- Email: [email protected]
Late-Onset Postpartum Eclampsia
CLINICAL ROUNDS Late-Onset Postpartum Eclampsia Ijeoma Azonobi, MD, Helen McBride-Richter, CNM, MSN, and Loretta Patrick, RN, Esq Eclampsia typically occurs in the antepartum or intrapartum period. Late-onset postpartum eclampsia is a controversial topic, which recently has been accepted as a true phenomenon. Late-onset postpartum eclampsia is a rare occurrence, although literature suggests that it is an increasing phenomenon. In this case study, an essentially healthy primigravida developed eclampsia 7 days postpartum after an unremarkable antepartum and intrapartum course. Because significant morbidity and mortality are associated with this disorder, it is imperative that efforts be made to prevent its occurrence. We recommend including patient education about the prodromal symptoms of late-onset postpartum eclampsia, including headache, visual changes, and abdominal pain at the time of hospital discharge. J Midwifery Womens Health 2006;51:51–53 © 2006 by the American College of Nurse-Midwives. keywords: eclampsia, hypertension, postpartum, preeclampsia, pregnancy-induced hypertension
CASE DESCRIPTION A 20-year-old primigravida presented for her initial prenatal visit at 18.3 weeks by dates, which were confirmed by second-trimester ultrasound. Her medical history was significant for mitral valve prolapse, for which she was monitored by a cardiologist and was advised to use prophylactic antibiotics when indicated. The patient also had sickle cell trait. Her family medical history was unremarkable, except for hypertension in her father, who was diagnosed at age 51. Her prenatal course was uneventful. At 5=5⬙, she experienced a total weight gain of 26 lb. She exhibited blood pressures within normal range (90 –110 mm Hg systolic 60 – 62 mm Hg diastolic). Laboratory studies at 18.3 weeks and at 26.2 weeks gestation revealed no hemoconcentration and normal platelet counts. She had not demonstrated proteinuria; however, one incidence of dependent edema was noted at her 37-week visit. She had no complaints of headaches or blurred vision. Her intrapartum course was unremarkable. At 39 and 5/7 weeks’ gestation, she presented to the hospital in active labor. On admission, her vital signs were stable, and laboratory findings were within normal range. She had an uncomplicated spontaneous vaginal delivery of a 6 lb, 1 oz girl. Her blood pressure remained within the normal range during hospitalization, and she was discharged to home on the third postpartum day. On postpartum day 7, she was brought into the emergency department by ambulance unresponsive. She had been found on the floor by her husband, who reported that she appeared to have suffered a seizure and then became
Address correspondence to Ijeoma Azonobi, MD, Duke University Medical Center, Department of OB/GYN, Box 3616 Med Cr, Durham, NC 27710. E-mail: [email protected]
Journal of Midwifery & Women’s Health • www.jmwh.org © 2006 by the American College of Nurse-Midwives Issued by Elsevier Inc.
unconscious. Vital signs on admission were temperature 97.0°F, pulse 115 bpm, blood pressure 138/67 mm Hg, and Sp O2 96%. Laboratory findings revealed normal chemistry, including negative drug screen and normal liver enzyme levels. Complete blood count revealed a WBC of 23.3 ⫻ 1000/cu mm, hemoglobin and hematocrit of 15.6 g/dL, and 46.1%, respectively, and platelets 415 ⫻ 1000/cu mm. She exhibited no proteinuria. ECG, chest x-ray, and CT scan of the brain were all normal. Magnesium sulfate and anticonvulsives were administered. When she regained consciousness, she had amnesia and was unable to recall any symptoms prior to the incident. Later, the patient did recall having a headache that entire day, which was not relieved by ibuprofen or other over-the-counter analgesics. She remained hospitalized for 3 days. Her blood pressure values remained stable, and she was discharged to home without a prescription for medication. Her final diagnosis was postpartum eclampsia. DISCUSSION Hypertensive disorders are the second leading cause of maternal mortality and the most common medical complication in pregnancy.1,2 Preeclampsia and eclampsia are forms of hypertension unique to human pregnancy. The incidence of preeclampsia ranges between 3% and 7% in nulliparas women and between 0.8% and 5.0% in multiparas.1 The so-called “classic triad” of preeclampsia includes hypertension, proteinuria, and edema. However, there is now universal agreement that edema should not be considered when making the diagnosis of preeclampsia.1 The guidelines for the diagnosis of preeclampsia accepted by the American College of Obstetricians and Gynecologists include a blood pressure of 140 mm Hg or greater systolic or 90 mm Hg or greater diastolic in a previously normotensive woman and proteinuria of 0.3 g in a 24-hour urine specimen.3 51 1526-9523/06/$32.00 • doi:10.1016/j.jmwh.2005.06.009
