Eclampsia can be defined as the encephalopathic complications of severe or imminent Preeclampsia toxaemia (PET). Eclampsia can occur in the ante-partum, intra-partum or immediate post-partum period.

This is usually manifests as:

  • Seizures
  • Coma and altered conscious state, but there can also be associated systemic disturbances in renal, hepatic and haematological systems.

See also


The eclamptic cerebral complications are thought to be due to a hypertensive encephalopathy, including the effects of cerebral vessel vasospasm.

Clinical Features

The diagnosis of eclampsia is made on clinical grounds based on the presence of the signs of PET with seizures.

The condition usually occurs from the second trimester to about 10 days post delivery.

The onset of eclampsia is unpredictable. It can arise from severe preeclampsia but it can also occur in a mildly hypertensive woman or even a previously normotensive woman.

Other possible causes of the clinical features such as hypertension and seizures, however, will always need to be considered and ruled out.

The event itself is unpredictable and occasionally  there may be a sudden onset of eclamptic seizures with only mild preceding clinical signs of PET – However, within 24 hours the typical signs of edema, hypertension and proteinuria will often be seen.

Eclamptic seizures are almost always self-limited to a few minutes only.


Blood tests:

  1. FBE
  2. U&Es and glucose
  3. LFTs
  4. Coagulation profile
  5. Calcium
  6. Uric acid
  7. Blood group and hold or cross matched, as clinically indicated


  • Dipstick (protein may also be due to infection or contamination)
  • MSU for M&C

CTG to monitor foetal well being.

CT Brain:

In general, women with typical eclamptic seizures who do not have focal neurologic deficits or prolonged coma will not routinely require a CT.

Any patient who has focal or ongoing CNS symptoms (coma and seizures) or any other features not typical for eclampsia must have a CT scan of the brain to rule out secondary problems (such as intracerebral haemorrhage) or other unsuspected preexisting pathology (such as a space occupying lesion).

  1. Resuscitation
    • Ensure the airway is patent
    • Oxygen administration via mask
    • IV access
    • Place in the left lateral position (to avoid IVC compression and circulatory compromise)
    • Check the bedside glucose
  2. Control of seizures:
    • IV Midazolam (0.1 – 0.2mg /kg IV or IM) if the seizure is prolonged
    • IV Magnesium Sulphate is the drug of choice for treatment
      • Loading dose: 4gm over 20 mins (rate 150 mL/hr for 20 mins only = 50mL).
  3. Prevention of further seizures
    • Magnesium sulphate infusion: generally at a rate of 2 grams per hour until at least 24 hours after delivery. This rate varies by hospital protocol.
    • All patients must be commenced on a MgSO4 infusion.
      • It is the first line agent for the treatment of eclampsia
      • It is sedating
      • Its vasodilatory effects are beneficial for the hypertension and will help control and prevent seizures.
      • Although not considered to be a true anticonvulsant it does cause cerebral vasodilation and hence treat the “root cause” of the encephalopathy.
  4. Establish monitoring
    • ECG
    • Pulse oximetry
    • Blood pressure: non-invasive or invasive depending on how unwell the patient is.
    • IDC
    • Fetal monitoring by continuous CTG
    • CVC is not routine but is considered when fluid balance needs to be more closely monitored.
  5. Control hypertension
    • Aim for a blood pressure below 160/100
    • The threshold for further seizures is lowered after eclampsia, and there is a real increased risk of cerebral haemorrhage.
    • Use:
      • IV Labetalol 20-80mg bolus dose over 2 minutes.
      • IV hydralazine 5-10mg over 2 minutes.
      • PO Nifedipine 10mg.
  6. Delivery
    • Delivery is the definitive management for patients suffering from eclampsia.
    • Urgent delivery (within hours) by c-section in cases of compromised maternal/ fetal condition.
    • If maternal and fetal conditions are stable then attempted induction and vaginal delivery within 12-24 hours may be considered. This time frame may be stretched to 48 hours to give steroids in cases of fetal immaturity, providing both mother and baby remain stable.
  7. Fluid resuscitation
    • Pre-eclamptic women, although peripherally edematous, are also intravascular depleted. Despite this, they are also susceptible to pulmonary edema with excessive fluid loading, so caution must be maintained when administering IV fluids. 
    • Maintenance fluids should in general be limited to 2 liters per day.
    • Fluid boluses of 250 mls -500 mls (saline or Hartman’s) may be indicated for:
      • Prior to the commencement of parenteral antihypertensive treatment.
      • Prior to epidural analgesia
      • Prior to delivery
      • Management of hypotension and oliguria
    • Diuretics must in general be avoided.
Magnesium Sulphate:

Close monitoring will be necessary for all patients on MgSO4 infusions:

  • Conscious state
  • Blood pressure
  • Respiratory rate (<16)
  • Temperature, (look for hypothermia)
  • Loss of deep tendon reflexes
  • ECG, (severe toxicity may result in arrhythmias)
  • Blood levels of Mg (2.0 – 3.5 mmol/L is therapeutic, > 3.5 mmol/L is toxic)

Note that MgS04 may also act as a tocolytic agent, necessitating increased doses of syntocinon, and in the event of postpartum haemorrhage, uterine atony may be a contributing factor. 

The antidote to magnesium toxicity is the slow IV administration of 10-20 mls of 10% calcium gluconate.

Post delivery:

Note that following delivery treatment must be continued for a period, as eclamptic complications such as seizures may still occur up to 10 days post delivery.

Magnesium infusions are continued for at least 24 hours post delivery.

Conversion to oral antihypertensives, such as labetolol or nifedipine as required


In addition to the encephalopathic complications of eclampsia the following clinical “crises” may also be seen in association with severe PET or eclampsia:

  1. Acute renal failure.
  2. Hypertensive emergencies such as SAH or intracerebral haemorrhage.
  3. Coagulopathy:
    • DIC
    • HELLP syndrome: “H” Hemolysis “E” Elevated liver enzymes “LP” Low platelets
  4. Hepatic: Impairment or failure
  5. Fetal crisis:
    • Placental abruptions
    • Growth retardation.
    • FDIU

In all cases notify the following urgently:

  • ED consultant
  • Obstetrics unit
  • ICU consultant
  • Anaesthetics Unit
  • Haematologist for any coagulopathy issues
  • Paediatric unit


In some cases it will be appropriate to refer to a physician postnatally to exclude any underlying pathology, which may have predisposed to the development of eclampsia, such as renal disease or hypertension.

This is especially important in those women who developed the disease early and for those who have presented with recurrent PET/eclampsia.




Fellowship Notes

Dr Lucy J Yarwood LITFL author

MSc, MBChB University of Manchester. Currently doctoring in sunny Western Australia, aspiring obstetrician and gynaecologist

Dr Jessica Hiller LITFL Author

Doctor at Sir Charles Gairdner Hospital in Western Australia. Graduated from Curtin University in 2023 with a Bachelor of Medicine, Bachelor of Surgery. I am passionate about Obstetrics and Gynaecology, with a special interest in rural health care.

Physician in training. German translator and lover of medical history.

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