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INTRODUCTION

Eclampsia is the convulsive manifestation of preeclampsia and one of several clinical manifestations at the severe end of the preeclampsia spectrum ( table 1 ). Despite advances in detection and management, preeclampsia/eclampsia remains a common cause of maternal morbidity and death, especially in resource-limited areas.

The clinical manifestations, diagnosis, and management of eclampsia will be reviewed here. Issues related to preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome are discussed separately:

● (See "Preeclampsia: Pathogenesis" .)

● (See "Preeclampsia: Clinical features and diagnosis" .)

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Management of Eclampsia

Video Clips on DVD 10-1 PowerPoint Discussion of Evaluation and Management of a Patient with Eclampsia 10-2 Discussion with Dr. Sibai on Emergent Management of a Woman Presenting with an Eclamptic Seizure Eclampsia is defined as the onset of seizures and/or unexplained coma during pregnancy (usually not before 20 weeks of gestation) or postpartum in patients with signs and symptoms of preeclampsia. In the Western world, the incidence ranges from 1 in 2000 to 1 in 3448 pregnancies. Incidence is higher in tertiary referral centers, in the developing countries, and in patients with no prenatal care. Although most cases (90%) present in the third trimester or 48 hours following delivery, there have been rare cases (1.5%) at or before 20 weeks and as late as 23 days postpartum. Risk factors for eclampsia are described in Table 10-1 . Table 10-1 Risk Factors for Eclampsia • First pregnancy • Previous eclampsia • Multifetal gestation • Chronic hypertension/renal disease • Collagen vascular disease • Molar pregnancy/partial mole • Gestational hypertension-preeclampsia plus • Severe headache • Persistent visual changes • Severe epigastric/right upper quadrant pain • Altered mental status   Case 1: Eclampsia with Eclamptic Seizure An ambulance rushes Jessica, a 19-year-old G1P0 with an intrauterine pregnancy at 36 weeks’ gestation, to labor and delivery. She’s had no prenatal care. Her family says she has been complaining of headache and visual disturbance for the last few days. They’ve witnessed a 3-minute seizure during which she drooled saliva but had no urinary or fecal incontinence. Her medical/surgical and social history are completely negative. On admission, her blood pressure is 170 mm Hg systolic over 110 mm Hg diastolic. She has 2+ protein on her urine dip. Bedside ultrasound confirms a singleton intrauterine pregnancy consistent with 36 weeks of gestation. Fetal heart rate tracing is reassuring, and cervical exam reveals a Bishop score of 7. The 19-year-old patient underwent immediate suctioning of secretions and was placed in a lateral semirecumbent position and given oxygen by face mask. IV access was secured and laboratory tests were obtained for complete blood count (CBC), including platelet count, liver enzymes, and a metabolic profile. A loading dose of 6 g of magnesium sulfate was given over 20 minutes and that was followed by a maintenance dose of 2 g/hr. Because of her severe hypertension, a 10-mg bolus of IV hydralazine was administered. Blood pressures were monitored every 5 to 10 minutes, and after 30 minutes, the systolic was 150 mm Hg and diastolic was 105 mm Hg. Maternal urine output and reflexes were monitored every hour. The results of the blood tests revealed a platelet count of 120,000/mm 3 , a hematocrit of 37%, and normal liver enzymes. Once maternal and fetal conditions were considered stable, IV oxytocin was started to initiate labor. The patient subsequently spontaneously delivered vaginally an infant weighing 2700 g with Apgar scores of 7 and 9 at 1 and 5 minutes, respectively. Postpartum magnesium sulfate was continued for 24 hours. In addition, maternal vital signs, intake and urine output and patellar reflexes, were monitored every hour. She was started on oral nifedipine, 10 mg every 6 hours, because of elevated blood pressures and asked to return within 1 week for postpartum follow-up. Discussion This is a typical presentation of a patient with eclampsia in the absence of prenatal care. It’s terrifying to witness a life-threatening eclamptic convulsion develop. First the patient’s face becomes distorted and her eyes bulge; then she becomes red faced. Lasting usually 60 to 75 seconds, convulsions occur in two phase. The first—which lasts for 15 to 20 seconds—begins with facial twitching; then the body becomes rigid with generalized muscular contractions. During the 60-second second phase, the muscles of the body alternately contract and relax in rapid succession starting in the jaw muscles, then moving to the eyelids and the other facial muscles before spreading throughout the whole body. Apnea develops not just during but also immediately after the seizure. Coma sometimes follows seizures and the woman usually remembers nothing of the recent events. The woman often foams at the mouth and usually bites her tongue, unless it’s protected. A period of hyperventilation occurs after the tonic-clonic seizure to compensate for the respiratory acidosis that developed during the apneic period. The majority of patients with eclampsia have hypertension (systolic blood pressure ≥140 and/or diastolic pressure ≥90 mm Hg), plus proteinuria (≥1+ on dipstick), and edema. In addition, as was the case in this patient, more than 50% will give a history of headaches, visual changes, and/or epigastric pain prior to seizures. Although hypertension is considered the hallmark for the diagnosis of eclampsia, it can be absent in 15% to 20% prior to seizures. In these cases, the patient will have proteinuria and associated central nervous system or epigastric pain with nausea and vomiting. There is no single laboratory test that is diagnostic of eclampsia. The patient usually has hemoconcentration and elevated serum creatinine and uric acid, but normal platelet count and liver enzymes. Thrombocytopenia (platelet count <100 K/mm 3 ) is seen in approximately 20% of cases, and the full HELLP ( h emolysis, e levated l iver enzymes, and l ow p latelet count) syndrome in 10% to 15% of cases. Most patients demonstrate reduced oxygen saturation during and immediately after the seizure. If these persist, consider aspiration or pulmonary edema. Although eclampsia is the most common cause of convulsions in association with hypertension in pregnancy and/or proteinuria, don’t overlook the other causes that—although rare—can produce convulsions in pregnancy or postpartum and can mimic eclampsia ( Table 10-2 ). Table 10-2 Differential Diagnosis of Eclampsia • Cerebrovascular accidents • Hemorrhage • Ruptured aneurysm or malformation • Arterial embolism or thrombosis • Cerebral venous thrombosis • Hypoxic ischemic encephalopathy • Angiomas • Hypertensive encephalopathy • Seizure disorder • Amniotic fluid embolism • Metabolic diseases • Hypoglycemia, hyponatremia, thyroid storm • Reversible posterior leukoencephalopathy syndrome • Thrombophilia • Thrombotic thrombocytopenic purpura • Postdural puncture syndrome • Cerebral vasculitis   The basic goals of therapy are to support maternal condition, prevent maternal injury and aspiration, prevent recurrent convulsions, and control blood pressure and other associated maternal complications. Once maternal and fetal conditions are optimized, the next step is to initiate process of delivery ( Fig. 10-1 ). Specifics of detailed steps are described following. Figure 10-1 Steps in managing an eclamptic seizure. Step 1. Support Maternal Respiratory and Cardiovascular Functions to Prevent Hypoxia Establish airway patency and maternal oxygenation during or immediately after the acute episode. Even if the initial seizure is short, it’s important to maintain oxygen levels by administering oxygen via face mask with or without reservoir at 8 to 10 L/min. The goal is to prevent the hypoxia and respiratory acidosis that often occur during the convulsions. I advise pulse oximetry to monitor oxygenation in these patients. Arterial blood gas analysis is required if the pulse oximetry is abnormal (oxygen saturation <92%), or aspiration or pulmonary edema is suspected. Sodium bicarbonate is not given unless the pH is less than 7.

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Eclampsia in the ED: Presentation, Differential Diagnosis, and Treatment

  • May 24th, 2021
  • Kyrra Engle
  • categories: practice updates

Authors: Kyrra Engle, ScM (@KyrraEngle, University of Miami Miller School of Medicine ); Alessandra Della Porta (@MedEdtweeter, University of Miami Miller School of Medicine ); Zoe Kornberg, MD, MPH ( Department of Obstetrics and Gynecology, University of Texas Rio Grande Valley) ; Kasha Bornstein (@BornsteinKasha) // Reviewed by: Marina Boushra, MD; Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

A 27-year-old P3G3 woman is found by her partner seizing at home one-week post-partum from a preterm (31 weeks + 4 days) pregnancy complicated by gestational hypertension. She was unable to schedule obstetric appointments during her second trimester due to loss of her insurance. She had been complaining of a headache earlier in the day, worsening prior to the seizure. On arrival to the patient’s home, paramedics find her altered, weak, and incontinent of urine. Pre-h ospital v ital signs included a heart rate of 110 bpm and a blood pressure of 180/110 mmHg . En route to the emergency department (ED) , paramedics witnessed a second generalized seizure, started an IV , and administered midazolam. She continued to seize, requiring a repeat dose of midazolam. As she is transferred from the stretcher to a hospital bed, she has a third seizure with tonic/clonic activity.

Introduction

Pregnancy-related conditions are the sixth most common reason for presentation to the ED in female patients of childbearing age, and account for 1.3% of ED visits overall. 1,2 Furthermore, of the four million patients that give birth in the United States each year, approximately 5% will present to the ED in the 6 weeks following delivery, highlighting the importance of emergency providers’ ability to recognize and acutely manage obstetric complications. 3,4

The most common neurologic complication of pregnancy is seizures, with a prevalence of 1.2% in the United States. 5,6 Although epilepsy is the most common cause of seizures in gravid patients, eclampsia remains a major cause of gestational morbidity and mortality due to the risk of hypoxic-ischemic brain injury and seizure-related intracranial hemorrhage 5,7-9 Eclampsia is among the top six causes of maternal death in the United States following postpartum hemorrhage, infection, and cardiovascular conditions. 10,11 Emergency providers can play a key role in recognizing and acutely managing patients with eclampsia, especially those who may not be able to access prenatal care or those who present in the postpartum period.

