Management of antenatal mother presented with pre-eclampsia

with severe features

Dr. U. D. B. S. Udugahapattuwa

Registrar in Anaesthesiology

Supervised by,

…………………………………………………..

Dr. Upul Ranjith (MBBS, MD)

Consultant Anaesthetist

Teaching Hospital Mahamodara

Abstract
Pre-eclampsia can be defined as new onset hypertension that is diagnosed after 20 weeks of gestation,
systolic blood pressure/SBP >140 mmHg, diastolic blood pressure/DBP >90 mmHg or both,
accompanied by one or more of the features of proteinuria, maternal organ dysfunction and
uteroplacental dysfunction1. (The international society for the study of hypertension in pregnancy
(ISSHP).

It’s a progressive disease that can be presented with or without severe symptoms. Pre-eclampsia is a
multi-system disorder of unknown etiology unique to pregnant women after 20 weeks of gestation.
The condition complicates 5 – 6% of pregnancies and is responsible for an estimated 50000 deaths
worldwide annually2. It remains a leading cause of maternal death. In Sri Lanka, it is the third
commonest cause of direct maternal death after obstetric haemorrhage and heart disease3.

This case highlights the management of a patient with pre-eclampsia with severe symptoms. In
addition, the management of acute non-cardiogenic pulmonary oedema is discussed with the
differential diagnosis of acute pulmonary edema in pregnancy.

Case history
Mrs. X 29 year old, house wife, primi mother at POA- 35weeks+4 days admitted to the antenatal ward
of the tertiary care hospital with high blood pressure BP-150/100 mmHg. Hypertension was detected
first time on this admission. She didn’t have any symptoms of headache, vertigo, visual scotomata and
shortness of breath. But she had two days history of epigastric pain and she had noticed reduced urine
output and concentrated urine.

The antenatal history was uncomplicated until 35 weeks of pregnancy and didn’t have any allergies to
food, plaster or drugs.

After admission to the ward, BP- 140/100mmHg, and urine ward test for protein 1+, initially managed
with oral Nifedipine 20mg stat, due to persistently high blood pressure, started with oral Labetalol
100mg tds increased up to 200mg tds. Following day early morning the patient complained of sudden
onset shortness of breath, with an on air saturation of 95%. Blood pressure was 190/130mmHg. She
didn’t have other pre-eclampsia features except epigastric pain. Oral Labetalol 200mg stat dose + IV
Hydralazine 5mg stat given, IV MgSO4 4g bolus started. The patient was sent to the ICU for further
management.

Examination
Height- 156cm Weight- 88kg BMI-39.1kgm-2

Conscious, rational and she had complained persistently about difficulty in breathing

She had facial puffiness, edema of fingers, hands and B/L ankles.

Afebrile, not pale, not cyanosed, not icteric

PR- 134bpm, BP- 190/130 mmHg urine dipstick- +

RR- 36cpm, tachypnoeic, using accessary muscles for breathing, B/L vesicular breathing + B/L fine
crepts++, saturation was 91%----> 55% with 4L of oxygen via face mask.

R/ hypochondrial tenderness+, no epigastric tenderness, no free fluid

FHS- 143bpm, adequate foetal movements

No papilledema, B/L knee reflexes+++, No ankle clonus

Investigations
8 / 2/23 9/2/23 10/2/23
3 3,
FBC WBC-12.6X10 N-73%, Plt-194x10 , WBC-18.13X10 N- WBC-19X103, N-78%,
Hb- 11.9g/dl 75%, PLT-2O5X103, PLT-221X103, Hb-
Hb- 10.3g/dl 10.6g/dl
Na+ 137.3mmol/l 135.3mmol/l 138mmol/l
K+ 4.21mmol/l 3.8mmol/l 3.6mmol/l
ALT 7.5U/L 25U/L 29U/L
AST 13.4U/L 20.6U/L 22.3U/L
Creatinine 0.52mg/dl 0.86mg/dl 0.66mg/dl
U.dipstick +1 trace NIl
UFR Albumin-nil, pus cells-4-5, red cells-
nil,
PT/INR 1.23
USS Fetal growth adequate for gestation,
umbilical artery Doppler-normal
study
ABG PH- 7.47, PCO2-50.6mmHg, PO2-
89mmHg, HCO3- 14, BE-(-6) SO2-
88%, LAC- 1.6
Blood group- A positive

ECG- HR- 112 bpm, t inversion in L 111

Bed side 2Decho- RV, RA not dilated, no hypokinetic segment in the R/V, EF- 60%, NO evidence of
pulmonary embolism or heart failure.