Eclampsia is the occurrence of seizures or coma in addition to proteinuria and hypertension. This disorder is even more rare, complicating approximately 3 in 1000 pregnancies, but higher incidences are observed in lower socioeconomic groups, women with multiple gestations, nulliparous women less than 20 years old, and multiparous women greater than 35 years of age.1,4 Most episodes of eclampsia occur between 20 weeks’ gestation and less than 48 hours postpartum, with approximately 50% occurring antepartum, 25% intrapartum, and 25% postpartum.1 Whether true eclamptic seizures can occur later than 48 hours has been the subject of much controversy, but it is now believed that this phenomenon does, in fact, exist. Lubarsky et al. reported that 16% of all postpartum eclampsia fall into the category of late postpartum eclampsia.5 Since that 1994 report, additional research on the incidence of these phenomena has been conducted. Chames et al. performed a 5-year, multicenter data analysis of 89 eclamptic patients to determine the timing of eclampsia in relation to delivery. This study demonstrated that 67.4% had convulsions before or during delivery, whereas 32.6% were diagnosed with postpartum eclampsia. Of those, 20.7% occurred 48 hours or less after delivery, and 79.3% occurred 48 hours or more after delivery.6 Further studies indicate that the incidence of postpartum eclampsia ranges from 11% to 44%, and that 5% to 26% of all cases of eclampsia will occur after 48 hours postpartum.7 It was noted in initial reports of case studies that late postpartum eclampsia does not always present in the manner of typical eclampsia because proteinuria and hypertension may not be detected in the patient during the antepartum evaluation.5,8 Several case reports have described women without a history of elevated blood pressures or proteinuria during their prenatal course who ultimately are diagnosed with late postpartum eclampsia.4,8 –10 In a study of 151 women without a history of gestational hypertension, who were diagnosed postpartum with preeclampsia, 11% became eclamptic.2 This is a phenomenon referred to as “eclampsia without preeclampsia.”8 Instead, these patients are more likely to present with headaches (87%), visual changes (44%), nausea or vomiting (22%), or epigastric pain (9%) prior to seizure.4,6,8 It has been noted in previous studies that many women who experienced late postpartum eclampsia also experienced these atypical symptoms but do not report these symptoms to their health care providers.2 Treatment for late postpartum eclampsia is similar to that of eclampsia, with the exception of the definitive treatment
of delivery of the infant. Traditionally, first-line treatment for eclamptic seizures is magnesium sulfate, although benzodiazepines and phenytoin may be used as well. Although hypertension usually resolves with the cessation of seizures, if they persist, both hydralazine and labetalol have been used successfully to control eclampsia-induced hypertension. Consultation with a neurologist may be required because women with late postpartum eclampsia may display the characteristic pattern of cerebral edema on imaging studies. Cerebral edema reverses with the resolution of symptoms. In summary, late-onset postpartum eclampsia is a disorder that is difficult to detect or prevent. It is important that health care providers take a role in improving patient education to increase the ability to swiftly diagnose and treat this condition. Two important factors play a role in our ability to prevent the occurrence of eclampsia in the postpartum period. First, in a case like the one presented here, women may not be aware of the need to report symptoms of headache or vision changes in the postpartum period. Second, because the signs and symptoms mirror those of fatigue and anxiety normal in the postpartum period, patients may tend to devalue their significance. Therefore, it is incumbent upon health care providers to appropriately educate patients before being discharged from care in the early postpartum period. We recommend the following precautions to assist in the prevention of this disorder and increase patient awareness: 1. Discharge instructions should be revised to include the immediate reporting of headache, vision changes, and abdominal pain. 2. All providers involved in the discharge process should be made aware of late postpartum eclampsia through an in-service process. This is very important because providers who do not know the signs or symptoms of late postpartum eclampsia may not give the appropriate instructions at discharge and may misinform a patient who calls back with symptoms. 3. Patients should be instructed to call immediately when symptoms occur. We thank the faculty and staff of the Primary Care Faculty Development Program at the Morehouse School of Medicine for their educational support that ultimately spurred the development of this article, and whose advice was crucial to its completion.
