Eclampsia
No Results
No Results
processing….
Ten percent of all pregnancies are complicated by hypertension. Eclampsia and preeclampsia account for about half of these cases worldwide, and these conditions have been recognized and described for years despite the general lack of understanding of the disease. [1] In the fifth century, Hippocrates noted that headaches, convulsions, and drowsiness were ominous signs associated with pregnancy. In 1619, Varandaeus coined the term eclampsia in a treatise on gynecology. [2, 3]
Eclampsia, which is considered a complication of severe preeclampsia, is commonly defined as new onset of grand mal seizure activity and/or unexplained coma during pregnancy or postpartum in a woman with signs or symptoms of preeclampsia. [4, 5] It typically occurs during or after the 20th week of gestation or in the postpartum period. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been demonstrated to occur in 38% of cases reported in the United Kingdom. [6] Similarly, hypertension was absent in 16% of cases reviewed in the United States. [4]
The clinical manifestations of maternal preeclampsia are hypertension and proteinuria with or without coexisting systemic abnormalities involving the kidneys, liver, or blood. There is also a fetal manifestation of preeclampsia involving fetal growth restriction, reduced amniotic fluid, and abnormal fetal oxygenation. [6] HELLP syndrome is a severe form of preeclampsia and involves hemolytic anemia, elevated liver function tests (LFTs), and low platelet count.
Most cases of eclampsia present in the third trimester of pregnancy, with about 80% of eclamptic seizures occurring intrapartum or within the first 48 hours following delivery. Rare cases have been reported before 20 weeks’ gestation or as late as 23 days’ postpartum. Other than early detection of preeclampsia, no reliable test or symptom complex predicts the development of eclampsia. In developed countries, many reported cases have been classified as unpreventable.
Eclampsia manifests as 1 seizure or more, with each seizure generally lasting 60-75 seconds. The patient’s face initially may become distorted, with protrusion of the eyes, and foaming at the mouth may occur. Respiration ceases for the duration of the seizure.
Eclamptic seizures may be divided into 2 phases. Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions.
Phase 2 lasts about 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence.
A coma or period of unconsciousness, lasting for a variable period, follows phase 2. After the coma phase, the patient may regain some consciousness, and she may become combative and very agitated. However, the patient will have no recollection of the seizure.
A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase.
Seizure-induced complications can include tongue biting, head trauma, broken bones, and aspiration.
The mechanism(s) responsible for the development eclampsia remain(s) unclear. [5] Genetic predisposition, immunology, endocrinology, nutrition, abnormal trophoblastic invasion, coagulation abnormalities, vascular endothelial damage, cardiovascular maladaptation, dietary deficiencies or excess, and infection have been proposed as etiologic factors for preeclampsia/eclampsia. [2] Imbalanced prostanoid production and increased plasma antiphospholipids have also been implicated in eclampsia. [2, 7] In murine models, placental ischemia appears to be associated with an increased susceptibility to seizures and cerebrospinal fluid (CSF) inflammation. [5]
The following are considered risk factors for eclampsia:
Nulliparity
Family history of preeclampsia, previous preeclampsia and eclampsia [2]
Poor outcome of previous pregnancy, including intrauterine growth retardation, abruptio placentae, or fetal death
Multifetal gestations, hydatid mole, fetal hydrops, primigravida
Teen pregnancy
Primigravida
Patient older than 35 years
Lower socioeconomic status
The following preexisting medical conditions are also considered risk factors [4] :
Obesity
Chronic hypertension
Renal disease
Thrombophilias-antiphospholipid antibody syndrome
Protein C deficiency and protein S deficiency
Antithrombin deficiency
Vascular and connective tissue disorders
Preeclampsia/eclampsia produces multiple systemic derangements that can involve a diversity of organ systems including hematologic, hepatic, renal, and cardiovascular systems as well as the central nervous system. The severity of these derangements often correlates with maternal medical (eg, preexisting renal or vascular pathology) or obstetric factors (eg, multifetal gestations or molar pregnancy).
Eclampsia is associated with cardiovascular derangements such as generalized vasospasm, increased peripheral vascular resistance, and increased left ventricular stroke work index. Pulmonary capillary wedge pressure (PCWP) may vary from low to elevated. Importantly, central venous pressure (CVP) may not correlate with PCWP in patients with severe preeclampsia or eclampsia. [8]
A prospective observational study by Vaught that included 63 women with pre-eclampsia with severe features reported higher systolic pressure, higher rates of abnormal diastolic function, decreased global right ventricular longitudinal systolic strain, increased left-sided chamber remodeling, and higher rates of peripartum pulmonary edema in these women when compared with healthy pregnant women. [36]
Hematologic problems associated with eclampsia can include decreased plasma volume, increased blood viscosity, hemoconcentration, and coagulopathy.
Eclampsia-associated renal abnormalities can include decreases in glomerular filtration rate, renal plasma flow, and uric acid clearance.
Hepatic derangements associated with eclampsia can include periportal necrosis, hepatocellular damage, and subcapsular hematoma.
Eclampsia can result in central nervous system (CNS) abnormalities such as cerebral overperfusion due to loss of autoregulation, cerebral edema, and cerebral hemorrhage.
Many uterovascular changes occur when a woman is pregnant. It is believed that these changes are due to the interaction between fetal and maternal allografts and result in systemic and local vascular changes. It has been shown that in patients with eclampsia, the development of uteroplacental arteries is hindered.