Bed side USS of lung - B lines+++, no evidence of pleural effusion

Management
1. Propped up the patient 45 degrees
2. CPAP applied Fio2- 80%, PEEP- 12cmH20, converted to BiPAP according to ABG result, PS-15,
Gradually requirement of non- invasive ventilation reduced over 3-4 hours and eventually put
her on 4L of Oxygen via face mask, So2 maintained > 95%
3. IV Frusemide 80mg stat+ 40mg+ 20mg
4. IV Hydralazine 5mg + 5mg
5. 0.9% saline 250ml bolus was given
6. Oral Prazocin 1mg stat
7. IV dexamethasone 12mg, 12 hourly, two doses were completed.
8. Patient was closely monitored for Conscious level, BP, HR, SO2, RR, urine albumin-dipstick and
UOP maintained 0.5ml/kg/h
9. Foetal monitoring continued- FHS and CTG monitoring
10. Once the patient was stabilized her delivery plan (when and mode of delivery) was decided by
multidisciplinary team – Obstetric anaesthetist, Obstetrician, Physician and Neonatalogist.
11. Since coagulation profile was within normal limits, Em/LSCS was planned under sub arachnoid
block once the patient was stabilized.
 She was kept fasting for solid 6hours and clear fluid for 2hours
 Gastric acid prophylaxis was given, IV Ranitidine 50mg stat, IV
Metoclopramide 10mg stat.
 Informed Neonatalogist
 Preserved 1 pint of RCC
 Patient was sent to the OT with 4l of 0xygen via face mask, SO2 maintained
>95%, Prepared portable CPAP machine and intubation equipment in case of
an emergency.
12. Em/LSCS was done under direct supervision of consultant anaesthetist
 The anaesthetic machine and suction apparatus were checked
 Laryngoscope with a long blade, endotracheal tubes(size 7, 7.5. 6.5mm)
and airways were kept ready
 Emergency drugs such as Epherdrine 5mg/ml and atropine 0.3mg/ml
were prepared.
 After patient was taken in to the operating table, all basic monitoring
were attached and basic values were obtained. ECG was in sinus rhythm,
BP-150/80 mmHg, SPO2- 97%
 The midwife checked fetal heart sounds and it was 130bpm
 17G IV cannula insitu on L/hand with 1pint of 0.9% saline started slowly
 Patient was in seated position and L3/L4 level was identified
 2% Lignocaine 3ml infiltrated into the skin of corresponding level
 0.5% Hyperbaric Bupivacaine 2.5ml injected into the intrathecal space
 After completion of injection, sterile gauze was placed and a plaster was
pasted and patient was kept supine with a pillow on lower border of the
scapulae.
 Sensory block was achieved up to the level of T4 ( cold sensation T4 and
light touch sensation T5)
 Bed was tilted to 15 degree left lateral position to avoid supine
hypotension syndrome.
  Oxygen via face mask was continued and the blood pressure was checked
every five minutes. BP dropped to 137/88 not further.
 Monitored- BP, HR, SO2 and UOP
 After delivering of the anterior shoulder of the baby slow bolus of IV
syntocinon 5U was given and 20U infusion was started over 4 hours.

