Eclampsia (Nursing)


Learning Outcome

This activity discusses preeclampsia and eclampsia, one of the four categories of hypertensive disorders of pregnancy. Eclampsia is a severe complication of preeclampsia and poses both a risk to the mother and fetus. Eclampsia is a disease process that needs to be emergently identified and treated promptly. This article reviews the topic of eclampsia and specifically focuses on etiology, epidemiology, pathophysiology, history and physical, evaluation and management of eclampsia by an interprofessional team.

Introduction

Hypertensive disorders of pregnancy are a heterogeneous group of conditions that include chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed on chronic hypertension.[1] Hypertension in pregnancy is defined as a systolic BP of 140 mm Hg and a diastolic BP of 90 mm Hg on two separate measurements at least 4–6 hours apart.[2] Diagnose women who develop hypertension after 20 weeks' gestation and who do not have proteinuria or other criteria for preeclampsia with gestational hypertension. Preeclampsia is a multiorgan disease process characterized by hypertension and proteinuria or one of the following features, which are diagnostic when they develop in the setting of new-onset hypertension after 20 weeks' gestation.

Preeclampsia is a multiorgan disease process characterized by new-onset elevated blood pressure and proteinuria or one of its severe features after 20 weeks' gestation.[3] Eclampsia is preeclampsia complicated by generalized tonic-clonic convulsions. [4] The progression of preeclampsia to eclampsia is sudden and without prediction.[5] The onset of eclamptic convulsions can be antepartum (38% to 53%), intrapartum (18% to 36%), or postpartum (11% to 44%).[6]

Onset is by definition after 20 weeks and although delivery usually resolves the condition, symptoms can present as late as 4-6 weeks postpartum.

Patients who meet the criteria for preeclampsia are at an increased risk of cerebral edema, stroke, pulmonary edema, disseminated intravascular coagulation, liver failure, and renal failure. Fetal risks include intrauterine demise, neonatal demise, placental abruption, prematurity, ischemic encephalopathy, and intrauterine growth restriction.

Nursing Diagnosis

  • Deficient fluid volume
  • Decreased cardiac output
  • Risk for maternal injury
  • Altered tissue perfusion (uteroplacental)
  • Risk for imbalanced nutrition: less than body requirements
  • Deficient knowledge

Causes

The exact cause of preeclampsia is still unknown, although is thought to be due to widespread vascular endothelial malfunction and vasospasm.

Risk Factors

Hypertensive disorders affect as many as 10% of all pregnancies worldwide.[1][7]These disorders account for a significant proportion of perinatal morbidity and mortality, nearly 10% of all maternal deaths in the United States.[1] Preeclampsia is one of the most serious pregnancy-specific medical conditions of increasing incidence. It remains a major cause of maternal and fetal morbidity and mortality.[8] The risk of preeclampsia is increased in women with a previous history of preeclampsia (particularly if severe or before 32 weeks' gestation)and in those with antiphospholipid antibodies, pre-existing diabetes mellitus, multiple gestation, nulliparity, family history of preeclampsia (first-generation relative), elevated body mass index, maternal age greater than 40 years, and chronic hypertension or renal disease.[3] Women with a history of eclampsia are at increased risk of eclampsia (1% to 2%) and preeclampsia (22% to 35%) in subsequent pregnancies.[6]

Although eclampsia is uncommon in developed countries, it is still a major cause of maternal morbidity and mortality worldwide.[4]

Eclampsia is defined as preeclampsia complicated by generalized tonic-clonic convulsions [4] that occurs in 0.5% of patients with mild preeclampsia, and 2% to 3% of those with severe preeclampsia.[2]

Assessment

Eclamptic seizures are a life-threatening emergency and can occur antepartum (53%), intrapartum (19%), or postpartum (28%). It may be preceded by central nervous system symptoms such as headache (80%) and visual changes (45%). However, seizures can occur without other severe features of preeclampsia and with a normal BP; 15% of women with eclampsia have a diastolic BP less than 90 mm Hg. Eclamptic seizures are usually generalized tonic-clonic 60- to 90-second seizures. Postictal confusion, agitation, or combativeness may follow.[3] 

The diagnosis of pre-eclampsia is made during routine screening at prenatal appointments as the condition is generally asymptomatic until severe features are present. Hypertension is defined as SBP>140 or DBP>90 on two separate readings. I should screen all women with hypertension during pregnancy for proteinuria it defines which as a 24hr urine protein measurement >0.3g, a protein to creatinine ratio >0.3, or a positive urine protein dipstick of >1+. Generalized edema was once considered the third diagnostic criteria but has now been removed.