REFERENCES Ijeoma Azonobi, MD, received her medical degree from Morehouse School of Medicine in May 2005. She has begun a residency program in obstetrics and gynecology. Helen McBride-Richter, CNM, MSN, is currently in private practice. Loretta Patrick, RN, JD, received her nursing degree from Purdue University and her law degree from Georgia State University College of Law.
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1. Sibai BM. Hypertension in pregnancy. In Gabbe Obstetrics— Normal and problem pregnancies, 4th ed. New York: Churchill Livingstone, 2002:950 – 83. 2. Matthys LA, Coppage KH, Lambers DS, Barton JR, Sibai BM. Delayed postpartum pre-eclampsia: An experience of 151 cases. Am J Obstet Gynecol 2004;190:1464 – 6.
Volume 51, No. 1, January/February 2006
3. ACOG Practice Bulletin. Diagnosis and management of preeclampsia and eclampsia. Obstet Gynecol 2002;99:159 – 65.
7. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol 2002;105:402–10.
4. Martin J, Sidman R. Late postpartum eclampsia: A common presentation of an uncommon diagnosis. J Emerg Med 2002;25:387– 90.
8. Veltkamp R, Kupsch A, Polasek, Yousry TA, Pfister HW. Late onset postpartum eclampsia without pre-eclamptic prodromi: Clinical and neuroradiological presentation in two patients. J Neurol Neurosurg Psychiatry 2000;69:824 –7.
5. Lubarsky SL, Barton JR, Friedman SA, Nasreddine S, Ramadan MK, Sibai BM. Late postpartum eclampsia revisited. Obstet Gynecol 1994;83:502– 4.
9. Dziewas R, Stogbauer F, Freund M, Ludemann P, Imai T, Holzapfel C, Ringelstein PB. Late onset postpartum eclampsia: a rare and difficult diagnosis. J Neurol 2002;249:1287–91.
6. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: A preventable disease? Am J Obstet Gynecol 2002;186:1174 –7.
10. Graeber B, Vanderwal T, Stiller RJ, Werdmann MJ. Late postpartum eclampsia as an obstetric complication seen in the ED. Am J Emerg Med 2005;23:168 –70.
Journal of Midwifery & Women’s Health • www.jmwh.org
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CASE DESCRIPTION A 20-year-old primigravida presented for her initial prenatal visit at 18.3 weeks by dates, which were confirmed by second-trimester ultrasound. Her medical history was significant for mitral valve prolapse, for which she was monitored by a cardiologist and was advised to use prophylactic antibiotics when indicated. The patient also had sickle cell trait. Her family medical history was unremarkable, except for hypertension in her father, who was diagnosed at age 51. Her prenatal course was uneventful. At 5=5⬙, she experienced a total weight gain of 26 lb. She exhibited blood pressures within normal range (90 –110 mm Hg systolic 60 – 62 mm Hg diastolic). Laboratory studies at 18.3 weeks and at 26.2 weeks gestation revealed no hemoconcentration and normal platelet counts. She had not demonstrated proteinuria; however, one incidence of dependent edema was noted at her 37-week visit. She had no complaints of headaches or blurred vision. Her intrapartum course was unremarkable. At 39 and 5/7 weeks’ gestation, she presented to the hospital in active labor. On admission, her vital signs were stable, and laboratory findings were within normal range. She had an uncomplicated spontaneous vaginal delivery of a 6 lb, 1 oz girl. Her blood pressure remained within the normal range during hospitalization, and she was discharged to home on the third postpartum day. On postpartum day 7, she was brought into the emergency department by ambulance unresponsive. She had been found on the floor by her husband, who reported that she appeared to have suffered a seizure and then became
Address correspondence to Ijeoma Azonobi, MD, Duke University Medical Center, Department of OB/GYN, Box 3616 Med Cr, Durham, NC 27710. E-mail: [email protected]
Journal of Midwifery & Women’s Health • www.jmwh.org © 2006 by the American College of Nurse-Midwives Issued by Elsevier Inc.