Eclampsia is defined as the occurrence of one or more generalized tonic-clonic convulsions unrelated to other medical conditions in pregnant or postpartum patients with hypertensive disorders of pregnancy. 8-10 Hypertensive disorders of pregnancy are a spectrum of clinical conditions including chronic hypertension, gestational hypertension, preeclampsia, preeclampsia superimposed on chronic hypertension, and Hemolysis, Elevated liver enzymes and Low platelets (HELLP) syndrome. 12,13 Defining characteristics of the hypertensive disorders of pregnancy can be observed in Table 1. As convulsions may be the presenting symptom of preeclampsia, seizures in pregnant or postpartum patients should be considered eclampsia until proven otherwise. 14

management of eclampsia presentation ppt

Epidemiology

In the United States, eclampsia occurs in approximately 0.3% of live births with significant variation in incidence between states. 15 This variation is likely due to differences in screening and the use of magnesium sulfate, economic inequity, quality and access to obstetric care, and the distribution of physical factors associated with eclampsia. 15 Socioeconomic status has been found to play an important role in the incidence of eclampsia with the presence of public insurance and fewer than five prenatal visits significantly increasing the risk of eclampsia. 16 Other factors associated with eclampsia are similar to those for preeclampsia, and include, extremes of maternal age, nulliparity, multiple gestations, obesity, diabetes, and preterm delivery at <32 weeks of gestation. 10,16-18 Eclampsia is also more common among women who self-identify as Black or Hispanic for reasons that are multifactorial and likely related to social determinants of health, including access to prenatal care and chronic stress associated with experiences of racial discrimination. 16,17,19,20

Maternal Fetal Outcomes

In the acute setting, complications associated with highest morbidity include stroke, coma or persistent loss of consciousness, heart failure, pulmonary edema, venous thrombosis, and disseminated intravascular coagulation. Pregnant patients with a history of eclampsia have a 25% risk of developing eclampsia in subsequent pregnancies and long term sequelae, including a 12-fold risk of cardiovascular-related pathologies, such as myocardial infarction, cerebrovascular disease and heart failure. 21 Neonates born to patients with eclampsia are at increased risk of being small for gestational age due to intrauterine growth restriction and complications associated with premature birth, including neonatal respiratory distress syndrome. 10,22,23

Time of Onset

Eclampsia can present during the antepartum, intrapartum, or postpartum period. 24-26 In the postpartum period, the onset of convulsions may occur within the first 48 hours (early postpartum) or up to six weeks following delivery (late postpartum). 24,27 Among eclampsia cases, 59-70% of occur during the antepartum period, around 20- 30% occur during labor (intrapartum), and 20- 30% occur in the postpartum period, including 15- 16% in the late postpartum period. 10,26,28,29 In the antepartum period, virtually all eclamptic seizures occur after 28 weeks of gestation. When seen before 20 weeks of gestation, eclampsia is usually associated with a molar pregnancy, multiple gestations, or severe maternal renal disease. 5,10,30,31

Presentation

More than 50% of eclamptic seizures are preceded by prodromal symptoms. 14,26,32 The most common reported symptoms are headache (66-82%), visual disturbances (27-44%), and epigastric pain (25%). 14,29,33 Visual disturbances include blurry vision, diplopia, scotoma, photopsia, and transient cortical blindness. 10,34,35 However, none of these symptoms have been found to accurately predict, or rule out, imminent eclampsia. 8,14,29,36 Additionally, if the patient is unresponsive and records or family members are unavailable, it may not be possible to evaluate for these prodromal symptoms. 5 For this reason, many clinicians rely on exam findings and laboratory evidence of eclampsia including hypertension and proteinuria.

While hypertension has long been recognized as a manifestation of preeclampsia and a warning sign for eclampsia, the degree of hypertension may not always predict the risk of eclampsia. 30 Approximately 20% of eclampsia cases occur in patients with only mild hypertension. Furthermore, hypertension may be absent in up to 25% of cases. 8-10,29 Severe hypertension is more common in pregnant patients who developed eclampsia in the antepartum period rather than the postpartum period. 26

Differential Diagnosis

While the evaluation of seizure in pregnant or postpartum patients should begin with a consideration of eclampsia, alternative diagnoses should also be considered in certain circumstances. 10 These circumstances include patients with normal blood pressure and the absence of proteinuria, focal neurologic deficits, onset before 20 weeks of gestation or >48 hours after delivery, or prolonged loss of consciousness. 10,37 In these cases, the differential diagnosis can generally be broken down into three categories of conditions: exacerbation of known pre-existing seizure disorder (mainly epilepsy), new onset of seizures due to non-pregnancy related problem (eg, metabolic alterations, brain tumors, infections), and neurologic conditions either specific to or frequently occurring during pregnancy. 14,38-40 A complete differential diagnosis of seizures that should be taken into consideration is listed in Figure 1. 5,7,10,14

Figure 1: Differential Diagnosis of Seizure During Pregnancy or After Delivery . 5,10

management of eclampsia presentation ppt

History and Physical Exam

A thorough history and physical examination are key to narrowing the differential diagnosis. Seizure activity in a pregnant or postpartum patient without a history of epilepsy should be considered eclampsia until proven otherwise. 5 In 78-83% of eclampsia cases, the seizures are preceded by signs of cerebral irritation, such as persistent headaches, blurred vision, photophobia, or altered mental status. 12 As eclamptic seizures are typically tonic-clonic in nature and often last less than one minute, obtaining as much history of the event, including any symptoms prior to the onset of seizure activity, length of time and bodily location of convulsions, and presence of post-ictal state can be useful in ruling out potential etiologies. 26,32 A full history may be difficult to obtain from the patient if there are alterations in mental status. However, when possible, information regarding the pregnancy, including gestational age, complications, mode of delivery if postpartum and maternal history should be obtained.

While all patients presenting with seizure—especially new onset—should have a full neurological examination in the ED, physical examination following eclamptic seizure may be unremarkable, apart from hypertension or residual confusion. Clonus or hyperreflexia may be found on focused neurology exam. 35,41 Patients who go on to develop eclamptic seizures often present with symptoms of headache, visual disturbance, or altered mental status. Neuroimaging is not recommended in the routine care or diagnosis of patients with eclampsia. However, in patients with atypical presentations, including recurrent convulsions, prolonged coma or focal neurologic deficits, neuroimaging may be warranted to rule out cerebral edema, infarction, and hemorrhage, which would require additional pharmacologic or surgical intervention. 10,41,42

Recognizing the manifestations of eclampsia is particularly important as eclampsia is one of the most preventable causes of gestational mortality, which occurs secondary to high rates of diagnostic delay, ineffective control of blood pressure, and lack of continuity of care. 43 A recent study among Ob/Gyn residents found that while all learners were familiar with the management of pre-eclampsia and emergent hypertension, none were able to stop an eclamptic seizure in a case-based simulation. 44 Furthermore, all participants indicated they had no exposure to patients with eclampsia and found the simulation immensely valuable, suggesting a gap in resident medical education and that exposure may contribute to the preventable deaths associated with eclampsia.

  Management

As with all patients who arrive at the emergency department with active seizure-like movements, initial consideration for respiratory and circulatory status should take precedence. Any concern for patency of the airway should be addressed immediately and obstruction with secretions should be addressed with suctioning of the oropharynx following cessation of seizure activity. 5 Oxygenation and prevention of hypoxia for both patient and fetus should be addressed with supplemental oxygen as appropriate. Additionally, maternal repositioning to the left lateral decubitus position can increase placental blood flow and reduce risk of aspiration. 45

In gravid or peripartum patients who present with seizure or concern for eclampsia, OB/GYN consult should be obtained early in emergency department evaluation. Following stabilization, patients should be admitted or transferred to a tertiary medical center with OB/GYN service for continuous monitoring, assurance of fetal wellbeing, and delivery planning ifprepartum. 10

Seizure activity

The mainstay of treatment for eclampsia is magnesium sulfate, both as seizure prophylaxis in patients with preeclampsia and as a first line antiepileptic when seizures occur. 44,46-49 A 2010 Cochrane review evaluating the evidence supporting magnesium sulfate vs. diazepam in the treatment of eclampsia demonstrated fewer maternal deaths and recurrence of seizures in patients receiving magnesium. There was no difference in neonatal outcomes. 50 The largest trials included in this review demonstrated a 52% lower risk of recurrent convulsions in patients receiving magnesium sulfate when compared with diazepam and a 67% lower risk when compared with phenytoin. 51 The American College of Obstetrics and Gynecology (ACOG) currently maintains a level A recommendation for the use of magnesium sulfate in the prevention and treatment of eclampsia. A summary of the following recommendations can be seen in Table 2.

Mechanistically, magnesium has many sites of action, but exerts its main therapeutic effect by stabilizing cell membrane potentials and inducing smooth muscle relaxation. 52 Therapeutic plasma levels of magnesium necessary to reduce and prevent seizures (3.5-7mEq/L) are much greater than those used in treatment of other conditions. 53 The most recent ACOG guidelines recommend initial dosing in any patient suspected to have eclampsia includes a loading dose of 4 or 6 grams over 15-20 minutes, followed by maintenance with continuous infusion at a rate of 2 g/hr. 10 If IV magnesium sulfate is not available or IV access cannot be established, administer a 10g loading dose IM (5g IM in each buttock) followed by 5g IM every 4 hours.

