Version of Record: https://www.sciencedirect.

com/science/article/pii/S0735675722003710
Manuscript_4b5509cc61eecbc4ebf851d289154921

Title: High Risk and Low Prevalence Diseases: Eclampsia

Authors:
Name, Degrees, ORCID ID Affiliations Best Email

Marina Boushra, MD East Carolina University [email protected]

Brody School of Medicine
Department of Emergency Medicine
600 Moye Blvd., Mailstop 625, Greenville,
NC, USA

Sreeja M. Natesan, MD Duke University School of Medicine [email protected]

Department of Surgery, Division of m
Emergency Medicine
2301 Erwin Rd.
Durham, NC, USA

Alex Koyfman, MD Department of Emergency Medicine, UT [email protected]

Southwestern, Dallas, TX, USA

Brit Long, MD SAUSHEC, Department of Emergency [email protected]

Medicine, Brooke Army Medical Center,
Fort Sam Houston, TX, USA

Corresponding Author:
Brit Long, MD
Present Address:
3841 Roger Brooke Dr
Fort Sam Houston, TX 78234
Email: [email protected]

Keywords: eclampsia; preeclampsia; seizures; pregnancy; postpartum

Conflicts of Interest: NONE

Acknowledgements: SN, MB, BL, and AK conceived the idea for this manuscript and
contributed substantially to the writing and editing of the review. This manuscript did not
utilize any grants, and it has not been presented in abstract form. This clinical review has
not been published, it is not under consideration for publication elsewhere, its publication
is approved by all authors and tacitly or explicitly by the responsible authorities where
the work was carried out, and that, if accepted, it will not be published elsewhere in the
same form, in English or in any other language, including electronically without the
written consent of the copyright-holder. This review does not reflect the views or
opinions of the U.S. government, Department of Defense, U.S. Army, U.S. Air Force, or
SAUSHEC EM Residency Program.

© 2022 published by Elsevier. This manuscript is made available under the Elsevier user license
https://www.elsevier.com/open-access/userlicense/1.0/
1 High Risk and Low Prevalence Diseases: Eclampsia

3 Abstract

4 Introduction: Eclampsia is a rare partum and puerperal condition that carries a high rate of

5 morbidity and mortality.

6 Objective: This review highlights the pearls and pitfalls of the care of patients with eclampsia,

7 including presentation, evaluation, and evidence-based management in the emergency

8 department.

9 Discussion: Eclampsia is a hypertensive disease of pregnancy defined by new onset tonic-clonic,

10 focal, or multifocal seizures or unexplained altered mental status in a pregnant or postpartum

11 patient in the absence of other causative etiologies. However, signs and symptoms of

12 preeclampsia and prodromes of eclampsia are often subtle and non-specific, making the

13 diagnosis difficult. Thus, it should be considered in pregnant and postpartum patients who

14 present to the ED. Laboratory testing including complete blood cell count, renal and liver

15 function panels, electrolytes, glucose, coagulation panel, fibrinogen, lactate dehydrogenase, uric

16 acid, and urinalysis, as well as imaging to include head computed tomography, can assist, but

17 these evaluations should not delay management. Components of treatment include emergent

18 obstetric specialist consultation, magnesium administration, and blood pressure control in

19 patients with hypertension. Definitive treatment of eclampsia requires emergent delivery in

20 pregnant patients. If consultants are not in-house, emergent stabilization and immediate transfer

21 is required.

22 Conclusions: An understanding of eclampsia can assist emergency clinicians in rapid

23 recognition and timely management of this potentially deadly disease.

24 Keywords: eclampsia; preeclampsia; seizures; pregnancy; postpartum

25

26 1. Introduction

27 This article series addresses high risk and low prevalence diseases that are encountered in the

28 emergency department (ED). Much of the primary literature evaluating these conditions is not

29 emergency medicine focused. By their very nature, many of these disease states and clinical

30 presentations have little useful evidence available to guide the emergency physician in diagnosis

31 and management. The format of each article defines the disease or clinical presentation to be

32 reviewed, provides an overview of the extent of what we currently understand, and finally

33 discusses pearls and pitfalls using a question-and-answer format. This article will discuss

34 eclampsia. This condition’s low prevalence but high morbidity and mortality, as well as its

35 variable atypical patient presentations and challenging diagnosis, makes it a high risk and low

36 prevalence disease.