Other than early detection of preeclampsia, there are no reliable tests or symptoms for predicting the development of eclampsia.[6]

Evaluation

Diagnosis of preeclampsia requires a systolic BP of at least 140 mm Hg or a diastolic BP of at least 90 mm Hg on at least two occasions, taken at least four hours apart, plus new-onset proteinuria or a severe feature. 

A single severe feature, in combination with hypertension, is sufficient for the diagnosis. Proteinuria is not essential for diagnosis if a severe feature is present. Severe features of preeclampsia include a systolic blood pressure of at least 160 mm Hg or a diastolic blood pressure of at least 110 mm Hg, platelet count less than 100 × 10^3 per microL, liver transaminase levels two times the upper limit of normal, a doubling of the serum creatinine level or level greater than 1.1 mg per dL, severe persistent right upper quadrant pain, pulmonary edema, or new-onset cerebral or visual disturbances.[3]

Medical Management

Regarding eclampsia, the drug of choice for prevention and management is magnesium sulfate. This drug reduces the risk of seizures in patients with severe preeclampsia.[9]

 Magnesium sulfate is the drug of choice for reducing the rate of eclampsia developing intrapartum and immediately postpartum.[6]

The goal of treatment is to prevent significant cerebrovascular and cardiovascular events in the mother without compromising fetal well-being.[2] 

If a woman is at greater than 34 weeks gestation and develops severe preeclampsia, delivery is still the treatment of choice, while expectant management may be reasonable in those with mild preeclampsia. At greater than 36 to 37 weeks gestation, the induction of labor should be pursued.[2]

The primary objective of magnesium sulfate prophylaxis in women with preeclampsia is to prevent or reduce the rate of eclampsia and complications associated with eclampsia.[10]

The overall management of preeclampsia includes supportive treatment with antihypertensives and anti-epileptics until definitive treatment - delivery. In preeclampsia without severe features, patients are often induced after 37 weeks gestation after with or without corticosteroids to accelerate lung maturity. These patients are monitored more closely with antenatal testing twice a week. If severe features are present, induction is considered as early as 34 weeks, although the benefits must outweigh the risks of preterm delivery. Patients with severe features are admitted and monitored on bed rest until delivery.First-line antihypertensives for preeclampsia/eclampsia include hydralazine, labetalol, and nicardipine.

  • Hydralazine: The recommended dose of hydralazine hydrochloride is 5-10 mg (IV/IM) given every 15 minutes up to a dose of 20 mg IV (or 30 mg IM). If no change in pressure after 20 minutes, should think about another agent.
  • Labetalol: Recommended initial dose of labetalol hydrochloride is 20 mg, slow injection. May be preferred because of a lack of reflex tachycardia and hypotension (if pushed slow), or increased intracranial pressure. Be cautious if a patient has a history of a previous myocardial disease or preexisting congestive heart failure or asthma.
  • Nicardipine: Nicardipine can cause less reflex tachycardia than nifedipine. Recommended initial rate is 5mg/hour and can be adjusted by 2.5 mg/hour every 5 minutes until the reduction of MAP of 15% has been achieved, or a maximum dose of 15 mg/hour has been reached. (*)

Medications are titrated to an average BP of 140/90. Seizures are treated with IV magnesium as a loading dose of 4 g over 5 to 10 minutes, followed by an infusion of 1g/hr maintained for 24 hours after the last seizure. Lorazepam and phenytoin may be used as second-line agents but are avoided due to fetal effects. Other supportive measures include sparing use of diuretics and fluid restriction to avoid pulmonary and cerebral edema.

Nursing Management

  • Monitor blood pressure.
  • Assess fetal heart rate.
  • Send blood and urine for testing.
  • Administer prescribed medications.
  • Monitor reflexes on patients on magnesium sulfate.
  • Neurologic checks regularly.
  • Seizure precautions if ordered.

When To Seek Help

  • Seizure
  • An altered state of consciousness
  • Blood pressure greater than 180/110 mmHg
  • Decreased urine output

Outcome Identification

Goal Outcomes

  • Delivery of a healthy neonate.
  • Discharge of mother and baby home.

