Preeclampsia and eclampsia nursing: complete reference guide

Preeclampsia complicates an estimated 2–8% of pregnancies worldwide and is among the leading causes of maternal and perinatal mortality (ACOG Practice Bulletin 222). In the United States, hypertensive disorders of pregnancy caused 7.0% of pregnancy-related deaths recorded by CDC’s Pregnancy Mortality Surveillance System from 2005 to 2024 (Njie 2026). Many of those deaths are preventable with early recognition and skilled nursing response. For nursing students, preeclampsia represents one of the most heavily tested obstetric topics on NCLEX, appearing in scenarios that test your knowledge of diagnostic criteria, magnesium sulfate toxicity, and emergency seizure management. This reference covers everything you need: the pathophysiology behind why the condition progresses as it does, how to recognize it across its clinical spectrum, how to manage magnesium therapy safely, and what the NCLEX consistently tests.

Quick reference: preeclampsia spectrum at a glance

Pathophysiology: why preeclampsia develops and progresses

Understanding why preeclampsia causes what it causes is more useful for NCLEX than memorizing a list of symptoms. The disorder originates in abnormal placentation.

In a normal pregnancy, extravillous trophoblast cells invade the maternal spiral arteries of the uterus during the first and second trimester. This invasion remodels the arteries from narrow, high-resistance vessels into wide, low-resistance conduits that can supply the growing placenta. In preeclampsia, this remodeling fails. The spiral arteries remain narrow and high-resistance, leading to chronic placental ischemia.

In response to ischemia, the placenta releases a cascade of anti-angiogenic factors – most importantly sFlt-1 (soluble fms-like tyrosine kinase-1), which neutralizes circulating vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). The result is widespread maternal endothelial dysfunction. Endothelial dysfunction explains essentially all of the clinical manifestations:

• Hypertension: vasospasm from loss of normal endothelial vasodilatory tone
• Proteinuria: glomerular endotheliosis – the glomerular capillary endothelium swells, increasing permeability to protein
• Cerebral involvement: disruption of cerebrovascular autoregulation, cerebral edema, and lowered seizure threshold – the mechanism for eclamptic seizures
• Hepatic involvement: hepatic sinusoidal obstruction from fibrin deposition causes the epigastric/RUQ pain and elevated liver enzymes seen in severe disease
• Thrombocytopenia: microangiopathic consumption of platelets as they encounter damaged endothelium

The seizure that defines eclampsia therefore grows out of cerebrovascular injury and lost autoregulation, with cerebral imaging findings that resemble hypertensive encephalopathy (Sibai 2005). This is why magnesium sulfate, which acts on the CNS rather than as an antihypertensive, is the preferred seizure prophylaxis and treatment.

Diagnostic criteria: what ACOG 2013 changed

ACOG’s 2013 hypertension task force removed proteinuria as a requirement for diagnosing preeclampsia, and Practice Bulletin 222 (2020, reaffirmed 2026) carries those criteria forward. The change matters for NCLEX.

Preeclampsia is diagnosed when a pregnant patient at ≥20 weeks gestation with previously normal BP has:

• BP ≥140 mmHg systolic OR ≥90 mmHg diastolic on at least 2 occasions, 4 hours apart

AND at least one of the following:

• Proteinuria ≥300 mg in a 24-hour collection, or protein:creatinine ratio ≥0.3, or a urine dipstick reading of 2+ (used only when quantitative methods are not available)
• OR any severe feature (see below) even without proteinuria

Severe features (any one qualifies as preeclampsia with severe features):

• Systolic BP ≥160 or diastolic BP ≥110 on 2 occasions at least 4 hours apart, unless antihypertensive therapy is started before then. In practice, severe-range BP is confirmed within minutes so treatment is not delayed.
• Thrombocytopenia: platelet count <100,000/μL
• Renal insufficiency: serum creatinine >1.1 mg/dL, or doubling of creatinine in the absence of other renal disease
• Impaired liver function: AST or ALT >2× the upper limit of normal, or severe persistent RUQ/epigastric pain unresponsive to medication
• Pulmonary edema
• New-onset headache unresponsive to medication and not explained by another diagnosis
• Visual disturbances

The BP cutoff matters: ≥140/90 defines the condition; ≥160/110 defines the severe range requiring urgent antihypertensive treatment.

