The document discusses eclampsia, its incidence, risk factors, pathophysiology, clinical presentation, and management strategies. It emphasizes the need for prompt delivery and appropriate maternal transport to reduce morbidity and mortality associated with eclampsia. The document also details the role of emergency medical services in facilitating maternal transport in case of complications during pregnancy.

1. ECLAMPSIA
AND
MATERNAL TRANSPORT

2. Dr. Niranjan Chavan
MD, FCPS, DGO, DFP, MICOG, DICOG, FICOG
Professor and Unit Chief, L.T.M.M.C & L.T.M.G.H
Chairperson, FOGSI Oncology and TT Committee (2012-2014)
Treasurer, MOGS (2017- 2018)
Chair and Convener, FOGSI Cell- Violence against Doctors (2015-2016)
Chief Editor, AFG Times (2015-2017)
Editorial Board, European Journal of Gynecologic Oncology
Editor of FOGSI FOCUS, MOGS, AFG & IAGE Newsletters
Member, Managing Committee, IAGE (2013-2017)
Member , Oncology Committee, AOFOG (2013 -2015)
Recipient of 6 National & International Awards
Author of 15 Research Papers and 19 Scientific Chapters
Course Co-Ordinator, of 11 batches, of MUHS recognized Certificate Course of
Basic Infertility Management Including Endoscopy (BIMIE) at LTMGH

3. INTRODUCTION
• Eclampsia refers to the occurrence of new-
onset, generalized, tonic-clonic seizures or
coma in a woman with preeclampsia.
• It is the convulsive manifestation of
preeclampsia
• It is often preceded by premonitory signs and
symptoms like severe headaches and
hyperreflexia.

4. INCIDENCE
Eclampsia occurs in:
• 2 to 3 percent of women with severe features of
preeclampsia not receiving anti-seizure prophylaxis
• 0.6 percent of women with preeclampsia without severe
features.
• 1.5 to 10 cases per 10,000 deliveries in developed.
• 6 to 157 cases per 10,000 deliveries in developing countries.
Jaatinen N, Ekholm E. Eclampsia in Finland; 2006 to 2010. Acta Obstet Gynecol Scand 2016; 95:787.
Miguil M, Chekairi A. Eclampsia, study of 342 cases. Hypertens Pregnancy 2008; 27:103.

5. RISK FACTORS
• Genetic
• Personal or family history (37% in
sisters)
• Endothelial dysfunction
• Maternal infection
• Chronic Hypertension
• Renal Disease
• Diabetes (50%)
• Androgen excess
• Obesity/Insulin Resistance
• Dyslipidemia
• Thrombophilias
• Immune-mediated invasion
and angiogenesis
• Nulliparity
• Primipaternity
• Twin gestation (20, 70%)
• Molar pregnancy (70%)
• Condom use
• Donor sperm fertilization

6. PATHOPHYSIOLOGY
Hindrance in cerebral
blood flow regulation
Endothelial
dysfunction

7. Reduced
trophoblastic
perfusion
Vascular
disease
Excessive
trophoblast
Extravillous,
Endovascular Idiopathic

9. Hypertension causes activation of the
autoregulatory system
Vasoconstriction of cerebral vessels
Hypo perfusion causing localized ischemia
Endothelial dysfunction
Vasogenic and/or cytotoxic edema
ECLAMPSIA

10. BIOMARKERS
• Serum Uric acid level above 5.2 mg/dl: marker of
oxidative stress, tissue injury and renal dysfunction.
• Ratio of soluble fms-like tyrosine kinase-1 (sFlt-1)and
placental growth factor (PlGF) more than 85 has 86%
positive predictive value for severe pre eclampsia
progressing to eclampsia
• Increased soluble endoglin (sENG)
• Decreased vascular endothelial growth factor VEGF

11. In a study published in 2012 in American Journal of Hypertension, authors studied
249 singleton pregnancies with associated hypertension. They found that that
higher the Uric Acid levels more is the chance to progression to severe form and
other complications including eclampsia.

12. In an article published in BJOG An International Journal of Obstetrics and Gynaecology
RCOG in 2012 , authors studied 34 published papers and found that placental growth
factor (PlGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1
(sFLT1) and soluble endoglin (sENG) are not only helpful in predicting early onset Pre
eclampsia but also sFLT1/PIGF ratio predicts its severity and progression to eclampsia.

