Eclampsia Case File

Eclampsia Case File

Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 35

An 18-year-old G1P0 woman at 34 weeks' gestation comes into the obstetrical triage unit complaining of a severe headache. She states that  bright lights are bothersome to her. Her prenatal history is unremarkable. Her blood pressures in the first trimester were in the 100/60 mm Hg range. On examination, her blood pressure (BP) is 180/105 mm Hg, heart rate (HR)  98 beats/minute, temperature 98.4°F, and respiratory rate (RR) 12/minute. Her heart and lung examinations are normal. The abdomen is nontender, and the fundal height is 27 cm. The fetal heart tones are in the 135 beats/minute range with occasional variable decelerations on external fetal monitoring. There are no uterine contractions. The vaginal examination  reveals that the cervix is closed, long, and posterior. During your examination,  you notice that she has some facial twitching and now is undergoing a tonic-clonic seizure involving both upper and lower extremities.

⯈What is the most likely diagnosis? 

⯈What are your next steps?

⯈What are the important considerations in managing her condition?

ANSWER TO CASE 35:

Eclampsia

Summary: An 18-year-old G1P0 female at 34 weeks' gestation complains of a severe headache and photophobia. Her BP is 180/105 mm Hg, and her fundal height is 27 cm. The fetal heart tones are in the 135 beats/minute range with occasional variable decelerations without contractions. The cervix is unfavorable. During your examination, you notice that she has some facial twitching, and now she is undergoing a tonic-clonic seizure involving both upper and lower extremities.

• Most likely diagnosis: Eclampsia. Other diagnoses to consider include epilepsy, drug intoxication, drug withdrawal, alcohol withdrawal, and CNS abnormalities including cerebral infarction, cerebral hemorrhage, venous thrombosis, head trauma, infections, neoplasms, and metabolic disorders.

• Your next steps: (1) Maintenance of airway patency, (2) prevention of aspiration via rolling the mother to her left side and elevating the head of the bed, (3) supplemental oxygen (8-10 L/min) via face mask during convulsive episode, (4) obtain IV access, (5) administer magnesium sulfate intravenously or intramuscularly, (6) constant monitoring of respiratory rate, pulse, and blood pressure, and (7) call obstetrician for delivery.

• Important considerations in managing her condition: The most important goal when managing a patient with eclampsia is to stabilize the mother.

Fetal bradycardia and/or decelerations in heart rate can occur during the seizure episode. Both generally resolve with cessation of eclamptic event.

ANALYSIS

Objectives

1. To list the hypertensive disorders of pregnancy.
2. To describe eclampsia and prioritize the management.
3. To describe the treatment of eclampsia.
4. To describe the common complications of preeclampsia.

Considerations

This 18-year-old pregnant patient presented with hypertension with a blood pressure of 180/105 mm Hg, headache, and photophobia, all of which are concerning for severe preeclampsia. Because she proceeds with a generalized tonic-clinic seizure, she now has progressed to eclampsia, which appreciably increases the risk to both the mother and the fetus.

• Her blood pressure will need to be controlled, and an obstetrician should be called, but first she must be stabilized and given magnesium sulfate to prevent further seizures.

• Eclamptic seizures may be violent; therefore this patient must be protected. Considering she just had a generalized tonic-clonic seizure, she is likely to become motionless and confused due to the post-ictal state that follows seizures. In some eclamptic patients, a coma of variable durations may ensue. Because eclamptic patients can become combative after a seizure or they may have another seizure, the railings of her bed should be raised and padding placed on the head board and rails. A padded tongue blade may be carefully inserted into her mouth to prevent biting the tongue, but should not cause a gag reflex or injure the teeth. Physical restraints should not be used.

• To prevent hypoxia to her and her baby, she needs supplemental oxygen via a face mask. Her vital signs should be frequently assessed, as well as urine output, proteinuria, and peripheral edema.

• To prevent further seizures and associated comorbidities, IV magnesium sulfate should be initiated. Treatment includes a loading dose of 6 g of magnesium sulfate over 15 minutes, followed by 2 to 3 g/h administered continuously. Since magnesium sulfate has a narrow therapeutic index of 2 to 3 .5 mmol/L, the patient must be monitored for hyporeflexia and respiratory depression. Because convulsions often continue during labor and delivery, as well as postpartum, the magnesium should be continued for 24 hours postpartum. In the event of status epilepticus that is resistant to magnesium sulfate, she should be intubated and deeply sedated.