unconscious. Vital signs on admission were temperature 97.0°F, pulse 115 bpm, blood pressure 138/67 mm Hg, and Sp O2 96%. Laboratory findings revealed normal chemistry, including negative drug screen and normal liver enzyme levels. Complete blood count revealed a WBC of 23.3 ⫻ 1000/cu mm, hemoglobin and hematocrit of 15.6 g/dL, and 46.1%, respectively, and platelets 415 ⫻ 1000/cu mm. She exhibited no proteinuria. ECG, chest x-ray, and CT scan of the brain were all normal. Magnesium sulfate and anticonvulsives were administered. When she regained consciousness, she had amnesia and was unable to recall any symptoms prior to the incident. Later, the patient did recall having a headache that entire day, which was not relieved by ibuprofen or other over-the-counter analgesics. She remained hospitalized for 3 days. Her blood pressure values remained stable, and she was discharged to home without a prescription for medication. Her final diagnosis was postpartum eclampsia. DISCUSSION Hypertensive disorders are the second leading cause of maternal mortality and the most common medical complication in pregnancy.1,2 Preeclampsia and eclampsia are forms of hypertension unique to human pregnancy. The incidence of preeclampsia ranges between 3% and 7% in nulliparas women and between 0.8% and 5.0% in multiparas.1 The so-called “classic triad” of preeclampsia includes hypertension, proteinuria, and edema. However, there is now universal agreement that edema should not be considered when making the diagnosis of preeclampsia.1 The guidelines for the diagnosis of preeclampsia accepted by the American College of Obstetricians and Gynecologists include a blood pressure of 140 mm Hg or greater systolic or 90 mm Hg or greater diastolic in a previously normotensive woman and proteinuria of 0.3 g in a 24-hour urine specimen.3 51 1526-9523/06/$32.00 • doi:10.1016/j.jmwh.2005.06.009
Eclampsia is the occurrence of seizures or coma in addition to proteinuria and hypertension. This disorder is even more rare, complicating approximately 3 in 1000 pregnancies, but higher incidences are observed in lower socioeconomic groups, women with multiple gestations, nulliparous women less than 20 years old, and multiparous women greater than 35 years of age.1,4 Most episodes of eclampsia occur between 20 weeks’ gestation and less than 48 hours postpartum, with approximately 50% occurring antepartum, 25% intrapartum, and 25% postpartum.1 Whether true eclamptic seizures can occur later than 48 hours has been the subject of much controversy, but it is now believed that this phenomenon does, in fact, exist. Lubarsky et al. reported that 16% of all postpartum eclampsia fall into the category of late postpartum eclampsia.5 Since that 1994 report, additional research on the incidence of these phenomena has been conducted. Chames et al. performed a 5-year, multicenter data analysis of 89 eclamptic patients to determine the timing of eclampsia in relation to delivery. This study demonstrated that 67.4% had convulsions before or during delivery, whereas 32.6% were diagnosed with postpartum eclampsia. Of those, 20.7% occurred 48 hours or less after delivery, and 79.3% occurred 48 hours or more after delivery.6 Further studies indicate that the incidence of postpartum eclampsia ranges from 11% to 44%, and that 5% to 26% of all cases of eclampsia will occur after 48 hours postpartum.7 It was noted in initial reports of case studies that late postpartum eclampsia does not always present in the manner of typical eclampsia because proteinuria and hypertension may not be detected in the patient during the antepartum evaluation.5,8 Several case reports have described women without a history of elevated blood pressures or proteinuria during their prenatal course who ultimately are diagnosed with late postpartum eclampsia.4,8 –10 In a study of 151 women without a history of gestational hypertension, who were diagnosed postpartum with preeclampsia, 11% became eclamptic.2 This is a phenomenon referred to as “eclampsia without preeclampsia.”8 Instead, these patients are more likely to present with headaches (87%), visual changes (44%), nausea or vomiting (22%), or epigastric pain (9%) prior to seizure.4,6,8 It has been noted in previous studies that many women who experienced late postpartum eclampsia also experienced these atypical symptoms but do not report these symptoms to their health care providers.2 Treatment for late postpartum eclampsia is similar to that of eclampsia, with the exception of the definitive treatment