It is believed that in eclampsia there is abnormal cerebral blood flow in the setting of extreme hypertension. The regulation of cerebral perfusion is inhibited, vessels become dilated with increased permeability, and cerebral edema occurs, resulting in ischemia and encephalopathy. In extreme hypertension, normal compensatory vasoconstriction may become defective. Several autopsy findings support this model and consistently reveal swelling and fibrinoid necrosis of vessel walls. [2]
Factors associated with endothelial dysfunction have been shown to be increased in the systemic circulation of women suffering from eclampsia. These include the following [1] :
Cellular fibronectin
Von Willebrand factor
Cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion molecule-1 [VCAM-1]
Intercellular adhesion molecule-1 [ICAM-1])
Cytokines (ie, interleukin-6 [IL-6])
Tumor necrosis factor-α [TNF-α]
In addition, it is believed that antiangiogenic factors, such as placental protein fms-like tyrosine kinase 1 (sFlt-1) and activin A, antagonize vascular endothelial growth factor (VEGF). [9] Elevated levels of these proteins cause a reduction of VEGF and induce systemic and local endothelial cell dysfunction. [1]
Leakage of proteins from the circulation and generalized edema are sequelae of the endothelial dysfunction and thus a defining factor associated with preeclampsia and eclampsia.
Evidence indicates that leptin molecules increase in the circulation of women with eclampsia, inducing oxidative stress, another factor in eclampsia, on cells. (The leptin increase also results in platelet aggregation, most likely contributing to the coagulopathy associated with eclampsia.) [2, 10]
Oxidative stress has been found to stimulate the production and secretion of the antiangiogenic factor activin A from placental and endothelial cells. [9] Studies in pregnant mouse models have proposed that there is a dysregulation in the reactive oxygen species (ROS) signaling pathway. [10, 11]
Studies also suggest that increased systemic leukocyte activity plays a role in the mediation of oxidative stress, inflammation, and endothelial cell dysfunction. Histochemistry studies indicate that there is predominantly an increase in neutrophil infiltration of vasculature in patients with eclampsia. [11]
Eclampsia always should be considered in a pregnant patient with a seizure episode. A pregnant patient who has been involved in an unexplained trauma (such as a single-vehicle auto accident) and has exhibited seizure activity should be evaluated for eclampsia. Eclampsia can occur during the antepartum, intrapartum, and postpartum periods. Ninety percent of eclampsia cases occur after 28 weeks’ gestation. [2]
Preeclampsia can quickly develop into eclampsia. The natural progression of the disease is from symptomatic severe preeclampsia (differentiated from preeclampsia by specific vital signs, symptoms, and laboratory abnormalities) to seizures.
Features of eclampsia include the following:
Seizure or postictal state (100%)
Headache (80%), usually frontal
Generalized edema (50%)
Vision disturbance (40%), such as blurred vision and photophobia
Right upper quadrant abdominal pain with nausea (20%)
Amnesia and other mental status changes
The incidences of signs or symptoms before seizure include the following:
Headache (83%)
Hyperactive reflexes (80%)
Marked proteinuria (52%)
Generalized edema (49%)
Visual disturbances (44%)
Right upper quadrant pain or epigastric pain (19%)
The absence of signs or symptoms before seizure include the following:
Lack of edema (39%)
Absence of proteinuria (21%)
Normal reflexes (20%)
The relation of seizure to delivery is as follows:
Before delivery (>70%)
Before labor (antepartum) (25%)
During labor (intrapartum) (50%)
After delivery (postpartum) (25%)
Although patients with severe preeclampsia are at greater risk for seizures, 25% of patients have symptoms consistent with mild preeclampsia (i.e., preeclampsia without severe features) before the seizures.
A study by Cooray et al found that the most common symptoms that immediately precede eclamptic seizures are neurologic symptoms (ie, headache, with or without visual disturbance), regardless of degree of hypertension. This suggests that closely monitoring patients with these symptoms may provide an early warning for eclampsia. [12]
A retrospective study by Nerenberg et al evaluated 1,565,733 births to determine the incidence rate and relative risk of a seizure disorder after eclampsia. The study reported that eclampsia exclusively affected 1,615 (0.10%) pregnancies, 17,264 (1.1%) with preeclampsia, 60,863 (3.9%) with gestational hypertension, and 1,485,991 (94.9%) remained unaffected. A future seizure disorder was more likely after a pregnancy with eclampsia (4.58/10,000 person-years) than a pregnancy without a hypertensive disorder (0.72/10,000 person-years) however the absolute risk was low (approximately one seizure/2,200 person-years). [13]
Most patients with eclampsia present with hypertension and seizures, along with some combination of proteinuria and edema. Findings at physical examination may include the following:
Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg
Tachycardia
Tachypnea
Rales
Mental status changes
Hyperreflexia
Clonus
Papilledema
Oliguria or anuria
Localizing neurologic deficits
Right upper quadrant or epigastric abdominal tenderness
Generalized edema
Small fundal height for the estimated gestational age
Apprehension
Cervical examination of the patient with eclampsia should not be overlooked, because the delivery mode may largely depend upon the patient’s cervical status.
Adrenal Insufficiency and Adrenal Crisis
Gestational Trophoblastic Neoplasia
Head Trauma
Seizures and Epilepsy: Overview and Classification
Thrombotic Thrombocytopenic Purpura
Angiomas
Cerebral Vasculitis
Drug Overdose
Metabolic Disorders
Undiagnosed Brain Tumors
Seizures in the first trimester or well into the postpartum period probably are due to CNS pathology and warrant full evaluation, including computed tomography (CT) scanning of the head, lumbar puncture (if clinical evidence of meningitis or concern for hemorrhage exists), determination of electrolyte levels, and urine or serum toxicologic screening. Do not overlook other neurologic causes of seizure, particularly if the seizure occurs more than 24 hours after delivery. In addition, rule out hypoglycemia as cause of seizure or result of seizure, and rule out hyperglycemia as a cause of mental status changes.
When preeclampsia occurs in the early second trimester (ie, 14-20 weeks’ gestation), the diagnosis of hydatiform mole or choriocarcinoma should be considered.