37

38 1.1 Epidemiology

39 Pregnancy-related conditions account for 1.3% of annual ED visits and are responsible for a

40 steeply increasing proportion of morbidity and mortality in women of childbearing age over the

41 last three decades.1–3 Hypertensive diseases of pregnancy (HDP) represent a broad but non-linear

42 spectrum of partum and puerperal conditions that account for nearly one fifth of maternal deaths

43 worldwide, with preeclampsia and eclampsia being the most severe manifestations of HDP and

44 accounting for the largest proportion of these deaths.4 Eclampsia is rare, occurring in

45 approximately of 0.3% of live births, though there is significant variability in incidence due to

46 factors such as maternal risk factors, economic inequity, and differences in access and quality of
47 obstetric care.5–9 Despite its rarity, eclampsia is associated with serious complications including

48 ischemic and hemorrhagic stroke, coma, heart failure, venous thrombosis, renal failure,

49 disseminated intravascular coagulation, and fetal demise.9 Maternal mortality rates range from

50 5.6% to 14%.10–12 Additionally, approximately 25% of patients develop long-term sequelae,

51 including cardiovascular-related pathologies (i.e., myocardial infarction, heart failure).9

52 Neonates born to eclamptic patients are also at risk of being small for gestational age, hypoxic-

53 ischemic brain injury, and neonatal respiratory distress syndrome.6,9

54

55 1.2 Definition

56 Eclampsia is a severe manifestation of HDP and is defined by new onset tonic-clonic, focal, or

57 multifocal seizures or unexplained altered mental status in a pregnant or postpartum patient in

58 the absence of other causative etiologies.13 The classic understanding of HDP is a linear

59 progression from gestational hypertension to preeclampsia to preeclampsia with severe features

60 to eclampsia in the absence of intervention.13,14 However, research increasingly supports the

61 notion that HDP may progress in a non-linear fashion.10,15,16 For example, in one study, 38% of

62 patients who developed acute-onset eclampsia had no signs or symptoms of preeclampsia during

63 their hospital stay.10 Conversely, other studies have shown that only 1.9% and 3.2% of patients

64 with preeclampsia and preeclampsia with severe features, respectively, develop eclampsia in the

65 absence of intervention.15,17 Nevertheless, patients with HDP are at increased risk of developing

66 eclampsia, and recognition of the conditions in the spectrum of HDP may aid in the diagnosis,

67 prevention, and management of eclampsia.9 Table 1 outlines the current diagnostic criteria for

68 the spectrum of HDP; however, it is important to recognize the diagnosis of preeclampsia is

69 increasingly becoming a clinical one and that emergent obstetric specialist involvement is

70 paramount as soon as these diagnoses are suspected.

71

72 Table 1. Diagnostic criteria for hypertensive disorders of pregnancy.13

73

74 According to The American College of Obstetricians and Gynecologists (ACOG), eclampsia can

75 occur during or after the 20th week of pregnancy and up to 6 weeks postpartum.13 Two thirds of

76 cases occur during the antepartum period, with the remainder of cases evenly distributed between

77 labor and the postpartum period.18–21 While the definition includes symptoms and signs past 20

78 weeks of gestation, eclampsia may occur in those less than 20 weeks of gestation in patients with

79 renal disease, molar pregnancy, or multiple gestations.21–24

80

81 2. Discussion

82 2.1 Presentation

83 While seizures are the defining symptom of eclampsia, the presentation of eclampsia is variable,

84 and many patients present atypically, making early diagnosis of this condition challenging.