Clinical presentation: recognizing the spectrum

Symptoms follow directly from the pathophysiology. Endothelial dysfunction affects every organ system, so presentation can be subtle early and rapidly life-threatening.

Central nervous system: Headache (often occipital, severe, persistent) and visual disturbances are the most NCLEX-relevant symptoms. Visual changes may include blurred vision, photophobia, or scotomata – visual blind spots caused by retinal vasospasm. Hyperreflexia (brisk DTRs) and clonus indicate CNS irritability and predict seizure risk. Assess patellar reflexes at every nursing encounter during MgSO4 therapy.

Hepatic: Right upper quadrant or epigastric pain from hepatic capsule distension is a warning sign. It often precedes either an eclamptic seizure or HELLP syndrome and should be reported immediately.

Renal: Oliguria (<30 mL/hr, or <500 mL/24 h) signals worsening renal involvement and is a key nursing monitoring parameter.

Edema: Generalized edema – including non-dependent edema of the face and hands – is associated with preeclampsia, though non-edematous preeclampsia occurs. Edema alone is insufficient for diagnosis.

Nursing assessment and monitoring

Structured, frequent assessment is the primary nursing intervention in preeclampsia. The purpose is early detection of clinical deterioration.

Blood pressure monitoring:

• Frequency follows unit protocol; checks are closer together during MgSO4 infusion, while BP is in the severe range, and after each antihypertensive dose
• Use an appropriately sized cuff with the arm at heart level; in hospital the patient may sit up or lie in the left lateral position (PB 222)
• Severe-range BP (≥160 systolic or ≥110 diastolic) that persists for 15 minutes or more is treated as soon as reasonably possible, ideally within 30–60 minutes. Do not wait 4 hours for a confirmatory reading.

Neurological assessment:

• Assess deep tendon reflexes (patellar) before each MgSO4 dose adjustment and at least every hour during infusion
• Grade reflexes: 0 = absent, 1+ = diminished, 2+ = normal, 3+ = brisk, 4+ = clonus
• Check for ankle clonus: briskly dorsiflex the foot and hold – sustained rhythmic oscillation indicates CNS irritability
• Report absent DTRs immediately – this is the earliest sign of magnesium toxicity

Urine output:

• Measure output hourly during MgSO4 infusion (an indwelling catheter is common in severe disease)
• Report output <30 mL/hr. ACOG advises reducing the maintenance dose to 1 g/hr when output stays below 30 mL/hr for more than 4 hours or creatinine is 1.0–1.5 mg/dL
• Oliguria during MgSO4 infusion matters because magnesium is excreted almost entirely by the kidneys; reduced clearance raises toxicity risk
• Do not push fluids on your own: PB 222 warns that aggressive fluid therapy in preeclampsia raises pulmonary capillary wedge pressure and the risk of pulmonary edema. Transient oliguria (<100 mL over 4 hours) is common in labor and the first 24 hours postpartum

Fetal monitoring:

• Continuous electronic fetal monitoring during labor and during MgSO4 infusion
• Variability may be modestly reduced (MgSO4 crosses the placenta; Duffy 2012)
• Late decelerations or absent variability require immediate provider notification

Respiratory monitoring:

• Respiratory rate at every MgSO4 assessment – many unit protocols use <12 breaths/min as the threshold to stop the infusion and notify the provider
• Pulse oximetry continuous during infusion

Magnesium sulfate therapy

Magnesium sulfate (MgSO4) is the cornerstone of seizure prophylaxis and treatment in preeclampsia. It is the single most NCLEX-tested pharmacologic topic in this clinical area.

Mechanism: Magnesium is a physiologic calcium antagonist. It crosses the blood-brain barrier and acts as a CNS depressant, raising the seizure threshold by blocking NMDA receptors and reducing neuronal excitability. Magnesium also causes peripheral vasodilation (which produces a mild BP-lowering effect) and relaxes smooth muscle.

