Eclampsia is a uniquely pregnancy-related disorder that manifests as new onset of generalized tonic colonic seizures. It typically occurs after 20 weeks of concluded gestation, although it may occur sooner with plural gestations or molar pregnancies, and may additionally occur in the 6-week postpartum window. It represents the severe end of the preeclampsia spectrum. Preeclampsia spectrum includes symptoms of the central nervous system (CNS), for example, severe headaches or vision changes, and may involve hepatic abnormalities (such as elevated liver transaminases with right upper quadrant/epigastric discomfort), elevated blood pressures, and also may include thrombocytopenia, renal abnormalities, and pulmonary edema. In developed countries, resultant maternal mortality may be as high as 1.8%, and in the developing countries, it may be as high as 14%.The etiology of the disorder remains elusive. The placenta seems to have a prime role in its etiology. An increase in placental mass, as in plural pregnancies, increases the risk for the preeclampsia-eclampsia spectrum, as does placental edema that occurs in pregnancies complicated by fetal hydrops. Molar pregnancies that impact placental architecture also have a higher risk of the complication. In the developed countries, the incidence of preeclampsia has been described to be between 1.5 to 10 cases in 100,000 deliveries. The condition is more prevalent in the developing countries. The risk factors of preeclampsia are similar to those of preeclampsia and include nulliparity, non-white, low socioeconomic backgrounds, plural pregnancies, and extremes of maternal age. Additionally, it is associated with and an array of maternal medical conditions such as chronic hypertension, chronic renal disease, and autoimmune disorders. Obesity and maternal diabetes are also recognized as increasingly important etiologies. Fetal conditions such as fetal hydrops have been associated with preeclampsia. Women known to have preeclampsia may develop eclamptic, generalized, tonic-clonic seizures that conclude with no persistent neurologic deficit, meaning they do not deserve diagnostic evaluation beyond that performed for preeclampsia. A preeclampsia workup would include an evaluation of renal function, liver function, complete blood count, and imaging of fetoplacental unit. Obstetric ultrasound imaging of the fetus includes an assessment of fetal growth as well as fetal health (biophysical profile and as indicated umbilical artery cord Doppler studies), including fetal heart rate stri Clinical monitoring for placental abruption is heightened and is maternal monitoring for evolving complications such as pulmonary edema or renal dysfunctionNeuroimaging should be considered if: • There are persistent neurologic deficits • The loss of consciousness is prolonged • The onset of seizures is 48 hours beyond delivery • An eclamptic seizure occurs before 20 weeks • Recurrent seizures in spite of adequate magnesium sulfate

1. ECLAMPSIA: LABOUR ROOM PROTOCOL
FOR MANAGEMENT
DR ALKA MUKHERJEE
MBBS DGO FICOG FICMCH PGDCR PGDMLS
MA(PSY)
DR APURVA MUKHERJEE
MBBS JR 2 (MS OBGY)
Dr Alka Mukherjee Nagpur 1

2. INTRODUCTION
• Pre-eclampsia/eclampsia is a pregnancy-specific disorder.
• It is the most important (and common) medical complication
of pregnancy.
• Devastating disease: about 50-60,000 pre eclampsia /
eclampsia related deaths per year reported worldwide.
• The deadly triad - Severe pre-eclampsia along with
hemolysis, elevated liver enzyme levels, and low platelet
levels (HELLP) syndrome and eclampsia
• Mortality is just the tip of the iceberg (what lies beneath is
the 'near miss' morbidity')

3. PRE-ECLAMPSIA WITH SEVERE FEATURES: EFFECTS ON THE HEART

4. • For every maternal death there are 50-100 women who
experience 'near miss' significant morbidity that results in
significant health risk and health care cost.
• The disease continues to challenge mankind.
• Eclampsia is a Greek word which translates to flash of
lightning.

5. DEFINITION
• Eclampsia is characterized by the occurrence of one or more
seizures (tonic and clonic convulsions) during pregnancy,
delivery or up to 10 days postpartum.
• By definition, two or more of the following features must
also be present within 24 hours of the seizure:
• 1. Hypertension, proteinuria
• 2. Thrombocytopenia, elevated serum aspartate
aminotransferase (AST) levels.

