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Reproductive & OB

Preeclampsia, Eclampsia & HELLP

HELLP High-yield Verified · Oct 2026

Preeclampsia is new-onset hypertension, usually with proteinuria, occurring most often after 20 weeks of gestation; eclampsia adds new-onset seizures, and HELLP adds hemolysis, elevated liver enzymes, and low platelets.

The highest-yield obstetric disorder: the diagnostic numbers, the seizure that can arrive without warning, HELLP hiding behind a nearly normal blood pressure, and the magnesium toxicity ladder every exam asks about.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 It begins in the placenta, not the blood pressure

In a normal pregnancy, invading trophoblasts remodel the mother’s spiral arteries to supply the placenta. In preeclampsia this physiologic transformation fails, with atherosis: trophoblast invasion is altered or inadequate, the spiral arteries fail to remodel, and the placenta is left hypoperfused — placental ischemia.

The ischemic placenta fights back chemically. It activates the endothelium and releases antiangiogenic factors, and these circulate through the mother’s entire vascular tree. The result is diffuse endothelial dysfunction: a whole-body microvascular injury that shows up as hypertension, leaky glomeruli (proteinuria), an inflamed liver capsule (RUQ pain), consumed platelets, and an irritable brain. Every finding on this page traces back to that one lesion.

The fetus shares it. Chronic placental hypoperfusion produces fetal growth restriction, oligohydramnios, abnormal umbilical-artery Doppler flow, and stillbirth risk — mother and fetus are two patients injured by the same vessel disease. Two phenotypes are described: early-onset disease is placentally driven (infarcts, arterial sclerosis, abnormal trophoblast invasion), while late-onset disease reflects maternal endothelial dysfunction with a comparatively healthy, still-perfused placenta.

One lesion, every finding: failed spiral-artery transformation starves the placenta, and the ischemic placenta’s chemical response injures the mother’s endothelium everywhere.

02 The spectrum — and the seizing brain

The hypertensive disorders of pregnancy sit on one spectrum, sorted by when the pressure appears and what else it brings. Chronic hypertension is ≥ 140/90 confirmed before 20 weeks. Gestational hypertension is new-onset ≥ 140/90 on two occasions at least 4 hours apart after 20 weeks. Add proteinuria — ≥ 300 mg on a 24-hour collection, protein/creatinine ratio ≥ 0.3, or dipstick ≥ 2+ — and it becomes preeclampsia. Proteinuria is not required: new hypertension after 20 weeks that arrives with new maternal organ dysfunction (or uteroplacental dysfunction) also meets the definition. Preeclampsia developing on top of chronic hypertension is superimposed preeclampsia.

Severe features mark the disease escalating: SBP ≥ 160 or DBP ≥ 110 (confirmable on readings just minutes apart to expedite treatment), platelets < 100 K/mm³, creatinine ≥ 1.1 mg/dL or doubling of baseline, liver enzymes > 2× the upper limit of normal, new-onset headache, visual disturbance, RUQ/epigastric pain, or pulmonary edema. Eclampsia is the sudden onset of seizures in a patient with a hypertensive disorder of pregnancy, in the absence of other neurological causes.

Why does the brain seize? Severe hypertension overwhelms cerebral blood-flow autoregulation — the same physiology as hypertensive encephalopathy. The blood–brain barrier fails, fluid and protein leak into brain tissue, and vasogenic edema, neuroinflammation, and neuronal injury follow. But eclampsia can occur without severe hypertension, so this is not the only mechanism — which is exactly why the warning symptoms matter more than any single BP reading, and why some seizures arrive with no warning at all.

The disease spectrum: pressure alone becomes preeclampsia when proteinuria or new organ dysfunction joins it, escalates through severe features, and ends in seizures or HELLP — and every arrow points toward delivery.

03 HELLP — when the liver and the platelets take the hit

HELLP = Hemolysis + Elevated Liver enzymes + Low Platelets, in a pregnant or postpartum patient. It is considered a severe form of preeclampsia, though recent evidence suggests the etiologies may be separate. Mechanically it is the microvascular injury at its most destructive: red cells shear apart squeezing through platelet-fibrin-clogged capillaries (microangiopathic hemolysis), hepatic microvascular injury and necrosis release liver enzymes and stretch the liver — the RUQ/epigastric pain — and platelets are consumed in the microvasculature.

