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Clinical Reviews


Managing an eclamptic patient

Most Ob/Gyns have little experience managing acute eclampsia, but all maternity units and obstetricians need to be prepared to diagnose and manage this grave threat.

May 2005 · Vol. 17, No. 5

An eclamptic convulsion is frightening to behold. First, the woman’s face becomes distorted, and her eyes protrude. Then her face acquires a congested expression, and foam may exude from her mouth. Breathing stops.

Because eclampsia is so frightening, the natural tendency is to try to stop a convulsion, but this is not the wisest strategy.

Rather, the foremost priorities are to avoid maternal injury and support cardiovascular functions. How to do this, and how to prevent further convulsions, monitor and deliver the fetus, and avert complications are the focus of this article.

Since eclampsia may be fatal for both mother and fetus, all labor and delivery units and all obstetricians should be prepared to diagnose and manage this grave threat. However, few obstetric units encounter more than 1 or 2 cases a year; most obstetricians have little or no experience managing acute eclampsia. In the Western world, it affects only 1 in 2,000 to 1 in 3,448 pregnancies. 1-4

How a convulsion happens

Most convulsions occur in 2 phases and last for 60 to 75 seconds. The first phase, lasting 15 to 20 seconds, begins with facial twitching, soon followed by a rigid body with generalized muscular contractions.

In the second phase, which lasts about a minute, the muscles of the body alternately contract and relax in rapid succession. This phase begins with the muscles of the jaw and rapidly encompasses eyelids, other facial muscles, and body. If the tongue is unprotected, the woman often bites it.

Coma sometimes follows the convulsion, and deep, rapid breathing usually begins as soon as the convulsion stops. In fact, maintaining oxygenation typically is not a problem after a single convulsion, and the risk of aspiration is low in a well managed patient.

Upon reviving, the woman typically remembers nothing about the seizure.

If convulsions recur, some degree of consciousness returns after each one, although the woman may become combative, agitated, and difficult to control.

Harbingers of complications

In the developed world, eclampsia increases the risk of maternal death (range: 0 to 1.8%).1-5 A recent review of all reported pregnancy-related deaths in the United States from 1979 to 1992 found 4,024 cases. 6 Of these, 790 (19.6%) were due to preeclampsia-eclampsia, 49% of which were caused by eclampsia. The risk of death from preeclampsia or eclampsia was higher for the following groups:

  • women over 30,
  • no prenatal care,
  • African Americans, and
  • onset of preeclampsia or eclampsia before 28 weeks.6

Maternal morbidity

Pregnancies complicated by eclampsia also have higher rates of maternal morbidity such as pulmonary edema and HELLP syndrome (TABLE 1). Complications are substantially higher among women who develop antepartum eclampsia, especially when it is remote from term.1-3

TABLE 1

Maternal complications

Antepartum eclampsia, especially when it is remote from term, is much more likely to lead to complications

COMPLICATION

RATE (%)

REMARKS

Death

0.5-–2

Risk of death is higher:

  • Older than 30 years of age
  • No prenatal care
  • African Americans
  • Onset of preeclampsia or eclampsia before 28 weeks’ gestation

Intracerebral hemorrhage

<1

Usually related to several risk factors

Aspiration pneumonia

2–3

Heightened risk of maternal hypoxemia and acidosis

Disseminated coagulopathy

3–5

Regional anesthesia is contraindicated in these patients, and there is a heightened risk of hemorrhagic shock

Pulmonary edema

3–5

Heightened risk of maternal hypoxemia and acidosis

Acute renal failure

5–9

Usually seen in association with abruptio placentae, maternal hemorrhage, and prolonged maternal hypotension

Abruptio placentae

7–10

Can occur after a convulsion; suspect it if fetal bradycardia or late decelerations persist

HELLP syndrome

10–15

 

Adverse perinatal outcomes

Perinatal mortality and morbidity are high in eclampsia, with a perinatal death rate in recent series of 5.6% to 11.8%.1,7 This high rate is related to prematurity, abruptio placentae, and severe growth restriction.1

Preterm deliveries occur in approximately 50% of cases, and about 25% occur before 32 weeks’ gestation.1