• Along with controlling the seizures, the blood pressure should also be controlled with hydralazine or labetalol with a goal systolic blood pressure <160 mm Hg and diastolic blood pressure <100 mm Hg. Additionally, the hemoglobin, platelets, serum creatinine, liver enzymes, and lactate dehydrogenase should be monitored for ensuing HELLP syndrome (hemlysis, elevate liver enzymes, and low platelets).

• The only curative treatment for eclampsia is delivery of the fetus. Once the mother is stabilized, vaginal delivery is initially pursued to avoid maternal risks from cesarean delivery.

• The patient's fundal height of 27 cm signifies that the fetus is small for gestational age, which is likely caused by deficiency in uteroplacental blood flow secondary to her hypertension. The fetus is at risk of intrauterine growth retardation and adverse fetal events, so regular surveillance is used for careful monitoring.

Approach To:

Hypertensive Disease in Pregnancy

DEFINITIONS

CHRONIC HYPERTENSION: Blood pressure >40/90 mm Hg before pregnancy or diagnosed before 20 weeks' gestation not attributable to gestational trophoblastic disease o r hypertension first diagnosed after 20 weeks' gestation and persistent after 12 weeks postpartum.

ECLAMPSIA: The development of grand mal seizures in pregnancy that are not related to a preexisting condition.

GESTATIONAL HYPERTENSION: New-onset hypertension >140/90 mm Hg after the 20th week of gestation without the development of proteinuria, and associated with normal blood pressure within 12 weeks postpartum.

HELLP SYNDROME: Hemolytic anemia, elevated liver enzymes, and low platelets.

MILD PREECLAMPSIA: The development of new-onset hypertension with BP >140/90 mm Hg and proteinuria that is >300 mg/24 h in the mother that occurs after the 20th week of gestation.

SEVERE GESTATIONAL HYPERTENSION: New-onset hypertension >160/105 mm Hg after the 20th week of gestation without the development of proteinuria, and associated with normal blood pressure within 12 weeks postpartum.

SEVERE PREECLAMPSIA: The development of new-onset hypertension with BP >160/110 mm Hg systolic, >5 g of urinary protein excretion per 24 hours, plus evidence of other organ system involvement such as impaired liver function, thrombocytopenia, oliguria (<500 mL in 24 hours) , pulmonary edema, epigastric or right upper quadrant pain, cerebral or visual disturbances, and/or fetal growth restriction.

SUPERIMPOSED PREECLAMPSIA ON CHRONIC HYPERTENSION: New-onset proteinuria >300 mg/24 h in a hypertensive woman but no proteinuria before 20 weeks gestation, or a sudden increase in proteinuria, blood pressure, or platelet count <100,000/μL in a woman with hypertension and proteinura before 20 weeks gestation

CLINICAL APPROACH

Epidemiology

The deadly triad of pregnancy consists of embolism, hypertensive disorders, and hemorrhage. These 3 complications contribute greatly to maternal morbidity and mortality rates with hypertensive disorders complicating 5 % to 10% of all pregnancies. Hypertensive disorders are the most dangerous and deadly complications of pregnancy. In the Western world, eclampsia ranges from 1 in 2000 to 1 in 3448 pregnancies and is higher in tertiary referral centers, in multifetal gestation, and in patients with no prenatal care. The onset of eclamptic convulsions in the antepartum period range from 38% to 53%, in the intrapartum period between 18% and 36%, and in the postpartum period from 11% to 44%.

Pathophysiology

The definitive pathophysiology of eclampsia is unknown but several investigations have implicated the placenta as the main cause. Likely, placental hypoperfusion secondary to abnormal modeling of the maternal-fetal interface is the key. Additionally, other factors such as maternal vasculature increased sensitivity to pressor agents lead to vasospasm (organ hypoperfusion) and capillary leakage (edema). Furthermore, activation of the coagulation cascade causes microthrombi that further aggravate perfusion. Though most patients remain asymptomatic, a myriad of complications may exist and involve multiple individual organ systems. Hypertension causes increased cardiac afterload, and the endothelium is injured with extravasation of intravascular fluid, leading to cardiac abnormalities, hemoconcentration, nondependent edema, and possible pulmonary edema. Complications of the baby include fetal growth restriction from uteroplacental perfusion deficiency caused by defects in trophoblastic invasion and placentation.