The exam trap: HELLP can present with minimal blood pressure elevation. Hypertension or proteinuria is absent in at least 15–20% of HELLP patients. The cue that should trigger a workup is colicky mid-epigastric or RUQ pain with nausea, vomiting, and malaise — a pregnant patient in the third trimester who "just feels awful with stomach pain" needs labs, not antacids. About 70% of cases occur in the third trimester (usually 28–37 weeks); the rest present within 48 hours of delivery.

04 The treatment tightrope — magnesium and the injured kidney

The drug at the center of this disorder is IV magnesium sulfate — first-line seizure prophylaxis for severe features, eclampsia, and HELLP. Its therapeutic window for seizure prophylaxis is 4–7 mEq/L (2.0–3.5 mmol/L), and above it lies a ladder the exam loves: patellar (deep-tendon) reflexes are lost FIRST at 8–10 mEq/L, respiratory depression follows at 10–15 mEq/L, and cardiac arrest at 25–30 mEq/L. The sequence is the testable fact — the knees warn you before the lungs fail, and the lungs fail before the heart stops.

Why does a standard infusion become toxic? Magnesium is renally cleared. The kidney holds magnesium in equilibrium until creatinine clearance falls below roughly 20 mL/min — and renal impairment is common in severe preeclampsia (creatinine ≥ 1.1 is a severe feature). The disease damages the very organ that clears its treatment, so the monitoring — reflexes, respirations, urine output — is not routine paperwork; it is the safety system. The stop rules and the antidote (IV calcium gluconate) live in the nursing section below.

The magnesium toxicity ladder: reflexes go first, breathing second, the heart last — and the injured preeclamptic kidney is what pushes a standard dose up the ladder.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Prior preeclampsia (high risk — recurs in ~25% of future pregnancies) Multifetal gestation (high risk) Chronic hypertension (high risk) modifiable Pregestational type 1 or 2 diabetes (high risk) modifiable Kidney disease (high risk) Autoimmune disease — SLE, antiphospholipid syndrome (high risk) Nulliparity — first pregnancy (moderate risk) Obesity, pre-pregnancy BMI > 30 (moderate risk — the main modifiable factor) modifiable Family history of preeclampsia — mother or sister (moderate risk) Age ≥ 35 (moderate risk) Black persons; lower income (moderate risk — USPSTF equity-based flags) In-vitro conception; > 10-year pregnancy interval; prior low-birth-weight/SGA or adverse outcome (moderate risk)

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

BP ≥ 140/90 after 20 weeks (×2, ≥ 4 h apart) early Expected
Why: Diffuse endothelial dysfunction from placental antiangiogenic factors — the defining (but least dangerous-looking) sign.
Proteinuria (≥ 300 mg/24 h · P/C ≥ 0.3 · dipstick ≥ 2+) early Expected
Why: Injured glomerular endothelium leaks protein — the kidney’s version of the same microvascular lesion.
Swelling of the face, hands, or around the eyes, or sudden weight gain Hold & notify
Why: Extreme swelling of the hands or face, unlike the usual slight swelling of pregnancy, is a CDC urgent warning sign — capillary leak from endothelial injury; swelling that is increasing beyond usual pregnancy swelling is the cue. Swollen feet alone are common in pregnancy and may not signal a problem; face and hand swelling and sudden weight gain are listed preeclampsia symptoms.
Shortness of breath or swelling worsening beyond baseline pregnancy symptoms early Hold & notify
Why: Capillary leak into the lungs and tissues — reported by patients with preeclampsia and worth a same-day evaluation.
Severe or persistent headache late Report immediately
Why: Cerebral microvascular involvement and failing autoregulation — a classic pre-seizure warning symptom.
Visual disturbances — scotomata, photophobia, blurred vision, temporary blindness or visual field defects late Report immediately
Why: The occipital cortex and retina sit downstream of the same failing cerebral microcirculation — another pre-seizure warning.
RUQ or epigastric pain, often with nausea/vomiting and malaise late Report immediately
Why: Hepatic microvascular injury stretching the liver — a severe feature, a pre-seizure warning, and the HELLP cue even when the BP looks tame.
Altered mental status late Report immediately
Why: Vasogenic cerebral edema — the brain announcing the blood–brain barrier is failing.
Severe-range BP ≥ 160/110 late Report immediately
Why: Pressure high enough to overwhelm cerebral autoregulation; persistent severe-range pressure is the treatment trigger.
Trouble breathing late Report immediately
Why: Pulmonary edema — leaky pulmonary capillaries plus rising vascular pressure; a severe feature.
Falling urine output on I&O Hold & notify
Why: The injured kidney failing — and the organ that clears magnesium sulfate going offline; urine output is one of the clinical magnesium checks.
Unusual or severe bleeding Hold & notify
Why: Platelets consumed in the damaged microvasculature — HELLP can present with severe bleeding, abruption, or liver hematoma.
Decreased fetal movement Report immediately
Why: The fetus lives downstream of the failing placenta — hypoperfusion shows up as reduced activity.
Vaginal bleeding with abdominal pain Report immediately
Why: Placental abruption — a complication of the ischemic, infarct-prone placenta.