13. Live non asphyxiated baby girl was delivered, Birth weight- 1.8kg, no evidence of placental
abruption.
14. Placenta was removed completely.
15. Estimated blood loss was 400ml.
16. There were no episodes of hypotension.
17. The urine output was 1085ml for 24 hours.
18. Post- operative care was given in the ICU
19. Head end was kept elevated for 30 degrees and bed rest > 6 hours
20. Oral Enalapril 5mg bd, dose was adjusted according to the BP , planned to add prazosin as
second line, target SBP < 135mmHg, DBP < 85 mmHg
21. IV morphine infusion 1mg/h
22. Oral Paracetamol 1g 6 hourly
23. Reduced rate of IV Syntocinon infusion to 5U/h
24. Oral Frusemide 40mg bd
25. Oral KCL 1tab bd
26. IV 0.9% saline 1ml/kg/hr until oral started.
27. FBC and SE post operatively
28. Urine albumin – dipstick twice a day, Planned to repeat RFT and LFT next day
29. Monitor ECG, PR, UOP, SPO2, reflexes
30. IV antibiotics- co-amoxyclav 1.2g 8 hourly and Metronidazole 500mg 8 hourly.
31. Observed for vaginal bleeding
32. Maintained input/out chart
33. The baby was sent to the ward.

ICU day 2
1. She was well looking, facial puffiness and generalized edema was reduced, no symptoms of
pre-eclampsia
2. Target BP was maintained with Enalapril 10mg bd and prazosin 2mg bd ( dose adjusted
according to BP)
3. There was negative fluid balance- 825ml overnight (21 hours), the frusemide dose was
reduced to 40mg mane and 20mg noct.
4. DVT prophylaxis - S/C Enoxaparin 40mg/daily was started
5. Urine albumin dipstick was trace
6. Gradually mobilized the patient
7. Express breast milk+ breast feeding and breast care continued

ICU day 3
 Discharged to the ward with same management plan
Discussion
Hypertensive disease in pregnancy comprises chronic hypertension, gestational hypertension and pre-
eclampsia. They are the significant causes of morbidity and mortality in worldwide affecting adversely
for both the mother and the baby. Pre-eclampsia in particular results in major perinatal and long term
complications.

Fetal implications such as incidence of placental abruption, preterm delivery and intra uterine growth
restriction are increased

Obstetric anaesthetist plays a leading role of managing mother at the ICU setting as well as improving
fetal outcome by providing timely, safe anaesthesia for delivering the baby.

Pre-eclampsia is defined as new onset hypertension (SBP >140MMHg, DBP > 90mmHg or both)
accompanied by one or more of the following features at or after 20 weeks of gestation1.

1 Proteinuria
 Considered positive if 1+ or more
 Significant proteinuria
 Urine protein: creatinine ratio (PCR) > 30 mg mmol-1
 Albumin: creatinine ratio (ACR) > 8 mg mmol-1
 24 hours urine protein > 300mg
 Pre-eclampsia can present without proteinuria.

2 Maternal organ dysfunction

 Acute kidney injury
 Increased serum creatinine > 90mic molL-1
 Liver involvement
 Elevated transaminases, increase in alanine transaminase > 70 IUL-1 or twice
upper limit of normal range
 Neurological complications
 Eclamptic seizures, severe headaches, persistent visual scotomata, clonus,
blindness, altered mental status, stroke
 Haematological complications
 Thrombocytopaenia- platelets count <150x103
 Disseminated intravascular coagulation
 Haemolysis

3 Uteroplacental dysfunction
a. Abnormal umbilical artery Doppler wave form analysis
b. Restricted fetal growth
c. Still birth
Pre-eclampsia represents a potentially progressive clinical condition, therefore former categorization
of mild and severe forms no longer be used. Instead, pre-eclampsia is described as being with or
without severe features4.

Severe features associated with pre-eclampsia

 SBP > 160 mmHg or DBP > 110 mmHg

 Thrombocytopaenia < 100x 103
 Impaired liver function- AST or ALT levels elevated to twice the upper limit of normal, severe
persistent right upper quadrant or epigastric pain not accounted for by alternative diagnoses.
 Renal insufficiency- doubling of the serum creatinine concentration in the absence of other
renal disease
 Pulmonary edema
 New onset headache, unresponsive to medication and not accounted for by alternative
diagnoses
 Visual disturbances

Numerous strong and moderate risk factors have been identified for development of pre-eclampsia4.