85 Unfortunately, studies have shown that more than one third of eclampsia cases occur acutely and

86 have no signs or symptoms of preeclampsia preceding the seizures. However, up to 83% of

87 eclampsia cases are associated with non-specific prodromal symptoms prior to seizure

88 occurrence.13 These prodromal symptoms include headache (66-82%), visual disturbances (27-

89 44%), and upper abdominal pain (25%).11,13,20,23,25,26 The headache associated with eclampsia

90 varies in the location and quality of pain, and documented vision disturbances include blurry

91 vision, scotoma, photopsia, diplopia, and transient blindness.21,26–28 Altered mental status may
 92 also occur prior to and/or after the seizure. Unfortunately, these symptoms cannot be used to rule

93 in or out the diagnosis, and in many situations, history will not be available, as the patient is

94 altered or actively seizing.18,25,26,29 Seizures associated with eclampsia are typically tonic-clonic

95 and last less than one minute.25

96

97 Similar to patient presentation, physical examination findings in eclampsia are variable. In

98 patients with preeclampsia preceding seizure, common findings include hypertension, edema,

99 clonus, and hyperreflexia.24,28 Accurate measurement of blood pressure using an appropriately

100 sized cuff is of paramount importance, but the degree of hypertension does not predict

101 eclampsia.24 Approximately 20% of eclampsia cases occur in the setting of mild hypertension,

102 and blood pressure may be normal in 25% of patients.10,18,21,26

103

104 2.2 ED Evaluation

105 While eclampsia is a clinical diagnosis, laboratory evaluation is recommended to evaluate for

106 complications and alternate or concurrent etiologic conditions, including complete blood cell

107 count (CBC), renal and liver function panels, electrolytes, glucose, coagulation panel, fibrinogen,

108 lactate dehydrogenase (LDH), uric acid, and urinalysis.8,13,21,23,30 Laboratory testing may reveal

109 thrombocytopenia, elevated creatinine, elevated aminotransferases, elevated LDH and uric acid,

110 and proteinuria (Table 1). Patients with new-onset seizure or focal neurologic deficits should

111 undergo non-contrast head computed tomography (CT) to evaluate for intracranial hemorrhage

112 or other intracranial pathology. Patients with cardiovascular or respiratory symptoms should

113 undergo electrocardiogram to evaluate for dysrhythmias and right heart strain and chest
114 radiography to assess for other processes such as pulmonary edema and pneumonia, among other

115 etiologies.8,13,21,23,30

116

117 2.3 ED Management

118 Key components of management include preventing maternal hypoxia, treatment of severe

119 hypertension if present, seizure discontinuation and prevention, and evaluation for emergent

120 delivery if the patient is pregnant. Emergent consultation of an obstetric specialist is

121 recommended as soon as the diagnosis of eclampsia is suspected. Delivery of the fetus is the

122 definitive treatment for eclampsia.31 In the ED setting, foundational emergency care should be

123 provided for stabilization, starting with airway, breathing and circulation. Assessment and

124 management of respiratory and circulatory compromise and seizure cessation should be

125 optimized while obtaining obstetric consultation. If the airway is not patent, airway protection is

126 recommended with endotracheal intubation. Supplemental oxygen is recommended to prevent

127 hypoxia for both the patient and fetus,23 and adequate intravenous (IV) access is necessary. The

128 patient should also be placed in the left lateral decubitus position to improve placental blood

129 flow and reduce aspiration risk. While eclampsia is an emergent diagnosis in a seizing pregnant

130 or postpartum patient, mimics must be considered, and thus, immediate assessment of serum

131 glucose is necessary. Evaluation for trauma, infection, and toxic ingestion is recommended.

132 Additionally, a thorough history and physical examination should be performed to evaluate for

133 an underlying cardiovascular, pulmonary, infectious, or neurologic emergency (i.e., elevated

134 intracranial pressure, central nervous system infection, etc.).

135
136 The treatment of choice for seizures in pregnancy is magnesium, which demonstrates greater

137 effectiveness compared to other medications in this patient population.32–35 If the patient is

138 actively seizing, intravenous (IV) magnesium sulfate is recommended at a loading dose of 4-6

139 grams over 15 minutes, followed by maintenance infusion of 1-3 g/hr, with a goal serum

140 magnesium of 2-3.5 mmol/L (4-5 mEq/L) (Table 2).21,23,31 If IV access is not available,

141 magnesium 10 g intramuscular (IM) can be administered (5 g in each buttock). Magnesium is

142 also recommended in patients with preeclampsia for seizure prophylaxis.13 Magnesium is

143 associated with reduced maternal mortality and risk of seizure recurrence.36–41 Absolute