Diagnosis can be tricky

When the patient has generalized edema, hypertension, proteinuria, and convulsions, diagnosis of eclampsia is straightforward. Unfortunately, women with eclampsia exhibit a broad spectrum of signs, ranging from severe hypertension, severe proteinuria, and generalized edema, to absent or minimal hypertension, nonexistent proteinuria, and no edema (TABLE 2).1

Hypertension is the hallmark of diagnosis. Hypertension is severe (at least 160 mm Hg systolic and/or at least 110 mm Hg diastolic) in 20% to 54% of cases, and it is mild (systolic pressure between 140 and 160 mm Hg or diastolic pressure between 90 and 110 mm Hg) in 30% to 60% of cases.2,3 In 16% of cases, there may be no hypertension at all.2

Proteinuria. Eclampsia usually is associated with proteinuria (at least 1+ on dipstick).1 However, when I studied a series of 399 women with eclampsia, I found substantial proteinuria (3+ or above on dipstick) in only 48% of cases; proteinuria was absent in 14%.2

Edema. A weight gain of more than 2 lb per week (with or without clinical edema) during the third trimester may be the first sign of eclampsia. However, in my series of 399 women, edema was absent in 26% of cases.2

TABLE 2

Signs and symptoms of eclampsia*

Hypertension and proteinuria in eclampsia may be severe, mild, or even absent

CONDITION

FREQUENCY (%) IN WOMEN WITH ECLAMPSIA

REMARKS

SIGNS

Hypertension

85

Should be documented on at least 2 occasions more than 6 hours apart

  Severe: 160/110 mm Hg or more

20–54

  Mild: 140–160/90–110 mm Hg

30–60

No hypertension2

16

Proteinuria

85

 

  At least 1+ on dipstick2

48

  At least 3+ on dipstick

14

No proteinuria

15

SYMPTOMS

At least 1 of the following:

33–75

Clinical symptoms may occur before or after a convulsion

Headache

30–70

Persistent, occipital, or frontal

Right upper quadrant or epigastric pain

12–20

 

Visual changes

19–32

Blurred vision, photophobia

Altered mental changes

4–5

 

* Summary of 5 series

Symptoms of eclampsia

Several clinical symptoms can occur before or after a convulsion1:

  • persistent occipital or frontal headaches,
  • blurred vision,
  • photophobia,
  • epigastric and/or right upper quadrant pain, and
  • altered mental status.

Usual times of onset

Eclamptic convulsions can occur during pregnancy or delivery, or after delivery ( TABLE 3).1-5

Approximately 91% of antepartum cases develop at 28 weeks or beyond. The remaining cases tend to occur between 21 and 27 weeks’ gestation (7.5%), or at or before 20 weeks (1.5%).2

When eclampsia occurs before 20 weeks, it usually involves molar or hydropic degeneration of the placenta, with or without a fetus.1 However, eclampsia can occur in the first half of pregnancy without molar degeneration of the placenta, although this is rare.1,2 These women are sometimes misdiagnosed as having hypertensive encephalopathy, seizure disorder, or thrombotic thrombocytopenia purpura. Thus, women who develop convulsions in association with hypertension and proteinuria in the first half of pregnancy should be assumed to have eclampsia until proven otherwise,1 and require ultrasound examination of the uterus to rule out molar pregnancy and/or hydropic or cystic degeneration of the placenta.

Postpartum cases tend to occur within the first 48 hours, although some develop beyond this limit and have been reported as late as 23 days postpartum.8

Late postpartum eclampsia occurs more than 48 hours but less than 4 weeks after delivery.8 These women have signs and symptoms consistent with preeclampsia along with their convulsions.8,9 Thus, women who develop convulsions with hypertension and/or proteinuria, or with headaches or blurred vision, after 48 hours postpartum should be assumed to have eclampsia and treated accordingly.8,9

When eclampsia occurs especially late, perform an extensive neurologic examination to rule out other cerebral pathology.1,10

Eclampsia is atypical if convulsions occur before 20 weeks’ gestation or beyond 48 hours postpartum. It also is atypical if convulsions develop or persist despite adequate magnesium sulfate, or if the patient develops focal neurologic deficits, disorientation, blindness, or coma. In these cases, conduct a neurologic exam and cerebral imaging to exclude neurologic pathology.8-10