Strong risk factors Moderate risk factors

Prior pre-eclampsia Primiparity
Chronic hypertension Primipaternity-changed paternity and
interpregnancy interval>5 years
Maternal BMI > 30 Advanced maternal age > 40 years
Pregestational diabetes Family history of pre-eclampsia
mellitus
Antiphospholipid Multiple gestation
syndrome/SLE
Assisted reproductive Chronic kidney disease
therapies

Pathogenesis
Poor invasion of the placental trophoblast cells of the maternal spiral arteries, is believed to be a major
pathophysiological mechanism of pre-eclampsia. This results in small muscular high resistance vessels
instead of large low resistance vessels, leading to limited distensibility of spiral arteries restricting
blood flow to the placenta and fetus.

A two stage process of pathogenesis has been described2.

In stage 1 abnormal placentation and vascular remodeling will lead to decreased placental perfusion.
This is progressed into stage 11 depending on genetic, behavioral and environmental factors of the
mother, eventually leads to maternal syndrome of pre-eclampsia with endothelial dysfunction. The
resulting endothelial dysfunction produces an imbalance of pro and anti-angiogenic factors, with an
increase in anti-angiogenic factors. This will result in failure of spiral arterial dilatation, leading to
placental hypoperfusion and consequently hypoxia. In response to hypoxia, the placenta releases
cytokines and inflammatory factors into maternal circulation triggering endothelial dysfunction. This
results in increased production of thromboxane A2/ TXA2 and endothelin-1, which are potent
vasoconstrictors and reduced production of prostacyclin/PGI2 and nitric oxide which are potent
vasodilators. TXA2 also promotes platelets aggregation and endothelin causes platelets activation.
PGI2 is an inhibitor of platelet aggregation. Ultimately it causes increased systemic vascular resistance
and capillary permeability.
Marked vascular reactivity, endothelial injury, increased vascular permeability and reduced placental
perfusion can lead to widespread systemic manifestations.

With regard to this patient, she had strong and moderate risk factors, being maternal BMI > 30 kgm-2
and primiparity respectively. At POA- 35 weeks she came out with high BP -150/100 and proteinuria
1+. According to investigation findings she didn’t have features of maternal organ dysfunction and no
ultrasonographic evidence of uteroplacental dysfunction. When concerned about her presentation
she didn’t have classical symptoms such as headache, visual scotomata, clonus except exaggerated
tendon reflexes, right hypochondrial pain, high BP and reduction in urine output.( ISSHP diagnostic
criteria includes clonus not hyperreflexia1)

On admission to intensive care unit she had severe shortness of breath, tachypnea – RR-36 cpm, SO2-
91% with 6L of oxygen via Hudson’s face mask and there were bilateral fine crepitations and
sonographic evidence of pulmonary edema as well. Also she had tachycardia in addition to high blood
pressure and urine dipstick was 1+. It would have been better if we have facility to do urine creatinine
ratio or urine albumin ratio. All other basic investigations findings were within the normal range. While
managing acute pulmonary edema status we expanded our diagnosis as;

 Pre – eclampsia with severe features

 Pulmonary embolism
 Peri-partum cardiomyopathy
 Heart failure
Pregnancy itself is a hypercoagulable state and venous thromboembolism/VTE is a major cause of
death in pregnancy and peri-partum period worldwide. Pregnancy increases the risk of VTE by four to
five times, but overall incidence of VTE is low, at 2 in 1000 pregnancies (0.2%)4. The vast majority of
VTE events occur in the postpartum period, most commonly in the first 6 weeks after delivery. Venous
stasis, vascular damage and hypercoagulability known as Virchow’s triad are three factors that
contribute to an increased risk of thromboembolism. All three are increased during pregnancy.
Signs and symptoms of deep vein thrombosis (DVT) are non-specific and often imitate standard
symptoms of pregnancy, especially lower limb edema and pain. In pregnant women occurrence of
DVT more common in left leg.

