the ecliptic patient and management: local and international practices dr. chisale mhango frcog 1...
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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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