TABLE 3

Usual times of onset*

91% of antepartum eclampsia cases occur at 28 weeks or later, although eclamptic convulsions can occur at any time during pregnancy or delivery, or postpartum

ONSET

FREQUENCY (%)

REMARKS

Antepartum

38–53

Maternal and perinatal mortality, and the incidence of complications and underlying disease, are higher in antepartum eclampsia, especially in early cases

  ≤20 weeks

1.5

  21 to 27 weeks

7.5

  ≥28 weeks

91

Intrapartum

18–36

Intrapartum eclampsia more closely resembles postpartum disease than antepartum cases

Postpartum

11–44

Late postpartum eclampsia occurs more than 48 hours but less than 4 weeks after delivery

  ≤48 hours

7–39

  >48 hours

5–26

* Summary of 5 series

Differential diagnosis

As with other aspects of preeclampsia, the presenting symptoms, clinical findings, and many laboratory results in eclampsia overlap several other medical and surgical conditions.1,10 Of course, eclampsia is the most common cause of convulsions in a woman with hypertension and/or proteinuria during pregnancy or immediately postpartum. On rare occasions, other causes of convulsions in pregnancy or postpartum may mimic eclampsia.1 These potential diagnoses are particularly important when the woman has focal neurologic deficits, prolonged coma, or atypical eclampsia.

The differential diagnosis encompasses a variety of cerebrovascular and metabolic disorders:

  • hemorrhage,
  • ruptured aneurysm or malformation,
  • arterial embolism, thrombosis,
  • venous thrombosis,
  • hypoxic ischemic encephalopathy,
  • angiomas,
  • hypertensive encephalopathy,
  • seizure disorder,
  • hypoglycemia, hyponatremia,
  • posterior leukoencephalopathy syndrome,
  • thrombotic thrombocytopenic purpura,
  • postdural puncture syndrome, and
  • cerebral vasculitis/angiopathy.

Other diseases may factor in

Some women develop gestational hypertension or preeclampsia in association with connective tissue disease, thrombophilias, seizure disorder, or hypertensive encephalopathy, further confounding the diagnosis.

Thus, make every effort to ensure a correct diagnosis, since management may differ among these conditions.

Managing convulsions

Do not try to stop the first convulsion

The natural tendency is to try and interrupt the convulsion, but this is not recommended. Nor should you give a drug such as diazepam to shorten or stop the convulsion, especially if the patient lacks an intravenous line and no one skilled in intubation is immediately available. If diazepam is given, do not exceed 5 mg over 60 seconds. Rapid administration of this drug may lead to apnea or cardiac arrest, or both.

Steps to prevent maternal injury

During or immediately after the acute convulsive episode, take steps to prevent serious maternal injury and aspiration, assess and establish airway patency, and ensure maternal oxygenation (TABLE 4).

Elevate and pad the bed’s side rails and insert a padded tongue blade between the patient’s teeth, taking care not to trigger the gag reflex.

Physical restraints also may be needed.

Prevent aspiration. To minimize the risk of aspiration, place the patient in the lateral decubitus position, and suction vomitus and oral secretions as needed. Be aware that aspiration can occur when the padded tongue blade is forced to the back of the throat, stimulating the gag reflex and resultant vomiting.

TABLE 4

During a convulsion, 3 spheres of concern

AVOID MATERNAL INJURY

Insert padded tongue blade

  Avoid inducing gag reflex

Elevate padded bedside rails

Use physical restraints as needed

MAINTAIN OXYGENATION TO MOTHER AND FETUS

Apply face mask with or without oxygen reservoir at 8–10 L/minute

Monitor oxygenation and metabolic status via

  Transcutaneous pulse oximetry

  Arterial blood gases (sodium bicarbonate administered accordingly)

Correct oxygenation and metabolic status before administering anesthetics that may depress myocardial function

MINIMIZE ASPIRATION

Place patient in lateral decubitus position (which also maximizes uterine blood flow and venous return)

Suction vomitus and oral secretions

Obtain chest x-ray after the convulsion is controlled to rule out aspiration

Tips on supplemental oxygenation

Although the initial seizure lasts only a minute or 2, it is important to maintain oxygenation by giving supplemental oxygen via a face mask, with or without an oxygen reservoir, at 8 to 10 L per minute. This is important because hypoventilation and respiratory acidosis often occur.

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