Though she had tachycardia, severe shortness of breath and low saturation which were favored for
clinically diagnosis of pulmonary embolism, other features like low BP, 2DECHO evidence
(MacConnell’s sign, 60-60 sign, RV dilatation, hypokinetic RV wall, interventricular septum flattening,
IVC distension) and ECG evidence though it is very rare (S1Q3T3), were not there. Therefore we
excluded pulmonary embolism.

Though we considered peri-partum cardiomyopathy and heart failure as differential diagnosis,

echocardiographic evidences were not supporting that. In addition the patient was drastically
improved with non- invasive ventilation/NIV and medical management of pulmonary edema and
eventually able to wean off the NIV within four to five hours.
Therefore diagnosis made as pre-eclampsia with severe features. Pulmonary edema is a one of the
severe feature of pre-eclampsia.
According to the pathophysiological changes in vascular system, resulting contracted vascular system
with leaky capillaries.
Also as a result of normal physiological changes to pregnancy results in increase in cardiac output by
30- 50% during the third trimester. This further contributes to the pulmonary edema during pre-
eclampsia. Low albumin level, sudden increase in BP can derange the normal Starling’s forces and can
precipitate pulmonary edema.

Management
The patient management can be discussed under following headings.
1. Acute pulmonary edema management
2. BP control
3. Prevention of seizures
4. Monitoring – maternal and fetal wellbeing
5. Delivery plan
6. Anaesthesia for pre-eclampsia patient
7. Management after delivery
8. Follow up
9. Prevention

1. Acute pulmonary edema management

Noninvasive ventilation/NIV is a delivery of ventilator support via the patient’s upper airway
using a mask or similar devices, without invasive airway adjuncts. By using NIV can avoid most
of the complications associated with invasive ventilation.
Acute pulmonary edema/APE can result either hypoxaemic respiratory failure or
hypercapnoeic respiratory failure. Both these conditions are highly recommended to manage
by using NIV to prevent intubation. By using NIV able to reduce need for sedation, improve
neurocognitive function, reduced nosocomial infection and avoid all the complication of
mechanical ventilation. There are several physiological benefits of NIV, such as improve
oxygenation and CO2 clearance, alveolar recruitment, reduction in atelectasis, preservation
of lung volume(FRC, tidal volume, vital capacity), reduced work of breathing, maintenance of
airway patency, reduced extravascular lung water/pulmonary edema and enhanced left
ventricular performance.
According to history, examination and investigation findings of the patient she had acute
onset hypercapnoeic respiratory failure with increased work of breathing. The patient’s
condition was improved over 4 to 5 hours after application of BiPAP. We were able to de-
escalate the management into face mask with 4L of oxygen and maintained SO2 > 95%.
Pharmacological management of acute pulmonary edema also carried out in hand in hand.
On arrival to ICU, IV frusemide 80mg bolus was given and depending on the progression of
symptoms, needed to escalate the diuretic treatment up to total dose of frusemide 120mg.

GTN in pulmonary edema- When there is evidence of pulmonary edema, it is recommended