13. PREMONITORY SIGNS/SYMPTOMS
• Hypertension (75%)
• Headache (persistent frontal or occipital headaches or
thunderclap headaches) (66 %)
• Visual disturbances (scotomata, loss of vision [cortical
blindness], blurred vision, diplopia, visual field defects [eg,
homonymous hemianopsia], photophobia) (27 %)
• Right upper quadrant or epigastric pain (25 %)
• Asymptomatic (25 %)
Berhan Y, Berhan A. Should magnesium sulfate be administered to women with mild pre-eclampsia? A systematic review of
published reports on eclampsia. J Obstet Gynaecol Res 2015; 41:831.

14. CLINICAL PRESENTATION
• Generalized tonic-clonic seizure or coma with or
without abrupt loss of consciousness.
• Tongue bite and frothy and bloody sputum may come
out of the mouth.
• Postictal confusion and drowsiness.
• Focal neurologic deficits are generally absent.
• Transient fetal bradycardia.

15. TIMING
• Antenatal within 20 – 30 weeks : 20%
• Antenatal within 30 – 37weeks :40%
• Intrapartum 20%
• Postpartum 21%
Berhan Y, Berhan A. Should magnesium sulfate be administered to women with mild pre-eclampsia? A systematic review of
published reports on eclampsia. J Obstet Gynaecol Res 2015; 41:831.

16. DIFFERENTIAL DIAGNOSIS
• Eclampsia before 20 weeks of gestation  Hydatidiform Mole
• Persistent neurologic deficits  stroke, intracranial hemorrhage, brain
mass lesion, toxic and metabolic encephalopathies and central nervous
system infection like Tuberculoma, neurocysticercosis.
• Metabolic abnormalities (eg, hypocalcemia, hyponatremia,
hypoglycemia)
• Pregnancy is a precipitating factor for some disorders associated with
seizure activity, such as TTP or HUS.
• Recent head trauma.

17. MANAGEMENT

18. KEY PRINCIPLES
• Prevention of maternal hypoxia and trauma
• Treatment of severe hypertension
• Prevention of recurrent seizures
• Evaluation for prompt delivery

19. PREVENTION OF HYPOXIA & TRAUMA
• Left lateral position with propped up position
• Oxygen by mask at 6L/min
• Mouth gag to prevent tongue bite
• Raised padded bed rails
• Patient can be restrained if become agitated
• Strict vitals monitoring

20. TREATMENT OF SEVERE HYPERTENSION
• Anti hypertensive therapy should be initiated to prevent stroke due to
acute hypertension.
• Targeted BP should be 140/90 mm of Hg.
• In the first instance, oral anti-hypertensive agents should be tried.
• If oral anti-hypertensive agents have failed to adequately control blood
pressure, intravenous anti-hypertensives should be considered.
Commonly used intravenous anti-hypertensives include labetalol,
hydralazine and glyceryl trinitrate.
* Arulkumaran N, Lightstone L. Severe pre-eclampsia and hypertensive crises. Best Pract Res Clin Obstet Gynaecol 2013;
27:877-884. Back to cited text no. 2

21. DRUG INITIAL DOSE FOLLOW UP DOSE
Labetalol 20 mg IV over 2 minutes. Repeat BP measurement at 10-minute intervals: If BP remains above target level at 10 minutes,
give 40 mg IV over 2 minutes.
If BP remains above target level at 20 minutes, give 80 mg IV over 2 minutes.
If BP remains above target level at 30 minutes, give 80 mg IV over 2 minutes.
If BP remains above target level at 40 minutes, give 80 mg IV over 2 minutes.
Cumulative maximum dose is 300 mg. If target BP is not achieved, switch to another agent.
Hydralazine 5 mg IV over 1 to 2
minutes.
Repeat BP measurement at 20-minute intervals:
If BP remains above target level at 20 minutes, give 5 or 10 mg IV over 2 minutes, depending on
the initial response.
If BP remains above target level at 40 minutes, give 10 mg IV over 2 minutes, depending on the
previous response.
Cumulative maximum dose is 20 mg.
Nifedipine
immediate release
10 mg orally If BP remains above target at 20 minutes, give 10 or 20 mg orally
Nifedipine
extended release
20 mg orally. If target BP is not achieved in 1 to 2 hours, another dose can be administered
Nicardipine
(parenteral)
A continuous IV infusion
of 3 to 9 mg/hour.
Onset of action is delayed
by 5 to 15 minutes
Adjust dose within this range to achieve target BP.