Ruling out eclampsia in an obstetric patient who has been involved in an unexplained trauma is important. Immediately consult an obstetrician/gynecologist when the diagnosis of eclampsia is being considered.
No single laboratory test or set of laboratory determinations is useful in predicting maternal or neonatal outcome in women with eclampsia. Imaging studies may be indicated after initial stabilization, especially if there is doubt about the diagnosis or possible injuries secondary to seizure activity.
Proteinuria is typically one of the presenting symptoms in patients with eclampsia. A timed collection has been the criterion standard for urinalysis to detect proteinuria (>300 mg/24 h or >1 g/L). Protein per unit time measured over 24 hours has been used traditionally; however, 12-hour collections have proved to be as accurate. [14] . In addition, it is now common to rely upon a spot protein to creatinine ratio to assess proteinuria, instead of a timed collection. The degree of proteinuria or change in proteinuria is helpful in diagnosing preeclampsia, but does not have any significant effect on clinical management.
Although investigational, Baweja et al suggest that when measuring intact urinary albumin levels using high-performance liquid chromatography in an early and uncomplicated pregnancy, spot urinary albumin:creatinine ratio (ACR) values are higher. If measured early in the second trimester, an ACR of 35.5 mg/mmol or higher may predict preeclampsia before symptoms arise. [15]
Uric acid levels may be mildly increased.
A complete blood cell (CBC) count may reveal the following:
Anemia due to microangiopathic hemolysis, hemoconcentration due to third spacing, or physiologic hemodilution of pregnancy
Peripheral smear (schistocytes, burr cells, echinocytes)
Increased bilirubin (>1.2 mg/dL)
Thrombocytopenia (< 100,000) due to hemolysis and low platelet count associated with HELLP syndrome (seen in 20-25% of patients with eclampsia) [4]
Low serum haptoglobin levels
Elevated lactate dehydrogenase (LDH) levels (threshold of 180–600 U/L)
The coagulation profile may reveal normal prothrombin (PT) and activated partial thromboplastin (aPTT) times, fibrin split products, and fibrinogen levels. Rule out associated disseminated intravascular coagulation (DIC). DIC is rare, unless there is an associated abruption.
The serum creatinine level is elevated in eclampsia because of a decreased intravascular volume and a reduced glomerular filtration rate (GFR). Creatinine clearance (CrCl) may be less than 90 mL/min/1.73 m2.
Liver function test results may reveal the following (20-25% of patients with eclampsia):
Aspartate aminotransferase (SGOT) level higher than 72 IU/L
Total bilirubin levels higher than 1.2 mg/dL
LDH level higher than 600 IU/L [2]
Elevated levels due to hepatocellular injury and HELLP syndrome
Computed tomography (CT) scanning of the head, with or without contrast, can exclude cerebral venous thrombosis, intracranial hemorrhage, and central nervous system lesions, all of which can occur in pregnancy and present with seizures.
Although obtaining a CT scan in eclampsia is not routine, abnormalities have been observed in up to 50% of women imaged.
Characteristic CT scan findings include cortical hypodense areas, particularly in the occipital lobes, and diffuse cerebral edema, which is believed to correspond to petechial hemorrhages and diffuse edema noted in postmortem studies.
CT scan findings may include the following:
Cerebral edema
Diffuse white matter low-density areas
Patchy area of low density
Occipital white matter edema
Loss of normal cortical sulci
Reduced ventricular size
Cerebral hemorrhage
Intraventricular hemorrhage
Parenchymal hemorrhage (high density)
Cerebral infarction
Low attenuation areas
Basal ganglia infarctions
Abnormal magnetic resonance imaging (MRI) findings of the head have been reported in up to 90% of women imaged. These include an increased signal at the gray-white matter junction on T2-weighted images, as well as cortical edema and hemorrhage. The syndrome of posterior reversible encephalopathy (PRES), indicative of central vasogenic edema, has been increasingly recognized as a component of eclampsia. [16]
One should consider CT scanning or MRI in patients who have been involved in trauma, are refractory to magnesium sulfate therapy, or have atypical presentations (eg, seizures >24 h after delivery, absence of severe hypertension).
Transabdominal ultrasonography is used to estimate gestational age and fetal well-being. Poor fetal growth, oligohydramnios, and/or abnormal umbilical artery Doppler velocimetry may be seen secondary to the hypertension associated with eclampsia. Ultrasound may also be used to assess for abruptio placentae, which can complicate eclampsia. However, the sensitivity of ultrasound to detect an abruption is poor.
Electroencephalograms and cerebrospinal fluid studies are rarely useful in management; however, they may be indicated if epilepsy or meningitis is considered in the diagnosis.
Eclamptic convulsions are life-threatening emergencies and require the proper treatment to decrease maternal morbidity and mortality. Delivery is the only definitive treatment for eclampsia.
The patient should be advised and educated on the course of the disease and any residual problems. She should also be educated on the importance of adequate prenatal care in subsequent pregnancies.
Several organizations have developed screening, treatment, and prevention guidelines for preeclampsia and eclampsia. [17, 18, 19] The American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) continue to support the short-term (usually < 48 hours) use of magnesium sulfate in obstetric care for conditions and treatment durations that include the following [19] :
An experienced obstetrician or maternal-fetal medicine specialist should be consulted. Patients with eclampsia require immediate obstetric consultation and admission to a labor and delivery unit capable of providing intensive care until delivery of the neonate. In the event of premature delivery or fetal compromise, a pediatrician or neonatologist should be consulted.
When initially evaluating a patient with eclampsia, become familiar with the level of care that the medical center can offer the patient, as eclampsia clearly poses a risk of considerable maternal and neonatal morbidity and mortality. Patients with eclampsia may benefit from management at a tertiary care center, a high-risk obstetric facility that provides neonatal and maternal intensive care.