144 contraindications include myasthenia gravis, severe hypocalcemia, complete heart block, and

145 myocarditis.13 Benzodiazepines and phenytoin are less effective than magnesium for seizure

146 prophylaxis in eclampsia but may be used if magnesium is not available or contraindicated.13,41

147 Up to 10% of patients will have recurrent seizure activity despite an initial bolus of

148 magnesium.42 If this occurs, a second bolus of magnesium 2g is recommended over 3-5

149 minutes.21 If further seizures occur, benzodiazepine therapy is recommended.13

150

151 Table 2. Magnesium dosing considerations for eclampsia.8,31

152

153 Following magnesium administration and seizure cessation, management of severe hypertension

154 is recommended, as blood pressures over 160/110 mm Hg increases the risk of poor outcome.21,43

155 Target blood pressure is based on patient baseline blood pressure and mental status, but typically

156 includes a systolic blood pressure (SBP) of 130-150 mm Hg and diastolic blood pressure (DBP)

157 80-100 mm Hg.14,44,45 Medications such as labetalol, nicardipine, hydralazine, or nifedipine may

158 be used, which will be further discussed in detail.13

159

160 3. Pearls and Pitfalls

161 3.1. Why is eclampsia missed, and what is a simplified means of identifying eclampsia?

162 One study of obstetric clinicians found a misdiagnosis rate of 31% for patients with

163 preeclampsia, which was associated with a higher rate of complications, re-hospitalization, and

164 patient cost.46 Misdiagnosis of eclampsia and other conditions in the spectrum of HDP is likely

165 secondary to their often variable and subtle presentations. Prodromal symptoms are present in the

166 majority of patients but are non-specific and include headache, visual disturbances, and

167 gastrointestinal symptoms.26 The non-specific nature of these prodromal symptoms may cause

168 them to be ignored by patients or misattributed to other more benign causes by healthcare

169 clinicians, leading to late presentation, diagnostic delay, or misdiagnosis. Elevations in blood

170 pressure that may otherwise be considered a reactive response to discomfort should trigger an

171 evaluation in pregnant women and those in the postpartum period. Aside from the development

172 of seizures, there is no correlation of physical examination findings, laboratory abnormalities, or

173 symptoms that can definitively rule in or rule out eclampsia. Thus, eclampsia should be

174 considered in pregnant and postpartum women presenting to the ED, especially in patients with

175 symptoms such as headache, confusion/altered mental status, vision changes, and hypertension.

176 Identification of maternal risk factors in the history may aid in risk stratification, but the absence

177 of risk factors does not exclude eclampsia as a potential diagnosis (Table 3).

178

179 Table 3. Maternal risk factors for eclampsia.9,13

180
181 3.2. What is the utility and limitations of the ED evaluation including laboratory assessment and

182 imaging?

183 Because the diagnosis of eclampsia is clinical, the primary utility of maternal laboratory and

184 imaging testing in the ED is to evaluate for other etiologic conditions and evidence of end-organ

185 damage, including CBC, renal and liver function panels, electrolytes, glucose, coagulation panel,

186 fibrinogen, LDH, uric acid, and urinalysis. Testing should not delay consultation with obstetrics

187 and the initiation of management for patients with suspected eclampsia. While the diagnostic

188 criteria does allow for the absence of protein in the urine, proteinuria identified by dipstick

189 urinalysis should be interpreted with caution, as it is 55% sensitive and 84% specific for >

190 300mg/ 24-hour urine protein, the diagnostic criterion for proteinuria in HDP.14 In addition to the

191 maternal testing, when possible, a fetal ultrasound and non-stress test should be performed to

192 evaluate for fetal distress, growth restriction, and oligohydamnios.8

193

194 Imaging to include head CT non-contrast can play an important role in the evaluation of patients

195 with severe headache, new seizure, or altered mental status. This may reveal reversible cerebral

196 vasoconstriction syndrome, cerebral venous thrombosis, posterior reversible encephalopathy

197 syndrome (PRES), subarachnoid hemorrhage, or other intracranial hemorrhage, which can

198 impact ED management.47-49 Of note, up to 90% of patients with eclampsia will demonstrate

