The Ecliptic Patient and

Management: local and

international practices

Dr. Chisale Mhango FRCOG

NPC Training in MNH 1

 Definition of Eclampsia
New onset of grand mal seizure activity
and/or unexplained coma during
pregnancy or postpartum in a woman with
signs or symptoms of preeclampsia
It typically occurs at ≥ 20th week of
gestation.
It is considered a complication of severe
preeclampsia.
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 Prevalence
• 10% of all pregnancies are complicated
by hypertension.
• Eclampsia and preeclampsia account for
about half of these cases worldwide.
• Preeclampsia affects approximately 4.5
to 11.2% of pregnancies in
industrialized countries [ 33]
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 Presentation
• Seizure or postictal state (100%)
– tonic-clonic spasms like epilepsy
• Headache (83%), usually frontal
• Vision disturbance (44%), such as blurred
vision and photophobia
– Nurse patient in a darkened room
• Amnesia and other mental status changes
• Coma (unconsciousness)
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 Presentation cont.
Physical signs Physical signs cont.
1. Sustained systolic BP 9. Oliguria or anuria
greater than 160 mm Hg or 10. Localizing neurologic deficits
diastolic BP greater than 11. Right upper quadrant or
110 mm Hg epigastric abdominal
2. Tachycardia tenderness with nausea
(20%)
3. Tachypnea
12. Generalized oedema (49%)
4. Rales
13. Small fundal height for the
5. Hyperreflexia (80%) estimated gestational age
6. Clonus 14. Apprehension
7. Papilledema 15. Marked proteinuria
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 Aetiology
1. Genetic predisposition, 7. Vascular endothelial
2. Immunology, damage,
3. Endocrinology, 8. Cardiovascular
4. Nutrition, maladaptation,
5. Abnormal trophoblastic 9. Dietary deficiencies or
invasion, excess, and infection
have been proposed as
6. Coagulation
etiologic factors for
abnormalities,
preeclampsia/eclampsia
[2]

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 Risk Factors for Eclampsia
The following are considered risk The following pre-existing medical
factors for eclampsia: conditions are also considered risk
factors[4] :
• Family history of • Low socioeconomic status
preeclampsia, previous • Obesity
preeclampsia and • Renal disease
eclampsia[2]
• Gestational diabetes
• Multifoetal gestations,
• underlying hypertension
• hydatidform mole,
• chronic illnesses such as
• foetal hydrops, – autoimmune disease
• Teen pregnancy – diabetes mellitus
• Primigravida/Nulliparity – renal disease.
• Patient older than 35 years
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 Diagnosis
1. Eclampsia manifests as 1 seizure or more, with each
seizure generally lasting 60-75 seconds.
2. Hypertension ≥ 140/90
3. Proteinuria ≥ 2+
• with or without coexisting systemic abnormalities of
the kidneys, liver, or blood
• Eclampsia in the absence of hypertension with
proteinuria occurs in 38% of cases reported in the
United Kingdom.[5]
• Similarly, hypertension was absent in 16% of cases
reviewed in the United States.[4]
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 Differential Diagnosis
1. Cerebral malaria 7. Meningitis
2. Subarachnoid Haemorr 8. Stroke, Haemorrhagic
hage 9. Stroke, Ischemic
3. Cerebellar 10. Metabolic Disorders
Haemorrhage
11. Undiagnosed Brain
4. Encephalopathy, Hyper Tumour e.g.
tensive
Gestational
5. Encephalitis Trophoblastic
6. Hypoglycaemia Neoplasia