Diagnostics

Test In this disorder Normal
Blood pressure Persistent severe-range pressure lasting ≥ 15 minutes is the treatment trigger — do not wait 4 hours to "confirm" a 160/110 ≥ 140/90 on 2 occasions ≥ 4 h apart after 20 weeks = diagnostic; ≥ 160/110 = severe range (may be confirmed on readings minutes apart to expedite treatment) StatPearls < 140/90
Urine protein The dipstick is the least reliable method — used when quantitative testing is unavailable. Proteinuria is not required for the diagnosis when new maternal organ dysfunction is present. ≥ 300 mg on 24-h collection, protein/creatinine ratio ≥ 0.3, or dipstick ≥ 2+ StatPearls —
Platelet count Falling platelets in a preeclamptic patient means the microvasculature is consuming them — recheck, don’t wait < 100 K/mm³ = severe feature — and one arm of the HELLP triad StatPearls —
Serum creatinine Doubles as the magnesium-safety lab: magnesium is renally cleared, so a rising creatinine raises toxicity risk on a standard infusion ≥ 1.1 mg/dL or doubling of baseline = severe feature StatPearls —
AST/ALT + hemolysis panel Order the panel for third-trimester RUQ/epigastric pain regardless of the BP Transaminases > 2× ULN = severe feature. HELLP = hemolysis (≥ 2 of: schistocytes/burr cells on smear, bilirubin > 1.2 mg/dL, haptoglobin < 25 mg/dL or LDH > 2× ULN, hemoglobin < 8–10 g/dL) + AST or ALT > 2× ULN + platelets < 100,000/µL Tennessee classification —
Serum magnesium (on therapy) Levels every 6–8 h or clinical checks of patellar reflexes and urine output — and remember that the kidney clears it Therapeutic for seizure prophylaxis: 4–7 mEq/L (2.0–3.5 mmol/L); DTRs lost at 8–10 · respiratory depression at 10–15 · cardiac arrest at 25–30 mEq/L StatPearls —