199 features of PRES on neuroimaging.48,49

200

201 3.3. What mistakes can be made with magnesium administration? How is magnesium toxicity

202 managed?
203 Magnesium is a safe and effective medication in patients with preeclampsia and eclampsia, and

204 maternal toxicity is rare with close monitoring (Table 4). However, most emergency clinicians

205 are unaccustomed to the management of a magnesium IV infusion and the potentially serious

206 complications that may occur if the patient is not closely monitored. Adverse effects of

207 magnesium infusion, which are rarely life-threatening, include flushing, headaches, nystagmus,

208 hypothermia, acute kidney injury, urinary retention, and constipation.16,42 These effects are

209 typically seen at magnesium levels of 3.8-5 mmol/L and are mild and self-limited in most

210 patients.16 Life-threatening complications are possible with magnesium toxicity, which

211 highlights the importance of close monitoring in patients on magnesium infusion. While

212 increasing serum magnesium concentrations correlate with the severity of magnesium toxicity,

213 the decision to continue magnesium infusion should be based on physical examination findings

214 rather than a serum magnesium level.16 The first physical examination finding of magnesium

215 toxicity is loss of deep tendon reflexes. A physical examination with testing of deep tendon

216 reflexes should be performed and documented upon completion of the loading dose of

217 magnesium and every two hours while on a magnesium infusion (Table 5).13,14,31 At therapeutic

218 magnesium levels of 2-3.5 mmol/L, deep tendon reflexes may be diminished but are rarely

219 absent, and the presence of deep tendon reflexes is highly sensitive for non-toxic serum

220 magnesium levels.13,16 Urine output should be measured and recorded hourly, and urine output

221 should be at least 100 mL/4 hours.13 This is critically important, as urinary retention can be seen

222 in magnesium toxicity, and decreased urine production may signal impairment of renal function,

223 both an adverse effect of magnesium administration and the primary means of magnesium

224 elimination in the body. Because 90% of magnesium is eliminated through the urine, dose

225 adjustments should be made in patients with existing renal disease and those who develop renal
226 injury in the course of treatment.50 Respiratory depression, cardiac conduction abnormalities, and

227 refractory hypotension are associated with severe toxicity and magnesium levels of 5-7.5

228 mmol/L.16

229

230 Table 4. Serum magnesium levels and correlating symptoms.16,41

231

232 Table 5. Patient monitoring during magnesium administration.14

233

234 If signs of magnesium toxicity occur, the magnesium infusion should be stopped immediately. If

235 evidence of cardiopulmonary compromise is present, calcium should be given as an antidote for

236 magnesium toxicity. This can be provided as a 1 g bolus of calcium gluconate over 2-5 minutes

237 and can be repeated every 5 minutes as necessary.16,51 Normal saline and loop diuretics can also

238 be administered to enhance renal clearance of magnesium.51 In severe cases and in patients with

239 severely impaired kidney function, hemodialysis may be necessary for magnesium clearance.51

240

241 3.4. How should blood pressure be managed?

242 In addition to seizure prophylaxis, management of blood pressure is paramount in patients with

243 preeclampsia and eclampsia. Pharmacologic therapy is necessary in patients with SBP >160 mm

244 Hg and DBP >110 mm Hg.13 There are several safe and effective regimens in the management of

245 hypertension in pregnancy, including labetalol, hydralazine, nicardipine, and nifedipine (Table

246 6). A large systematic analysis found no difference in efficacy or safety between hydralazine and

247 labetalol or hydralazine and calcium channel blockers.52 Of note, angiotensin converting enzyme
248 (ACE) inhibitors and angiotensin receptor blockers should be avoided in pregnant patients, as

249 these medications have teratogenic effects including fetal renal agenesis and dysfunction.14

250

251 Table 6. Blood pressure medication regimens and considerations.8,14,30,31,44,53

252

253 3.5 How should patients refractory to standard treatment be managed?