There are few absolute contraindications to magnesium sulfate therapy, including myasthenia gravis, severe hypocalcemia, complete heart block, and myocarditis. 12 Renal failure is a relative contraindication. Magnesium is fully excreted by the kidneys and therefore dosing should be adjusted in patients with potential for reduced clearance. 44 Patients with serum creatinine > 1.2mg/dL should receive a standard loading dose of 4 to 6 grams, but a maintenance infusion at a lower rate of 1g/hr. 54 Caution is advised in patients taking labetalol and nifedipine; administration of magnesium sulfate may produce a synergistic effect leading to bradycardia and/or hypotension. 55 Monitoring of magnesium levels is not universally recommended, except in patients with renal dysfunction or those showing signs of toxicity, such as loss of deep tendon reflexes, respiratory depression, or cardiac arrest. 10 Attention should be taken to limit total IV fluid administration to an average of <125 mL/hr to avoid pulmonary edema, a common complication of severe preeclampsia. 56

Despite proper dosing and monitoring, approximately 10% of eclamptic patients will have recurrence of seizure activity following administration of magnesium sulfate. 55 Return of convulsions should be addressed with a second 2g bolus of magnesium sulfate given over a course of 3 to 5 minutes. While rare, seizures resistant to magnesium sulfate, or with recurrence following a second magnesium bolus, treatment with benzodiazepines can be considered, with recent reviews recommending dosing 4 mg lorazepam over 3 to 5 minutes. 10 In cases where magnesium sulfate is unavailable, or there is a significant delay in preparation, patients may be initiated on benzodiazepine therapy with intravenous diazepam at a rate of 2mg/min with a maximum of 10mg, or clonazepam 1-2mg over 2-5 minutes. 57 In patients of childbearing age with recurrent seizure activity and unknown history of recent or current pregnancy, magnesium sulfate therapy should be considered, especially if seizures are refractory to typical therapy.

management of eclampsia presentation ppt

Hypertension

Severe range hypertension in pregnancy is defined as systolic blood pressures >160 mmHg and/or diastolic blood pressures >110 mmHg. 10,58 This is the range at which the likelihood of the patient developing eclampsia, stroke, and/or vasogenic edema, rises precipitously. 46 Note that these threshold values for hypertensive emergency in pregnancy are much lower than the blood pressure ranges considered to be emergent in non-pregnant adults. Prior research has demonstrated that increased cerebral perfusion and vasogenic edema secondary to hypertension can independently produce seizure activity, thus, increasing the importance of maintaining blood pressures below the severe range. 59

While definitive management of severe hypertension from preeclampsia is delivery of the fetus and placenta, temporizing antihypertensive medications should be administered as soon as possible. 58 Anti-hypertensive agents other than labetalol, hydralazine, and nifedipine (immediate release formulation) have either not been tested in pregnant populations or are associated with fetal toxicity and should be avoided whenever possible. Immediately following administration, blood pressures should be reassessed at 10-minute intervals, with additional dosing as described in Figure 2.

management of eclampsia presentation ppt

  • Eclampsia is among the top six causes of maternal death in the United States
  • Eclampsia should be in the differential in any female or antepartum or postpartum patient presenting with altered mental status, persistent headache, visual changes, or convulsive symptoms.
  • The immediate management of eclampsia for both seizure treatment and prophylaxis is IV magnesium sulfate.
  • Hypertension of greater than or equal to 160/110 in the pregnant patient is an emergency and should be managed with immediate administration of antihypertensive medications safe for use in pregnancy.

From Dr. Katy Hanson at Hanson’s Anatomy :

management of eclampsia presentation ppt

References/Further Reading:

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  • Abraham C, Kusheleva N. Management of pre-eclampsia and eclampsia: a simulation. MedEdPORTAL. 2019;15:10832. https://doi.org/10.15766/mep_2374-8265.10832 .
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  • Garg D, Rahaman B, Stein EG, Dickman E. Late Postpartum Eclampsia with Postpartum Angiopathy: An Uncommon Diagnosis in the Emergency Department. J Emerg Med. 2015;49(6):e187-191.
  • Sibai BM. Magnesium sulfate prophylaxis in preeclampsia: Lessons learned from recent trials. Am J Obstet Gynecol. 2004;190(6):1520-1526.
  • Eclampsia checklist. In ACOG safe motherhood initiative. 2017. Available at: https://www.acog.org/-/media/Districts/District-II/Public/SMI/v2/sm02a170713EclampsiaCheckRev072017.pdf?dmc51&ts520170928T0147570258 . Accessed January 18, 2021.
  • Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995;333(4):201-205.
  • Duley L, Henderson-Smart DJ, Walker GJ, Chou D. Magnesium sulphate versus diazepam for eclampsia. Cochrane Database Syst Rev. 2010(12):CD000127.
  • The Eclampsia Trial Collaborative G. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial. The Lancet. 1995;345(8963):1455-1463.
  • Tso E, Reid RP, Barish RA, Browne BJ. Late postpartum eclampsia. Ann Emerg Med. 1987;16(8):907-909.
  • Euser AG, Cipolla MJ. Magnesium sulfate for the treatment of eclampsia: a brief review. Stroke. 2009;40(4):1169-1175.
  • Alexander JM, McIntire DD, Leveno KJ, Cunningham FG. Selective magnesium sulfate prophylaxis for the prevention of eclampsia in women with gestational hypertension. Obstet Gynecol. 2006;108(4):826-832.
  • Gilardi E, Marsiliani D, Nicolo R, et al. Magnesium sulphate in the Emergency Department: an old, new friend. Eur Rev Med Pharmacol Sci. 2019;23(9):4052-4063.
  • Anthony J, Schoeman LK. Fluid management in pre-eclampsia. Obstet Med. 2013;6(3):100-104.
  • Lowe SA, Bowyer L, Lust K, et al. SOMANZ guidelines for the management of hypertensive disorders of pregnancy 2014. Aust N Z J Obstet Gynaecol. 2015;55(5):e1-29.
  • Kattah AG, Garovic VD. The management of hypertension in pregnancy. Adv Chronic Kidney Dis. 2013;20(3):229-239.
  • Zeeman GG, Hatab M, Twickler DM. Maternal cerebral blood flow changes in pregnancy. Am J Obstet Gynecol. 2003;189(4):968-972.

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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StatPearls [Internet].

Acute eclampsia.

Prabhcharan Gill ; Anita P. Tamirisa ; James W. Van Hook .

Affiliations

Last Update: February 27, 2023 .

  • Continuing Education Activity

Eclampsia is a pregnancy-related disorder that manifests as new-onset generalized tonic colonic seizures. Typically eclampsia occurs after gestational week 20, although it may occur sooner with multi-gestational or molar pregnancies and may occur in the 6-week postpartum window. In developed countries, resultant maternal mortality may be as high as 1.8%, and in developing countries, it may be as high as 14%. This activity reviews the presentation, evaluation, and management of patients with eclampsia and highlights the interprofessional team's role in caring for patients with this condition.

  • Identify risk factors associated with eclampsia and preeclampsia.
  • Explain how a patient with eclampsia might present.
  • Explain how to treat a patient with eclampsia.
  • Outline the role of a collaborative interprofessional team in coordinating care for patients with eclampsia.
  • Introduction

Eclampsia is a uniquely pregnancy-related disorder that manifests as a new onset of generalized tonic colonic seizures. It typically occurs after 20 weeks of concluded gestation, although it may occur sooner with plural gestations or molar pregnancies, and may additionally occur in the 6-week postpartum window. It represents the severe end of the preeclampsia spectrum. Preeclampsia spectrum includes symptoms of the central nervous system (CNS), for example, severe headaches or vision changes, and may involve hepatic abnormalities (such as elevated liver transaminases with right upper quadrant/epigastric discomfort), elevated blood pressures, and also may include thrombocytopenia, renal abnormalities, and pulmonary edema. In developed countries, resultant maternal mortality may be as high as 1.8%, and in developing countries, it may be as high as 14%. [1]

The etiology of the disorder remains elusive. The placenta seems to have a prime role in its etiology. An increase in placental mass, as in plural pregnancies, increases the risk for the preeclampsia-eclampsia spectrum, as does placental edema that occurs in pregnancies complicated by fetal hydrops. Molar pregnancies that impact placental architecture also have a higher risk of the complication.

  • Epidemiology

In developed countries, the incidence of preeclampsia has been described to be between 1.5 to 10 cases in 100,000 deliveries. The condition is more prevalent in developing countries. The risk factors of preeclampsia are similar to those of preeclampsia and include nulliparity, non-White race, low socioeconomic backgrounds, plural pregnancies, and extremes of maternal age. Additionally, it is associated with an array of maternal medical conditions such as chronic hypertension, chronic renal disease, and autoimmune disorders. Obesity and maternal diabetes are also recognized as increasingly important etiologies. Fetal conditions, such as fetal hydrops, have been associated with preeclampsia. 

  • Pathophysiology

Some have suggested hypertension causes breakdown of the autoregulatory mechanisms of cerebral circulation, inducing endothelial dysfunction that concludes in cytotoxic edema and expression of a generalized seizure. Inflammation of the cerebrum seems to play a role in the pathophysiology. In some scenarios, it may be associated with posterior reversible encephalopathy syndrome due to posterior circulation's inability to autoregulate itself in response to acute hypertension. [2]

  • Histopathology

In a 1973 report, autopsy findings included more than 50% of women who died within 2 days of seizures had evidence of cerebral hemorrhages. It also described brain histopathology. Occipital lobe petechial hemorrhages were a common finding. Cerebral venous thrombosis was also frequently observed. Since then, some studies have used free radical stains to demonstrate endothelial, histiocytic, and platelet markers suggestive of capillary injury in otherwise intact brain parenchyma.