Complications

Warning: Eclamptic seizure Report immediately
New-onset seizures — heralded by headache, visual changes, RUQ pain, or altered mentation, or by nothing at all.
During the seizure: turn her onto one side to keep the airway clear, do not restrain, and keep the bed rails elevated and padded; call for help. Establish the airway and give oxygen by face mask at more than 8–10 L/min to treat the hypoxemia of seizure hypoventilation, and suction oral secretions as needed. The lateral decubitus position lowers aspiration risk and improves uterine blood flow by lifting the gravid uterus off the vena cava. About 10% of patients seize again after receiving magnesium; a second 2 g IV magnesium bolus over 3–5 minutes can be given. If seizures persist past 20 minutes or more than 2 occur despite magnesium, lorazepam 4 mg IV over 3–5 minutes is recommended. Magnesium continues 24 hours after delivery or the last seizure, and eclampsia is among the findings that call for expedited delivery after stabilization.
Warning: HELLP progression — DIC, hepatic hematoma/rupture Report immediately
DIC complicates 15–62.5% of HELLP; worsening RUQ pain may herald hepatic hematoma or rupture; acute renal failure in 36–50%.
Escalating RUQ pain in a HELLP patient is a report-now finding, not "expected discomfort." Transfusion support: red cells if hemoglobin < 7 g/dL (or ecchymosis, severe hematuria, suspected abruption); platelets for any actively bleeding thrombocytopenic patient.
Warning: Placental abruption Report immediately
Vaginal bleeding with abdominal pain — the ischemic placenta separating. Complicates 11–25% of HELLP.
Bleeding + pain + a rigid or tender uterus = emergent OB evaluation; abruption threatens both patients at once and is on the patient’s report-immediately list for a reason.
Caution: Pulmonary edema Report immediately
New dyspnea in a preeclamptic patient — leaky capillaries plus rising pressures flooding the lungs; itself a severe feature.
New or worsening trouble breathing moves the patient into severe-features territory and changes the delivery-timing calculus — report immediately.
Caution: Postpartum presentation — the danger outlasts the birth Report immediately
Eclampsia most frequently develops in the first 48 hours postpartum, risk stays elevated through the first week, and late-onset eclampsia (more than 48 hours after delivery) can still pose a significant risk. Late postpartum preeclampsia (new-onset hypertension from 48 hours up to 6 weeks after delivery) should be considered, and eclampsia has been reported in 10–15% of people with delayed-onset postpartum preeclampsia.
Close monitoring continues after delivery — eclamptic seizures typically occur from labor through 72 hours postpartum, with a large portion within the first 7 to 10 days, often heralded by headache — and discharge teaching must include the warning-sign list (symptoms after delivery mean calling the provider or 911 right away) — the patient who delivered "fine" is still not out of the woods.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Magnesium Sulfate (Obstetric) First-line High-alert
Reproductive & OB

First-line seizure prophylaxis in preeclampsia with severe features, eclampsia, and HELLP (started at admission in HELLP; also fetal/neonatal neuroprotection), continued 24 hours after delivery or the last seizure. It is the first-line treatment for preventing and controlling eclamptic seizures; about 10% seize again after receiving it, and a second 2 g IV bolus over 3–5 minutes can be given; if seizures persist past 20 minutes or more than 2 occur despite magnesium, lorazepam 4 mg IV over 3–5 minutes is recommended. The nurse owns the toxicity ladder: DTRs lost first → respiratory depression → cardiac arrest; stop rules and the calcium gluconate antidote are in the nursing section.
Other Antihypertensives First-line
Cardiovascular

For sustained severe-range BP ≥ 160/110 (persisting ≥ 15 minutes): the exam triad is IV labetalol (10–20 mg IV over 2 min, then 20–80 mg every 20–30 min to a maximum of 300 mg in 24 h; preferred over hydralazine for its faster onset, about 5 min, and lower risk of reflex tachycardia; contraindicated in severe asthma, heart failure, and AV block), IV hydralazine (5–10 mg q20 min, max 20 mg), and PO immediate-release nifedipine (10–20 mg, repeat in 20 min; max 180 mg/day). The goal is gradual reduction to 140–160/90–110 — never normalization, because placental perfusion rides on maternal pressure. ACE inhibitors, ARBs, MRAs, and nitroprusside are contraindicated in pregnancy — teratogenic.