Critical distinction for NCLEX: magnesium sulfate is given for seizure prophylaxis. Its mild vasodilating effect does not control severe-range BP, so labetalol, hydralazine, or nifedipine is given separately for that.

Who gets it: ACOG recommends MgSO4 for gestational hypertension with severe features, preeclampsia with severe features, and eclampsia. For preeclampsia without severe features there is no consensus, and PB 222 leaves the decision to the physician or institution. In the Magpie trial (10,110 participants), magnesium more than halved the risk of eclampsia.

Dosing (PB 222):

• Loading dose: 4–6 g IV over 20–30 minutes
• Maintenance dose: 1–2 g/hr continuous IV infusion
• Duration: through labor and for 24 hours after delivery. For a cesarean before labor, the infusion ideally starts before surgery, continues during it, and runs for 24 hours afterward
• If IV access cannot be established: 10 g IM (5 g in each buttock), then 5 g IM every 4 hours

Therapeutic serum range: 4–7 mEq/L (5–9 mg/dL) per PB 222 Table 2. ACOG notes that the evidence behind any exact therapeutic range is weak, so clinical assessment of reflexes, respirations, and urine output drives care.

Because reflexes disappear well before breathing or the heart is affected, ACOG notes that serious toxicity is avoided as long as deep tendon reflexes are present. When renal function is impaired, serum magnesium is checked every 4 hours; if it exceeds 9.6 mg/dL (8 mEq/L) the infusion is stopped and levels are rechecked every 2 hours, restarting at a lower rate once the level falls below 8.4 mg/dL (7 mEq/L).

Antidote: calcium gluconate 10% solution, 10 mL (1 g) IV over 3 minutes (PB 222). Keep it at the bedside for every patient receiving MgSO4. A patient with impending respiratory depression may also need intubation, and IV furosemide can be given to speed urinary excretion of magnesium.

Assessment before and during infusion (COAT mnemonic):

• Clonus/DTRs present? (absent = stop)
• Output adequate? (<30 mL/hr = notify the provider; ACOG lowers the maintenance dose if it persists beyond 4 hours)
• Airway/respirations? (RR <12 = stop)
• Toxicity signs? (flushing and warmth are expected; somnolence, absent DTRs, RR <12 are not)

Antihypertensive management

Treating hypertension in preeclampsia serves a different goal than treating it in non-pregnant patients. ACOG frames the objective as preventing congestive heart failure, myocardial ischemia, renal injury, and ischemic or hemorrhagic stroke, while avoiding drops in BP steep enough to compromise uteroplacental perfusion.

When to treat: ACOG recommends starting antihypertensive therapy for acute-onset severe hypertension (systolic ≥160 or diastolic ≥110) that persists for 15 minutes or more. The literature supports giving it within 30–60 minutes, and PB 222 says to give it as soon as reasonably possible once the criteria are met. This is a medical urgency.

First-line agents (PB 222, Table 3):

• Labetalol: 10–20 mg IV, then 20–80 mg every 10–30 minutes to a maximum cumulative dose of 300 mg, or a continuous infusion of 1–2 mg/min. Onset 1–2 minutes. Avoid in asthma, preexisting myocardial disease, decompensated cardiac function, heart block, and bradycardia.
• Hydralazine: 5 mg IV or IM, then 5–10 mg IV every 20–40 minutes to a maximum cumulative dose of 20 mg. Onset 10–20 minutes. Higher or frequent doses are associated with maternal hypotension, headache, and abnormal fetal heart rate tracings.
• Nifedipine (immediate release, oral): 10–20 mg, repeated in 20 minutes if needed, then 10–20 mg every 2–6 hours; maximum 180 mg/day. Onset 5–10 minutes. Useful when IV access is unavailable. Case reports described neuromuscular blockade with nifedipine plus MgSO4, but a cohort study found no increase in serious magnesium-related effects with the combination (Magee 2005), so the expected nursing response is close monitoring rather than avoidance.

Avoid in pregnancy:

• ACE inhibitors (captopril, lisinopril, enalapril) – fetotoxic in the second and third trimesters (fetal renal injury, oligohydramnios)
• Angiotensin receptor blockers (ARBs) – same mechanism of fetal harm
• Atenolol – generally avoided because of its association with fetal growth restriction

HELLP syndrome

HELLP syndrome represents the most severe end of the preeclampsia spectrum. The name is a diagnostic triad, and each component has specific laboratory thresholds that are tested on NCLEX.