22. The current study published in 2015 studied use NTG and Hydralazine drip in 180 eclamptic
or severe pre eclamptic patient and found that, although both hydralazine and nitroglycerin
infusions are effective in acute control of hypertension in patients with severe PE before
delivery, the therapeutic goal is reached faster with nitroglycerin and with greater safety
profile than with hydralazine.

23. PREVENTION OF RECURRENT SEIZURES
• Magnesium sulphate is drug of choice for
prevention of recurrent seizures as it is a
neuroprotectant.
• Persistent seizures are managed with
diazepam, lorazepam or midazolam.
• There is no role for mannitol in the routine
care of women with eclampsia.

24. Continuous Intravenous Infusion (ZUSPAN REGIMEN)
Magnesium sulfate 4 gm to 6 gm loading dose diluted in 100 mL fluid administered
intravenously over 15 minutes, followed by continuous intravenous infusion at 1 to 2 gm
per hour. Discontinue 24 hours after delivery or last seizure.
OR
Intermittent Intramuscular Injections (PRITCHARD REGIMEN)
Magnesium sulfate 4 gm as 20% solution intravenously at rate not to exceed 1g/min,
followed immediately by magnesium sulfate 5 gm (as 50% solution) into the upper outer
quadrant of each buttock. then 5 gm in alternate buttocks every 4 hours . Use 20 gauge, 3
inch long needle.
For Recurrent Convulsions (either IV or IM regimen)
If convulsions persist after 15 min, give up to 2 gm more intravenously as a 20% solution at a rate
not to exceed 1gm/min. If the woman is large (> 70 kg) then an additional 2 gm may be given
slowly

25. MAGNESIUM TOXICITY
SERUM MAGNESIUM EFFECT
>mmol/L mEq/L mg/dL
2 to 3.5 4 - 7 5 – 9 Therapeutic range
> 3.5 > 7 > 9 Loss of patellar reflexes
> 5 > 10 > 12 Respiratory paralysis
> 12.5 > 25 > 30 Cardiac arrest

26. MAGNESIUM TOXICITY
• Urine output < 100 ml in 4 h and there are no other signs
of magnesium toxicity  reduce the next IM dose of
magnesium sulfate to 2.5 g, or the IV infusion to 0.5 g/h
• Patellar reflexes are depressed and respiration is normal
 withhold further doses of magnesium sulfate until the
reflexes return and request magnesium level.
• Respiratory depression stop magnesium, give oxygen by
mask and give: Calcium gluconate (10mL of 10% solution
over 10 minutes)

27. EVALUATION FOR PROMPT DELIVERY
The definitive treatment
for eclampsia is prompt
delivery.

28. INDUCTION VS CAESAREAN SECTION
• Induction is a reasonable for pregnancies 32 weeks of
gestation or more with a favorable Bishop score.
• Long inductions should be avoided and a clear endpoint
for delivery planned eg, within 24 hours.
• Induction is not advisable eclamptic women less than 32
to 34 weeks of gestation with an unfavorable cervix.

29. In a trial that randomly assigned 200 rural Indian women at ≥34 weeks with eclampsia to cesarean
delivery or induction after initial stabilization, planned cesarean delivery did not significantly
reduce the rate of adverse maternal or fetal outcomes, and almost three-quarters of women in the
planned vaginal delivery group succeeded in delivering vaginally.

30. INTRAPARTUM FOETAL MONITORING:
MONICA WIRELESS NST
• It records Wireless FHS , Maternal Heart Sound and
Uterine contractions simultaneously upto 10 patients
on a single workstation.
• The tracings can be monitored and send in real time to
the Lecturer on call, Senior consultant for his opinion
and advice on a smart phone , laptop.
• Started on 8/4/2015 in Sion Hospital in Dr N N Chavan
Unit.

31. MONICA : WIRELESS NST

32. COMPLICATION
Outcome Frequency, percent
Abruption 7 to 10
Disseminated intravascular coagulation 7 to 11
Pulmonary edema 3 to 5
Acute renal failure 5 to 9
Aspiration pneumonia 2 to 3
Cardiopulmonary arrest 2 to 5
Liver hematoma 1
HELLP syndrome 10 to 15
Perinatal death 5.6 to 11.8
Preterm birth 50

33. A population-based cohort study from Canada including 1481 cases of
eclampsia from 2003 to 2009 reported a case mortality rate of 0.34
percent (5/1481) . Severe morbidity included acute renal failure, need for
assisted ventilation, embolism, shock, and adult respiratory distress syndrome.