  • History and Physical

There may be a history of worsening headaches with vision changes such as blurred vision or “spots.” Hypertension and proteinuria may be present or absent. Impending eclampsia may have clonus. Eclampsia is a clinical diagnosis described by the occurrence of new-onset generalized tonic-clonic seizures in a woman with preeclampsia; however, on occasion, it may be the first presentation of preeclampsia. Clinical findings may include posterior reversible encephalopathy syndrome (due to vasogenic edema predominantly localized in the posterior cerebral hemispheres), including headaches, confusion, visual symptoms, and seizure.

Women known to have preeclampsia may develop eclamptic, generalized, tonic-clonic seizures that conclude with no persistent neurologic deficit, meaning they do not deserve diagnostic evaluation beyond that performed for preeclampsia. A preeclampsia workup would include evaluating renal function, liver function, complete blood count, and imaging of the fetoplacental unit. Obstetric ultrasound imaging of the fetus includes an assessment of fetal growth as well as fetal health (biophysical profile and as indicated umbilical artery cord Doppler studies), including fetal heart rate strip. [3]  Clinical monitoring for placental abruption is heightened, as is maternal monitoring for evolving complications such as pulmonary edema or renal dysfunction. Neuroimaging should be considered if:

  • Persistent neurologic deficits
  • Prolonged loss of consciousness
  • The onset of seizures is 48 hours beyond delivery.
  • An eclamptic seizure occurs before 20 weeks.
  • Recurrent seizures despite adequate magnesium sulfate therapy
  • Treatment / Management

Acute care is prioritized to maintain the airway, prevent aspiration, and prevent maternal injury. The patient should be shifted onto her left side, and once the seizures have concluded, maternal oxygenation is optimized with the supplemental oxygen of 8 to 10 liters per minute administered via a nonrebreathing face mask to treat hypoxemia that occurs from hypoventilation during the seizure activity. [3]

Magnesium sulfate is a treatment of choice to prevent recurrent seizures; however, approximately 10% will have a repeat seizure despite magnesium sulfate therapy. Recurrent seizures require surveillance for rhabdomyolysis, metabolic acidosis, aspiration pneumonia, and neurogenic pulmonary edema. Magnesium sulfate remains superior for recurrent seizure activity (an additional 2 gm bolus can be considered in those already on magnesium sulfate therapy), but intravenous lorazepam 2mg intravenously over 3 to 5 minutes may also be considered. The initial loading bolus of magnesium sulfate is 4 gm to 6 gm intravenously over 15 to 20 minutes with a maintenance dose of 1 gm to 3 gm an hour, depending on renal function. Blood levels of magnesium are monitored every four hours and targeted at four mEq/L to -7 mEq/L or 5 mg/dl to 9 mg/dl. Urine output is closely monitored. Should magnesium sulfate toxicity occur calcium, gluconate 1 gm intravenously can be administered.

Management of severe hypertension is the next focus of patient care. A preferred agent for the treatment of severe hypertension is intravenous labetalol (initial dose of 20 mg and for recalcitrant severe hypertension follow-up dose of 40 mg and 80 mg every 15 minutes). Maintaining systolic blood pressure between 140 mm Hg to 160 mmHg and diastolic blood pressure between 90 mmHg to 105 mmHg are targeted treatment goals.

Fetal bradycardia lasting 3 to 5 minutes is a common finding during and immediately after the seizure and does not indicate emergency cesarean delivery. Stabilization of the mother by stabilizing the seizure activity and correction of maternal hypertension if present and oxygen to treat hypoxemia and hypercarbia is the mainstay of initial supportive therapies are part of fetal intrauterine fetal resuscitation.  However, if the fetal heart rate strip does not improve after 15 minutes of maternal and fetal resuscitative interventions, then a differential diagnosis of occult abruption should be considered, and emergent cesarean delivery may be indicated. Eclampsia represents an absolute contraindication to expectant management. Once the maternal-fetal condition is stabilized, delivery should be accomplished by labor induction. This is a particularly reasonable option after 32 weeks of gestation. It may be an option at early gestations with a favorable Bishop score; however, long induction-delivery intervals are best avoided with a clear end-point for delivery to be concluded within 24 hours.

  • Differential Diagnosis
  • Adrenal insufficiency and adrenal crisis
  • Cerebral hemorrhage
  • Cerebral aneurysms
  • Cerebral venous thrombosis
  • Encephalopathy
  • Encephalitis
  • Gestational trophoblastic neoplasia
  • Head trauma
  • Hypertensive emergencies
  • Hypoglycemia

Most females with mild preeclampsia have positive pregnancy outcomes. Eclampsia has an overall 2% mortality rate, so it is a serious condition. The recurrence risk for preeclampsia depends on the severity of the condition.

Patients with eclampsia may demonstrate an increased risk for cardiovascular disease later in life; this risk is increased in more severe cases or those with early-onset.

  • Complications
  • Cortical blindness
  • Neurological deficits
  • Coronary event
  • Renal failure
  • Liver dysfunction
  • Intrauterine growth retardation
  • Deterrence and Patient Education

Women need to continue to receive education and counsel regarding eclampsia into the post-partum period to understand and recognize the symptoms that accompany post-partum eclampsia. Post-partum women who present for treatment (usually at an emergency department) should be provided a consult with an OB/GYN specialist, not merely emergency medicine clinicians.

  • Pearls and Other Issues

As a point of caution, when an eclamptic seizure is diagnosed before 20 weeks, it deserves careful exclusion of non-obstetric etiologies such as brain tumor or ruptured aneurysm, as does the diagnosis of delayed postpartum eclampsia. Approximately 60% of the cases occur antepartum, and 20% occur intrapartum, and finally, 20% of the cases occur postpartum. Approximately 90% of the postpartum seizures occur within one week of delivery.

  • Enhancing Healthcare Team Outcomes

Eclampsia is a serious disorder of pregnancy that can jeopardize the lives of both the mother and the fetus. Because the condition can affect many organ systems, an interprofessional approach to management is highly recommended. The nurse looking after a patient with eclampsia must be aware of the potential complications to make a prompt physician referral. The nurse should monitor vital signs and for progression. Any untoward complications should be immediately addressed with the clinical team. The pharmacist should assist in medication reconciliation and in making sure appropriate treatment doses are ordered. This is a challenging disease and relatively uncommon. The clinical team, including nurses, pharmacists, and clinicians, need to assist in patient and family education. Only through an interprofessional approach will the best outcomes be achieved. [Level 5]

Over the past 3 decades, the outcomes of eclampsia have improved chiefly due to improvements in healthcare. However, morbidity from the disorder still occurs. At least 20% of women with eclampsia will go on to develop hypertension in subsequent pregnancies, and another 2 to 5% will develop eclampsia in a future pregnancy. Overall, multiparous females are not only likely to develop hypertension but also have higher mortality compared to primiparous women. Because there is no reliable test to predict who will develop pre-eclampsia, all high-risk women are urged to take low-dose aspirin during pregnancy. Finally, all pregnant women should be educated about the signs and symptoms of preeclampsia and when to seek medical help.

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Disclosure: Prabhcharan Gill declares no relevant financial relationships with ineligible companies.

Disclosure: Anita Tamirisa declares no relevant financial relationships with ineligible companies.

Disclosure: James Van Hook declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

  • Cite this Page Gill P, Tamirisa AP, Van Hook JW. Acute Eclampsia. [Updated 2023 Feb 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Preeclampsia: Pathophysiology and Clinical Presentations

The following are key points to remember from this JACC state-of-the-art review on preeclampsia—pathophysiology and clinical presentations:

  • Preeclampsia is a hypertensive disorder of pregnancy that occurs in 2-8% of pregnancies and causes substantial morbidity and mortality.
  • Preeclampsia is defined as new-onset hypertension and new-onset end-organ damage after 20 weeks’ gestation. Proteinuria is no longer required for the diagnosis.
  • The complex pathophysiology of preeclampsia begins with abnormal placental development, endothelial dysfunction, and immunologic aberrations, possibly related to genetic susceptibility. Clinical features of preeclampsia include hypertension, proteinuria, renal dysfunction, neurological abnormalities, eclampsia, cardiac dysfunction, pulmonary edema, hepatic dysfunction, hematologic dysfunction, and fetal growth restriction.
  • Hypertension is necessary for the diagnosis of preeclampsia, defined as systolic blood pressure (SBP) ≥140 mm Hg or diastolic BP (DBP) ≥90 mm Hg on two occasions ≥4 hours apart after 20 weeks’ gestation in a woman with previously normal BP; or SBP ≥160 mm Hg or DBP ≥110 mm Hg on one occasion.
  • Proteinuria: The imbalance between proangiogenic and antiangiogenic factors likely causes podocyte injury leading to increased risk of hypertension and chronic kidney disease. Proteinuria can take up to 2 years to resolve after preeclampsia.
  • Renal dysfunction in preeclampsia is defined as serum creatinine >1.1 mg/dl or a doubling of baseline creatinine. Inflammatory cytokines lead to endothelial dysfunction and thrombotic microangiopathy of the kidneys, and decreased intravascular volumes in preeclampsia increases sodium and free-water retention.
  • Neurologic dysfunction includes headaches, visual disturbances, seizure, posterior reversible encephalopathy syndrome, and hemorrhagic stroke. The classic preeclampsia headache is progressive, bilateral, pulsating/throbbing, associated with visual changes, worse with higher BP, worsened by physical activity, and not relieved by over-the-counter medications.
  • Eclampsia is defined as new-onset tonic-clonic, focal or multifocal seizures in the setting of pregnancy-related hypertension. Magnesium reduces the risk of eclampsia by 59%.
  • Cardiac dysfunction: Impaired placentation in preeclampsia causes increased vascular resistance and higher afterload, resulting in mild-to-moderate left ventricular diastolic dysfunction with concentric left ventricular hypertrophy. Preeclampsia is also a risk factor for peripartum cardiomyopathy (defined as left ventricular systolic function <45%).
  • Pulmonary edema is rare in preeclampsia and is related to: 1) increased vascular permeability, 2) cardiac dysfunction, 3) corticosteroids/tocolytics, and 4) iatrogenic volume overload.
  • Hepatic dysfunction is defined as transaminases ≥2x the upper limit of normal (AST typically < ALT) with right upper quadrant or epigastric tenderness.
  • Hematologic disturbances in preeclampsia include thrombocytopenia (due to increased platelet activation, aggregation, and consumption) and disseminated intravascular coagulopathy (due to consumption coagulopathy, hepatic injury and decreased clotting factors, and/or inflammatory response).
  • Fetal growth restriction (defined as an estimated fetal weight <10th percentile for gestational age) occurs commonly in pregnancies complicated by preeclampsia. Several mechanisms of uterine and placental dysfunction contribute to intrauterine growth restriction.
  • Low-dose aspirin is recommended for prevention of preeclampsia in high-risk women. Possible benefits of exercise, pravastatin, and metformin are being investigated. The definitive treatment for preeclampsia is delivery.
  • Further research to understand the link between preeclampsia and subsequent short- and long-term cardiovascular disease is needed.

Clinical Topics: Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Prevention, Vascular Medicine, Acute Heart Failure, Hypertension

Keywords: Aspirin, Cardiomyopathies, Eclampsia, Fetal Growth Retardation, Headache, Hypertension, Hypertension, Pregnancy-Induced, Hypertrophy, Left Ventricular, Pre-Eclampsia, Kidney Diseases, Pregnancy, Primary Prevention, Proteinuria, Pulmonary Edema, Renal Insufficiency, Seizures, Stroke, Thrombocytopenia, Vascular Diseases

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critical care management of preeclampsia and eclampsia

Critical care management of preeclampsia and eclampsia

Jan 04, 2020

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Critical care management of preeclampsia and eclampsia. Gunnar Dahlgren, MD, PhD Department of Anesthesia and Intensive Care Karolinska University Hospital Stockholm. [email protected]. The obstetric ICU patient. Intensive Care Unit. Delivery room. Post Anesthesia Care Unit.

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Critical care management of preeclampsia and eclampsia Gunnar Dahlgren, MD, PhD Department of Anesthesia and Intensive Care Karolinska University Hospital Stockholm [email protected]

The obstetric ICU patient Intensive Care Unit Delivery room Post Anesthesia Care Unit Operating room

The cause of preeclampsia is unknown • Primary placental causes • Secondary maternal systemic illness • Ill-defined links between the two (maternal systemic inflammatory response?)

Primary changes in the vasculature • Impaired endothelial production of prostacylin, and possibly NO • Release of platelet-derived factors as thromboxane and serotonin • Release of endothelial procoagulant factors Vasoconstriction Low grade DIC

Pathology • Placenta: Spiral arteries fail to undergo physiological dilatation and show luminal disease similar to acute atherosis in non-pregnant patients • Kidney: Glomerular capillary endotheliosus. Might progress to ATN or acute cortical necrosis • Placenta, kidney, brain, and liver show features consistent with chronic ischemia

Inadequate cellular oxygenation • Low cardiac filling pressures (CVP, PCWP), decreased plasma volume • Vasoconstriction - increased SVR • Low cardiac output • Tissue oxygen extraction impaired Inadequate oxygen delivery and consumption

Hypertension in pregnancy • Pre-existing hypertension (3-5% of pregnancies) • Pregnancy-associated hypertension (12%) (occurring de novo after the 20th week of pregnancy and settling within 6 weeks after delivery) • Gestational hypertension (6-7%) • Preeclampsia (5-6%) • Superimposed preeclampsia (25% of women with pre-existing hypertension) Lancet 2000: 356: 1260-1265

Preeclampsia/eclampsia definitions • Preeclampsia: Hypertension >140/90 with proteinuria of at least 0.3g/24h • Severe preeclampsia: Preeclampsia with hypertension >160/110 or proteinuria >5g/24h or multiorgan involvement • Eclampsia: Convulsions in any woman who has, or then presents with, hypertension in pregnancy of any cause

Symptoms other than hypertension and proteinuria in severe preeclampsia • Oliguria (<400 ml/24h) • Cerebral signs (headache, blurred vision, altered consciousness) • Pulmonary edema, cyanosis • Epigastric or right upper quadrant pain • Impaired liver function • Hepatic rupture • Trombocytopenia • HELLP syndrome

Fetal complications of severe preeclampsia • Intrauterine growth retardation • Premature delivery • Abruptio placentae • Fetal distress/fetal demise Associated maternal risks General/regional anesthesia DIC Hemorrhage

Maternal complications of severe preeclampsia • Cardiovascular dysfunction (cardiac failure, hypertension) • Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis) • Respiratory dysfunction (ARDS, pulmonary edema) • Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome) • Cerebral dysfunction (encephalopathy, ischemia, cortical blindness, retinal detachment, infarction, hemorrhage, edema, eclampsia)

”Delivery of the fetus and placenta is the definitive management of severe preeclampsia. Once severe disease has been established and is progressing, delivery of the fetus and placenta must be accomplished to limit maternal risk.” Int Care Med 1997: 23: 248-255

Invasive hemodynamic monitoring • There are no data from randomized controlled clinical studies illustrating the usefulness of PA-catheters or echocardiographic techniques in patients with preeclampsia • Echocardiography shows good agreement with PA-catheter measurements of cardiac output • CVP may be misleading and needs cautious interpretation, particularly in patients treated with vasoactive agents or plasma volume augmentation • Invasive monitoring could still be considered in patients with persistant oliguria, pulmonary edema and significant blood loss in order to guide therapy Best Pract Res Clin Obst Gyn 2001: 15: 605-622

Maternal complications of severe preeclampsia • Cardiovascular dysfunction (cardiac failure, hypertension) • Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis) • Respiratory dysfunction (ARDS, pulmonary edema) • Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome) • Cerebral dysfunction (encephalopathy, ischemia, cortical blindness, retinal detachment, infarction, hemorrhage, eclampsia)

Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation

Untreated pre-eclampsia Best Pract Res Clin Obst Gyn 2001: 15: 605-622

Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable

Treated pre-eclampsia Best Pract Res Clin Obst Gyn 2001: 15: 605-622

Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable • In patients with pulmonary edema a significant part of the women has a depressed cardiac performance

Pulmonary edema Best Pract Res Clin Obst Gyn 2001: 15: 605-622

Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable • In patients with pulmonary edema a significant part of the women has a depressed cardiac performance • Diastolic dysfunction, estimated with echocardiography, is not uncommon in preeclamptic patients with pulmonary edema • There is an association between preeclampsia and peripartem cardiomyopathy

Hypertension • Untreated severe hypertension increases the risk for cerebral hemorrhage, renal/liver dysfunction, pulmonary congestion, decreased placental perfusion, placental detachment • Treatment indicated in severe hypertension • Hydralazine less effective than nifedipine and equally effective as labetalol for reducing blood pressure* • Side-effects (eg maternal hypotension, placental abruption, cesarean section) more frequent with hydralazine than with labetalol and nifedipine* * BMJ 2003: 327: 955-964

Oliguria • Decreased plasma volume • Decreased renal perfusion and glomerular filtration • Pre-renal oliguria may develop to acute tubular necrosis, most often with a good prognosis • Acute cortical necrosis is rare; poor prognosis Diuresis <100 ml/4h Plasma volume expansion if CVP is <5 mmHg Furosemide if fluid balance is positive Echocardiography PA catheter to optimize left ventricular preload (PCWP 12-14 mmHg) and reduce afterload appropriately

Pulmonary edema • Incidence 6% in severe preeclampsia • Reduced COP (from 22 in normotensive patients at term to 15 mmHg in severe preeclampsia), a further reduction in COP after delivery. • A COP-PCWP difference of 4 mmHg or less is associated with pulmonary edema in critically ill non-pregnant patients (Chest 1977: 72: 709) • Increased capillary permeability • Possible left ventricular dysfunction (systolic and/or diastolic) • Increased risk during the first day(s) post partem

HELLP syndrome • Microangiopathic hemolytic anemia, consumptive thrombocytopenia, liver dysfunction • 4-12% of patients with severe preeclampsia, 30% occur postpartum • DIC often secondary to placental abruption, sepsis or fetal death • Platelet count indirectly proportional to severity of disease • Differential diagnoses: TTP, HUS, SLE, sepsis, acute fatty liver of pregnancy • Complications: ARF, ARDS, hemorrhage, placental abruption, rarely liver hematoma with rupture

Lancet 1995: 345: 1455-1463

Lancet 2002: 359: 1877-1890

Eclampsia • The treatment of choice for eclampsia and prophylaxis against recurrent convulsions is magnesium sulphate (Lancet 1995: 345: 1456-1463) • Magnesium sulphate is also the drug of choice for seizure prophylaxis in patients with preeclampsia (Lancet 2002: 359: 1877-1890) • Prophylaxis in patients with preeclampsia is however in many departments limited to patients with severe preeclampsia or impending eclampsia • Stabilize maternal condition before vaginal or cesarean delivery!