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 Laboratory studies to guide management
[60]:
1. FBC with platelet count
2. Liver function test
i. Aspartate aminotransferase
(SGOT) >72 IU/L
ii. Plasma albumin (decrease
because of hemodilution)
1. Total bilirubin > 1.2
mg/dL
iii. LDH >600 IU/L[2]
iv. Elevated levels due to
hepatocellular injury and
HELLP syndrome
v. Fibrinogen levels, and fibrin
degradation products and
vi. Prothrombin time,(abruptio
placentae, or microangiopathic
haemolytic anaemia),
vii. Activated partial
thromboplastin time
3. Kidney function tests
a. Blood Urea Nitrogen,
b. Creatinine clearance,
c. Uric acid,
d. 24-hour urine collection for
protein excretion
10
 Maternal and Neonatal Outcomes
Maternal mortality
Maternal death is largely a
result of
• complications from
abruptio placentae,
• hepatic rupture, and
• Eclampsia
– Cerebral oedema
Neonatal mortality
• Delivery likely to be
preterm. Sequelae of
prematurity include
– respiratory distress
syndrome,
– chronic lung disease,
– intraventricular haemorrhage,
– cerebral palsy,
– sepsis,
– necrotizing enterocolitis.
11
 Management
• Delivery is only
definitive treatment
for eclampsia (i.e. removal
of the placenta from the uterus).
• Admit to intensive
care setting for
supportive care and
treatment until
delivery (do not leave woman
alone).
NPC Training in MNH
Supportive care
1. Secure an intravenous (IV) line
with a large-bore catheter, -
Ringer lactate or normal saline 30
drops/min. or 1 litre in 6-8 hrs.
2. Administer oxygen, and (iii) keep
patient in left lateral decubitus
position.
3. Supportive care for ecliptic
convulsions includes the
following:
–
–
Close monitoring
Maintain airway at all times
– Anticonvulsant therapy
– Blood pressure (BP) control
12
 Management cont.
1. BP should be assessed with the goal of maintaining the
systolic BP at ≤ 170 mmHg; diastolic BP ≤ 110 mm Hg with
antihypertensive medications as needed (e.g., hydralazine
(apresoline), labetalol, nifedipine).
– NB: Excessive decrease of BP can cause inadequate uteroplacental
perfusion and foetal distress.[13]
2. Antenatal steroids may be administered in anticipation of
delivery at less than 34 weeks gestation.
– Betamethasone (12 mg IM q24h × 2 doses) or dexamethasone (6 mg IM
q12h × 4 doses) is recommended.
3. Keep nil by mouth (including medications) until patient is
stabilized or delivered, to reduce risk for aspiration when
postictal.
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 Management cont.
Foetal monitoring
Maternal monitoring

• Monitor • Foetal heart rate should

be monitored
– (a) fluid intake and
continuously.
urine output
– If the foetal heart tracing
– (b) maternal does not improve following
respiratory rate, and a seizure, further
evaluation should be
– (c) uterine undertaken.
contractions status. • Abruption may be
present where uterine
hyperactivity and foetal
NPC Training in MNH
bradycardia persists. 14
 Management cont.
Pharmacotherapy goals The drug of choice
• reduce morbidity, • MgSO4 is drug of
• prevent complications, choice.[13]
and • Control of hypertension
• correct eclampsia. is essential to prevent
further morbidity or
possible mortality.
– Most recommended
antihypertensive agents
are hydralazine, labetalol,
and nifedipine.
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 Management of Hypertension
1. Hydralazine 5 mg IV over 3-4 minutes, if not
possible give IM every 30 minutes until BP ≤
170/90. MAXIMUM total dose 20 mg.
2. If hydralazine not available give Labetalol 10 mg
IV
a. If inadequate response after 10 minutes, repeat 20
mg, if ten minutes later still adequate increase to
40mg, then 80 mg ten minutes later if still inadequate
3. Nifedipine 5 mg orally. If no response after 10
minutes, repeat dose
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16
 Monitor patient closely
1. Assess pregnancy status. If pregnant
a. Deliver as soon as patient is stabilised
b. Deliver regardless of gestation
2. Measure temperature 4 hrly
a. If ≥ 38 degrees C, treat for fever (antimalarial or
antibiotic)
3. Assess the cervix
a. If soft, thin and partially dilated do ARM (Bishop score
4)
b. If unfavourable, ripen cervix with cytotec/misoprostol
c. If there is foetal distress do C/S
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 Delivery (antepartum or intrapartum eclampsia)

• Adequate pain relief for labour and delivery is vital and may
be provided with either systemic opioids or epidural
anaesthesia.
• In the absence of foetal malpresentation or foetal distress,
oxytocin or prostaglandins may be initiated to induce
labour.
• Caesarean delivery recommended in patients with an
unfavourable cervix and a gestational age of 30 weeks or
less.
– When emergency caesarean delivery is indicated, substantiating
the absence of coagulopathy before the procedure is important.
[16]

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 Anaesthesia
• For non-emergency caesarean delivery, epidural or
combined techniques of regional anaesthesia are
preferred.
• Regional anaesthesia is contraindicated in the presence
of coagulopathy or severe thrombocytopenia (< 50,000
platelets/µL).
• General anaesthesia in women with eclampsia increases
the risk of aspiration, and airway oedema may make
intubation difficult. It also can produce significant
increases in systemic and cerebral pressures during
intubation and extubation.
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 Management of Preeclampsia-Eclampsia
According to Severity (1)
Gestational age at
Severity diagnosis Management
Mild preeclampsia <38 wk without maternal Hospitalization for bed
(≥140mm Hg/90mm Hg – or foetal compromise (a) rest and close observation
≤160mm Hg/110mm Hg)
Maternal glucocorticoid
therapy at 24-34 wk for
foetal lung maturation