Beyond medications

  • Delivery is the definitive cure — timing by severity: at 37 weeks or later, delivery is usual; before 37 weeks, treatment options that give the fetus more time may be considered depending on severity, with close maternal and fetal surveillance, and severe preeclampsia is managed in hospital with close, continuous monitoring. Delivery is expedited after stabilization regardless of gestational age for uncontrolled BP, persistent headache, visual symptoms or RUQ pain despite treatment, pulmonary edema, HELLP, eclampsia, suspected abruption, or abnormal fetal testing.
  • Antenatal corticosteroids (betamethasone) for fetal lung maturity when delivery is anticipated < 34 weeks — never delaying delivery when unstable. In HELLP, dexamethasone showed no maternal benefit in two large randomized trials: the steroids are for the baby’s lungs, not the mother’s platelets.
  • Low-dose aspirin 81 mg/day, started after 12 weeks, for anyone with ≥ 1 high-risk factor — and considered with ≥ 2 moderate-risk factors (USPSTF 2021, Grade B; pooled risk ratio for preeclampsia 0.85).
  • Fetal surveillance: ultrasound with amniotic-fluid index and estimated fetal weight, non-stress tests and biophysical profiles; umbilical-artery Doppler abnormality flags placental insufficiency/growth restriction. Expectant management runs up to twice-weekly BP checks with NST, AFI, and labs.
  • HELLP transfusion support: red cells for hemoglobin < 7 g/dL (or ecchymosis, severe hematuria, suspected abruption); platelets for any actively bleeding patient with thrombocytopenia.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Trend the BP against the two thresholds that change everything: ≥ 140/90 (diagnosis) and ≥ 160/110 (severe range — treat when it persists ≥ 15 minutes).
Why: Severe-range readings may be confirmed only minutes apart specifically so treatment isn’t delayed — waiting hours to "reconfirm" a 165/112 is the error the criteria were written to prevent.
On magnesium: check patellar (deep-tendon) reflexes, respiratory rate, and urine output at every assessment, and draw levels every 6–8 h or follow clinical checks per protocol.
Why: The toxicity ladder announces itself in order — DTRs vanish first (8–10 mEq/L), breathing slows next (10–15), the heart stops last (25–30) — so the reflex hammer is the early-warning system.
Track urine output closely and flag oliguria; know the creatinine.
Why: Magnesium is renally cleared — the preeclamptic kidney (creatinine ≥ 1.1 is a severe feature) is the exact organ that clears the drug, so falling output means the infusion is accumulating.
Ask about the warning trio every time: headache, visual changes, RUQ/epigastric pain — plus mental status.
Why: These are the classic pre-seizure warnings (cerebral and hepatic microvascular involvement). But eclampsia can strike without warning — their absence is reassuring, never a guarantee.
Ask about and assess edema in the legs, hands, or face, and swelling or shortness of breath worsening beyond baseline pregnancy symptoms.
Why: Swelling of the hands or face beyond the usual pregnancy swelling is a listed warning sign (CDC) — a "yes" goes to the provider for evaluation.
Monitor FHR continuously during instability, and during a maternal seizure protect her airway first — she is the fetus’s oxygen supply.
Why: Fetal evaluation (antenatal testing, abnormal umbilical-artery flow) is part of every delivery decision, and abnormal fetal testing is itself an indication for expedited delivery after the mother is stabilized.
The acute phase — severe features, magnesium, seizures
Keep full seizure precautions in place: bed rails elevated and padded, and be ready to turn her onto one side.
Why: Side-lying keeps the airway clear; padded rails protect her from injury when a seizure arrives — possibly without any warning symptoms.
During a seizure: do not restrain, turn her onto one side with the mouth toward the ground, cushion her head, call for help, and give face-mask oxygen at more than 8–10 L/min.
Why: Holding someone down during a seizure can injure the patient or the nurse; side-lying keeps the airway clear, lowers aspiration risk, and improves uterine blood flow by relieving vena cava compression; oxygen treats the hypoxemia caused by hypoventilation during the seizure.
Before each dose, confirm the FDA labels’ safe-dose checks: patellar reflex present, respirations about 16/min or more, and urine output at least 100 mL in the preceding 4 hours — if the reflex is absent, give no more magnesium until it returns. Stop the magnesium infusion for StatPearls’ stop-rule findings — absent DTRs, respiratory rate < 12/min, or urine output < 80 mL over 4 hours — then notify the provider.
Why: Both sets of numbers are sourced: the drug labels set the safe-dose checks before each dose, which come earlier than the StatPearls stop rule, so checking against the label numbers catches toxicity sooner. Stopping the infusion removes the source instantly; the drug already on board still has to clear through the kidneys, so the antidote may be next.
Know the antidote: IV calcium gluconate 1 g (10 mL of a 10% solution) over ~3 minutes, repeatable after 5 minutes, as ordered.
Why: Calcium directly counters magnesium’s neuromuscular blockade — it is the reversal for respiratory depression and the step before arrest.
For sustained severe-range BP, give the ordered IV labetalol, IV hydralazine, or PO nifedipine and recheck per protocol — aiming for 140–160/90–110, not a normal BP.
Why: Placental perfusion depends on maternal pressure; dropping her to 118/70 trades the mother’s stroke risk for the fetus’s perfusion.
Recognize expected magnesium effects — facial flushing, warmth, transient hypotension — and don’t treat them as toxicity.
Why: These are benign; the toxicity signals are the reflexes, respirations, and urine output. Confusing the two either alarms the patient or numbs the team to real warnings.
If seizures persist past 20 minutes or more than 2 occur despite magnesium, anticipate lorazepam 4 mg IV over 3–5 minutes; then anticipate delivery planning.
Why: Magnesium is the first-line agent for preventing and controlling eclamptic seizures, and eclampsia is among the findings that call for expedited delivery after stabilization.
Patient teaching (home management & discharge)
Teach the report-immediately list: severe or worsening headache, vision changes, RUQ or upper-abdominal pain, nausea or vomiting, trouble breathing, swelling of the legs, hands, or face, sudden weight gain, persistent vomiting, decreased fetal movement, and any vaginal bleeding or leaking of fluid.
Why: Each item maps to an organ the disease is injuring — the patient at home is the monitoring system between visits.
Support the home plan: BP checks as scheduled, tracking how many times she feels the baby kick each day (fetal movement; there is no single normal number, and movement that stops or slows is reported at once), and antihypertensives as prescribed — and report any warning sign rather than waiting for the next visit.
Why: Expectant management lives or dies on early detection — the numbers she collects at home decide when management changes.
Before discharge after delivery, teach that preeclampsia and eclampsia can start or worsen postpartum — highest risk in the first 48 hours, elevated through the first week, with a large portion of postpartum seizures in the first 7 to 10 days — and review the same warning signs. Preeclampsia can, rarely, begin after the birth, and new high blood pressure up to 6 weeks after delivery still counts: symptoms after delivery mean calling the provider or 911 right away.
Why: Late-onset eclampsia (more than 48 hours after delivery) can still pose a significant risk, often heralded by headache; the patient who thinks delivery ended the disease won’t call about the headache that matters.
Counsel for the future: prior preeclampsia is itself a high-risk factor (recurrence ~25%; HELLP 19–27%) → the next pregnancy needs early low-dose aspirin (81 mg after 12 weeks) and closer surveillance.
Why: Aspirin prophylaxis is USPSTF Grade B for exactly this patient — the history she just acquired is the indication.
Discuss cardiovascular risk after eclampsia and confirm the activity plan with the provider.
Why: An eclampsia hospitalization carries a 12-fold increased risk of cardiovascular complications (MI, stroke, heart failure) during that hospitalization — this is a vascular disease with a long shadow.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    Three findings changed since 2200: patellar DTRs went from 2+ to absent, RR fell from 16 to 11, and urine output is 60 mL over 4 hours. The chart also holds the setup: creatinine 1.2 mg/dL on a continuous magnesium infusion. The BP of 152/96 (below severe range), the reassuring FHR, and her drowsiness-but-arousable state are context, not the headline.

