Eclampsia

Eclampsia is a known complication of preeclampsia during pregnancy and is associated with morbidity and mortality in both mother and fetus if not properly diagnosed. Preeclampsia and eclampsia belong to four categories of hypertensive disorders of pregnancy. [ 1 ] The other three categories include chronic hypertension, gestational hypertension, and preeclampsia superimposed on chronic hypertension.

Preeclampsia, a precursor to eclampsia, has been redefined in recent years. The original definition of preeclampsia included proteinuria as a diagnostic criterion, but this is no longer the case because some patients already had advanced disease before proteinuria was detected. Preeclampsia is defined as new-onset hypertension with a systolic blood pressure greater than or equal to 140 mmHg and/or a diastolic blood pressure greater than or equal to 90 mmHg after 20 weeks of gestation with proteinuria and/or end-organ dysfunction ( renal failure, liver dysfunction, central nervous system abnormalities, pulmonary edema, and thrombocytopenia ). [ 2 ]

Eclampsia is defined as the new onset of generalized tonic-clonic seizures in a woman with preeclampsia. Eclamptic seizures may occur before delivery, after 20 weeks of pregnancy, during labor, and after delivery. Seizures before 20 weeks are rare but have been reported in gestational trophoblastic disease.[ 3 ]

Epidemiology

Most often (91%), eclampsia occurs after the 28th week of pregnancy. Less often, it is observed between the 21st and 27th (7.5%) or before the 20th week of pregnancy (1.5%). At the same time, eclampsia occurs during pregnancy in 38-53%, during childbirth - in 18-36% and in the postpartum period - in 11-44% of cases, and this can occur both in the first 48 hours and within 28 days after childbirth, which is called late eclampsia.

Hypertensive disorders, including chronic hypertension, gestational hypertension, preeclampsia, eclampsia, and chronic hypertension superimposed on preeclampsia, affect up to 10% of all pregnancies worldwide and are responsible for approximately 10% of all maternal deaths in the United States. The incidence of preeclampsia has increased over the past several decades, resulting in increased morbidity and mortality among mothers and newborns. In the United States, African American women are more likely to have preeclampsia and have a maternal mortality rate three times higher than their white counterparts. Additional risk factors associated with preeclampsia include maternal age over 40 years, prior preeclampsia, multiple gestations, obesity, chronic hypertension, pregestational diabetes, kidney disease, antiphospholipid syndrome, thrombophilia, lupus, and in vitro fertilization.

Causes eclampsia

The exact etiology of eclampsia remains unclear despite advances in understanding preeclampsia. It has been suggested that the permeability of the blood-brain barrier increases in gestosis, causing changes in cerebral blood flow due to impaired autoregulation.[ 4 ]

Pathogenesis

There are two proposed pathophysiological mechanisms of eclampsia, both related to the initial disease process, preeclampsia. The pathogenesis of preeclampsia is related to abnormal placentation. In normal pregnancy, fetal cytotrophoblasts migrate into the maternal uterus and induce remodeling of the endometrial vasculature to supply the placenta. In preeclampsia, inadequate cytotrophoblast invasion occurs, resulting in poor remodeling of the spiral arteries, which reduces the blood supply to the placenta. The impaired blood supply leads to increased uterine arterial resistance and vasoconstriction, which ultimately leads to placental ischemia and oxidative stress. Free radicals and cytokines such as vascular endothelial growth factor 1 or VEGF are released as a result of oxidative stress, leading to endothelial injury. [ 5 ] In addition, angiogenic or proinflammatory proteins negatively affect maternal endothelial function. [ 6 ] Endothelial destruction occurs not only in the uterine region but also in the cerebral endothelium, leading to neurological disorders including eclampsia. Another proposed mechanism is that elevated blood pressure resulting from preeclampsia causes dysfunction of autoregulation of the cerebral vasculature, leading to hypoperfusion, endothelial injury, or edema.

Symptoms eclampsia

Eclampsia is a disease process, primarily associated with the diagnosis of preeclampsia, that can occur before labor, during labor, and for 6 weeks after delivery. Women with eclampsia typically present to their physician after 20 weeks of pregnancy, with most cases occurring after 28 weeks of pregnancy. The hallmark of eclampsia on physical examination is generalized tonic-clonic seizures that typically last 60 to 90 seconds. A postictal state often follows the seizure activity. Before the onset of seizure activity, patients may experience warning symptoms such as headaches, vision changes, abdominal pain, and increased blood pressure.