Emergency medical services personnel should (1) secure an intravenous (IV) line with a large-bore catheter, (2) initiate cardiac monitoring and administer oxygen, and (3) transport the patient in the left lateral decubitus position. Supportive care for eclamptic convulsions includes the following:
Close monitoring (invasive, if clinically indicated)
Airway support
Adequate oxygenation
Anticonvulsant therapy
Blood pressure (BP) control
Place the patient in the left lateral position. This positioning decreases the risk of aspiration and will help to improve uterine blood flow by relieving obstruction of the vena cava by the gravid uterus. Protect the patient against injury during the seizure by padding and raising guardrails, using a padded tongue blade between the teeth, and suctioning the oral secretions as needed.
After the seizure has ended, a 16- to 18-gauge IV line should be established for drawing specimens and administering fluids and medications. (Fluid management is critical in patients with eclampsia.) IV fluids should be limited to isotonic solutions to replace urine output plus about 700 mL/d to replace insensible losses.
Pharmacotherapy goals are to reduce morbidity, prevent complications, and correct eclampsia. The drug of choice to treat and prevent eclampsia is magnesium sulfate. [19, 20] Familiarity with second-line medications phenytoin and diazepam/lorazepam is required for cases in which magnesium sulfate may be contraindicated (eg, myasthenia gravis) or ineffective. Control of hypertension is essential to prevent further morbidity or possible mortality. The most commonly used antihypertensive agents are hydralazine, labetalol, and nifedipine.
IV magnesium sulfate is the initial drug administered to terminate seizures. Seizures usually terminate after the loading dose of magnesium. A loading dose of 4-6 g (15-20 min) and a maintenance dose of 1-2 g per hour as a continuous IV solution should be administered. Alternatively, lorazepam (Ativan; 4 mg IV over 2-5 minutes) or diazepam (Valium; 5-10 mg IV slowly) can be used to terminate the seizure, after which magnesium sulfate is administered. While benzodiazepines can be used to treat the seizures due to eclampsia magnesium remains the preferred choice. There exist over 50 years of data and experience using magnesium for this purpose with excellent safety and efficacy. Once the seizures terminate, 85% of patients note improved BP control. [18, 21] Note: Magnesium toxicity can cause coma, and, if mental status changes with these infusion rates, this should be considered. [2]
Benzodiazepines or phenytoin can be used for seizures that are not responsive to magnesium sulfate. Avoid the use of multiple agents to abate eclamptic seizures, unless necessary.
Severe hypertension must be addressed after magnesium infusions. Hydralazine or labetalol can be administered IV for BP control. The goal is to maintain systolic BP between 140 and 160 mm Hg and diastolic BP between 90 and 110 mm Hg. An IV bolus of hydralazine (5-10 mg q20min prn) or labetalol (20-40 mg q15min prn) is recommended. Other potent antihypertensive medications, such as sodium nitroprusside or nitroglycerin, can be used but are rarely required. [2]
Diuretics are used only in the setting of pulmonary edema prior to delivery.
Care must be taken not to decrease the BP too drastically; an excessive decrease can cause inadequate uteroplacental perfusion and fetal compromise. [20]
A dose of antenatal steroids may be administered in anticipation of emergent delivery when gestational age is less than 32 weeks. Betamethasone (12 mg IM q24h × 2 doses) or dexamethasone (6 mg IM q12h × 4 doses) is recommended.
About 10% of women with eclampsia will have an additional seizure after receiving magnesium sulfate. Another 2 g bolus of magnesium may be given in these cases. For the rare patient who continues to have seizure activity while receiving adequate magnesium therapy, seizures may be treated with sodium amobarbital, 250 mg IV over 3-5 minutes. [22] Alternatively, lorazepam or diazepam may be administered (as described above) for status epilepticus. However, these drugs can be associated with prolonged neonatal neurologic depression.
BP should be assessed with the goal of maintaining the diastolic BP at less than 110 mm Hg with administration of antihypertensive medications as needed (eg, hydralazine, labetalol, nifedipine).
Keep nothing by mouth (including medications) until the patient is medically stabilized or delivered, because she is at risk for aspiration when postictal and may have recurrent seizures. Anjum et al reported that following a loading dose of magnesium sulfate, a reduced duration of maintenance doses (12 hours vs 24 hours) for women with eclampsia may be effective for preventing recurrent seizures. [23]
Depending on the clinical course, regularly check the patient’s neurologic status for signs of increased intracranial pressure or bleeding (eg, funduscopic examination, cranial nerves)
Monitor fluid intake and urine output, maternal respiratory rate, and oxygenation, as indicated, and continuously monitor fetal status. Pulmonary arterial pressure monitoring is rarely indicated but may be helpful in patients who have evidence of pulmonary edema or oliguria/anuria.
Once the seizure is controlled and the patient has regained consciousness, the patient’s general medical condition should be assessed to identify any other causes for seizures.
Induction of labor may be initiated when the patient is stable.
Fetal heart rate and uterine contractions should be continuously monitored. Fetal bradycardia is common following the eclamptic seizure and has been reported to last from 30 seconds to 9 minutes. The interval from the onset of the seizure to the fall in the fetal heart rate is typically 5 minutes or less. Transitory fetal tachycardia may occur following the bradycardia. Typically, emergent cesarean delivery is not indicated for this postseizure transient bradycardia; it spontaneously resolves.
After the initial bradycardia, during the recovery phase, the fetal heart rate tracing may reveal a loss of short- and long-term variability and the presence of late decelerations. These abnormalities are most likely due to the decrease in uterine blood flow caused by the intense vasospasm and uterine hyperactivity during the convulsion. If the fetal heart tracing does not improve following a seizure, further evaluation should be undertaken. Growth-restricted and preterm fetuses may take longer to recover following a seizure. Placental abruption may be present if uterine hyperactivity remains and fetal bradycardia persists.