Assessment of Blood Pressure

During an obstetric evaluation of a patient, the blood pressure should be measured with an appropriately fitting blood pressure cuff (cuff bladder should encompass two thirds of the arm). To diagnose hypertension, there must be 2 separate elevated recordings that exceed 140/90 mm Hg. Hypertension is considered chronic if it is elevated before 20 weeks' gestation (see Table 35-1).

Gestational Hypertension

If a woman develops hypertension with a blood pressure >140/90 mm Hg after 20 weeks of gestation on 2 separate occasions without evidence of preeclampsia (including proteinuria) , she will be diagnosed with gestational hypertension. As indicated, gestational hypertension is diagnosed based on clinical examinations and she should be evaluated for other signs including severe headache, visual changes, epigastric or right upper quadrant pain, nausea, vomiting, or decreased urine output. Once diagnosed, it is treated with careful surveillance of the mother and fetus. However if the hypertension is >160/110 mm Hg without proteinuria, then the mother has severe gestational hypertension and should be treated with antihypertensive and magnesium sulfate for seizure prophylaxis. Generally 20% of patients with severe gestational hypertension are actually preeclamptic and will need termination of the pregnancy with delivery.

Preeclampsia

As defined earlier, preeclampsia means a woman develops hypertension and proteinuria after 20 weeks' gestation. Further subcategories include mild and severe preeclampsia depending on the extent of blood pressure elevation. Mild preeclampsia involves a blood pressure that is >140/90 mm Hg with proteinuria >300 mg in 24 hours while severe preeclampsia causes >5 g of proteinuria and signs of organ involvement. Treatment for both depends on the gestation of the mother. If she is >34 weeks then delivery is preferred while if she is <34 weeks gestation, then corticosteroids are given to the mother to aid in lung development of the fetus followed with expectant management and delivery.

Eclampsia

Although preeclampsia can progress to eclampsia, this is not always the case. That is, eclampsia may not develop or it may occur without the setting of preeclampsia. The cause of preeclampsia still remains unknown, though it is thought to be secondary to vasospasm, endothelial dysfunction, and ischemia. Preeclampsia has progressed to 

eclampsia once a patient convulses. Speculations maintain that the pathogenesis of eclamptic convulsions include cerebral vasoconstriction and vasospasms, hyper­tensive encephalopathy, cerebral edema or infarction, cerebral hemorrhage, and metabolic encephalopathy. Seizures likely result from excessive release of excit­atory neurotransmitters, massive depolarization, and bursts of action potentials. In a normal pregnancy, renal blood flow and glomerular filtration rate increase, but patients wit h eclampsia have decreased renal perfusion and glomerular filtra­tion resulting from a reduced plasma volume and increased renal afferent arteriolar resistance. This elevates the blood pressure and causes oliguria and proteinuria. Proteinuria is not always seen before a woman develops seizures but will appear at some point in an eclamptic patient. Hepatic changes that take place are periportal hemorrhage in the liver periphery with  more severe cases leading to hepatic infarc­tion and death (see Table 35-2 for other complications).

A straightforward diagnosis of eclampsia occurs when a gravida has general­ized edema, hypertension, proteinuria, and convulsions, but it may not always be this clear since there is a broad spectrum of these signs. The hallmark is the convulsion which can occur at any time during pregnancy, delivery, or postpar­tum. Hypertension is generally severe around 160/110 mm Hg in 20% to 54% of cases but has been shown to be absent in 16%. Symptoms that may occur before or after a convulsion include persistent occipital or frontal headache, blurred vision, photophobia, epigastric and/or right upper quadrant pain, and altered mental status. 

Management of Eclampsia

During or immediately after the acute convulsive episode, steps should be taken to ensure the safety of the mother. A padded tongue blade should be inserted to prevent trauma to her tongue, her bedside rails should be padded and raised, and physical restraints may be used as needed. She should also be placed in the lat­eral decubitus position with suction available to prevent aspiration. Her airway, breathing, and circulation should be carefully monitored and an intravenous line started. Apply a facemask with 8 to 10 L/min oxygen and monitor oxygenation and metabolic status via pulse oximetry and arterial blood gases. An obstetrician should be notified immediately. After stabilizing the mother, the next step is to manage the convulsions. It is important not to try and stop the first convulsion, but to stabilize the patient and then administer magnesium sulfate with a loading dose of 6 g  over 15 to 20 minutes followed by a continuous maintenance dose of 2 g/h to prevent recurrences. Out of the eclamptic women receiving magnesium sulfate, 10% will have another seizure and should be given another 2 g bolus intravenously over 3 to 5 minutes. 