7. INCIDENCE
• Eclampsia complicates approximately
1 in 2,000 pregnancies in developed countries and
1 in 68-500 pregnancies in developing countries.
It is one of the leading causes of maternal mortality in both
industrialized and developing countries.

13. TYPES
• Types of eclampsia are given
• Intercurrent eclampsia : when fits are controlled &
pregnancy continues for 48 hours or more (maximum 7-10
days)
• Antenatal (50%) – Status eclampticus – rapid succession of
convulsions without control
• - Eclampsism – patient with gestational
hypertention goes into coma without any convulsions
• Intranatal (30%)
• Postnatal (20%)

16. Some criteria that are used to denote the severity of
eclampsia is given
• Coma of 6 or more hours
• Temperature 39 degree C or more
• Pulse over 120/minute
• Systolic BP>200 mm Hg
• Respiratory rate over 40/min
• More than 10 convulsions

17. MANAGEMENT
“Pre-eclampsia/eclampsia patient must be delivered at the
appropriate time, in an appropriate place in an appropriate
manner.”
• Eclampsia is an obstetric emergency – aims of management:
• To control and prevent further convulsions
• To decrease maternal morbidity and mortality to minimum .
• To deliver surviving infant with minimal trauma. Patient
must deliver in a tertiary care hospital with neonatal care
facilities

18. ECLAMPSIA KIT
• Every hospital must have ready to use medication box for
treatment. It should contain following drugs with dose
recommendations.
• Labetalol: 200 mg tablets; 100 mg/20ml vial
• Hydralazine 20mg/vial
• Nifedepine 10 mg tablets
• Magnesium sulfate 20g/50g vials/IV infusion bags
(20g/500ml)
• Injection Atropine, Frusemide, Adrenaline
• Syringes, long needles, infusion sets
• IV fluids: RL, NS, Distilled water

19. General nursing care
• Ecalampsia patient should be
kept on low cot next to the
nursing station where she can
be seen frequently
• Mouth gag to prevent tongue
bite
• Moist nasal O2 – 6 Lit/min
• Put antibiotic eye drop &
cover eyes with a shield/pad
• Self-retaining foley’s cathetor
• Repeated suction –
immediately after convulsion
& every 15 min
• Constant supervision & good
nursing care
• TPR/15min, BP ½ Hourly,
Urine albumin 4-6 hourly
• I-O chart, CVP every 2 hourly
• 6 hourly inv – CBC, Platelets,
coagulation profile, urea,
electrolytes, LFT, Uric acid

20. STABILISATION OF THE PATIENT
MYTHS
• Many obstetricians are under the
wrong impression that an
eclampsia patient must be
delivered immediately following
an eclamptic seizure.
• Such patients should be
delegated to separate dark quiet
corner room far away from the
nursing station and away from
the other normal patients.
TRUTH
• it is very important to stabilise
the patient hemodynamically
before delivering her. Adequate
nursing care of these patients is
very important. They should be
treated like an unconscious
patient.
• "Eclamptics Need Silence, Not
Darkness".

21. CONTROL OF BLOOD PRESSURE - that antihypertensive drugs are given only
to prevent cardiovascular and cerebral complications of hypertensive crisis.
They do not alter the course of the disease.
• The ACOG now suggests stricter BP control for prevention of
strokes:
• Antihypertensive drugs :
• Labetalol 100-200mg 8-12 hourly, maximum 2400mg/day
• Nifedipine 10-20mg 8-12 hourly, maximum 80mg/day: it
should be noted that , if administered to patients receiving
concomitant magnesium sulfate, nifedipine may exaggerate
the hypotensive response.
• Hydrallazine – 20-50mg 8 hourly, maximum 200 mg/day
• For hypertensive crisis injectable labetalol or hydralazine
are used.

22. SEIZURE CONTROL AND PREVENTION
• Intravenous diazepam can be used to stop the convulsion.
• Magnesium sulfate is generally accepted – DRUG OF CHOICE
• maintenance dosage is not fixed, it must be adjusted according to
patient response.
• If there is recurrent seizure whilst on magnesium sulfate:
• Further bolus of 4 ml MgSO4 (2 g) diluted with 6 mL normal saline
(0.9%). Give IV over 5 minutes. If possible take blood for
magnesium levels before bolus. If further convulsions occur.
• Consider other causes of fits including intracranial haemorrhage
• Consider using other drugs (diazepam, phenytoin), including
general anaesthesia.