Delivery is the treatment for eclampsia after the patient has been stabilized. No attempt should be made to deliver the infant either vaginally or by cesarean delivery until the acute phase of the seizure or coma has passed. The mode of delivery should be based on obstetric indications but should be chosen with an awareness that vaginal delivery is preferable from a maternal standpoint.
Adequate maternal pain relief for labor and delivery is vital and may be provided with either systemic opioids or epidural anesthesia.
In the absence of fetal malpresentation or fetal distress, oxytocin or prostaglandins may be initiated to induce labor.
Cesarean delivery may be considered in patients with an unfavorable cervix and a gestational age of 30 weeks or less, as induction under these circumstances may result in a prolonged intrapartum course and is frequently unsuccessful in avoiding cesarean delivery, given the high rate of intrapartum complications. When emergent cesarean delivery is indicated, substantiating the absence of coagulopathy before the procedure is important. (See Surgical Therapy.) [24]
Intrapartum complications include the following:
Fetal growth retardation (30%)
Nonreassuring fetal heart rate patterns (30%)
Placental abruption (23%)
Irrespective of gestational age, a prolonged induction with clinically significant worsening of maternal cardiovascular, hematologic, renal, hepatic, and/or neural status is generally an indication for cesarean delivery when the anticipated delivery time is remote.
Cesarean delivery may be necessary for obstetric indications or a deteriorating maternal condition. The patient should be stabilized with respect to seizures, oxygenation, and hemodynamic status before the initiation of cesarean delivery. BP should be controlled and coagulopathies monitored or corrected.
An anesthesiology consultation should be obtained. Early evaluation is recommended to assist with cardiopulmonary stabilization and to prepare for a possible operative delivery or endotracheal intubation.
For nonemergency cesarean delivery, epidural or combined techniques of regional anesthesia are preferred. Regional anesthesia is contraindicated in the presence of coagulopathy or severe thrombocytopenia (< 50,000 platelets/µL). General anesthesia in women with eclampsia increases the risk of aspiration, and airway edema may make intubation difficult. It also can produce significant increases in systemic and cerebral pressures during intubation and extubation.
The use of spinal anesthesia requires caution because of the possibility of total sympathetic blockade, resulting in maternal hypotension and uteroplacental insufficiency.
Follow up 1-2 weeks after delivery to evaluate the patient for BP control and any residual deficits from the eclamptic seizure. Patients with persistent hypertension past 8 weeks’ puerperium or neurologic changes may need medical referral.
Al-Safi et al suggest that the first week after discharge is the most critical period for the development of postpartum eclampsia. Discussing the risks and educating patients about the possibility of delayed postpartum preeclampsia is important, regardless of whether they develop hypertensive disease prior to discharge. [25]
Preventing the development of preeclampsia in high-risk patients could theoretically decrease the risk of eclampsia and its complications later in pregnancy. Aspirin blocks platelet aggregation and vasospasm in preeclampsia, and it may be effective in preventing preeclampsia. Studies have shown that low-dose aspirin in women at high risk for preeclampsia can contribute to a decreased risk of preeclampsia, a reduction in preterm delivery rates, and a reduction in fetal death rates, without increasing the risk of placental abruption. An obstetrician should directly supervise low-dose aspirin therapy in high-risk patients.
If the patient has preexisting hypertension, she should have good control before conception and throughout her pregnancy. Her case should be followed for recognition and treatment of preeclampsia.
A study by Vadillo-Ortega et al suggests that in a high-risk population (eg, previous pregnancy complicated by preeclampsia, preeclampsia in a first-degree relative), supplementation during pregnancy with a special food (eg, bars) containing L-arginine and antioxidant vitamins may reduce the risk of preeclampsia. Notably, the beneficial effect was greatest when supplementation was started prior to 24 weeks’ gestation. Antioxidant vitamin supplementation alone did not protect against preeclampsia. More studies performed on low-risk populations are needed. [26]
As many as 56% of patients with eclampsia may have transient deficits, including cortical blindness. However, studies have failed to demonstrate evidence of persisting neurologic deficits after uncomplicated eclamptic seizures during the follow-up period. [27] Studies suggest that there is an increased risk for cerebrovascular accidents (CVAs) and coronary artery disease (CAD) in eclamptic mothers later in life.
Other potential complications of eclampsia include the following:
Permanent neurologic damage from recurrent seizures or intracranial bleeding
Renal insufficiency and acute renal failure
Fetal changes – IUGR, abruptio placentae, oligohydramnios
Hepatic damage and rarely hepatic rupture
Hematologic compromise and DIC
Increased risk of recurrent preeclampsia/eclampsia with subsequent pregnancy
Maternal or fetal death: Eclampsia is associated with approximately 13% of maternal deaths worldwide [5]
Although some women who have had eclampsia or preeclampsia have reported subsequent cognitive difficulties even years later, a long-term follow-up study by Postma et al utilizing standardized testing was unable to find objective evidence of such problems. The reported neurocognitive difficulties have seemingly been associated with concentration and memory, as well as with vision-related tasks of daily living. In the study, 46 women who had been eclamptic and 51 who had been preeclamptic were given neurocognitive tests an average of about seven years following the index pregnancy; 48 controls, who had normotensive pregnancies, were also involved. [28, 29]
The eclamptic and preeclamptic women in the study did not perform as well as the controls on motor-function tests. (They also performed more poorly on the Hospital Anxiety and Depression Scale.) However, they scored similarly to the control subjects with regard to attention, executive functioning, visual perception, and working and long-term memory. The investigators suggested that the reported cognitive difficulties in previously eclamptic or preeclamptic women occur during complex, stressful situations of daily life and may be exacerbated by anxiety and depression. [28, 29]
Although the incidence of eclampsia has declined in recent years, mainly due to the improvement of healthcare, serious adverse outcomes still exist. [30] Five percent of patients with hypertension develop severe preeclampsia, and about 25% of women with eclampsia have hypertension in subsequent pregnancies. About 2% of women with eclampsia develop eclampsia with future pregnancies.