to commence GTN early7. GTN produces vasodilatation predominantly in the capacitance
vessels by the production of nitric oxide. This causes reduction in preload and venous return,
there by reduces pulmonary venous congestion and pulmonary edema.
 2. BP control
Main aim of controlling blood pressure is prevention of intracerebral haemorrhage and stroke.
The rate of stroke during the peripartum period in women with pre-eclampsia is 133 per
100,000, with haemorrhagic stroke being more common than ischaemic stroke. The sustained
blood pressure more than 140/90 mmHg warrants treatment, targeting BP is < 135/85 mmHg.
NICE recommends offering oral labetalol as initial therapy, followed by nifedipine and then
methyldopa as alternative4. Second and third line agents include hydralazine and prazosin.
Severe hypertension can be defined as an acute onset BP > 160/110 mmHg persisting for > 15
min4. It’s a hypertensive emergency, may present with end organ damage such as myocardial
infarction, pulmonary edema, respiratory failure or stroke.
Treatment of severe hypertension, can start with oral drugs, Labetalol 200mg and Nifedipine
20mg. If no response within 30 minutes, advices to start intra venous drugs.
First line intra venous drugs
1. Labetalol 20mg slow bolus over 2-3 minutes, can repeat every 15 minutes up to
200mg, followed
by infusion 20mg/hr double every 30 min if necessary to a maximum of 160 mg/hr.
Labetalol is a selective alfa 1 and non- selective beta adrenoceptor antagonist. The
ratio of alpha:beta blocking effects depend on the route of administration- 1:3 for oral
and 1:7 for IV.
Side effects: bradycardia, bronchospasm, gastrointestinal disturbances
Contraindication and caution- Asthma, Cardiac disease, phaeochromocytoma

or

2. Hydralazine 5mg slow bolus over 5 min, fluid bolus of 5ml/kg over 20- 30 min should
be given with the bolus if SO2 is normal. Another bolus can be given if blood pressure
still high, followed by infusion 5- 6 mic/kg/min reducing to 1- 3 mic/kg/min as BP is
coming down.
Mode of action of Hydralazine is activation of guanylate cyclase and increase in
intracellular cyclic GMP leading to decrease in intracellular calcium causing arteriolar
dilatation reduces pheripheral vascular resistance.
Side effects- fluid retention, flushing, palpitation, tachycardia, headache, dizziness,
SLE like syndrome, peripheral neuropathy
Contraindication and caution: severe tachycardia.

Second line drugs

Labetalol and Hydralazine both

Third line drugs

To be considered when the patient is on maximum first line drug infusion and BP is
still very high.

When evidence of pulmonary edema is present, Glyceryl trinitrate /GTN should be commenced early.

Also it’s better to consider intra-arterial blood pressure monitoring for resistant hypertension.
 She had managed in the ward with oral Labetalol, Hydralazine and Nifedipine. She was admitted to
ICU with severe hypertension and pulmonary edema. During the ward management, she had not been
given appropriate doses of Labetalol and Hydralazine. So she was given a repeated doses of a
Hydralazine and oral Labetalol, didn’t have IV preparation of Labetalol. Also she had a low level of SO2
91 %-> 55%, but she was given repeated doses of IV hydralazine which is not recommended in
Obstetric anaesthesia guidelines- CSHW/ Castle street hospital for women- updated in 20227. The
patient was improved symptomatically and BP was 150/100 mmHg. It would have been better if
commenced GTN early considering both pulmonary edema+ severe hypertension not much
responding to available drugs.

3. Prevention of seizures

Eclamptic seizures complicate 1-2% of pre-eclamptic prgnancies2. Magnesium sulphate is now the
drug of choice for reducing the risk of seizures in severe pre-eclampsia, controlling new onset seizures
and reducing the risk of their recurrence.

Mode of action- It antagonists at calcium channels reducing systemic and cerebral vasospasm, also
antagonists N-methyl D-aspartate receptor antagonist and increases production of endothelial
prostacyclin, which in turn, may restore thromboxane-prostacyclin imbalance. The vasodilator
property of magnesium is thought to revert the cerebral vasospasm and increase cerebral blood flow,
thus preventing convulsions.

How to give Magnesium Sulphate?

70mg/kg or 4 g slow bolus diluted in 0.9% saline 100ml over 5- 15 minutes. In eclampsia, its given over
5 minutes. Following the bolus, 1g/h infusion to be commenced only if urine output is normal. The
infusion to be continued for 24 hours if baby is not delivered or 24 hours after delivery or 24 hours
after last convulsion. If the patient is oliguric or if the serum magnesium levels are higher than the
therapeutic range (2-4mmol/L, 4-8mg/dl) maintenance dose of Magnesium sulphate infusion should
be reduced to 0.5g/h.