Complications and consequences

Eclampsia can lead to a number of complications. The patient may require intubation after the attack due to decreased level of consciousness. When the patient does require intubation, blood pressure control is critical as laryngoscopy causes a hypertensive response and may lead to intracranial hemorrhage. Patients with preeclampsia are also at risk for respiratory failure in the form of acute respiratory distress syndrome as well as pulmonary edema. Additionally, women may experience renal and hepatic failure in severe forms of preeclampsia. Posterior reversible encephalopathy syndrome (PRES), a neurological condition, is another complication that can lead to eclampsia in patients. Patients with PRES may present with a variety of symptoms including headaches, seizures, mental status changes, cortical blindness, and other visual disturbances.[ 7 ] Most cases of PRES resolve within a couple of weeks if blood pressure and other precipitating factors are controlled; However, there is always a risk that the patient will develop cerebral edema and other fatal complications. Patients with preeclampsia and eclampsia also have an increased risk of developing cardiovascular disease later in life.[ 8 ]

Diagnostics eclampsia

Patients with eclampsia present with generalized tonic-clonic seizures. The evaluation of eclampsia focuses on the diagnosis of preeclampsia, as it is a known life-threatening complication of this disease process. The diagnosis of preeclampsia is primarily based on blood pressure, as the patient develops hypertension for the first time after 20 weeks of gestation. Patients with a systolic blood pressure greater than or equal to 140 mmHg and/or a diastolic blood pressure greater than or equal to 90 mmHg meet the criteria for new-onset hypertension. In addition to elevated blood pressure, patients also have one of the following: proteinuria, renal dysfunction, liver dysfunction, central nervous system symptoms, pulmonary edema, and thrombocytopenia. Proteinuria is no longer an essential factor in the diagnosis of preeclampsia; however, this criterion is often still included in the current diagnosis. Proteinuria is defined as at least 300 mg of protein in a 24-hour urine specimen or a urine protein/creatinine ratio of 0.3 or greater. Other important laboratories include a liver panel to evaluate liver function, a complete blood count to evaluate platelet function, and a basic metabolic profile to evaluate eGFR and renal function. Transaminase levels greater than twice the upper limit of normal, with or without right upper quadrant or epigastric pain, are consistent with preeclampsia. Platelet levels greater than 100,000 are also included in the diagnosis of preeclampsia. The presence of pulmonary edema on chest radiograph or physical examination, along with elevated blood pressure, suggests the development of preeclampsia. Central nervous system symptoms associated with a diagnosis of preeclampsia include headache and visual disturbances.

Obstetric ultrasound imaging with Doppler is useful to assess the impact of preeclampsia on the fetus, such as intrauterine growth restriction. Ultrasound is also useful to monitor for further complications, such as placental abruption. Non-stress fetal testing should be performed to assess fetal well-being in the antenatal period.

Differential diagnosis

The list of differential diagnoses should be based on the patient's history and physical examination. Differential diagnoses to consider include electrolyte disturbances, toxins, infections, head trauma, ruptured aneurysm, and malignant brain tumors. If the patient has persistent neurologic symptoms, stroke and intracranial hemorrhage should also be considered.

• Chronic hypertension.
• Chronic kidney disease.
• Primary seizure disorders.
• Gallbladder diseases.
• Antiphospholipid syndrome.
• Hemolytic uremic syndrome.
• Pancreatic disease.
• Immune thrombocytopenic purpura.
• Thrombotic thrombocytopenic purpura.
• Toxins.
• Aneurysm rupture.
• Brain tumor.
• Intracranial hemorrhage.

Treatment eclampsia

Eclamptic seizures are a medical emergency and require immediate treatment to prevent mortality of both mother and fetus. In actively seizing patients, the airway should be secured to avoid aspiration. The patient should be placed in the left lateral position and suction applied to remove secretions from the oral cavity. Other airway aids should also be readily available in case the patient's condition worsens and intubation is required. Magnesium sulfate should be given to control seizures and is the first-line drug for eclamptic seizures. A loading dose of 4 to 6 grams should be given intravenously over 15 to 20 minutes. A maintenance dose of 2 grams per hour should be given thereafter. Magnesium therapy should be continued for at least 24 hours after the patient's last seizure. Care must be taken when administering this drug because it can be toxic and cause respiratory paralysis, central nervous system depression, and cardiac arrest. When using magnesium, it is important to monitor reflexes, creatinine function, and urine output. Other antiepileptic drugs include diazepam or phenytoin. Benzodiazepines and barbiturates are used for refractory seizures that do not respond to magnesium. Levetiracetam or valproic acid are alternatives for patients with myasthenia gravis and eclampsia, as magnesium and phenytoin cause increased muscle weakness, which may lead to myasthenic crisis. [ 9 ] Ultimately, immediate obstetric consultation is required. Women with severe preeclampsia, who are more than 34 weeks pregnant and unstable from both a maternal and fetal perspective, should deliver as soon as the mother's condition is stabilized. [ 10 ] Corticosteroids should be given to women less than 34 weeks pregnant if time and circumstances permit to help accelerate lung maturation. Delivery should not be delayed due to steroid use. Ultimately, the definitive treatment for preeclampsia/eclampsia is delivery of the fetus. The route of delivery and timing depend on maternal and fetal factors.