Multiparous women with eclampsia have a higher risk for the development of essential hypertension; they also have a higher mortality rate in subsequent pregnancies than do primiparous women.
Maternal complications from eclampsia include the following:
Permanent CNS damage from recurrent seizures or intracranial bleeds
Disseminated intravascular coagulopathy
Renal insufficiency
Pulmonary edema
Cardiopulmonary arrest
The most significant maternal complication of eclampsia is permanent CNS damage secondary to recurrent seizures or intracranial bleeding. The maternal mortality rate is 8-36% in these cases. [21] A loading dose of magnesium sulfate followed by maintenance doses for 12-24 hours may be effective in preventing recurrent seizures. [23]
Eclampsia and preeclampsia account for approximately 63,000 maternal deaths annually worldwide. [31] In developed countries, the maternal death rate is reportedly 0-1.8%. The perinatal mortality rate from eclampsia in the United States and Great Britain ranges from 5.6% to 11.8%. The maternal mortality rate is as high as 14% in developing countries. [6, 22, 27]
A study from the US Centers for Disease Control and Prevention (CDC) found an overall preeclampsia/eclampsia case-fatality rate of 6.4 per 10,000 cases at delivery. The study also found a particularly high risk of maternal death at 20-28 weeks’ gestation. [32]
Black woman have twice the risk that white women have for mortality associated with preeclampsia/eclampsia. This is most likely due to inadequate access to prenatal care among black women, as well as to increased incidences in black women of genetic diseases associated with circulating antiphospholipids. It has been proven that patients with elevated antiphospholipid plasma levels have a higher incidence of preeclampsia and eclampsia. [2] However, whether this is due to the antiphospholipids themselves or to some other underlying process is not clear. [7]
A majority of women who suffer eclampsia-associated death have concurrent HELLP syndrome. [31]
A report of an international study demonstrated that serious complications among patients with eclampsia (including maternal mortality) may be predicted by the use of a model that incorporates gestational age, chest pain or dyspnea, oxygen saturation, platelet count, and creatinine and aspartate transaminase concentrations. Although clinical use of the model awaits future validation, the identification of the predictive variables may aid in management decisions. [33]
The fetal mortality rate varies from 13-30% due to premature delivery and its complications. Placental infarcts, abruptio placentae, intrauterine growth retardation, and fetal hypoxia also contribute to fetal demise. [2]
Overview
What is the prevalence of eclampsia?
What are the clinical manifestations of preeclampsia?
When during the pregnancy is eclampsia most likely to occur?
What is the duration of seizures associated with eclampsia?
What are the phases of eclampsia seizures?
What follows phase 2 of eclampsia seizures?
What occurs after tonic-clonic seizures in eclampsia?
What are the general seizure induced complications of eclampsia?
What are the risk factors for eclampsia?
Which preexisting medical conditions are risk factors for eclampsia?
What are the multiorgan system effects of eclampsia?
What are the cardiovascular effects of eclampsia?
What are the hematologic effects of eclampsia?
What are the renal effects of eclampsia?
What are the hepatic effects of eclampsia?
What are the central nervous system effects of eclampsia?
How does eclampsia affect uterovascular development?
What causes cerebral edema in eclampsia?
What are the factors associated with endothelial dysfunction in eclampsia?
What is the role of antiangiogenic factors in the pathophysiology of eclampsia?
What are the roles of protein leakage from edema in the pathophysiology of eclampsia?
What is the role of oxidative stress in the pathophysiology of eclampsia?
When should a pregnant woman be evaluated for eclampsia?
How is preeclampsia differentiated from eclampsia?
What are the signs and symptoms of eclampsia?
What is the frequency of the most common signs or symptoms of eclampsia?
How frequently are signs or symptoms absent before eclampsia seizure?
When are eclampsia seizures most likely to occur?
Which symptoms are most common before eclampsia seizure?
Which physical findings are characteristic of eclampsia?
How is CNS pathology of eclampsia evaluated?
What are the diagnostic considerations in an obstetric patient with eclampsia?
How are lab tests and imaging tests used in the diagnosis of eclampsia?
What is the role of urinalysis in the diagnosis of eclampsia?
What is the role of urinary albumin measurement in the diagnosis of eclampsia?
How are uric acid levels affected by eclampsia?
What is the role of CBC count in the diagnosis of eclampsia?
What is the role of a coagulation profile in the diagnosis of eclampsia?
What is the role of serum creatinine measurement in the diagnosis of eclampsia?
What is the role of liver function tests in the evaluation of eclampsia?
Which conditions can be excluded with CT scanning of the head during the evaluation for eclampsia?
What is the prevalence of abnormalities on CT scan in patients with eclampsia?
Which CT findings are characteristic of eclampsia?
What are less common CT scan findings in patients with eclampsia?
What is the role of MRI in the evaluation of eclampsia?
When are MRI or CT scans indicated in the evaluation for eclampsia?
What is the role of transabdominal ultrasonography in the diagnosis and management of eclampsia?
How are eclamptic convulsions treated?
What should be included in patient education about eclampsia?
What is the role of magnesium sulfate in the treatment of eclampsia?
Which specialist consultations may be beneficial in the treatment of eclampsia?
What is transfer indicated for the treatment of eclampsia?
What is included in the initial treatment of eclamptic convulsions?
How is a patient with eclampsia positioned during a seizure?
What is included in treatment of eclampsia following a seizure?
What are the goals of drug treatment for eclampsia?
Which medications are used in the treatment of eclampsia?
What is the role of benzodiazepines or phenytoin in the treatment of eclampsia?
How is hypertension treated in patients with eclampsia?