  2. 2
    Analyze cues

    This is the magnesium toxicity ladder, climbing in order: reflexes are lost first (8–10 mEq/L) and respiratory depression follows (10–15 mEq/L) — she has both, and RR 11 is below the < 12/min threshold. The why is on the lab sheet: magnesium is renally cleared, her creatinine of 1.2 marks the renal injury of severe preeclampsia, and 60 mL over 4 hours (< 80 mL/4 h) means the drug is accumulating faster than her kidneys can dump it. Every one of the three stop rules — absent DTRs, RR < 12, urine output < 80 mL/4 h — is met.

  3. 3
    Prioritize

    The next rung of the ladder is cardiac arrest — this outranks everything else on the unit. Breathing is threatened and the threat is still infusing into her arm, so the sequence is: remove the source (stop the infusion) → protect breathing → reverse (antidote) → reassess. Nothing about the BP or the delivery plan comes before that.

  4. 4
    Generate solutions

    Stop the magnesium infusion (the stop rules are the nurse’s authority to act). Notify the provider immediately with the three findings and the creatinine, anticipating IV calcium gluconate 1 g (10 mL of 10%) over ~3 minutes and a stat serum magnesium level. Keep her side-lying with padded rails up — stopping the prophylaxis does not stop the disease, and she remains at seizure risk. Keep continuous FHR monitoring running.