If recurrent convulsions occur;

1. Repeat MgSO4 2g in 50 ml 0.9% saline over 2.5min

2. If third fit develops – check for correct dose given or not. consider another 2g MgSO4,
look for other causes
3. Endotracheal intubation if
 >3 convulsions over 20-30 min
 GCS < 8 in between fits
 Severe pulmonary edema/ aspiration with SPO2 < 90% with high flow oxygen
& not showing any improvement to treatment

Monitoring during MgSO4 therapy is important, BP, ECG, SPO2, respiratory rate hourly, urine output
hourly- maintain >0.3- 0.5ml/kg/h, patella reflex, observe for slurred speech, muscle weakness,
change in GCS, visual disturbances, nausea and vomiting.

Advice to stop MgSO4 infusion if one or more of following appears

 Patella reflex Absent
Respiratory rate < 10/ min
Systolic blood pressure < 100mmHg
ECG Peaked T, prolonged PR, QT, AV Block, HR<
50/min
UOP < 0.5 ml/kg
2+
Mg level only when suspecting >4 mmol/L
toxicity
Other features Nausea, double vision, slurred speech,
weakness, coma

Contraindications to MgSO4 – Acute kidney injury, liver failure, myasthenia gravis, pulmonary edema

IV magnesium sulphate 4 g bolus was given in the ward and started 1 g/h infusion. But in the ICU after
confirmation of acute onset of pulmonary edema, it was withheld due to contraindication.

4. Monitoring-maternal and fetal

Monitoring of maternal and fetal well-being is the one of the important part of the managing pre-
eclampsia. As this is a progressive disease, monitoring helps to early identification of at risk patients
for eclampsia, deteriorating patients and developing complications. Monitoring of heart rate, blood
pressure, saturation, urine albumin, urine output, side effects of the drugs and features of magnesium
toxicity. Fetal monitoring such as fetal heart rate, fetal movements and umbilical arterial doppler have
to concern.

5. Fluid management

Pre-eclampsia causes a contracted vascular system with increased vascular permeability. This
influences fluid management in two main ways. Due to the generalized vasoconstriction, there may
be a sudden drop in blood pressure following administration of certain antihypertensive agents
(Hydralazine). Secondly, due to increased capillary permeability there is a higher predisposition to
pulmonary edema. Therefore carefully balanced fluid intake and output should be maintained.

The patient initially had noticed reduction in urine output at home. On admission to ICU she was
catheterized and started to monitor urine output. With IV hydralazine, 250 ml of 0.9% saline bolus
was administered and thereafter intake adjusted according to output after frusemide boluses. After
initial resuscitation phase maintenance fluid intake should be continued as 1ml/kg/h, urine output of
0.5ml/kg/h was accepted as minimum. In between fluid challenges can be given to maintain this
output cautiously.

6. Delivery plan

Delivery is the definitive mode of treatment, the decision to deliver depends largely on maternal
rather than fetal wellbeing as delivery improves the maternal disease. It should be a multidisciplinary
team approach, involve, obstetric anaesthetist, obstetrician, neonatologist and family members. Time
and mode of delivery is also dependent on the severity of the condition and the gestation of the fetus.
In women < 34 weeks gestation, if fetus is viable, unless the woman is very sick, measures should be
aimed at stabilizing and gaining time to obtain the maximum possible fetal lung maturity.

The patient was at 35 weeks, dexamethasone two doses were completed, the team decided to deliver
the baby.
 7. Anaesthesia for pre-eclampsia patient

Analgesia

Women with pre-eclampsia with severe features would benefit from neuraxial analgesia during labour
as this can help to reduce the sympathetic response to pain and facilitate cardiovascular stability, and
offers the facility to top up the epidural for operative delivery. Neuraxial techniques are
contraindicated in the presence of coagulopathy or thrombocytopaenia because of the increased risk
of epidural haematoma. The platelet count should be obtained within 6 hours of performing regional
analgesia or more, recently in those with HELLP (haemolysis, elevated liver enzymes, low platelets)
syndrome or disseminated intravascular coagulation.

