Late Postpartum Eclampsia Late Postpartum Eclampsia

Zoila Velastegui M.D.; Miguel Luna M. D.; Donald Ross M.D.; Abraham Hamaoui M.D. ; Ray Mercado D.O;

Department of Obstetrics and Gynecology, Weill Medical College of Cornell Univer sity and Lincoln Medical and Mental Health Center, Bronx, New York

BACKGROUND: The blood pressure of pregnant patients has been measure accurately since the ea rly 1900s with the advent of the blood-pressure cuff. Eclampsia, then called toxe mia of pregnancy has been a well-known obstetric complication for many centuries. Early on, pregnant patients presenting with elevated blood pressure were consi dered to be at risk for seizure and labeled pre-eclamptic. Because both condition

s, eclampsia and pre-eclampsia share common symptoms and have a common name, the y are intrinsically linked. When in fact, we are likely dealing with quite a fe w pathologies broadly labeled under either name. A further derivation of these pathologies is Late Postpartum Eclampsia. Late Postpartum Eclampsia, is a dangerous enigma. It is characterized by seizur es associated with pregnancy occurring sometimes weeks after delivery. The path ophysiology is vascular in nature with initial symptoms related to angioedema in the occipital lobes, causing visual disturbances and headache followed by seizu res. The similarity in names is confusing and intertwines all three conditions. Alth ough Eclampsia, Pre-Eclampsia and Late Postpartum Eclampsia share similar chara cteristics they are separate and distinct conditions. CASE REPORT: 23 yo G1P1 Hispanic female s/p vaginal delivery six days prior a t another facility, arrived in ED via ambulance for two seizure episodes: one at home and a second one witnessed by EMS for which she recieved diazapam. First seizure episode was preceded by a short period of headache upon awakening. Pati ent arrived to hospital in post-ictal state, disoriented. VS significant for mi ld tachycardia and BP 142/91. Pt was admitted to MICU with diagnosis of postpar tum emclampsia, for magnesium sulfate therapy. No prior h/o seizure or antepartum, intrapartum or immediate post partum preclam psia referred by patient or family members. Her post-partum period was complica ted with headache, nausea and blurry vision that was managed as epidural headach e. No history of substance abuse or psychiatric issues. During hospital stay patient was without seizures. BP ranged from a systolic hi gh of 165/84 and a diastolic high of 137/94. The lowest pressure recorded was 1 07/58. Although hepatomegaly was found on CT scan, labs were significant only f or mildly elevatd LDH and proteinuria 1+. After 24 hrs magnesium sulfate was di scontunued, lebetalol initiated and patient was discharged home 3 days later wit h BP 129/58 and lebetalol 200mg BID. On follow-up visit patient still complaine d fo occasional headaches and blurry vision. Lebetalol was contunued. Pt did n ot retrun for more follow-up visits. DISCUSSION: Eclampsia is seizure occurring during or after pregnancy attributable to no othe r cause in a preeclamptic patient. In the past late postpartum eclampsia (LPPE) was considered to occur between 48 hours and 10 days postpartum[1]. However, L PPE has been reported in one case 8 weeks postpartum.[2] The ethology of eclamp sia is unknown. A study at NYU in 2004 found eclampsia may be a risk factor for future temporal lobe epilepsy and hippocampal sclerosis in the birth mother.[4] It is importan t to control subsequent seizures in eclamptic patients for many reasons includin g the emerging evidence showing its association with epilepsy. Magnesium sulfate is the medication of choice. Phenytoin, Diazepam and a cockta il mixture of chlorpromazine, promethazine and pethidine have proven inferior to magnesium sulfate in reducing the risk of recurrent seizures in three Cochrane Library meta-analysis studies. [5] [6] [7]

