m1_c._mhango_-_eclamptic_patient_and_management.pptx

Mgt of eclampsia

1. The Ecliptic Patient and Management : local and international practices Dr. Chisale Mhango FRCOG 1 NPC Training in MNH

2. 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. 2 NPC Training in MNH

3. 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] 3 NPC Training in MNH

4. 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) 4 NPC Training in MNH

5. Presentation cont. Physical signs Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg Tachycardia Tachypnea Rales Hyperreflexia (80%) Clonus Papilledema Physical signs cont. Oliguria or anuria Localizing neurologic deficits Right upper quadrant or epigastric abdominal tenderness with nausea (20%) Generalized oedema (49%) Small fundal height for the estimated gestational age Apprehension Marked proteinuria 5 NPC Training in MNH

6. Aetiology Genetic predisposition, Immunology, Endocrinology, Nutrition, Abnormal trophoblastic invasion, Coagulation abnormalities, Vascular endothelial damage, Cardiovascular maladaptation, Dietary deficiencies or excess, and infection have been proposed as etiologic factors for preeclampsia/eclampsia [2] 6 NPC Training in MNH

7. Risk Factors for Eclampsia The 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. 7 NPC Training in MNH

8. Diagnosis Eclampsia manifests as 1 seizure or more, with each seizure generally lasting 60-75 seconds. Hypertension ≥ 140/90 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] 8 NPC Training in MNH

9. Differential Diagnosis Cerebral malaria Subarachnoid Haemorrhage Cerebellar Haemorrhage Encephalopathy, Hypertensive Encephalitis Hypoglycaemia Meningitis Stroke, Haemorrhagic Stroke, Ischemic Metabolic Disorders Undiagnosed Brain Tumour e.g . Gestational Trophoblastic Neoplasia 9 NPC Training in MNH

10. Laboratory studies to guide management [60]: FBC with platelet count Liver function test Aspartate aminotransferase (SGOT) >72 IU/L Plasma albumin (decrease because of hemodilution) Total bilirubin > 1.2 mg/ dL LDH >600 IU/L [2] Elevated levels due to hepatocellular injury and HELLP syndrome Fibrinogen levels , and fibrin degradation products and Prothrombin time ,( abruptio placentae, or microangiopathic haemolytic anaemia), Activated partial thromboplastin time Kidney function tests Blood Urea Nitrogen, Creatinine clearance, Uric acid, 24-hour urine collection for protein excretion 10

11. 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

12. 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 care 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. Administer oxygen, and (iii) keep patient in left lateral decubitus position. Supportive care for ecliptic convulsions includes the following: Close monitoring Maintain airway at all times Anticonvulsant therapy Blood pressure (BP) control 12 NPC Training in MNH

13. Management cont. 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] 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. Keep nil by mouth (including medications) until patient is stabilized or delivered, to reduce risk for aspiration when postictal . 13 NPC Training in MNH

14. 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 . 14 NPC Training in MNH

15. 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. 15 NPC Training in MNH

16. Management of Hypertension 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. If hydralazine not available give Labetalol 10 mg IV 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 Nifedipine 5 mg orally. If no response after 10 minutes, repeat dose 16 NPC Training in MNH

17. Monitor patient closely Assess pregnancy status. If pregnant Deliver as soon as patient is stabilised Deliver regardless of gestation Measure temperature 4 hrly If ≥ 38 degrees C, treat for fever (antimalarial or antibiotic) Assess the cervix If soft, thin and partially dilated do ARM (Bishop score 4) If unfavourable, ripen cervix with cytotec/misoprostol If there is foetal distress do C/S 17 NPC Training in MNH

18. 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 ] 18 NPC Training in MNH

19. 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. 19 NPC Training in MNH

20. Management of Preeclampsia-Eclampsia According to Severity (1) Severity Gestational 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 20

21. 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 21

22. 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 22

23. 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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