34. IS NEUROIMAGING REQUIRED IN ALL CASES OF
ECLAMPSIA?
• Eclampsia patients unresponsive to conventional treatment
should be screened by neuroimaging (CT Scan/MRI Brain) to
exclude serious morbid CNS pathological conditions. *
• Neuroimaging have found various CNS abnormalities such as
Venous infarct, Cortical Venous Sinus Thrombosis and
infections such as Tuberculomas/ Neurocysticercosis.
*Patil MM. Role of Neuroimaging in Patients with Atypical Eclampsia. Journal of Obstetrics and
Gynaecology of India. 2012;62(5):526-530. doi:10.1007/s13224-012-0181-5.

35. WHAT IS PRES (POSTERIOR REVERSIBLE
ENCEPHALOPATHY SYNDROME)?
• Reversible posterior leukoencephalopathy syndrome is a clinicoradiologic entity
characterized by
1. Headaches
2. Altered mental status
3. Seizures
4. May or may not be Visual loss
5. White matter vasogenic oedema predominantly affecting the posterior
occipital and parietal lobes of the brain

36. HOW SHOULD BE PRES MANAGED IN
PREGNANCY?
• Magnesium therapy
• Preventing fluctuation in Blood Pressure
• Maintaining Electrolyte balance , especially magnesium levels.
• Critical care and monitoring
• Corticosteroids and Mannitol should theoretically reduce
Vasogenic oedema, however there are very trials proving there
efficacy.

37. PREVENTION
• Prompt and early diagnosis of Pre eclampsia.
• Vigilant for severe features of Pre eclampsia.
• Weekly Routine investigations to rule out HELLP .
• All high risk cases should be evaluated by senior consultant.
• Counselling patients and relatives together about Home BP
Monitoring.
• Educating patient about the pre monitory symptoms.
Sibai BM, Abdella TN, Spinnato JA, Anderson GD. Eclampsia. V. The incidence of nonpreventable eclampsia. Am J Obstet
Gynecol 1986; 154:581.

38. RECURRENCE RATE AND LATER LIFE
SEQUALAE
• Recurrent eclampsia occurs in 2 percent of subsequent
pregnancies.
• The risk appears to be reduced by close maternal monitoring
and timely intervention if preeclampsia develops.
• In 2011, American Heart Association added Pre eclampsia as a
major risk factor for development of cardiovascular disease.
• Pre eclampsia associated with IUGR and Eclampsia and recurrent
eclampsia is more strongly associated cardiovascular sequale
later in life.

39. ATYPICAL PRE ECLAMPSIA - ECLAMPSIA
• Atypical pre eclampsia – eclampsia is with minimal or no
proteinuria, but with hypertension, or proteinuria with no or
marginally elevated blood pressure (BP), or without
hypertension or proteinuria.
• Atypical can also be Convulsion with HELLP
• Presentations before 20 weeks or more than 48 h
postpartum.
• Resistant to MgSO4 therapy

40. MATERNAL TRANSPORT
• Transfer of the complicated pregnant patient to a facility with
appropriate medical, surgical, obstetric, or paediatric
resources can reduce maternal, foetal, and/or neonatal
morbidity and mortality.
• The most common reason for maternal transfer is Non
availability of neonatal tertiary care.
• Severe pre eclampsia and eclampsia should be managed at a
tertiary centre.

41. MATERNAL TRANSPORT
PATIENT STABILITY
RECORDS AND
DOCUMENTATION
COMMUNICATION
EQUIPMENT AND
SUPPLIESMODE OF
TRANSPORT
TRANSPORT
TEAM
PERSONNEL
EN ROUTE CARE

44. MAHARASHTRA EMERGENCY MEDICAL
SERVICES (MEMS) 108
• Maharashtra Emergency Medical Services (MEMS) is
a project of Government of Maharashtra under
National Rural Health Mission (NRHM) and
implemented and operated by BVG India Ltd.
• Citizens across Maharashtra can avail free ambulance
in case of any medical emergency by dialing toll free
number ‘108’.

45. MAHARASHTRA EMERGENCY MEDICAL
SERVICES (MEMS) 108
• BVG has implemented a network of around
1000 ambulances across the state of Maharashtra, well
equipped with medicines, life saving equipment and a
doctor on call 24 X 7.
• BVG has set up a state of the art “Emergency Response
Centre” (ERC) is developed at Aundh Chest Hospital
Pune.
• ERC operates 24 x 7 and all calls dialed to 108 from
across Maharashtra from any mobile or landline.