Impending eclampsia Severe preeclampsia with signs of cerebral affection like visual disturbancies, headache, increased reflexes, and clonus BJA 1996: 76: 133-148

Summary • Preeclampsia is a syndrome of unknown etiology with multiorgan involvement • It presents with a wide spectrum of symptoms • It is sometimes difficult to distinguish from other systemic diseases • Severe cases may progress to MOF and death • Delivery of the child and placenta is the only specific treatment – other lines of teatment are only supportive • There are several issues regarding diagnostic techniques and treatment options that need further evaluation

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Management of Medicines and Pharmaceutical Supplies for use in the prevention and treatment of Pre-eclampsia and Eclampsia PowerPoint PPT Presentation

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LANA K. WAGNER, M.D.

Am Fam Physician. 2004;70(12):2317-2324

Preeclampsia is a pregnancy-specific multisystem disorder of unknown etiology. The disorder affects approximately 5 to 7 percent of pregnancies and is a significant cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by the new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. It is considered severe if blood pressure and proteinuria are increased substantially or symptoms of end-organ damage (including fetal growth restriction) occur. There is no single reliable, cost-effective screening test for preeclampsia, and there are no well-established measures for primary prevention. Management before the onset of labor includes close monitoring of maternal and fetal status. Management during delivery includes seizure prophylaxis with magnesium sulfate and, if necessary, medical management of hypertension. Delivery remains the ultimate treatment. Access to prenatal care, early detection of the disorder, careful monitoring, and appropriate management are crucial elements in the prevention of preeclampsia-related deaths.

Preeclampsia is a pregnancy-specific, multisystem disorder that is characterized by the development of hypertension and proteinuria after 20 weeks of gestation. The disorder complicates approximately 5 to 7 percent of pregnancies, 1 with an incidence of 23.6 cases per 1,000 deliveries in the United States. 2

Complications of hypertension are the third leading cause of pregnancy-related deaths, superseded only by hemorrhage and associated with increased risks of placental abruption, acute renal failure, cerebrovascular and cardiovascular complications, disseminated intravascular coagulation, and maternal death. 3 Consequently, early diagnosis of preeclampsia and close observation are imperative.

Diagnostic criteria for preeclampsia include new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. Features such as edema and blood pressure elevation above the patient’s baseline no longer are diagnostic criteria. 4 , 5 Severe preeclampsia is indicated by more substantial blood pressure elevations and a greater degree of proteinuria. Other features of severe preeclampsia include oliguria, cerebral or visual disturbances, and pulmonary edema or cyanosis ( Table 1 ). 4 , 5

Diagnosis becomes less difficult if physicians understand where preeclampsia “fits” into the hypertensive disorders of pregnancy. These disorders include chronic hypertension, preeclampsia-eclampsia, preeclampsia superimposed on chronic hypertension, and gestational hypertension ( Figure 1 ). 5

Chronic hypertension is defined by elevated blood pressure that predates the pregnancy, is documented before 20 weeks of gestation, or is present 12 weeks after delivery. 5 In contrast, preeclampsia-eclampsia is defined by elevated blood pressure and proteinuria that occur after 20 weeks of gestation. Eclampsia, a severe complication of preeclampsia, is the new onset of seizures in a woman with preeclampsia. Eclamptic seizures are relatively rare and occur in less than 1 percent of women with preeclampsia. 1

Preeclampsia superimposed on chronic hypertension is characterized by new-onset proteinuria (or by a sudden increase in the protein level if proteinuria already is present), an acute increase in the level of hypertension (assuming proteinuria already exists), or development of the HELLP ( h emolysis, e levated l iver enzymes, l ow p latelet count) syndrome. 4

Gestational hypertension is diagnosed when elevated blood pressure without proteinuria develops after 20 weeks of gestation and blood pressure returns to normal within 12 weeks after delivery. 4 One fourth of women with gestational hypertension develop proteinuria and thus progress to preeclampsia. 6 , 7

Risk Factors

Risk factors for preeclampsia include medical conditions with the potential to cause microvascular disease (e.g., diabetes mellitus, chronic hypertension, vascular and connective tissue disorders), antiphospholipid antibody syndrome, and nephropathy. 4 , 8 Other risk factors are associated with pregnancy itself or may be specific to the mother or father of the fetus ( Table 2 ). 4 , 8

Pathophysiology

Although the exact cause of preeclampsia remains unclear, 4 , 5 many theories center on problems of placental implantation and the level of trophoblastic invasion. 9 , 10 It is important to remember that although hypertension and proteinuria are the diagnostic criteria for preeclampsia, they are only symptoms of the pathophysiologic changes that occur in the disorder. One of the most striking physiologic changes is intense systemic vasospasm, which is responsible for decreased perfusion of virtually all organ systems. 11 Perfusion also is diminished because of vascular hemoconcentration and third spacing of intravascular fluids. In addition, preeclampsia is accompanied by an exaggerated inflammatory response and inappropriate endothelial activation. 10 Activation of the coagulation cascade and resultant microthrombi formation further compromise blood flow to organs. 11

Clinical Presentation

The clinical presentation of preeclampsia may be insidious or fulminant. Some women may be asymptomatic at the time they are found to have hypertension and proteinuria; others may present with symptoms of severe preeclampsia, such as visual disturbances, severe headache, or upper abdominal pain. From 4 to 14 percent of women with preeclampsia present with superimposed HELLP syndrome. 12 HELLP syndrome may be a variant of preeclampsia or a separate entity, but its development is ominous because mortality or serious morbidity occurs in 25 percent of affected women. 13

Preeclampsia-eclampsia may develop before, during, or after delivery. Up to 40 percent of eclamptic seizures occur before delivery; approximately 16 percent occur more than 48 hours after delivery. 1 Death associated with preeclampsia-eclampsia may be due to cerebrovascular events, renal or hepatic failure, HELLP syndrome, or other complications of hypertension. 3

Diagnostic Evaluation

As part of the initial prenatal assessment, pregnant women should be questioned about potential risk factors for preeclampsia. They should be asked about their obstetric history, specifically the occurrence of hypertension or preeclampsia during previous pregnancies. A thorough medical history should be obtained to identify medical conditions that increase the risk for preeclampsia, including diabetes mellitus, hypertension, vascular and connective tissue disease, nephropathy, and antiphospholipid antibody syndrome.

During prenatal visits after 20 weeks of gestation, pregnant women should be asked about specific symptoms, including visual disturbances, persistent headaches, epigastric or right upper quadrant pain, and increased edema. Questions about these symptoms are included in many standardized prenatal documentation forms.

PHYSICAL EXAMINATION

Blood pressure should be measured at each prenatal visit. As mentioned previously, increases above the patient’s baseline (greater than 30 mm Hg systolic or 15 mm Hg diastolic) are no longer considered to be criteria for the diagnosis of preeclampsia. However, such increases warrant close observation. 5 To ensure accurate readings, an appropriate-size blood pressure cuff should be used, and blood pressure should be measured after a rest period of 10 minutes or more. During the blood pressure measurement, the patient should be in an upright or left lateral recumbent position with the arm at the level of the heart. 4

Fundal height should be measured at each prenatal visit because size less than dates may indicate intrauterine growth retardation or oligohydramnios. These conditions may become apparent long before diagnostic criteria for preeclampsia are met. Increasing maternal facial edema and rapid weight gain also should be noted because fluid retention often is associated with preeclampsia. Although these symptoms (e.g., facial edema, rapid weight gain) are not unique to preeclampsia, it is wise to follow affected patients for hypertension and proteinuria. 5 Edema involving the lower extremities frequently occurs during normal pregnancy and therefore is of less concern.

LABORATORY EVALUATION

There currently is no single reliable, cost-effective screening test for preeclampsia. 4 The serum uric acid level once was used as an indicator of preeclampsia but has been found to lack sensitivity and specificity as a diagnostic tool. 14 However, an elevated serum uric acid level may be of some use in identifying pregnant women with chronic hypertension who have an increased likelihood of having superimposed preeclampsia. 14

A baseline laboratory evaluation should be performed early in pregnancy in women who are at high risk for preeclampsia. Tests should include a hepatic enzyme level, a platelet count, a serum creatinine level, and a 12- to 24-hour urine collection for total protein measurement. Once the diagnosis of preeclampsia has been made, an expanded set of laboratory tests should be performed ( Table 3 ). 15 In women who have preeclampsia with no suspected progression, all laboratory tests should be conducted weekly. 4 , 5 If progression of eclampsia is suspected, the tests should be repeated more frequently.