We will review two cases of late postpartum eclampsia in which there is a delay in administering magnesium sulfate in patients presenting without a history of p reeclampsia after uncomplicated pregnancies. The first case comes from the University of Michigan.[8] A healthy 21 year old G3P1, African American woman with no history of hypertension or preeclampsia awo ke with severe bilateral frontal headaches and blurry vision which progressed to bilateral cortical blindness with a BP of 169/99, eight days after giving birth . Her perinatal blood pressure had risen to 130/80 one week prior to delivery w ith no proteinuria. In the acute postpartum period her blood pressure remained mostly in the 120/60s to 130/70s. It occasionally jumped to 140/80 and 150/90 m m Hg. After readmission a CT scan showed bilateral low attenuation lesions in t he cerebral hemispheres. MRI showed diffuse altered T2 signals in the posterior . Angiogram was normal. Magnesium was withheld for 20 hours. Only after the p atient suffered two tonic-clonic seizures was it administered. Phenytoin was al so added. Vision returned to normal over two days, however her blood pressure r emained elevated with reading as high as 200/110 mmHg. She was sent home on met aprolol after a three day stay. The second case we will review comes from the University of Munster, Germany[9]. A 30 year old G5P5 with medical history of migraine preceded by aura arrived t o the hospital complaining of left hemianopia and a severe headache which develo ped rapidly and a BP of 180/90. This occurred 53 days after delivering a health y child following an uncomplicated pregnancy. CT scan showed hypodensities in t he cerebellum and an MRI revealed hyperintense signal on T2-weighted images in t he left cerebellar hemisphere. A false diagnosis of ischemic stroke in the post erior circulation was made. Later it was found the changes in imaging studies w ere due to vasogenic edema. On day 3 of her stay she suffered two tonic-clonic seizures and urinalysis showed proteinuria. A diagnosis of late postpartum ecla mpsia was made. She was given magnesium and valproic acid, later switched to le vetiracetam. Urapidil was added. During her four week stay she developed a pul monary embolism and had a positive lupus anticoagulant test. Upon discharge she was without sequele. Diagnosing a patient with eclampsia without prior preeclampsia goes against the basic definition of eclampsia which is the presence of new-onset grand mal seizur es in a woman with preeclampsia according to The American College of Obstetrician s and Gynecologists.[10] This leaves inexperienced physicians in a diagnostic c onundrum and may contribute to a delay in administering magnesium to patients wi th no history of preeclampsia. A change in clinical thinking and training is necessary. Eclampsia can occur wi thout antecedent preeclampsia, so the definition of eclampsia should be changed. Also, eclampsia can occur many weeks after delivery well beyond the standard t hinking of 10 days postpartum.

Reference List: American College of Obstetricians and Gynecologists, (2002). Diagnosis and manag ement of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Obstet Gynec ol Vol. 99, p159167 Cunningham, F.G. (2001). Hypertensive Disorders in Pregnancy. In A. Seils, S. No ujaim & K. Davis (Eds.), Williams Obstetrics, (p 459). New York, USA: McGraw-Hi ll Duley L, Glmezoglu AM, Chou D. (2010). Magnesium sulphate versus lytic cocktail f

or eclampsia. Cochrane Database of Systematic Reviews, Issue 9. Art. No.: CD002 960. DOI: 10.1002/14651858.CD002960.pub2. Duley L, Henderson-Smart DJ, Chou D. (2010). Magnesium sulphate versus phenytoin for eclampsia. Cochrane Database of Systematic Reviews, Issue 10. Art. No.: CD0 00128. DOI: 10.1002/14651858.CD000128.pub2. Duley L, Henderson-Smart DJ, Walker GJA, Chou D. (2010). Magnesium sulphate vers us diazepam for eclampsia. Cochrane Database of Systematic Reviews, Issue 12. A rt. No.: CD000127. DOI:10.1002/14651858.CD000127.pub2. Gold, K.J., (2005). Case report: late-onset eclampsia presents as bilateral cort ical blindness, American Family Physician, Lawn N., (2004). Eclampsia, hippocampal sclerosis, and temporal lobe epilepsy, N eurology, Vol. 62 No. 8 1352-1356 Minnerup J., Kleffner I., (2010). Late Onset Postpartum: It is Really Never Too Late - A Case of Eclampsia 8 Weeks after Delivery, Stroke Research and Treatment , Article ID 798616, 1-4p [1] Cunningham, F.G. (2001). Hypertensive Disorders in Pregnancy. In A. Seils, S . Noujaim & K. Davis (Eds.), Williams Obstetrics, (p 459). New York, USA: McGra w-Hill. [2] Minnerup J., Kleffner I., (2010). Late Onset Postpartum: It is Really Never Too Late - A Case of Eclampsia 8 Weeks after Delivery, Stroke Research and Trea tment, Article ID 798616, 1-4p [4] Lawn N., (2004). Eclampsia, hippocampal sclerosis, and temporal lobe epileps y, Neurology, Vol. 62 No. 8 1352-1356 [5] Duley L, Henderson-Smart DJ, Chou D. (2010). Magnesium sulphate versus pheny toin for eclampsia. Cochrane Database of Systematic Reviews, Issue 10. Art. No.: CD000128. DOI: 10.1002/14651858.CD000128.pub2. [6] Duley L, Henderson-Smart DJ, Walker GJA, Chou D. (2010). Magnesium sulphate versus diazepam for eclampsia. Cochrane Database of Systematic Reviews, Issue 1 2. Art. No.: CD000127. DOI:10.1002/14651858.CD000127.pub2. [7] Duley L, Glmezoglu AM, Chou D. (2010). Magnesium sulphate versus lytic cockta il for eclampsia. Cochrane Database of Systematic Reviews, Issue 9. Art. No.: C D002960. DOI: 10.1002/14651858.CD002960.pub2. [8] Gold, K.J., (2005). Case report: late-onset eclampsia presents as bilateral cortical blindness, American Family Physician [9] Minnerup J., Kleffner I., (2010). Late Onset Postpartum: It is Really Never Too Late - A Case of Eclampsia 8 Weeks after Delivery, Stroke Research and Treat ment, Article ID 798616, 1-4p. [10] American College of Obstetricians and Gynecologists, (2002). Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Obstet Gynecol Vol. 99, p159167.