≥38 wk without maternal Delivery

or foetal compromise
Magnesium sulphate
seizure prophylaxis
intrapartum and 20
postpartum
 Management of Preeclampsia-Eclampsia
According to Severity (2)
Severity Gestational age at Management
diagnosis
<32 wk Hospitalization with close maternal
and foetal surveillance, ideally in a
tertiary care centre
Maternal glucocorticoid therapy for
foetal lung maturation if ≥24 weeks

Delivery if maternal or foetal

compromise

32-36 wk Delivery
Severe preeclampsia (b)
(≥ 160 mm Hg/110 mm Hg) Magnesium sulphate

Antihypertensive therapy

Maternal glucocorticoid therapy for

foetal lung maturation if <34 weeks

In selected women, cautious delay in

21
delivery until foetal lung maturity is
 Management of Preeclampsia-Eclampsia
According to Severity (3)
Severity Gestational age at Management
diagnosis
≥36 wk Delivery

Magnesium sulphate
seizure

Antihypertensive therapy

≥20 wk Stabilization and

expedient delivery
Eclampsia
Magnesium sulphate
seizure

22
Antihypertensive therapy
 References
2. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol
2000; 183: S1-S22.
4. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol 2001; 97: 533-538.
5. Committee on Technical Bulletins of the American College of Obstetricians and Gynecologists. ACOG technical bulletin: Hypertension in
pregnancy-Number 219: January 1996 (replaces no. 91, February 1986). Int J Gynaecol Obstet 1996; 53: 175-183.
12. National High Blood Pressure Education Program. Working Group Report on High Blood Pressure in Pregnancy (NIH Publication No. 00-
3029). Bethesda, MD, National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health and Human
Services, revised July 2000. Available at: http://www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_preg.pdf. Accessed June 24, 2003.
13. Pridjian G. Placental transfer, fetomaternal interaction: Placental physiology and its role as go between, in Avery GB, Fletcher MA,
MacDonald MG (eds): Neonatology: Pathophysiology and Management of the Newborn. Philadelphia, Lippincott Williams & Wilkins, 1999,
ed 5, pp 125-131.
14. Pirani BB, Campbell DM, MacGillivray I. Plasma volume in normal first pregnancy. J Obstet Gynaecol Br Commonw 1973; 80: 884-887.
16. Hunter S, Robson SC. Adaptation of the maternal heart in pregnancy. Br Heart J 1992; 68: 540-543.
19. Robson SC, Hunter S, Boys RJ, et al. Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol
1989; 256: H1060-H1065.
32. Centers for Disease Control and Prevention. Maternal mortality: United States, 1982-1996. MMWR Morb Mortal Wkly Rep 1998; 47: 705-
707.
33. U.S. Department of Health, Education, and Welfare. The Collaborative Perinatal Study of the National Institute of Neurological Diseases
and Stroke: The Women and their Pregnancies(DHEW Publication No. (NIH) 73-379). Bethesda, MD, U.S. Department of Health, Education,
and Welfare, Public Health Service, National Institutes of Health, 1972.
35. Trupin LS, Simon LP, Eskenazi B. Change in paternity: A risk factor for preeclampsia in multiparas. Epidemiology 1996; 7: 240-244.
43. Tyni T, Ekholm E, Pihko H. Pregnancy complications are frequent in long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Am J
Obstet Gynecol 1998; 178: 603-608.
44. Pridjian G, Puschett JB. Preeclampsia: Part 2-Experimental and genetic considerations. Obstet Gynecol Surv 2002; 57: 619-640.
45. Pridjian G, Puschett JB. Preeclampsia: Part 1-Clinical and pathophysiologic considerations. Obstet Gynecol Surv 2002; 57: 598-618.
53. Katz M, Berlyne GM. Differential renal protein clearance in toxaemia of pregnancy. Nephron 1974; 13: 212-220.
54. Cunningham FG, Gant NF, Leveno KJ, et al. Hypertensive disorders in pregnancy, in Williams Obstetrics. New York, McGraw-Hill Health
Professions Division, 2001, ed 21, pp 567-618
60. Barron WM, Heckerling P, Hibbard JU, et al. Reducing unnecessary coagulation testing in hypertensive disorders of pregnancy. Obstet
Gynecol 1999; 94: 364-370. 23
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