Small studies 16 – 18 have shown that random There currently is no single reliable, cost-effective screening test for preeclampsia. urinary protein-to-creatinine ratios predict the 24-hour urine total protein level and may provide a faster, simplified method of estimating proteinuria, providing that the protein values are less than 1 g in 24 hours. 19 The urinary protein-to-creatinine ratio is not sensitive enough to differentiate mild and severe preeclampsia if significant proteinuria exists. However, a ratio of less than 0.2 effectively excludes the presence of significant proteinuria. 20 A cutoff ratio of greater than 0.19 is a good predictor of significant proteinuria, with a sensitivity of 90 percent and a specificity of 70 percent. The negative predictive value of the urinary protein-to-creatinine ratio is 87 percent. 17

OTHER STUDIES

A baseline sonogram should be considered at 25 to 28 weeks of gestation to evaluate fetal growth in pregnant women at high risk for preeclampsia. 5 In women who have already been diagnosed with preeclampsia, antepartum testing with a nonstress test, a biophysical profile, or both should be performed on a weekly basis starting at the time of diagnosis. 5 If intrauterine growth retardation or oligohydramnios is suspected, the tests should be performed at least twice weekly, and delivery should be contemplated if there are any signs of fetal compromise. 4 , 5 Immediate antepartum testing or delivery is indicated for suspected placental abruption and nonreassuring fetal surveillance. 5

Delivery remains the ultimate treatment for preeclampsia. 4 , 5 Although maternal and fetal risks must be weighed in determining the timing of delivery, clear indications for delivery exist ( Table 4 ). 15 When possible, vaginal delivery is preferable to avoid the added physiologic stressors of cesarean delivery. 5 If cesarean delivery must be used, regional anesthesia is preferred because it carries less maternal risk. 5 In the presence of coagulopathy, use of regional anesthesia generally is contraindicated. 5

Women with preeclampsia and preterm pregnancy can be observed on an outpatient basis, with frequent assessment of maternal and fetal well-being. Women who are noncompliant, who do not have ready access to medical care, or who have progressive or severe preeclampsia should be hospitalized. Women whose pregnancy is remote from term should be cared for in a tertiary care setting or in consultation with an obstetrician or family physician who is experienced in the management of high-risk pregnancies. 4

During labor, the management goals are to prevent seizures and control hypertension. 4 Magnesium sulfate is the medication of choice for the prevention of eclamptic seizures in women with severe preeclampsia and for the treatment of women with eclamptic seizures. 1 , 21 One commonly used regimen is a 6-g loading dose of magnesium sulfate followed by a continuous infusion at a rate of 2 g per hour. 1 Magnesium sulfate has been shown to be superior to phenytoin (Dilantin) and diazepam (Valium) for the treatment of eclamptic seizures. 1 Although magnesium sulfate commonly is used in women with preeclampsia, studies to date have been inadequate to show that it prevents progression of the disorder. 22 , 23

Antihypertensive drug therapy is recommended for pregnant women with systolic blood pressures of 160 to 180 mm Hg or higher 24 and diastolic blood pressures of 105 to 110 mm Hg or higher 4 , 5 , 25 The treatment goal is to lower systolic pressure to 140 to 155 mm Hg and diastolic pressure to 90 to 105 mm Hg. To avoid hypotension, blood pressure should be lowered gradually. 5

Although evidence about the potential adverse effects of most antihypertensive drugs has been poorly quantified, use of many of these agents is contraindicated during pregnancy. 7 Hydralazine (Apresoline) and labetalol (Normodyne, Trandate) are the antihypertensive drugs most commonly used in women with severe preeclampsia ( Table 5 ). 15 Nifedipine (Procardia) and sodium nitroprusside (Nitropress) are potential alternatives, but significant risks are associated with their use. 5 Note that labetalol therapy should not be used in women with asthma or congestive heart failure. 5 Use of angiotensin-converting enzyme inhibitors is contraindicated in pregnant women.

In women with preeclampsia, blood pressure usually normalizes within a few hours after delivery but may remain elevated for two to four weeks. 26 As previously noted, a diagnosis of chronic hypertension is made if blood pressure remains elevated at 12 weeks postpartum. 5

Women with preeclampsia should be counseled about future pregnancies. In nulliparous women with preeclampsia before 30 weeks of gestation, the recurrence rate for the disorder may be as high as 40 percent in future pregnancies. 5 Multiparous women have even higher rates of recurrence. 5

There currently are no well-established measures for preventing preeclampsia. 4 , 8 Both low-dose aspirin therapy and daily calcium supplementation have been studied as preventive measures but have not been shown to be beneficial in the general pregnant population and are not recommended for primary prevention of preeclampsia. 4 , 5 Some evidence does support the use of low-dose aspirin therapy and daily calcium supplementation in certain high-risk women. Calcium supplementation has been shown to produce modest blood pressure reductions in pregnant women who are at above-average risk for hypertensive disorders of pregnancy and in pregnant women with low dietary calcium intake. 27 An optimum calcium dosage for these women has not been established. 27 Low-dose aspirin therapy (100 mg per day or less) has been shown to reduce the incidence of preeclampsia in women who were found to have an abnormal uterine artery on Doppler ultrasound examination performed in the second trimester. 28

Research on the use of antioxidants in the prevention of preeclampsia is promising. 29 However, further study is needed, and antioxidant therapy currently is not recommended. 4 , 5 , 29

Although preeclampsia is not preventable, many deaths from the disorder can be prevented. Women who do not receive prenatal care are seven times more likely to die from complications related to preeclampsia-eclampsia than women who receive some level of prenatal care. 3 Some studies indicate that preeclampsia-related fatalities occur three times more often in black women than in white women. 3 Although the precise reasons for the racial differences remain elusive, the differences may be indicative of disparities in health status, as well as access to, and quality of, prenatal care. 3 To decrease preeclampsia-related mortality, appropriate prenatal care must be available to all women. Early detection, careful monitoring, and treatment of preeclampsia are crucial in preventing mortality related to this disorder. 3 , 8

Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol. 1998;92:883-9.

Samadi AR, Mayberry RM, Zaidi AA, Pleasant JC, McGhee N, Rice RJ. Maternal hypertension and associated pregnancy complications among African-American and other women in the United States. Obstet Gynecol. 1996;87:557-63.

Mackay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. 2001;97:533-8.

ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. No. 33, January 2002. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2002;99:159-67.

Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol. 2000;183:S1-22.

Saudan P, Brown MA, Buddle ML, Jones M. Does gestational hypertension become preeclampsia?. Br J Obstet Gynaecol. 1998;105:1177-84.

Sibai BM. Chronic hypertension in pregnancy. Obstet Gynecol. 2002;100:369-77.

Dekker G, Sibai B. Primary, secondary, and tertiary prevention of preeclampsia. Lancet. 2001;357:209-15.

Postovit LM, Adams MA, Graham CH. Does nitric oxide play a role in the aetiology of preeclampsia?. Placenta. 2001;22(suppl A):S51-5.

Dekker GA, Sibai BM. Etiology and pathogenesis of preeclampsia: current concepts. Am J Obstet Gynecol. 1998;179:1359-75.

Roberts JM, Cooper DW. Pathogenesis and genetics of pre–eclampsia. Lancet. 2001;357:53-6.

Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): subsequent pregnancy outcome and long-term prognosis. Am J Obstet Gynecol. 1995;172(1 pt 1):125-9.

Padden MO. HELLP syndrome: recognition and perinatal management. Am Fam Physician. 1999;60:829-36.

Lim KH, Friedman SA, Ecker JL, Kao L, Kilpatrick SJ. The clinical utility of serum uric acid measurements in hypertensive diseases of pregnancy. Am J Obstet Gynecol. 1998;178:1067-71.

National High Blood Pressure Education Program. Working Group on High Blood Pressure in Pregnancy. Working group report on high blood pressure in pregnancy. Bethesda, Md.: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institutes, 2000; NIH publication no. 00-3029. Accessed online July 19, 2004, at: http://www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_preg.pdf.

Robert M, Sepandj RM, Liston RM, Dooley KC. Random protein-creatinine ratio for the quantitation of proteinuria in pregnancy. Obstet Gynecol. 1997;90:893-5.

Rodriquez-Thompson D, Lieberman ES. Use of a random urinary protein-to-creatinine ratio for the diagnosis of significant proteinuria during pregnancy. Am J Obstet Gynecol. 2001;185:808-11.

Neithardt AB, Dooley SL, Borensztajn J. Prediction of 24-hour protein excretion in pregnancy with a single voided urine protein-to-creatinine ratio. Am J Obstet Gynecol. 2002;186:883-6.

Adelberg AM, Miller J, Doerzbacher M, Lambers DS. Correlation of quantitative protein measurements in 8-, 12-, and 24-hour urine samples for the diagnosis of preeclampsia. Am J Obstet Gynecol. 2001;185:804-7.

Neithardt A, Dooley SL, Borensztajn J. Prediction of 24-hour protein excretion in pregnancy with a single voided urine protein-to-creatinine ratio. Am J Obstet Gynecol. 2002;186:883-6.

Magpie Trial Collaboration Group. Do women with preeclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359:1877-90.

Scott JR. Magnesium sulfate for mild preeclampsia [Editorial]. Obstet Gynecol. 2003;101:213.

Livingston JC, Livingston LW, Ramsey R, Mabie BC, Sibai BM. Magnesium sulfate in women with mild preeclampsia: a randomized controlled trial. Obstet Gynecol. 2003;101:217-20.

Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003;102:181-92.

Guide to clinical preventive services: report of the U.S. Preventive Services Task Force. 2d ed. Washington, D.C.: U.S. Dept. of Health and Human Services, Office of Public Health and Science, Office of Disease Prevention and Health Promotion, 1996.

Ferrazzani S, DeCarolis S, Pomini F, Testa AC, Mastromarino C, Caruso A. The duration of hypertension in the puerperium of preeclamptic women: relationship with renal impairment and week of delivery. Am J Obstet Gynecol. 1994;171:506-12.

Atallah AN, Hofmeyr GJ, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Database Syst Rev. 2004(2):CD001059.