What is the role of diuretics in the treatment of eclampsia?
How is the blood pressure maintained in the treatment of eclampsia?
What is the role of antenatal steroids in the treatment of eclampsia?
How are eclamptic seizures unresponsive to magnesium sulfate managed?
How is blood pressure (BP) assessed in patients with eclampsia?
What are the risks of aspiration in patients with eclampsia?
How is the neurologic status monitored in women with eclampsia?
What is included in maternal monitoring of patients with eclampsia?
When should other causes of seizures be assessed in women with eclampsia?
When is labor induced in patients with eclampsia?
How are the fetal heart rate and uterine contractions monitored in patients with eclampsia?
What is the significance of fetal bradycardia in patients with eclampsia?
What should be considered prior to delivery in patients with eclampsia?
How is maternal pain relief administered during delivery of women with eclampsia?
How is labor induced in women with eclampsia?
When is cesarean delivery considered in patients with eclampsia?
What are the intrapartum complications of eclampsia?
What are the indications for cesarean delivery in patients with eclampsia?
How are patients with eclampsia prepared for Caesarean delivery?
What are the anesthesiology concerns for a patient with eclampsia?
Which anesthesia should be used for nonemergency cesarean delivery in patients with eclampsia?
What are the cautions for the use of spinal anesthesia in patients with eclampsia?
What are the postpartum outpatient monitoring protocols for patients with eclampsia?
What is the role of aspirin in the prevention of eclampsia?
How should hypertension be managed during pregnancy?
What is the role of L-arginine and antioxidant vitamins in the prevention of eclampsia?
What is the prevalence of transient deficits in patients with eclampsia?
What are potential complications of eclampsia?
What is the incidence of cognitive deficits following eclampsia?
What is the prevalence of the serious adverse outcomes due to eclampsia?
What risks are increased in multiparous women with eclampsia?
What are the maternal complications from eclampsia?
What is the most significant maternal complication of eclampsia?
What is the mortality rate associated with eclampsia?
How does the mortality rate for eclampsia vary by race?
What is the prevalence of HELLP syndrome in eclampsia-associated death?
What models are used to predict the risk for complications in women with eclampsia?
What is the fetal mortality rate in women with eclampsia?
Craici I, Wagner S, Garovic VD. Preeclampsia and future cardiovascular risk: formal risk factor or failed stress test?. Ther Adv Cardiovasc Dis. 2008 Aug. 2(4):249-59. [Medline]. [Full Text].
Gabbe. Obstetrics: Normal and Problem Pregnancies. Hypertension. 5th ed. Churchill Livingstone, An Imprint of Elsevier; 2007. [Full Text].
ACOG. ACOG Practice Bulletin: Diagnosis and Management of Preeclampsia and Eclampsia: The American College of Obstetricians and Gynecologists Number 33. Jan 2002.
Mattar F, Sibai BM. Eclampsia. VIII. Risk factors for maternal morbidity. Am J Obstet Gynecol. 2000 Feb. 182(2):307-12. [Medline].
Warrington JP. Placental ischemia increases seizure susceptibility and cerebrospinal fluid cytokines. Physiol Rep. 2015 Nov. 3 (11):[Medline].
Douglas KA, Redman CW. Eclampsia in the United Kingdom. BMJ. 1994 Nov 26. 309(6966):1395-400. [Medline].
Nodler J, Moolamalla SR, Ledger EM, Nuwayhid BS, Mulla ZD. Elevated antiphospholipid antibody titers and adverse pregnancy outcomes: analysis of a population-based hospital dataset. BMC Pregnancy Childbirth. 2009 Mar 16. 9:11. [Medline]. [Full Text].
Bolte AC, Dekker GA, van Eyck J, van Schijndel RS, van Geijn HP. Lack of agreement between central venous pressure and pulmonary capillary wedge pressure in preeclampsia. Hypertens Pregnancy. 2000. 19 (3):261-71. [Medline].
Reddy A, Suri S, Sargent IL, Redman CW, Muttukrishna S. Maternal circulating levels of activin A, inhibin A, sFlt-1 and endoglin at parturition in normal pregnancy and pre-eclampsia. PLoS One. 2009. 4(2):e4453. [Medline]. [Full Text].
Banerjee S, Randeva H, Chambers AE. Mouse models for preeclampsia: disruption of redox-regulated signaling. Reprod Biol Endocrinol. 2009 Jan 15. 7:4. [Medline]. [Full Text].
Cadden KA, Walsh SW. Neutrophils, but not lymphocytes or monocytes, infiltrate maternal systemic vasculature in women with preeclampsia. Hypertens Pregnancy. 2008. 27(4):396-405. [Medline]. [Full Text].
Cooray SD, Edmonds SM, Tong S, et al. Characterization of symptoms immediately preceding eclampsia. Obstet Gynecol. 2011 Nov. 118(5):995-9. [Medline].
Nerenberg KA, Park AL, Vigod SN, Saposnik G, Berger H, Hladunewich MA, et al. Long-term Risk of a Seizure Disorder After Eclampsia. Obstet Gynecol. 2017 Nov 3. [Medline].
Hofmeyr GJ, Belfort M. Proteinuria as a predictor of complications of pre-eclampsia. BMC Med. 2009. 7:11. [Medline]. [Full Text].
Baweja S, Kent A, Masterson R, Roberts S, McMahon L. Prediction of pre-eclampsia in early pregnancy by estimating the spot urinary albumin: creatinine ratio using high-performance liquid chromatography. BJOG. 2011 Aug. 118(9):1126-32. [Medline].
Brewer J, Owens MY, Wallace K, Reeves AA, Morris R, Khan M, et al. Posterior reversible encephalopathy syndrome in 46 of 47 patients with eclampsia. Am J Obstet Gynecol. 2013 Jun. 208(6):468.e1-6. [Medline].