23. MGSO4 REGIMEN S FOR ECLAMSIA
NAME LOADING DOSE MAITAINANCE DOSE
PRITCHAR
PROTOCOL
4 GM IV OVER 5-10MIN, CONC
NOT > THAN 20%
10GM DEEP IM, 5 GM IN EACH
BUTTOCKS; TOTAL LOADING DOSE
14GM
5 GM DEEP IM EVERY 4
HOURS FOR > OR EQUAL
TO 24 HOURS AFTER THE
LAST SEIZURE IN
ALTERNATE BUTTOCKS
DHAKA REGIMEN 4 GM IV OVER 5-10MIN, CONC
NOT > THAN 20% + 8 GM DEEP
IM, 4 GM IN EACH BUTTOCK;
TOTAL LOADING DOSE 12GM
5 GM DEEP IM EVERY 4
HOURS FOR > OR EQUAL
TO 24 HOURS AFTER THE
LAST SEIZURE IN
ALTERNATE BUTTOCKS
BM SIBAI REGIMEN 6GM IN 100 ML OF 5% D OVER
10-15 MIN ()30ML OF 20%
SOLUTION
2GM/HOUR INFUSION;
20G OF 50% MGSO4
ADDED TO 1000 ML OF
DEXTROSE AS IV INFUSION
AS 100 ML/HOURS
IM INJECTION - VERY PAINFUL – 1 ML OF 2% LIGNOCAINE MAY BE
ADDED TO IM SYRINGE

24. MONITORING OF PATIENT ON PARENTERAL
MGSO.
• Each subsequent dose should only be given after monitoring
for clinical signs o hypermagnesemia: .
• DTR - Tendon reflexes should be present. The first sign of
impending MgSO, toxicity is disappearance of patellar reflex
(>5 mmol/L).
• Respiratory rate: Should be at least 16/minute.
• Urine output should be at least 100 ml in 4 hours (in the
presence of oliguria the rate of magnesium administration
should be reduced by 50%).
• Serum magnesium levels. .
• Pulse oxymetry: Slight fall in oxygen saturation below 95%
indicates the risk of onset of respiratory depression.

25. • The first three parameters should be monitored hourly. If
any of them are deranged prior to administration of the next
maintenance dose, the dose should be delayed till they
become normal.
• To counter the side effects of the drug, following must be
ready:
• Calcium gluconate (10%): 10 mL given slow IV over 3
minutes
• Ambu bag.

26. TREATMENT OF MGSO, TOXICITY
• If magnesium toxicity is suspected,
• Immediately discontinue the infusion,
• Start basic life support and
• Administer supplemental oxygen along with
• 10 ml of 10% calcium gluconate (1 g total) intravenously
slowly over 5 minutes.
• Calcium chloride can also be used.
• If respiratory arrest occurs - prompt resuscitation including
endotracheal intubation and assisted ventilation

27. OTHER ANTICONVULSANT DRUGS
• Diazepam: Initially, it is given in the dose of 40 mg IV stat;
followed by 40 mg in 500 cc of 5% dextrose at 30
drops/minute
• Phenytoin is another antiepileptic drug which can be used to
pre Vent recurrence of fits but not for their termination as it
acts after about 20 minutes Dose: 18 g/kg body weight (15-
25 mg/kg) slowly intravenously.
• Sodium thiopentone is a short acting general anaesthetic
used in emergency . Dose: 25 mg increments IV until
convulsions are controlled.
• An important dictum to remember in anticonvulsant
treatment is to 'Avoid Poly-pharmacy

28. INTRAVENOUS FLUIDS
• During fluid administration one should be very cautious
because the eclamptic patient is very readily overloaded.
Colloids should NOT be used for intravascular volume
expansion.
• Crystalloids (Ringer's lactate or Hartmann's solution)
therefore provide the mainstay of fluid therapy. Intravenous
fluid should be given at a rate of 80 ml/hour (1 ml/kg/hour)
or the previous hour's urine output plus 30 ml.