  5. 5
    Take action

    Stop the infusion first — it takes seconds and halts accumulation instantly. Then the SBAR: "34-week severe preeclampsia on a magnesium infusion — patellar reflexes now absent, RR 11, urine output 60 mL over 4 hours, creatinine 1.2. I have stopped the infusion. Requesting calcium gluconate and a stat magnesium level." Give the calcium gluconate as ordered over ~3 minutes; it can be repeated after 5 minutes. Monitor her respirations continuously — the magnesium already on board still has to clear through impaired kidneys.

  6. 6
    Evaluate

    Improvement looks like: RR climbing back above 12 (the labels’ safe-dose check before any further magnesium is about 16/min or more), DTRs returning, the stat level confirming the picture (a value like 10 mEq/L fits absent reflexes plus respiratory depression), and urine output recovering. She is still a severe-features patient headed for delivery, so seizure precautions stay up and the team re-plans her seizure prophylaxis and delivery timing. No improvement — or any further respiratory decline — re-escalates immediately.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Labor & delivery, antepartum room · 0200

A 26-year-old G1P0 at 34 weeks, admitted for preeclampsia with severe features (admission BP 168/112 with new headache). She received an IV magnesium sulfate loading dose and is on a continuous maintenance infusion; betamethasone has been given and delivery is planned for later today. At the 2200 assessment her patellar reflexes were 2+ and RR was 16.

0200 vitals — BP 152/96 · HR 88 · RR 11 · SpO₂ 95% on room air
Neuro — drowsy but arousable; patellar DTRs absent bilaterally (2+ at 2200)
I&O — Foley: urine output 60 mL over the past 4 hours
2000 labs — creatinine 1.2 mg/dL · platelets 118 K/mm³ · AST 52 U/L
Fetal monitor — FHR 140s, moderate variability
Infusing — magnesium sulfate maintenance infusion
Q1 Select all that apply
Which 0200 findings indicate magnesium toxicity? Select all that apply.
  1. A. Patellar reflexes absent bilaterally
  2. B. Respiratory rate 11/min
  3. C. Urine output 60 mL over 4 hours
  4. D. Facial flushing and a feeling of warmth
  5. E. BP 152/96 mmHg
Reveal answer & rationale
Answer: A, B, C
Absent DTRs are the first rung of the toxicity ladder, RR 11 is respiratory depression below the < 12/min threshold, and 60 mL/4 h is below the < 80 mL/4 h urine-output rule — each one alone is a stop-the-infusion criterion. Facial flushing and warmth (D) are expected benign effects of magnesium, not toxicity. BP 152/96 (E) is below severe range and is the disease, not the drug — magnesium is seizure prophylaxis, not an antihypertensive.
Q2 Multiple choice
Given the absent reflexes, RR of 11, and low urine output, the nurse’s first action is to:
  1. A. Halve the magnesium infusion rate and reassess in 30 minutes
  2. B. Stop the magnesium infusion
  3. C. Administer calcium gluconate from the medication supply
  4. D. Draw a stat serum magnesium level and await the result
Reveal answer & rationale
Answer: B
All three stop rules are met — the source of the harm is still running into her vein, and stopping it is instant and within the nurse’s authority (B). Slowing the rate (A) continues dosing a drug her injured kidneys cannot clear. Calcium gluconate (C) is the anticipated next step with a provider order — reversal follows removal of the source. Waiting on a lab (D) leaves the infusion running while the ladder’s next rung is cardiac arrest; the clinical stop rules exist precisely so the nurse does not wait for a number.
Q3 Put in order
Place the nurse’s actions in priority order:
  1. A. Notify the provider, anticipating calcium gluconate and a stat magnesium level
  2. B. Stop the magnesium infusion
  3. C. Confirm she is side-lying with padded rails up and monitor respirations continuously
  4. D. Document the findings and the time the infusion was stopped
Reveal answer & rationale
Correct order: B → C → A → D
Stop the infusion first — seconds, no order needed, halts accumulation. Positioning and continuous respiratory monitoring (C) protect her breathing and maintain seizure precautions — stopping the prophylaxis did not stop the disease. Then the SBAR call (A) sets up the antidote and the stat level. Documentation (D) matters but never precedes stabilizing her. Calling first leaves magnesium infusing while you talk.
Q4 Multiple choice
The provider orders the antidote. The nurse prepares:
  1. A. Naloxone 0.4 mg IV push
  2. B. Lorazepam 4 mg IV over 3–5 minutes
  3. C. Calcium gluconate 1 g (10 mL of a 10% solution) IV over about 3 minutes
  4. D. Protamine sulfate 50 mg IV
Reveal answer & rationale
Answer: C
Calcium gluconate is the magnesium antidote — 10 mL of a 10% solution equals 1 g, given over ~3 minutes and repeatable after 5 (C). Naloxone (A) reverses opioids; her respiratory depression is neuromuscular blockade from magnesium, not narcosis. Lorazepam (B) belongs to a different branch of this disorder — seizures persisting on magnesium — and would worsen respiratory depression here. Protamine (D) reverses heparin.
Q5 Multiple choice
Which chart finding best explains why this patient reached toxic magnesium levels on a standard maintenance infusion?
  1. A. Creatinine 1.2 mg/dL with urine output of 60 mL over 4 hours
  2. B. Platelets of 118 K/mm³
  3. C. Her age of 26
  4. D. The betamethasone she received for fetal lung maturity
Reveal answer & rationale
Answer: A
Magnesium is renally cleared, and severe preeclampsia injures the kidney — her creatinine ≥ 1.1 and falling urine output mean a standard infusion accumulates (A) — the kidney holds magnesium in equilibrium only until creatinine clearance falls below about 20 mL/min. Platelets of 118 (B) reflect the disease trending toward the < 100 K severe-feature threshold but do not affect drug clearance. Age (C) is irrelevant to clearance here. Betamethasone (D) matures fetal lungs and has no role in magnesium elimination.