[Guideline] Magee LA, Helewa M, Moutquin JM, von Dadelszen P,. Hypertension Guideline Committee, Society of Obstetricians and Gynaecologists of Canada. Prediction, prevention, and prognosis of preeclampsia. In: Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. J Obstet Gynaecol Can. Mar 2008. 30(3 Suppl 1):S16-23.
[Guideline] Milne F, Redman C, Walker J, Baker P, Bradley J, Cooper C, et al. The pre-eclampsia community guideline (PRECOG): how to screen for and detect onset of pre-eclampsia in the community. BMJ. 2005 Mar 12. 330(7491):576-80. [Medline]. [Full Text].
Committee opinion no 652: magnesium sulfate use in obstetrics. Obstet Gynecol. 2016 Jan. 127 (1):e52-3. [Medline].
Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995 Jul 27. 333(4):201-5. [Medline].
Rivers EP. The Clinical Practice of Emergency Medicine. Preeclampsia, eclampsia, and other hypertensive disorders of pregnancy. 2nd ed. 1996. 315-21.
Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005 Feb. 105(2):402-10. [Medline].
Anjum S, Goel N, Sharma R, Mohsin Z, Garg N. Maternal outcomes after 12 hours and 24 hours of magnesium sulfate therapy for eclampsia. Int J Gynaecol Obstet. 2015 Oct 14. [Medline].
Zhang J, Meikle S, Trumble A. Severe maternal morbidity associated with hypertensive disorders in pregnancy in the United States. Hypertens Pregnancy. 2003. 22(2):203-12. [Medline].
Al-Safi Z, Imudia AN, Filetti LC, et al. Delayed postpartum preeclampsia and eclampsia: demographics, clinical course, and complications. Obstet Gynecol. 2011 Nov. 118(5):1102-7. [Medline].
Vadillo-Ortega F, Perichart-Perera O, Espino S, et al. Effect of supplementation during pregnancy with L-arginine and antioxidant vitamins in medical food on pre-eclampsia in high risk population: randomised controlled trial. BMJ. 2011 May 19. 342:d2901. [Medline]. [Full Text].
Sibai BM, Sarinoglu C, Mercer BM. Eclampsia. VII. Pregnancy outcome after eclampsia and long-term prognosis. Am J Obstet Gynecol. 1992 Jun. 166(6 Pt 1):1757-61; discussion 1761-3. [Medline].
Janeczko LL. Formal Testing Fails to Confirm Cognitive Problems Years After Eclampsia or Preeclampsia. Medscape. Feb 24 2014. [Full Text].
Postma IR, Bouma A, Ankersmit IF, et al. Neurocognitive functioning following preeclampsia and eclampsia: a long-term follow-up study. Am J Obstet Gynecol. 2014 Jul. 211(1):37.e1-9. [Medline].
Liu S, Joseph KS, Liston RM, et al. Incidence, Risk Factors, and Associated Complications of Eclampsia. Obstet Gynecol. 2011 Nov. 118(5):987-994. [Medline].
Vigil-De Gracia P. Maternal deaths due to eclampsia and HELLP syndrome. Int J Gynaecol Obstet. 2009 Feb. 104(2):90-4. [Medline].
MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. 2001 Apr. 97(4):533-8. [Medline].
von Dadelszen P, Payne B, Li J, et al. Prediction of adverse maternal outcomes in pre-eclampsia: development and validation of the fullPIERS model. Lancet. 2011 Jan 15. 377(9761):219-27. [Medline].
Okusanya BO, Oladapo OT, Long Q, et al. Clinical pharmacokinetic properties of magnesium sulphate in women with pre-eclampsia and eclampsia: a systematic review. BJOG. 2015 Nov 24. [Medline].
Bond DM, Gordon A, Hyett J, de Vries B, Carberry AE, Morris J. Planned early delivery versus expectant management of the term suspected compromised baby for improving outcomes. Cochrane Database Syst Rev. 2015 Nov 24. 11:CD009433. [Medline].
Vaught AJ, Kovell LC, Szymanski LM, Mayer SA, Seifert SM, Vaidya D, et al. Acute Cardiac Effects of Severe Pre-Eclampsia. J Am Coll Cardiol. 2018 Jul 3. 72 (1):1-11. [Medline].
Michael G Ross, MD, MPH Distinguished Professor of Obstetrics and Gynecology, University of California, Los Angeles, David Geffen School of Medicine; Distinguished Professor, Department of Community Health Sciences, Fielding School of Public Health at University of California at Los Angeles
Michael G Ross, MD, MPH is a member of the following medical societies: American Association for the Advancement of Science, American College of Obstetricians and Gynecologists, American Federation for Clinical Research, American Gynecological and Obstetrical Society, American Physiological Society, American Public Health Association, Association of Professors of Gynecology and Obstetrics, Perinatal Research Society, Phi Beta Kappa, Society for Maternal-Fetal Medicine, Society for Neuroscience, Society for Reproductive Investigation
Disclosure: Nothing to disclose.
John G Pierce, Jr, MD Associate Professor, Departments of Obstetrics/Gynecology and Internal Medicine, Medical College of Virginia at Virginia Commonwealth University
John G Pierce, Jr, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Association of Professors of Gynecology and Obstetrics, Christian Medical and Dental Associations, Medical Society of Virginia, Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.
Ronald M Ramus, MD Professor of Obstetrics and Gynecology, Director, Division of Maternal-Fetal Medicine, Virginia Commonwealth University School of Medicine
Ronald M Ramus, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, Medical Society of Virginia, Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.
Bruce A Meyer, MD, MBA Executive Vice President for Health System Affairs, Executive Director, Faculty Practice Plan, Interim CEO, University Hospitals; Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School
Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Eclampsia
Research & References of Eclampsia|A&C Accounting And Tax Services
Source
0 Comments