The risk of epidural haematoma is extremely low (0.2%) in the presence of a platelet count> 70 x103 1.
When regional anaesthesia is contraindicated, inhalation and parenteral analgesia may be
used.Remifentanyl patient-controlled analgesia (PCA) is a good alternative to regional analgesia7.

Anaesthesia

When operative delivery is required, central neuraxial anaesthesia is preferred over general
anaesthesia for most women with pre-eclampsia. Spinal, epidural or a combined spinal/epidural
anaesthesia can all be used with good effect. Those techniques provide better haemodynamic stability
and avoidance of complications associated with general anaesthesia. General anaesthesia in
pregnancy is associated with multiple risks (difficult intubation, failed intubation, response to
laryngoscopy, airway trauma, and pulmonary aspiration). The pressor response to laryngoscopy can
lead to a dangerously high surge in blood pressure that may lead to intracranial haemorrhage. To
attenuate this response, magnesium bolus/increase infusion rate, labetalol/esmolol, potent
parenteral opioid/alfentanyl can be used successfully. Antacid and antiemetic premedication should
be administered prior to surgery. If patient is on MgSO4 infusion, muscle relaxation must be carefully
monitored and non-depolarizing muscle relaxant dose should be carefully titrated.

Syntocinon bolus should be avoided or can give slowly. The use of ergometrine and syntometrine
should be avoided due to their propensity to cause hypertension. Non-steroidal anti-inflammatory
drugs should be avoided due to potential adverse effects on renal and platelet function.

Though mother presented with pre-eclampsia with severe features, there was no coagulopathy,
therefore proceeded with sub arachnoid block. At the time of delivery of the baby 5U of syntocinon
slow bolus was given and followed by 20 U in 500ml of 0.9% saline infusion.

8. Management after delivery

Postoperative care in patients with pre-eclampsia is equally important as pre and intraoperative care.
There is a risk of post-partum seizures in up to 44% of women with severe pre-eclampsia3. Therefore
MgSO4 infusion should be continued for 24 hours following delivery. Postoperative care should
provide in maternal high dependency unit or intensive care unit. Careful attention to fluid balance,
antihypertensive therapy and blood and biochemical status should be maintained. With regard to
antihypertensives, can start angiotensin converting enzyme inhibitors or angiotensin receptor
blockers with other agents. Post-partum antihypertensive treatment may be required for 2-6 weeks
after which it may wean off with careful review.

The patient was managed in the ICU with careful monitoring. There was significant improvement of
BP after delivery. Antihypertensives changed over to Enalapril and Prazosin.
 9. Follow up

Post-partum hypertension can persist for up to 6- 8 weeks, so all women should be offered follow up
6- 8 weeks after the birth. These women are at increased risk of cardiovascular disease, stroke,
diabetes, chronic kidney disease and venous thromboembolism.

Educated the patient regarding future risks and importance of continuous follow up.

Conclusion
Hypertensive disorders of pregnancy continue to be a considerable cause of morbidity and mortality
to both the mother and the fetus. Anaesthetists play a leading role in the care of these women,
providing analgesia, anaesthesia and critical care during hypertensive emergencies. Understanding
these disorders and management of their complications is vital for improving outcomes for mothers
and babies.

References
1. The international society for the study of hypertension in pregnancy(ISSHP)

2. Krishnachetty B, Plaat F, Management of hypertensive disorders of pregnancy, ATOW 2014; 304

3. Annual health bulletine 2020, Ministry of health, Sri Lanka.

4. Goddard J, Wee MYK, Vinayakarao L, Update on hypertensive disorders in pregnancy, BMJ 2020;
411- 416.

5. Leslie D, Collis RE, Hypertension in pregnancy, BJA 2016; 33-37.

6. Kearsley R, Stocks G, Venous thromboembolism in pregnancy- diagnosis, management and
treatment, BJA 2021; 117-123

7. Obstetric anaesthesia guidelines- CSHW- update in 2022