46. MAHARASHTRA EMERGENCY MEDICAL SERVICES
(MEMS) 108
• Emergency Response Centre Physician (ERCP)
provides On-line Medical direction for the doctors
on ambulance during emergency calls.
• There is a network of around 1000 state of the
art ambulances operational across Maharashtra
capable to provide competent care for the sick or
injured in emergency medical situations.
• All professionals working with MEMS are certified
by Symbiosis International University.

47. TRANSPORT OF ECLAMPTIC PATIENT
• Assess maternal symptoms of headache, scotomata, epigastric
pain, vomiting and deep tendon reflexes.
• Obtain maternal vital signs and assess foetal status.
• Administer a loading dose of magnesium sulphate prior to
transport.
• Administer antihypertensive medications.
• Place a bladder catheter and monitor intake and output to avoid
excessive fluid administration.
• Provide supplemental oxygen to maintain O2 saturation ≥95
percent.

48. CONCLUSION
• Eclampsia is conclusive and convulsive phase of a wide spectrum disease pre
eclampsia.
• More conclusive RCT are required to assert the efficacy of biomarkers as a
sensitive predictability of eclampsia.
• Key management issues are:
Prevention of maternal hypoxia and trauma,
Treatment of severe hypertension (if present),
Prevention of recurrent seizures with magnesium sulphate and
Evaluation for prompt delivery.

49. CONCLUSION
• Seizures resistant to Magnesium sulphate should be evaluated with CT Scan or MRI for
other organic causes like Tuberculoma , Neurocysticercosis etc
• Eclampsia can be avoided by early diagnosis of pre eclampsia, vigilant monitoring and
good patient counselling.
• Key components to the successful transport of a patient at risk for delivery include:
 Good communication.
 Written documentation.
 Timely response/arrival by the transport team.
 Experienced and trained transport personnel to assess patient status and
determine appropriateness of transport.
 Rapid mode of transport to the receiving facility.

50. REFERENCES
• American college of obstetrics and gynaecology task force , hypertensive disorders in pregnancy,
2013.
• NICE clinical guidelines (CG 107) hypertension in pregnancy2011
• Arulkumaran N, Lightstone L. Severe pre-eclampsia and hypertensive crises. Best Pract Res Clin
Obstet Gynaecol 2013; 27:877-884. Back to cited text no. 2
• Jaatinen N, Ekholm E. Eclampsia in Finland; 2006 to 2010. Acta Obstet Gynecol Scand 2016; 95:787.
• Miguil M, Chekairi A. Eclampsia, study of 342 cases. Hypertens Pregnancy 2008; 27:103.
• Eke AC, Ezebialu IU, Okafor C. Presentation and outcome of eclampsia at a tertiary center in South
East Nigeria--a 6-year review. Hypertens Pregnancy 2011; 30:125.

51. REFERENCES
• Liu S, Joseph KS, Liston RM, et al. Incidence, risk factors, and associated complications of eclampsia.
Obstet Gynecol 2011; 118:987.
• Seal SL, Ghosh D, Kamilya G, et al. Does route of delivery affect maternal and perinatal outcome in
women with eclampsia? A randomized controlled pilot study. Am J Obstet Gynecol 2012; 206:484.e1.
• Postma IR, Bouma A, Ankersmit IF, Zeeman GG. Neurocognitive functioning following preeclampsia
and eclampsia: a long-term follow-up study. Am J Obstet Gynecol 2014; 211:37.e1.
• Johnson AC, Tremble SM, Chan SL, et al. Magnesium sulfate treatment reverses seizure susceptibility
and decreases neuroinflammation in a rat model of severe preeclampsia. PLoS One 2014; 9:e113670.
• Albayrak M, Ȯzdemir İ, Demiraran Y, Dikici S. Atypical preeclampsia and eclampsia: report of four cases
and review of the literature. Journal of the Turkish German Gynecological Association. 2010;11(2):115-
117. doi:10.5152/jtgga.2010.014.
• Patil MM. Role of Neuroimaging in Patients with Atypical Eclampsia. Journal of Obstetrics and
Gynaecology of India. 2012;62(5):526-530. doi:10.1007/s13224-012-0181-5.