Patients with severe preeclampsia should be given prophylactic magnesium sulfate to prevent eclamptic seizures. In addition, blood pressure control is important in pregnant women with preeclampsia. The American College of Obstetrics and Gynecology recommends initiating antihypertensive treatment in women with systolic blood pressure greater than 160 mm Hg or diastolic blood pressure greater than 110 mm Hg or greater on two occasions at least 4 hours apart (if antihypertensive therapy has not already been initiated). First-line pharmacologic treatment for hypertension in pregnancy includes labetalol, nifedipine, and hydralazine. The initial dose of labetalol is 20 mg intravenously. This dose can be doubled to 40 mg, then increased to 80 mg at 10-minute intervals until the target blood pressure is achieved. Hydralazine is given 5 to 10 mg intravenously over two minutes. An additional 10 mg intravenously may be given after twenty minutes if the systolic blood pressure exceeds 160 mmHg or the diastolic blood pressure exceeds 110 mmHg. Nifedipine is given orally at an initial dose of 10 mg. If after thirty minutes the systolic blood pressure exceeds 160 mmHg or the diastolic blood pressure exceeds 110, an additional 20 mg of nifedipine may be given. A second dose of nifedipine 20 mg may be given after another 30 minutes.

Blood pressure monitoring is also critical in the postpartum period, as the risk of eclampsia is highest within 48 hours of birth. Systolic blood pressure should be less than 150 mmHg and diastolic blood pressure should be less than 100 mmHg on two readings at least four hours apart. Treatment should also be initiated if systolic blood pressure exceeds 160 mmHg or diastolic blood pressure exceeds 110 mmHg after one hour. Magnesium sulfate should be continued for 12 to 24 hours after birth.

Forecast

Hypertensive disorders, including preeclampsia and eclampsia, occur in 10% of pregnancies in the United States and worldwide. Despite advances in medical treatment, it remains a leading cause of maternal and perinatal morbidity and mortality worldwide. [ 11 ] Although the incidence of eclampsia has decreased, it remains a very serious complication of pregnancy.

Sources

1. Wilkerson RG, Ogunbodede AC. Hypertensive Disorders of Pregnancy. Emerg Med Clin North Am. 2019 May;37(2):301-316.
2. Sutton ALM, Harper LM, Tita ATN. Hypertensive Disorders in Pregnancy. Obstet Gynecol Clin North Am. 2018 Jun;45(2):333-347.
3. Leeman L, Dresang LT, Fontaine P. Hypertensive Disorders of Pregnancy. Am Fam Physician. 2016 Jan 15;93(2):121-7.
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. Curr Hypertens Rep. 2019 Aug 02;21(9):72.
5. Uzan J, Carbonnel M, Piconne O, Asmar R, Ayoubi JM. Pre-eclampsia: pathophysiology, diagnosis, and management. Vasc Health Risk Manag. 2011;7:467-74.
6. Burton GJ, Redman CW, Roberts JM, Moffett A. Pre-eclampsia: pathophysiology and clinical implications. BMJ. 2019 Jul 15;366:l2381.
7. Waters J. Management of Myasthenia Gravis in Pregnancy. Neurol Clin. 2019 Feb;37(1):113-120.
8. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013 Nov;122(5):1122-1131.
9. Arulkumaran N, Lightstone L. Severe pre-eclampsia and hypertensive crises. Best Pract Res Clin Obstet Gynaecol. 2013 Dec;27(6):877-84.
10. Sesar A, Cavar I, Sesar AP, Sesar I. Transient cortical blindness in posterior reversible encephalopathy syndrome after postpartum eclampsia. Taiwan J Ophthalmol. 2018 Apr-Jun;8(2):111-114.
11. Amaral LM, Cunningham MW, Cornelius DC, LaMarca B. Preeclampsia: long-term consequences for vascular health. Vasc Health Risk Manag. 2015;11:403-15.
12. Aylamazyan, E. K. Obstetrics. National leadership. Brief edition / ed. E. K. Ailamazyan, V. N. Serov, V. E. Radzinsky, G. M. Savelyeva. - Moscow: GEOTAR-Media, 2021. - 608 p.