The Ecliptic Patient and Management : local and international practices

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

5. Presentation cont. Physical signs 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 • Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg • Tachycardia • Tachypnea • Rales • Hyperreflexia (80%) • Clonus • Papilledema 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] NPC Training in MNH

7. Risk Factors for Eclampsia The following are considered risk factors for eclampsia: 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. • Family history of preeclampsia, previous preeclampsia and eclampsia[2] • Multifoetalgestations, • hydatidformmole, • foetal hydrops, • Teen pregnancy • Primigravida/Nulliparity • Patient older than 35 years 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] 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 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 thromboplastintime • Kidney function tests • Blood Urea Nitrogen, • Creatinine clearance, • Uric acid, • 24-hour urine collection for protein excretion

11. Maternal and Neonatal Outcomes Maternal mortality Neonatal mortality Delivery likely to be preterm. Sequelae of prematurity include respiratory distress syndrome, chronic lung disease, intraventricular haemorrhage, cerebral palsy, sepsis, necrotizing enterocolitis. Maternal death is largely a result of • complications from abruptio placentae, • hepatic rupture, and • Eclampsia • Cerebral oedema

12. Management 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 • 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

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 whenpostictal. NPC Training in MNH

14. Management cont. Maternal monitoring 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. • Monitor • (a) fluid intake and urine output • (b) maternal respiratory rate, and • (c) uterine contractions status. NPC Training in MNH

15. Management cont. Pharmacotherapy goals 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. • reduce morbidity, • prevent complications, and • correct eclampsia. 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 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 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] 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. NPC Training in MNH

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

21. Management of Preeclampsia-Eclampsia According to Severity (2)

22. Management of Preeclampsia-Eclampsia According to Severity (3)

23. References 2. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J ObstetGynecol 2000; 183: S1-S22. 4. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. ObstetGynecol 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 GynaecolObstet 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. PridjianG. 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. PiraniBB, Campbell DM, MacGillivray I. Plasma volume in normal first pregnancy. J ObstetGynaecol 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. Centersfor 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. TrupinLS, Simon LP, Eskenazi B. Change in paternity: A risk factor for preeclampsia in multiparas. Epidemiology 1996; 7: 240-244. 43. TyniT, Ekholm E, Pihko H. Pregnancy complications are frequent in long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Am J ObstetGynecol 1998; 178: 603-608. 44. PridjianG, Puschett JB. Preeclampsia: Part 2-Experimental and genetic considerations. ObstetGynecolSurv 2002; 57: 619-640. 45. PridjianG, Puschett JB. Preeclampsia: Part 1-Clinical and pathophysiologic considerations. ObstetGynecolSurv 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, pp567-618 60. Barron WM, Heckerling P, Hibbard JU, et al. Reducing unnecessary coagulation testing in hypertensive disorders of pregnancy. ObstetGynecol 1999; 94: 364-370.