HELLP criteria used by many clinicians (ACOG PB 222):

• H – Hemolysis: LDH ≥600 IU/L; supporting signs include schistocytes or burr cells on the peripheral smear and elevated bilirubin
• EL – Elevated liver enzymes: AST and ALT more than 2× the upper limit of normal (the older Tennessee classification uses AST ≥70 U/L)
• LP – Low platelets: <100,000/μL

Clinical features that distinguish HELLP from severe preeclampsia:

• RUQ pain and generalized malaise in up to 90% of cases, nausea and vomiting in about 50% (PB 222)
• Up to 15% of patients lack hypertension or proteinuria, so normal BP does not rule HELLP out
• Jaundice in advanced cases
• DIC (disseminated intravascular coagulation) – a life-threatening complication; monitor fibrinogen, PT/INR, and D-dimer
• Spontaneous hepatic rupture (rare but catastrophic)

Key nursing actions in HELLP:

• Serial CBC, liver enzymes, and coagulation studies at least every 12 hours until delivery and into the postpartum period (PB 222)
• Type and crossmatch; platelet transfusion may be ordered before delivery, especially before cesarean. Neuraxial anesthesia is generally considered acceptable with a platelet count above 70,000/μL if no other coagulopathy is present (PB 222)
• Corticosteroids (betamethasone) if <34 weeks for fetal lung maturity; delivery is still required
• Delivery is the definitive treatment, and HELLP is one of the conditions that rule out expectant management

HELLP can present postpartum – in about 30% of cases it first appears or progresses after delivery (PB 222). Consider it in any postpartum patient with malaise, nausea, RUQ pain, and rising liver enzymes. See the HELLP syndrome nursing guide for the full lab and monitoring detail.

Delivery and postpartum considerations

Delivery of the fetus and placenta is the only definitive treatment for preeclampsia. All other management is supportive and temporizing.

Timing:

• Gestational hypertension or preeclampsia without severe features: delivery at 37 0/7 weeks rather than continued expectant management
• Preeclampsia with severe features: delivery at or beyond 34 0/7 weeks after maternal stabilization. Before 34 weeks, expectant management may be considered for a stable mother and fetus at a center with appropriate resources; deliver at any gestational age if maternal or fetal condition deteriorates
• Eclampsia: delivery after maternal stabilization – seizure management and airway first, then delivery planning. Eclampsia by itself is not an indication for cesarean

Postpartum magnesium: ACOG recommends continuing MgSO4 for 24 hours after delivery in patients receiving it for severe features or eclampsia. Eclampsia can occur before, during, or after labor: in Sibai’s review, 38–53% of eclamptic seizures were antepartum, 18–36% intrapartum, and 11–44% postpartum (Sibai 2005).

Late postpartum eclampsia: A growing share of eclampsia cases occur more than 48 hours after delivery (Sibai 2005), and late cases have been reported up to about 4 weeks postpartum. PB 222 adds that new seizures after 48–72 hours postpartum should also prompt a search for other causes. Educate postpartum patients to return immediately for:

• Severe or persistent headache
• Visual changes
• Right upper quadrant pain
• Facial or hand swelling that develops after discharge
• Seizure activity

BP management postpartum: BP often falls in the first 48 hours and then rises again, typically peaking 3–6 days postpartum (Sibai 2012). ACOG recommends a BP check no later than 7–10 days postpartum for anyone with a hypertensive disorder of pregnancy, and within 72 hours for those with severe hypertension (Committee Opinion 736).

NSAIDs postpartum: PB 222 states that NSAIDs should continue to be used in preference to opioid analgesics, and that the data support their safe use in postpartum patients with blood pressure problems. In a randomized trial of patients with preeclampsia with severe features, ibuprofen did not lengthen the duration of severe-range BP compared with acetaminophen (Blue 2018), and a cohort of 399 patients found no association between NSAID use and postpartum BP elevation (Viteri 2017). Patients with chronic hypertension may need closer BP monitoring and regimen adjustment while taking them.