254 While patients with eclampsia typically improve with seizure and blood pressure management,

255 clinicians must consider other conditions and treatment options if the patient does not improve

256 within 10-20 minutes following blood pressure and seizure control. Non-convulsive status

257 epilepticus, central nervous infection, PRES, and other intracranial pathologies should be

258 considered in those with continued altered mental status or seizure, and neurologic consultation

259 and neuroimaging, if not obtained previously, are recommended. Recurrent seizures in the

260 patient receiving a magnesium infusion should be treated with a second bolus of magnesium.13

261 Benzodiazepines such as lorazepam 4 mg IV can also be administered.54–57 If seizures continue

262 despite these interventions, phenytoin, levetiracetam, ketamine, or propofol can be administered.

263 Endotracheal intubation is likely necessary at this stage as well. 54–57

264

265 Table 7 lists pearls for the ED evaluation and management of eclampsia.

266

267 Table 7. Eclampsia pearls.

268

269

270
271 4. Conclusions

272 Eclampsia is a hypertensive disease of pregnancy defined by new onset tonic-clonic, focal, or

273 multifocal seizures or unexplained altered mental status in a pregnant or postpartum patient in

274 the absence of other causative etiologies. The diagnosis is not always clear, as signs and

275 symptoms of preeclampsia and prodromes of eclampsia can be subtle and non-specific.

276 Emergency clinicians must consider these conditions in pregnant and postpartum patients who

277 present to the ED. Laboratory testing including CBC, renal and liver function panels,

278 electrolytes, glucose, coagulation panel, fibrinogen, LDH, uric acid, and urinalysis, as well as

279 imaging to include head computed tomography, can assist. However, laboratory and imaging

280 should not delay management and stabilization. Management includes emergent obstetric

281 specialist consultation, magnesium administration, and reduction of blood pressure in patients

282 with hypertension.

283

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Table 1. Diagnostic criteria for hypertensive disorders of pregnancy.13
Condition Diagnostic Criteria Comments
Chronic (pre- BP >140/90 mmHg BEFORE 20 weeks Higher risk for development of
gestational) gestation preeclampsia and eclampsia.
hypertension
Gestational BP >140/90 mmHg on two occasions 4 50% develop preeclampsia, and
hypertension hours apart AFTER 20 weeks gestation there is increasing doubt that
without associated proteinuria or other gestational hypertension and
features of preeclampsia preeclampsia are distinct
disorders.**
Preeclampsia BP >140/90 mmHg on two occasions 4 1.9% develop eclampsia.
hours apart AFTER 20 weeks gestation
with associated proteinuria or signs of end-
organ dysfunction.
-Proteinuria > 300 mg in a 24-hour urine
collection or spot protein
(mg/dL)/creatinine (mg/dL) ratio > 0.3
-Protein > 2+ on urine dipstick may be
used if quantitative measurement is not
available
Preeclampsia with In the absence of proteinuria, new 3.2% develop eclampsia
severe features hypertension with any of the following:
-BP >160/110 mmHg
-New thrombocytopenia
-Laboratory evidence of liver dysfunction
not accounted for by other pathology or
intractable right upper quadrant or
epigastric abdominal pain
-New or worsening renal insufficiency in
the absence of other renal pathology
-Pulmonary edema not accounted for by
other pathology
-New intractable headache not accounted
for by other pathology
-Visual disturbances
Syndrome of In the absence of other causative A variant of preeclampsia with
Hemolysis, Elevated etiologies: severe features that is associated
Liver Enzymes, and -Lactate dehydrogenase > 600 IU/L with increased morbidity and
Low Platelets -Transaminitis 2X upper limit of normal mortality. Associated with more
(HELLP) -Platelets <100 x 109 insidious onset and nearly 15%
present without hypertension or
proteinuria. Abdominal pain and
nausea/vomiting often present.
**The most recent ACOG guidelines recommend that patients with severe range hypertension
(>160/110 mm Hg) without proteinuria should be managed similar to those with severe
preeclampsia.13
Table 2. Magnesium dosing considerations for eclampsia.8,31
Dose IV IM Serum Cr > Refractory Refractory to Mg not
1.2 mg/dL or to initial 2nd bolus available or
GFR <60 bolus contraindicated
mL/min

Initial Bolus 4-6 g 10 g (5 g 4-6 g over 15- 2 g over 3-5 Benzodiazepine Benzodiazepine
over each 20 min min (lorazepam 4
15-20 buttock) mg IV)
min