Common questions

What causes preeclampsia, eclampsia & hellp?
Common causes and risk factors include prior preeclampsia (high risk — recurs in ~25% of future pregnancies), multifetal gestation (high risk), chronic hypertension (high risk), pregestational type 1 or 2 diabetes (high risk), kidney disease (high risk), and others.
What are the early signs of preeclampsia, eclampsia & hellp?
Early findings include BP ≥ 140/90 after 20 weeks (×2, ≥ 4 h apart), Proteinuria (≥ 300 mg/24 h · P/C ≥ 0.3 · dipstick ≥ 2+), Shortness of breath or swelling worsening beyond baseline pregnancy symptoms.
Which findings should a nurse report immediately in preeclampsia, eclampsia & hellp?
Report immediately: Severe or persistent headache, Visual disturbances — scotomata, photophobia, blurred vision, temporary blindness or visual field defects, RUQ or epigastric pain, often with nausea/vomiting and malaise, Altered mental status, Severe-range BP ≥ 160/110, and others. These signal deterioration that needs rapid intervention.
Can preeclampsia or eclampsia happen after the baby is born?
Yes — and this is a critical teaching point. Eclampsia most frequently develops in the first 48 hours postpartum, risk stays elevated through the first week, and late-onset eclampsia (more than 48 hours after delivery) can still pose a significant risk. Seizures typically occur from labor through the first 72 hours postpartum, with a large portion in the first 7 to 10 days, which is why close monitoring continues after delivery and every discharge includes the warning-sign list: unrelenting headache, vision changes, RUQ pain, trouble breathing, swelling of the hands and face. New-onset hypertension between 48 hours and 6 weeks after delivery should raise concern for late postpartum preeclampsia, and anyone with symptoms after delivery should call the provider or 911 right away.
What is magnesium sulfate for, and how long does it continue?
Magnesium sulfate is the first-line treatment for preventing and controlling eclamptic seizures — in HELLP it is started at admission, and it also has neuroprotective effects for the fetus. During an active seizure the nurse protects the patient: turn her onto one side, no restraints, padded rails. If seizures persist past 20 minutes or more than 2 occur despite magnesium, lorazepam 4 mg IV over 3–5 minutes is recommended. The infusion continues 24 hours after delivery or after the last seizure, because the risk doesn’t end at birth.
How is HELLP different from preeclampsia?
HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) is considered a variant of severe preeclampsia in which the microvascular injury concentrates in the liver and the platelets — but hypertension or proteinuria is absent in at least 15–20% of HELLP patients. The cue is RUQ or epigastric pain with nausea, vomiting, and malaise in the third trimester or within 48 hours of delivery: that patient needs a CBC, smear, and liver panel even if her blood pressure looks unimpressive.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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