29. MANAGEMENT OF BLOOD CLOTTING
DISORDERS
• Consult a haematologist early where there is clinical or
haematological evidence of coagulopathy.
• If patient requires Caesarean delivery in presence of
coagulopathy - one adult dose of platelets prior to incision,
plus a further adult dose at uterine closure.
• If the platelet count is less than 50 x 109/L, - platelet
transfusion
• Crvoprecipitate – for bleeding and hypofibrinogenemia.
• Fresh frozen plasma - to correct a prolonged prothrombin
time (PT) or activated partial thromboplastin time (APTT) if
bleeding is not controlled.

30. DELIVERY
• The only definitive treatment of eclampsia is 'delivery of the
foetus'. But this is easier said than done: it is not always
possible. It is a clinical dilemma
• After convulsions are under control:
• Induce labour if patient is not already in Labour.
(spontaneous labour usually commences within 6 hours).
• If cervix is not ripe lower segment Caesarean section (LSCS)
may be required.

31. Important points in labour management are:
• First stage. Close monitoring of progress of labour
and condition of baby (intrapartum foetal
monitoring). Maintain a partogram.
• Second Stage : Cut short with generous episiotomy, outlet
forceps or vacuum extraction. A neonatologist must be
present at the time of delivery.
• Third stage. Intravenous Methergine is relatively
contraindicated. Active management of third stage is
important .

32. • Indications for caesarean section in eclampsia
• Uncontrolled seizures
• Cervix unfavourable
• Foetal distress,
• Abruptio placentae
• Failed induction/augmentation of labour.

33. CHOICE OF ANAESTHESIA
Most prefer general or epidural anaesthesia
(spinal anaesthesia is contraindicated)
Important points to be noted while inducing general
anaesthesia (GA) are:
• Routine invasive monitoring is not needed
• Induction commonly leads to transient rise in blood
pressure
• Good ventilatory support is important
• Do not under infuse
• Mgso, treatment reduces the amount of muscle relaxants
needed
• Nephrotoxic and hepatotoxic drugs should be avoided.

36. POSTPARTUM SURVEILLANCE
The definitive management of pre-eclampsia is to deliver the
foetus BUT we should - Remember patients are not cured by
delivery of the baby. One must continue to monitor the
following closely:
• Close BP monitoring in hospital for 72 hours.
• Intravenous antihypertensive therapy can be gradually
withdrawn and replaced with oral treatment;
• Magnesium sulfate should be continued after delivery for
at least 24 hours; it may be given at 6 hourly instead of 4
hourly intervals.

37. • BP must have been <140/90 for at least 24 hours prior to
discharge.
• After discharge, outpatient monitoring for 6 weeks
postpartum is also important.

38. “LACK OF” SYNDROME
• Even today eclampsia is associated with a
- High maternal mortality (Urban India: 4-22% and Rural India: 28%)
and
- Perinatal mortality (30-50%).
The reasons for such a high maternal/foetal mortality and morbidity
in both developing (India) and developed countries are:
• Lack of and/or poor antennal care: Resulting in delay in early
diagnosis and treatment
• Lack of access to hospital care
• Lack of well-trained staff and personnel
• Lack of proper resources: Medications, equipment, laboratory,
ICU facilities
• Lack of transportation.

39. CONCLUSION
• Most eclamptic patients die in our country of logistic causes
like inadequate healthcare facilities, lack of transport, social,
cultural and political factors. The obstetrician too is however
responsible for death in a few cases. It is the quality of
overall management rather than specific therapy which is
likely to be the important factor in reducing the mortality
rates.
• Today pre-eclampsia/eclampsia is considered as a stress test
of cardiovascular profile of women. In other words, pre-
eclampsia is a window to future cardiovascular risk. Pre-
eclampsia is a multisystem disorder. Its pathophysiology is
poorly understood.

40. • The first decade of this millennium has witnessed major
advances in our understanding about the pathophysiology of
pre-eclampsia.
• Recent observations SUDDOIT de hypothesis that altered
expression of placental antiangiogenic factors are
responsible for the clinical manifestations of the disease.

41. LONG-TERM RISKS OF PRE-ECLAMPSIA
• Recent studies (prospective/retrospective cohort meta-
analysis) have shown that pre-eclampsia/eclampsia (both
types) is associated with following long term cardiovascular
risks.