NCLEX tips: highest-yield testable points

1. Magnesium toxicity sequence – loss of DTRs comes first. On NCLEX, if the question asks what sign appears first in magnesium toxicity, the answer is loss of patellar reflexes (above 7 mEq/L, or 9 mg/dL). Respiratory paralysis follows above 10 mEq/L (12 mg/dL), and cardiac arrest above 25 mEq/L (30 mg/dL), per ACOG PB 222 Table 2. The antidote is calcium gluconate 1 g IV (10 mL of 10%) over 3 minutes – it must be at the bedside before the infusion starts.

2. BP ≥160/110 sustained = medical urgency requiring treatment within 30–60 minutes. NCLEX tests whether you know that waiting is not acceptable. Antihypertensive treatment must begin promptly to prevent maternal stroke and abruption.

3. HELLP triad with specific lab thresholds. Memorize: LDH ≥600 IU/L (hemolysis), AST/ALT more than 2× the upper limit of normal (liver enzymes; the Tennessee criteria use AST ≥70), platelets <100,000. NCLEX frequently uses an SATA or priority question that requires you to distinguish HELLP from routine preeclampsia based on the lab values.

4. Eclampsia can occur without proteinuria. Since ACOG 2013, proteinuria is not required for either preeclampsia or eclampsia. A patient who seizes after 20 weeks of pregnancy without prior proteinuria may still have eclampsia; PB 222 notes that 20–38% of patients show neither hypertension nor proteinuria before the seizure. Do not let the absence of proteinuria rule out the diagnosis.

5. Magnesium sulfate is for seizure prophylaxis. Treating it as a BP drug is one of the most common NCLEX distractors in preeclampsia questions. Magnesium acts on the CNS; labetalol, hydralazine, and nifedipine are the agents that lower severe-range BP.

6. Postpartum eclampsia is most common early, and late cases occur. A rising share of cases occur more than 48 hours after delivery, with late cases reported up to about 4 weeks. If a NCLEX question presents a patient who developed a seizure 5 days after a normal delivery with no prior preeclampsia diagnosis, consider late postpartum eclampsia. Discharge teaching must include return-to-care warning signs.

7. Lateral decubitus (left side-lying) position improves uteroplacental blood flow. The gravid uterus compresses the inferior vena cava in the supine position. Left lateral positioning relieves this, improving venous return and placental perfusion. This is the standard positioning for any preeclamptic patient in labor.

8. No ACE inhibitors or ARBs in pregnancy. These drug classes cause fetal renal dysplasia, oligohydramnios, and neonatal renal failure. Captopril, lisinopril, enalapril, losartan, and valsartan are all contraindicated. If a NCLEX question gives a preeclamptic patient a medication history that includes an ACEI or ARB, the priority action is to flag the medication.

9. Oliguria threshold is <30 mL/hr. This signals worsening renal involvement and, during MgSO4 infusion, impaired magnesium clearance (raising toxicity risk). Report urine output <30 mL/hr to the provider promptly. Do not increase IV fluids without a provider order – aggressive fluid therapy in preeclampsia can precipitate pulmonary edema (PB 222).

10. NSAIDs are not off-limits postpartum. PB 222 says NSAIDs should continue to be preferred over opioids, including in patients with preeclampsia. An answer choice that withholds ibuprofen from a postpartum preeclamptic patient purely because of BP is outdated.

Related resources

For the broader context of obstetric nursing care, the obstetric nursing reference covers the complete labor and delivery nursing framework. Preeclampsia frequently coexists with or precedes postpartum hemorrhage, and the nursing priorities in both conditions overlap significantly. For antepartum bleeding comparison, see the placenta previa and abruption nursing reference.

HELLP syndrome lab interpretation requires familiarity with normal lab ranges – the nursing lab values cheat sheet covers LDH, platelet counts, and liver function reference ranges. Because magnesium sulfate affects serum electrolyte balance, the electrolyte imbalances nursing reference provides useful context for understanding magnesium physiology and toxicity. For ectopic pregnancy nursing – another OB emergency with overlapping triage considerations – see the ectopic pregnancy nursing reference.