Maintenance 2 g/hr 5g 1 g/hr - -

Drip every 4
hr
Table 3. Maternal risk factors for eclampsia.9,13
High-risk
• Previous preeclampsia/eclampsia
• Multifetal gestation
• Renal disease
• Autoimmune disorder
• Type 1 or type 2 diabetes mellitus
• Chronic hypertension

Moderate-risk
• First pregnancy
• Maternal age >35 years
• Family history of preeclampsia
• Body mass index >30
Table 4. Serum magnesium levels and correlating symptoms.16,41
Serum Magnesium Symptoms
Concentration
(mmol/L)
2-3.5 (therapeutic) Flushing, headaches, nystagmus, acute kidney injury, urinary
retention, constipation (all self-limited)
>3.5 Loss of patellar reflexes
>5 Respiratory arrest, cardiac conduction abnormalities,
refractory hypotension
>12.5 Cardiac arrest
Table 5. Patient monitoring during magnesium administration.14
Parameter Frequency

Respiratory rate, heart rate, and Every 30 minutes

blood pressure

Urine output Hourly

Deep tendon reflexes At end of loading dose and then every two hours while
on magnesium infusion
Table 6. Blood pressure medication regimens and considerations.8,14,30,31,44,53
Medication Initial Dose Considerations

Labetalol 20 mg IV - If no response, repeat dose in 20 minutes

- If suboptimal/no response within 10 minutes of
second dose, give third dose of 40 mg IV
- If suboptimal/no response within 10 minutes of third
dose, give fourth dose of 80 mg IV
- Maximum cumulative dose is 220-300 mg
- Once control is obtained, start infusion at 1-2
mg/kg/hr
- 200 mg PO can be administered if IV access is
unavailable
- Side effect: bronchoconstriction, heart block, sleep
disturbances, bradycardia, orthostatic hypotension,
fatigue
- Avoid in patients with asthma or congestive heart
failure or heart rate < 60bpm

Nicardipine Start at 3-5 mg/hr - Side effects: tachycardia, flushing, headaches

continuous drip;
titrate by 2.5
mg/hr every 5-15
minutes until
blood pressure
controlled
(maximum 15
mg/hr), then
reduce infusion

Hydralazine 5-20 mg IV - Repeat dose in 20 minutes if no response

- If no response after 3 doses, consider another agent
- Maximum cumulative dose is 20-30 mg
- If response is achieved, repeat bolus every 3 hours
- Side effects: labile blood pressures, headache,
lightheadedness, flushing, nausea, palpitations, reflex
tachycardia

Nifedipine 10 mg PO - Repeat BP in 20 minutes; if BP >160/110 mm Hg,

readminister 20 mg PO
- Side effects: reflex tachycardia, headache,
hypotension
- Use with caution with patients receiving magnesium
sulfate (theoretical risk of neuromuscular blockade
and hypotension when combined)
Table 7. Eclampsia pearls.
- Eclampsia is a severe manifestation of HDP and is defined by new onset tonic-clonic,
focal, or multifocal seizures or unexplained altered mental status in a pregnant or
postpartum patient in the absence of other causative etiologies.
- Eclampsia should be considered in pregnant and postpartum patients presenting to the ED,
even in the absence of the classic symptoms of preeclampsia. Symptoms of preeclampsia
and prodromes of eclampsia are often subtle and non-specific.
- Laboratory testing can assist, but it should not delay diagnosis and management of
eclampsia.
- Management focuses on emergent obstetric specialist consultation, magnesium
administration, and reduction of blood pressure in patients with hypertension.
- Monitor patients on magnesium drip closely to identify early signs and symptoms of
toxicity. Reduce magnesium dose in patients with renal dysfunction.
- Consider maternal medical history when selecting a blood pressure agent, as some may
exacerbate underlying conditions. Do not use ACE-I or ARB medications in pregnant
patients. Labetalol, hydralazine, nicardipine, and nifedipine may be used.
- For patients who do not improve with seizure control and blood pressure management and
display continued altered mental status or seizure, non-convulsive status epilepticus,
central nervous infection, PRES, and other intracranial pathologies should be considered.
In these patients, neurologic consultation and neuroimaging are recommended.