., a 250 mL fluid challenge)
may suggest renal insufficiency. Persistent oliguria may be an indication for judicious  diuretic use. In
the immediate postpartum period, oliguria is common, and does not require additional fluid

Coagulopathy

Thrombocytopenia and other coagulopathies may develop precluding neuraxial anaesthesia

techniques because of the risk of epidural haematoma. Spinal anaesthesia should not be attempted if
platelet count is less than 50,000/micol. 

Convulsion control

Magnesium sulphate is the first-line treatment for the prevention of eclamptic seizures. (Diazepam is
still widely used but magnesium sulphate is the preferred agent). It is usually given as an initial
loading dose of 4g i.v. over 20–30 minutes followed by a continuous infusion of 1g/hour until
delivery for 24 hours. A further 2–4 g bolus can be given for recurrent seizures. An alternative
regimen (described by Lucas, Leveno & Cunningham in 1995) is to give 10 g of magnesium sulphate
intramuscularly, given as 5 g i.m. into each buttock, followed by 5 g intramuscularly every 4 hours
until 24 hours post delivery. Ideally, magnesium blood levels should be monitored. The aim is to
maintain magnesium levels at 2 to 4 mmol/l. Feeling of warmth, flushing, double vision and slurred
speech occurs at 3.8 - 5 mmol/l. Deep tendon reflexes diminish at 5 mmol/l and respiratory depression
occurs at greater than 6 mmol/l, with respiratory arrest at 6.3 - 7.0 mml/l and cardiac arrest at greater
than 12 mmol/l. If blood magnesium levels cannot be monitored then the patient must have frequent
observation of their deep tendon (patellar) reflexes, respiratory rate, oximetry, heart rate and urine
output. If depression of reflexes or respiratory depression occurs, stop the infusion until the reflexes
return. Administer 10 mls 10% calcium gluconate, monitor ECG for heart block/arrhythmias and
check electrolyte and creatinine levels. If the urine output is less than 100 mL over 4 hours, check
magnesium levels and consider reducing magnesium sulphate infusion to 0.5 g/hour.

The differential diagnosis of maternal seizures includes epilepsy, cerebral infarction, cerebral
haemorrhage, subarachnoid haemorrhage, cerebral venous thrombosis, cerebral oedema, malignant
hypertension, benign and malignant cerebral tumours, cerebral abscess, viral, bacterial, parasitic
infestations, hyponatremia, hypocalcaemia, hypoglycaemia, and hyperglycaemia. Persistent coma and
localizing signs may indicate major intracranial pathology.

Choice of Anaesthesia

Regional anaesthetic techniques (spinal, epidural or combined spinal-epidural), in the absence of

contraindications, are useful for labour analgesia and are the preferred method of anaesthesia for
caesarean delivery. Previous concerns of uncontrolled hypotension with spinal anaesthesia have been
largely dispelled. General anaesthesia will be necessary in cases of coagulopathy, eclampsia and
altered conscious state. If general anaesthesia is used, particular attention should be taken to blunting
the hypertensive response to intubation as this is a cause of maternal mortality. Blood pressure may
increase by 50% and heart rate by 20%. Drugs that have been used to blunt the hypertensive response
include alfentanil (10 - 20 mcg/kg), fentanyl (1 - 3 mcg/kg), and remifentanil (1 mcg/kg), though
these may cause foetal respiratory depression.  A bolus dose of MgSO4 (30 mg/kg) in women
receiving maintenance MgSO4 may risk magnesium toxicity. Lidocaine (1.5 mg/kg) appears to be
less efficacious than other agents including labetalol (10 mg), esmolol (1 mg/kg) and nitrates.
The upper airway oedema of the pre-eclamptic patient may necessitate a smaller than predicted
tracheal tube diameter. The action of succinylcholine is unaffected by magnesium sulphate. All the
non-depolarizing neuromuscular blocking agents are potentiated by magnesium sulphate, and a
smaller dose than usual may be required with careful monitoring of adequate reversal into the
postoperative period.

Post Delivery Care

The anaesthesia provider must be aware that the patient remains at risk from pre-eclampsia for up to
48 hours after delivery including seizures, pulmonary oedema, stroke, venous thromboembolism, and
airway obstruction due to airway oedema.