References

1. American College of Obstetricians and Gynecologists. Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstetrics & Gynecology. 2020;135(6):e237–e260. https://doi.org/10.1097/AOG.0000000000003891 (Reaffirmed 2026.)
2. Magee LA, von Dadelszen P, Rey E, et al. Less-Tight versus Tight Control of Hypertension in Pregnancy. New England Journal of Medicine. 2015;372(5):407–417. https://doi.org/10.1056/NEJMoa1404595
3. Rana S, Lemoine E, Granger JP, Karumanchi SA. Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circulation Research. 2019;124(7):1094–1112. https://doi.org/10.1161/CIRCRESAHA.118.313276
4. American College of Obstetricians and Gynecologists. Practice Bulletin No. 202: Gestational Hypertension and Preeclampsia. Obstetrics & Gynecology. 2019;133(1):e1–e25. [Superseded by Practice Bulletin No. 222 (2020); see reference 1. No whole-document DOI is deposited for this bulletin.]
5. Njie F, Hollier LM, Gibson C, Syverson C, et al. Trends in Pregnancy-Related Mortality in the United States: Pregnancy Mortality Surveillance System, 2005–2024. Obstetrics & Gynecology. Published online August 7, 2026. https://doi.org/10.1097/AOG.0000000000006396 (PMID 42561415)
6. Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstetrics & Gynecology. 2004;103(5 Pt 1):981–991. https://doi.org/10.1097/01.AOG.0000126245.35811.2a
7. National Institute of Child Health and Human Development (NICHD). Preeclampsia and Eclampsia. NIH; 2023. https://www.nichd.nih.gov/health/topics/preeclampsia
8. Duley L, Gülmezoglu AM, Chou D. Magnesium sulphate versus lytic cocktail for eclampsia. Cochrane Database of Systematic Reviews. 2010;(9):CD002960. https://doi.org/10.1002/14651858.CD002960.pub2
9. Magpie Trial Collaborative Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359(9321):1877–1890. https://doi.org/10.1016/S0140-6736(02)08778-0
10. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstetrics & Gynecology. 2005;105(2):402–410. https://doi.org/10.1097/01.AOG.0000152351.13671.99
11. Lu JF, Nightingale CH. Magnesium sulfate in eclampsia and pre-eclampsia: pharmacokinetic principles. Clinical Pharmacokinetics. 2000;38(4):305–314. https://doi.org/10.2165/00003088-200038040-00002
12. Magee LA, Miremadi S, Li J, et al. Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with preeclampsia. American Journal of Obstetrics and Gynecology. 2005;193(1):153–163. https://doi.org/10.1016/j.ajog.2004.11.059
13. Duffy CR, Odibo AO, Roehl KA, Macones GA, Cahill AG. Effect of magnesium sulfate on fetal heart rate patterns in the second stage of labor. Obstetrics & Gynecology. 2012;119(6):1129–1136. https://doi.org/10.1097/AOG.0b013e318257181e
14. Sibai BM. Etiology and management of postpartum hypertension-preeclampsia. American Journal of Obstetrics and Gynecology. 2012;206(6):470–475. https://doi.org/10.1016/j.ajog.2011.09.002
15. American College of Obstetricians and Gynecologists. Committee Opinion No. 736: Optimizing Postpartum Care. Obstetrics & Gynecology. 2018;131(5):e140–e150. https://doi.org/10.1097/AOG.0000000000002633 (Reaffirmed 2025.)
16. Blue NR, Murray-Krezan C, Drake-Lavelle S, et al. Effect of ibuprofen vs acetaminophen on postpartum hypertension in preeclampsia with severe features: a double-masked, randomized controlled trial. American Journal of Obstetrics and Gynecology. 2018;218(6):616.e1–616.e8. https://doi.org/10.1016/j.ajog.2018.02.016
17. Viteri OA, England JA, Alrais MA, et al. Association of nonsteroidal antiinflammatory drugs and postpartum hypertension in women with preeclampsia with severe features. Obstetrics & Gynecology. 2017;130(4):830–835. https://doi.org/10.1097/AOG.0000000000002247