If the patient continues to convulse, she may need to be  intubated and sedated. The next step is to control the blood pressure while preserving cerebral, cardiac, and placental perfusion. The goal is to maintain the blood pressure between 140 to 160 mm Hg systolic, and 90 to 105 mm Hg diastolic. This is generally achieved with hydralazine, labetalol, or nifedipine. Diuretics are only used in the case of pul­monary edema. During a seizure the fetus may experience bradycardia, transient late decelerations, decreased beat-to-beat variability, and compensatory tachycardia, but usually returns to normal after the convulsion. However if fetal bradycardia or  repetitive late  decelerations persist, placental abruption may have occurred which is a surgical emergency needing a stat cesarean. Once the mother is stabilized and has regained consciousness, is oriented to name, place, and time, and her con­vulsions are controlled, delivery is the definitive treatment. 

Eclampsia is not an indication for cesarean unless the patient is <30 weeks' ges­tation or her Bishop score is below 5, indicating that the cervix is unfavorable for induction of labor. After delivery, the patient must remain on magnesium sulfate for 24 hours and requires close monitoring of vitals, fluid intake and output, and symptoms of end organ damage (headache, blurry vision, epigastric pain). Because of the endothelial damage and repair and vasospasm that occur in eclamptic women, they are very sensitive to vigorous fluid therapy and to blood loss at delivery. 

Brain pathology was described during the  era when mortality was high, prior to the widespread use of magnesium sulfate and anti-hypertensive agents. These studies showed that though gross intracerebral hemorrhage was seen in up to 60% of eclamp­tic patients, and was fatal in   about half of these cases. Other neurologic symptoms besides seizures that are seen in severe preeclampsia include headache and scotoma, blindness, and generalized cerebral edema that can cause confusion or coma.

HELLP Syndrome 

Hematological abnormalities may develop in some women, including thrombocy­topenia and hemolysis. The thrombocytopenia may lead to life-threatening coagu­lopathy.  When accompanied with  elevated liver enzymes indicative of hepatic necrosis, the combination of events is referred to as HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) syndrome. Other changes that may take place in HELLP syndrome include decreased plasma clotting factors, increased Factor VIII consump­tion, increased fibrin degradation products that in severe cases can lead to DIC. Hepatic hematomas can develop from hepatic infarctions and can bleed profusely they rupture; when unruptured, they can be observed and treated conservatively.

CLINICAL CASE CORRELATION

• See also Case 30 (Altered Mental Status), 31 (Status Epilepticus), Case 32 (Stroke), and Case 36 (Critical Care and Obstetrical Issues).

COMPREHENSION QUESTIONS

35.1  A 27-year-old G3P1102 at 29 weeks' gestation comes into the obstetric triage room with her husband who states that 15 minutes ago she had a seizure involving her entire body. She is lethargic and unable to answer questions. Her husband says her second pregnancy was complicated by high blood pressure and their son was delivered preterm. This pregnancy has not had any complications. Her blood pressures in the first trimester was in the 100/60 mm Hg range. On examination, her BP is 180/105 mm Hg, HR 97 beats/minute, temperature 98.4°F, and RR 12 breaths/minute. What is the most important first step in management?

A. Administer loading dose of magnesium sulfate.

B. Help her into a hospital bed and assess her airway, place a face mask with oxygen, and obtain IV access.

C. Deliver the baby by immediate C-section.

D. Give the mother a dose of corticosteroids and wait to deliver the baby for 48 hours.

35.2  A 26-year-old G2P1001 at 38 weeks' gestation presents with headache and contractions every 5 minutes. She is admitted to labor and delivery. She has not had any complications with her pregnancy. On examination, her BP is 180/110 mm Hg, HR 97 beats/minute, temperature 98.4°F, RR 12 breaths/ minute, and cervix is 3 cm dilated. Her urinalysis shows 2 + proteinuria. She is started on magnesium sulfate and hydralazine. Two hours later she is afebrile, her BP is 140/90 mm Hg, HR 100 beats/minute, RR is 8 breaths/minute, and she has decreased deep tendon reflexes. What is your next step in management?

A. CT scan of head

B. Stop hydralazine

C. Ca gluconate

D. Stop magnesium sulfate

35.3  A 30-year-old G3P1102 at 29 weeks' gestation comes in for her prenatal appointment. She has not had any complications with her pregnancy. On examination, her BP is 150/95 mm Hg, HR 97 beats/minute, temperature 98.4°F, and RR 12 breaths/minute. Her urinalysis reveals no proteinuria and she denies shortness of breath, headache, changes in vision, or right upper quadrant pain. What is her most likely diagnosis?