Coomarasamy A, Papaioannou S, Gee H, Khan KS. Aspirin for the prevention of preeclampsia in women with abnormal uterine artery Doppler: a meta-analysis. Obstet Gynecol. 2001;98(5 pt 1):861-6.

Chappell LC, Seed PT, Briley AL, Kelly FJ, Lee R, Hunt B, et al. Effect of antioxidants on the occurrence of preeclampsia in women at increased risk: a randomised trial. Lancet. 1999;354:810-6.

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Preeclampsia Clinical Case

Preeclampsia clinical case presentation, free google slides theme and powerpoint template.

Preeclampsia is a condition that affects people who are pregnant. It causes high blood pressure, kidney damage and even other signs of organ damage. When should you expect it? You should be looking for these symptoms around the 20th week of pregnancy. Now you might be worried about how this can affect your baby, but thanks to medical advances, new treatments offer a hopeful prospect for the pregnancy. Speak about your last patient with this clinical case template and share your findings with the medical community. Knowledge equals health!

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  1. PPT

    management of eclampsia presentation ppt

  2. PPT

    management of eclampsia presentation ppt

  3. Eclampsia ppt

    management of eclampsia presentation ppt

  4. PPT

    management of eclampsia presentation ppt

  5. PPT

    management of eclampsia presentation ppt

  6. PPT

    management of eclampsia presentation ppt

VIDEO

  1. PRE -ECLAMPSIA Ppt

  2. Eclampsia Management Tray .#obstetricsandgynecology #medicalshorts

  3. Eclampsia ER Management

  4. Pré-eclâmpsia na dieta vegana 😱

  5. case presentation ♡♡♡ midwifery @@ Eclampsia

  6. Part 4 Management of a patient of Pre eclampsia with breathlessness

COMMENTS

  1. Managment of eclampsia

    The management of eclampsia involves six stages: 1. Making sure the airways are clear and the woman can breathe. 2. Controlling the fits. 3. Controlling the blood pressure. 4. General care and monitoring. 5. Delivering the baby. 6. Care after delivery.

  2. Eclampsia ppt

    2) Eclampsia is defined as „A new onset of grandmal seizure activity in pregnancy & post partum period. 3) Pre-eclampsia when complicated with generalized tonicclonic seizures &/ or coma is called eclampsia. 4) In most of cases over 80% ,disease preceded by features of severe pre-eclampsia. 4.

  3. Eclampsia

    Eclampsia refers to the occurrence of new-onset, generalized, tonic-clonic seizures or coma in a patient with preeclampsia (including HELLP syndrome [hemolysis, elevated liver enzymes, low platelets]) or gestational hypertension (in those cases where, in retrospective, it was a temporary [provisional] diagnosis for a hypertensive pregnant ...

  4. PDF Eclampsia: an overview clinical presentation, diagnosis and management

    Eclampsia diagnosis. Eclampsia is defined as the occurrence of grand mal seizures during pregnancy or during/after delivery in a woman with preeclampsia, not attributable to other causes. Almost all cases occur in the third trimester (91%), after 28weeks of pregnancy.12 Preeclampsia or eclampsia occurring before 20weeks of pregnancy can occur in.

  5. eclampsia presentation

    eclampsia presentation. 4. INTRODUCTION Hypertension is the most common medical problem encountered during pregnancy. Hypertensive disorders in pregnancy may cause maternal & fetal morbidity & leading cause of maternal mortality. Hypertensive disorders are : 1.

  6. PPT Critical care management of preeclampsia and eclampsia

    Times New Roman Arial Standardformgivning Critical care management of preeclampsia and eclampsia The obstetric ICU patient The cause of preeclampsia is unknown Primary changes in the vasculature Pathology Hypertension in pregnancy Preeclampsia/eclampsia definitions Symptoms other than hypertension and proteinuria in severe preeclampsia Fetal ...

  7. Eclampsia

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

  8. Eclampsia: an overview clinical presentation, diagnosis and management

    The incidence of eclampsia varies between 0.2-0.5 percent of all deliveries according to the 1988 World Health Organization's International Collaborative Study of Hypertensive Disorders of Pregnancy. 6 The reported incidence is usually much higher in tertiary referral medical centers and in patients that do not obtain prenatal care.

  9. Management of Eclampsia

    PowerPoint Discussion of Evaluation and Management of a Patient with Eclampsia . 10-2. ... This is a typical presentation of a patient with eclampsia in the absence of prenatal care. It's terrifying to witness a life-threatening eclamptic convulsion develop. First the patient's face becomes distorted and her eyes bulge; then she becomes red ...

  10. Eclampsia in the ED: Presentation, Differential Diagnosis, and

    History and Physical Exam. A thorough history and physical examination are key to narrowing the differential diagnosis. Seizure activity in a pregnant or postpartum patient without a history of epilepsy should be considered eclampsia until proven otherwise. 5 In 78-83% of eclampsia cases, the seizures are preceded by signs of cerebral irritation, such as persistent headaches, blurred vision ...

  11. Clinical presentation and outcomes of pre-eclampsia and eclampsia at a

    Early detection and management of pre-eclampsia is essential, but few studies have examined prevalence or incidence of early versus late onset of pre-eclampsia in LMICs, including Kenya. Late detection and poor management of pre-eclampsia in primary healthcare facilities negatively affect newborn and maternal health outcomes.

  12. Acute Eclampsia

    In developed countries, resultant maternal mortality may be as high as 1.8%, and in developing countries, it may be as high as 14%. This activity reviews the presentation, evaluation, and management of patients with eclampsia and highlights the interprofessional team's role in caring for patients with this condition. Objectives:

  13. PPT

    Presentation Transcript. Eclampsia Pathophysiology Management Anesthetic implications Dr. InduBodh University College of Medical Sciences & GTB Hospital, Delhi www.anaesthesia.co.in email: [email protected]. Eclampsia • Associated with - maternal mortality of ~ 10% perinatal mortality and morbidity of 13 - 30 % • Life ...

  14. Preeclampsia—Pathophysiology and Clinical Presentations:

    Introduction. Preeclampsia is a hypertensive disorder of pregnancy (HDP). It impacts 2% to 8% of all pregnancies and is a major cause of maternal and perinatal morbidity and mortality ().In the United States, HDP were responsible for 212 (7%) of approximately 3,000 pregnancy-related deaths between 2011 and 2015 ().Preeclampsia is a complex disease process originating at the maternal-fetal ...

  15. Preeclampsia: Pathophysiology and Clinical Presentations

    Preeclampsia is a hypertensive disorder of pregnancy that occurs in 2-8% of pregnancies and causes substantial morbidity and mortality. Preeclampsia is defined as new-onset hypertension and new-onset end-organ damage after 20 weeks' gestation. Proteinuria is no longer required for the diagnosis. The complex pathophysiology of preeclampsia ...

  16. Critical care management of preeclampsia and eclampsia

    Management Of Mild Preeclampsia. Management Of Mild Preeclampsia. Dr . Mirzamoradi. Preeclampsia. Preeclampsia refers to the new onset of hypertension and either proteinuria or end organ dysfunction after 20 weeks of gestation in a previously normotensive woman. Preeclampsia. 803 views • 55 slides

  17. Eclampsia ppt

    Eclampsia ppt - Download as a PDF or view online for free ... Non-stress test, and contraction stress test, presentation Kanchan Mehra ... ANC coverage should be strengthened to detect pre-eclampsia, and prevent eclampsia. Management in the hospital should be optimized to prevent recurrent convulsion and complication after admission.

  18. Management Of Eclampsia PowerPoint PPT Presentations

    View Management Of Eclampsia PPTs online, safely and virus-free! Many are downloadable. Learn new and interesting things. Get ideas for your own presentations. ... PowerPoint Presentation Last modified by: Hennie Lombaard Created Date: 1/1/1601 12:00:00 AM Document presentation format: On-screen Show (4:3)

  19. Diagnosis and Management of Preeclampsia

    Am Fam Physician. 2004;70 (12):2317-2324. Preeclampsia is a pregnancy-specific multisystem disorder of unknown etiology. The disorder affects approximately 5 to 7 percent of pregnancies and is a ...

  20. PRE -ECLAMPSIA

    eclampsia presentation. eclampsia presentation Kavitha Kaleshan ... Pre Eclampsia Powerpoint Template - SlideWorld ... SCHEME OF MANAGEMENT OF PRE- ECLAMPSIA 3/28/201722 23. HEELLP SYNDROME This is an acronym for haemolysis, elevated liver enzymes and low platelet count (< 100000 mm3) ...

  21. Preeclampsia Clinical Case

    Green Modern Gradient Colorful Geometric Medical Health Minimalist Abstract Case Report Background. Present a clinical case on preeclampsia and speak about the symptoms, treatment and outcomes of this condition with this Google Slides & PowerPoint template.

  22. pre eclampsia

    Breech presentation. Breech presentation Ayman Shehata ... pre_and_eclampsia.ppt. pre_and_eclampsia.ppt ... clinical classification of preeclampsia is arbitrary and in principally dependent on the level of blood pressure for management purpose. 1) MILD 2) SEVERE 15 16.

  23. MANAGEMENT OF PREECLAMPSIA BY DR SHASHWAT JANI

    Severe Preeclampsia ( Hypertensive Crisis ) 09-Jul-18 Dr Shashwat Jani. 99099 44160. 45. 46. Remember : • Lower BP promptly but slowly: AIM for BP < 150/100 mm Hg • Loading Dose of MgSO4 is Recommended to Prevent Eclampsia in all Severe Preeclampsia. • No need of maintenance dose here.