of delivery of the infant. Traditionally, first-line treatment for eclamptic seizures is magnesium sulfate, although benzodiazepines and phenytoin may be used as well. Although hypertension usually resolves with the cessation of seizures, if they persist, both hydralazine and labetalol have been used successfully to control eclampsia-induced hypertension. Consultation with a neurologist may be required because women with late postpartum eclampsia may display the characteristic pattern of cerebral edema on imaging studies. Cerebral edema reverses with the resolution of symptoms. In summary, late-onset postpartum eclampsia is a disorder that is difficult to detect or prevent. It is important that health care providers take a role in improving patient education to increase the ability to swiftly diagnose and treat this condition. Two important factors play a role in our ability to prevent the occurrence of eclampsia in the postpartum period. First, in a case like the one presented here, women may not be aware of the need to report symptoms of headache or vision changes in the postpartum period. Second, because the signs and symptoms mirror those of fatigue and anxiety normal in the postpartum period, patients may tend to devalue their significance. Therefore, it is incumbent upon health care providers to appropriately educate patients before being discharged from care in the early postpartum period. We recommend the following precautions to assist in the prevention of this disorder and increase patient awareness: 1. Discharge instructions should be revised to include the immediate reporting of headache, vision changes, and abdominal pain. 2. All providers involved in the discharge process should be made aware of late postpartum eclampsia through an in-service process. This is very important because providers who do not know the signs or symptoms of late postpartum eclampsia may not give the appropriate instructions at discharge and may misinform a patient who calls back with symptoms. 3. Patients should be instructed to call immediately when symptoms occur. We thank the faculty and staff of the Primary Care Faculty Development Program at the Morehouse School of Medicine for their educational support that ultimately spurred the development of this article, and whose advice was crucial to its completion.
REFERENCES Ijeoma Azonobi, MD, received her medical degree from Morehouse School of Medicine in May 2005. She has begun a residency program in obstetrics and gynecology. Helen McBride-Richter, CNM, MSN, is currently in private practice. Loretta Patrick, RN, JD, received her nursing degree from Purdue University and her law degree from Georgia State University College of Law.
52
1. Sibai BM. Hypertension in pregnancy. In Gabbe Obstetrics— Normal and problem pregnancies, 4th ed. New York: Churchill Livingstone, 2002:950 – 83. 2. Matthys LA, Coppage KH, Lambers DS, Barton JR, Sibai BM. Delayed postpartum pre-eclampsia: An experience of 151 cases. Am J Obstet Gynecol 2004;190:1464 – 6.
Volume 51, No. 1, January/February 2006
3. ACOG Practice Bulletin. Diagnosis and management of preeclampsia and eclampsia. Obstet Gynecol 2002;99:159 – 65.
7. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol 2002;105:402–10.
4. Martin J, Sidman R. Late postpartum eclampsia: A common presentation of an uncommon diagnosis. J Emerg Med 2002;25:387– 90.
8. Veltkamp R, Kupsch A, Polasek, Yousry TA, Pfister HW. Late onset postpartum eclampsia without pre-eclamptic prodromi: Clinical and neuroradiological presentation in two patients. J Neurol Neurosurg Psychiatry 2000;69:824 –7.
5. Lubarsky SL, Barton JR, Friedman SA, Nasreddine S, Ramadan MK, Sibai BM. Late postpartum eclampsia revisited. Obstet Gynecol 1994;83:502– 4.
9. Dziewas R, Stogbauer F, Freund M, Ludemann P, Imai T, Holzapfel C, Ringelstein PB. Late onset postpartum eclampsia: a rare and difficult diagnosis. J Neurol 2002;249:1287–91.
6. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: A preventable disease? Am J Obstet Gynecol 2002;186:1174 –7.
10. Graeber B, Vanderwal T, Stiller RJ, Werdmann MJ. Late postpartum eclampsia as an obstetric complication seen in the ED. Am J Emerg Med 2005;23:168 –70.
Journal of Midwifery & Women’s Health • www.jmwh.org
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