Adverse Outcomes

  • Prolonged unconsciousness
  • Acute renal failure
  • Cerebrovascular accident
  • HELLP syndrome
  • Pulmonary edema
  • Pneumonia
  • Coagulopathy
  • Abruptio placenta
  • Cortical blindness
  • Cardiomegaly
  • Vesicovaginal fistula
  • Death

Monitoring

  • Blood pressure and heart rate
  • Urine protein
  • Fetal heart rate
  • Oxygen saturation
  • Liver function tests and CBCs
  • Neurologic checks

Coordination of Care

Eclampsia is a medical condition that requires prompt diagnosis and treatment to prevent morbidity and mortality in pregnant women. The health care team must work efficiently together to provide optimal care to both the mother and the unborn child. Nurses or providers triaging patients in the emergency department need to be cognizant of signs and symptoms of eclampsia. They must notify the attending physicians treating the patient as quickly as possible, especially if they are actively seizing and require medication to abort the seizure. The communication between nursing and physicians is vital to ensure that the patients are getting proper intervention. Communication is also important between emergency physicians and obstetricians as the delivery of the fetus may be emergent. Pharmacists review the dosage of medications and check for drug-drug interactions. Ultimately, care must be patient-centered.

Health Teaching and Health Promotion

Patients diagnosed with hypertension or preeclampsia during pregnancy, as well as their family members, need to be educated on the signs and symptoms of eclampsia. They need to be instructed to call emergency services immediately and should bring the patient to the hospital as soon as possible. Patients should be counseled about the importance of their hypertensive medication and should regularly follow up with their obstetrician.

Discharge Planning

Patients should be counseled about the importance of their hypertensive medication and should regularly follow up with their obstetrician.

Pearls and Other issues

Hypertensive disorders of pregnancy result in a substantial health burden, accounting fora large proportion of maternal and neonatal morbidity and mortality. Strategies to prevent preeclampsia include the identification of high-risk patients and the initiation of low-dose aspirin in early gestation.[1]


Details

Nurse Editor

Lisa M. Haddad

Updated:

1/30/2023 4:29:07 PM

References

[1]

Wilkerson RG,Ogunbodede AC, Hypertensive Disorders of Pregnancy. Emergency medicine clinics of North America. 2019 May;     [PubMed PMID: 30940374]

[2]

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[3]

Leeman L,Dresang LT,Fontaine P, Hypertensive Disorders of Pregnancy. American family physician. 2016 Jan 15     [PubMed PMID: 26926408]

[4]

Bergman L,Torres-Vergara P,Penny J,Wikström J,Nelander M,Leon J,Tolcher M,Roberts JM,Wikström AK,Escudero C, Investigating Maternal Brain Alterations in Preeclampsia: the Need for a Multidisciplinary Effort. Current hypertension reports. 2019 Aug 2;     [PubMed PMID: 31375930]

[5]

Uzan J,Carbonnel M,Piconne O,Asmar R,Ayoubi JM, Pre-eclampsia: pathophysiology, diagnosis, and management. Vascular health and risk management. 2011;     [PubMed PMID: 21822394]

[6]

Burton GJ,Redman CW,Roberts JM,Moffett A, Pre-eclampsia: pathophysiology and clinical implications. BMJ (Clinical research ed.). 2019 Jul 15;     [PubMed PMID: 31307997]

[7]

Waters J, Management of Myasthenia Gravis in Pregnancy. Neurologic clinics. 2019 Feb;     [PubMed PMID: 30470270]

[8]

Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstetrics and gynecology. 2013 Nov;     [PubMed PMID: 24150027]

[9]

Arulkumaran N,Lightstone L, Severe pre-eclampsia and hypertensive crises. Best practice     [PubMed PMID: 23962474]

[10]

Sesar A,Cavar I,Sesar AP,Sesar I, Transient cortical blindness in posterior reversible encephalopathy syndrome after postpartum eclampsia. Taiwan journal of ophthalmology. 2018 Apr-Jun;     [PubMed PMID: 30038892]

[11]

Amaral LM,Cunningham MW Jr,Cornelius DC,LaMarca B, Preeclampsia: long-term consequences for vascular health. Vascular health and risk management. 2015;     [PubMed PMID: 26203257]