A. Moderate preeclampsia

B. Superimposed preeclampsia on chronic hypertension

C. Severe gestational hypertension

D. Gestational hypertension

35.4  What is the next step in management of the patient in Question 35.3?

A . Weekly antepartum visits monitoring blood pressure and urinalysis

B. Start labetalol

C. Start hydralazine

D. IV magnesium sulfate

ANSWERS TO QUESTIONS

35.1  B. This patient presents with a tonic-clonic seizure and therefore has eclampsia until proven otherwise. Considering she has a history of hypertension in a previous pregnancy, high blood pressure on presentation, severe headache, and history of generalized tonic-clonic seizure, she most likely has eclampsia and should first be stabilized. She will need magnesium sulfate and delivery of her baby but first she must be stabilized.

35.2  D. This patient has severe preeclampsia since her systolic blood pressure is >160 mm Hg and she has 2 + proteinuria. She is appropriately treated with magnesium sulfate, which has a narrow therapeutic index. Toxic levels of magnesium sulfate can cause decreased deep tendon reflexes and respiratory depression to the point of respiratory compromise and death. Therefore, the patient must be vigilantly monitored when on magnesium. In the event of magnesium toxicity, the magnesium should be stopped and then the patient should receive calcium gluconate. CT scan of the head and hydralazine have no effect on magnesium toxicity.

35.3  D. This patient has an elevated blood pressure but no proteinuria. Since her blood pressure is <160/110 mm Hg, she has gestational hypertension and not severe gestational hypertension. Moderate preeclampsia not only has an elevated blood pressure, but also involves proteinuria. Superimposed preeclampsia on chronic hypertension occurs in patient with known hypertension before 20 weeks' gestation, with proteinuria occurring after 20 weeks' gestation.

35.4  A. The treatment of gestational hypertension involves weekly antepartum monitoring of the mother and the fetus. Hydralazine and labetalol are used for severe hypertension but are not used for hypertension <160/110 mm Hg. Women with gestational hypertension are accustomed to this elevated blood pressure, and decreasing their blood pressure to normal may cause hypoperfusion of vital organs such as the placenta and the brain. Magnesium sulfate is administered for seizure prophylaxis and is usually not given until the blood pressure is >160/110 mm Hg or the patient is experiencing signs of organ dysfunction including headache, changes in vision, oliguria, or right upper quadrant pain.

CLINICAL PEARLS

⯈ Epilepsy is the recurrence of seizures that are unprovoked by any immedi­ate identifiable cause. This diagnosis cannot be made based on a single seizure, even if anticonvulsant treatment is administered. 

⯈ Women with eclampsia should be treated with magnesium sulfate rather than other anticonvulsants because it more effectively reduces the rate of recurrent seizures and reduces the rate of maternal death. 

⯈ Intravascular magnesium sulfate has a  faster therapeutic effect and is less painful compared to intramuscular administration. 

⯈ Calcium gluconate 1 g IV should be given to reverse toxicity symptoms of magnesium sulfate such as hyporeflexia and respiratory  depression. 

⯈ Though delivery is the only curative treatment, the mother should be sta­bilized after a seizure  before proceeding with delivery. 

⯈ Cesarean delivery is reasonable in women who are <32 weeks of gestation and have an unfavorable cervix.

References

American College of Obstetricians and Gynecologists. Diagnosis and management of preeclampsia and eclampsia, ACOG Practice Bulletin. 2002;33. 

Benbadis SR. Differential diagnosis of epilepsy: a critical review. Epilepsy Behav. 2009;15:15-21. 

Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY. Chapter 34. Pregnancy hypertension. Williams Obstetrics. 23e. New York: McGraw-Hill Publishers, 2012. http://www.access­medicine.com.foyer.swmed.edu/content.aspx ?aiD= 603 2899, accessed Oct 14, 2013. 

Haddad B, Sibai BM. Expectant management in pregnancies with severe pre-eclampsia. Semin Perinatal. 2009;33:143-151. 

Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005;105:402-410. 

Sibai BM. Managing an eclamptic patient. OBG Management. 2005;17(5):37-50. 

Yoder SR, Thornburg LL, Bisognango JD. Hypertension in pregnancy and women of childbearing age. Am] Med. 2009;122:890.

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