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The Ecliptic Patient and Management: local and international practices

Dr. Chisale Mhango FRCOG

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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 preeclampsiaIt typically occurs at ≥ 20th week of

gestation.It is considered a complication of severe

preeclampsia.NPC Training in MNH

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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 signs1. Sustained systolic BP

greater than 160 mm Hg or diastolic BP greater than 110 mm Hg

2. Tachycardia3. Tachypnea4. Rales5. Hyperreflexia (80%)6. Clonus7. Papilledema

Physical signs cont.9. Oliguria or anuria10. Localizing neurologic deficits11. Right upper quadrant or

epigastric abdominal tenderness with nausea (20%)

12. Generalized oedema (49%)13. Small fundal height for the

estimated gestational age14. Apprehension15. Marked proteinuria

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Aetiology

1. Genetic predisposition,2. Immunology,3. Endocrinology,4. Nutrition,5. Abnormal trophoblastic

invasion,6. Coagulation

abnormalities,

7. Vascular endothelial damage,

8. Cardiovascular maladaptation,

9. Dietary deficiencies or excess, and infection have been proposed as etiologic factors for preeclampsia/eclampsia[2]

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Risk Factors for EclampsiaThe following are considered risk factors for eclampsia:

• Family history of preeclampsia, previous preeclampsia and eclampsia[2]

• Multifoetal gestations,• hydatidform mole,• foetal hydrops,• Teen pregnancy• Primigravida/Nulliparity• Patient older than 35 years

The following pre-existing medical conditions are also considered risk factors[4] :

• Low socioeconomic status• Obesity• Renal disease• Gestational diabetes• underlying hypertension• chronic illnesses such as

– autoimmune disease– diabetes mellitus– renal disease.

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Diagnosis1. Eclampsia manifests as 1 seizure or more, with each

seizure generally lasting 60-75 seconds.2. Hypertension ≥ 140/903. 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 malaria2. Subarachnoid Haemorr

hage3. Cerebellar

Haemorrhage4. Encephalopathy, Hyper

tensive5. Encephalitis6. Hypoglycaemia

7. Meningitis8. Stroke, Haemorrhagic9. Stroke, Ischemic10. Metabolic Disorders11. Undiagnosed Brain

Tumour e.g. Gestational Trophoblastic Neoplasia

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Laboratory studies to guide management [60]:

1. FBC with platelet count

2. Liver function testi. Aspartate aminotransferase

(SGOT) >72 IU/Lii. Plasma albumin (decrease

because of hemodilution)1. Total bilirubin > 1.2

mg/dLiii. 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 testsa. Blood Urea Nitrogen,b. Creatinine clearance,c. Uric acid,d. 24-hour urine collection for

protein excretion

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Maternal and Neonatal Outcomes

Maternal mortalityMaternal 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.

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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).

Supportive care1. 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

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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.Maternal monitoring

• Monitor– (a) fluid intake and

urine output– (b) maternal

respiratory rate, and– (c) uterine

contractions status.

Foetal monitoring

• Foetal heart rate should be monitored continuously.– If the foetal heart tracing

does not improve following a seizure, further evaluation should be undertaken.

• Abruption may be present where uterine hyperactivity and foetal bradycardia persists.

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Management cont.

Pharmacotherapy goals• reduce morbidity, • prevent complications,

and • correct eclampsia.

The drug of choice• MgSO4 is drug of

choice.[13] • Control of hypertension

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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Monitor patient closely

1. Assess pregnancy status. If pregnanta. Deliver as soon as patient is stabilisedb. Deliver regardless of gestation

2. Measure temperature 4 hrlya. If ≥ 38 degrees C, treat for fever (antimalarial or

antibiotic)

3. Assess the cervixa. If soft, thin and partially dilated do ARM (Bishop score

4)b. If unfavourable, ripen cervix with cytotec/misoprostolc. 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)

SeverityGestational age at diagnosis Management

Mild preeclampsia

(≥140mm Hg/90mm Hg – ≤160mm Hg/110mm Hg)

<38 wk without maternal or foetal compromise (a)

Hospitalization for bed rest and close observation

Maternal glucocorticoid therapy at 24-34 wk for foetal lung maturation

≥38 wk without maternal or foetal compromise

Delivery

Magnesium sulphate seizure prophylaxis intrapartum and postpartum

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Management of Preeclampsia-Eclampsia According to Severity (2)

Severity Gestational age at diagnosis

Management

Severe preeclampsia (b)

(≥ 160 mm Hg/110 mm Hg)

<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

Magnesium sulphate

Antihypertensive therapy

Maternal glucocorticoid therapy for foetal lung maturation if <34 weeks

In selected women, cautious delay in delivery until foetal lung maturity is documented by amniocentesis

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Management of Preeclampsia-Eclampsia According to Severity (3)

Severity Gestational age at diagnosis

Management

≥36 wk Delivery

Magnesium sulphate seizure

Antihypertensive therapy

Eclampsia

≥20 wk Stabilization and expedient delivery

Magnesium sulphate seizure

Antihypertensive therapy

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References2. 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 567-61860. Barron WM, Heckerling P, Hibbard JU, et al. Reducing unnecessary coagulation testing in hypertensive disorders of pregnancy. Obstet Gynecol 1999; 94: 364-370.

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