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Preeclampsia

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Preeclampsia

Key Points

  • Preeclampsia is new-onset hypertension (≥140/90 mmHg) with proteinuria or end-organ dysfunction after 20 weeks’ gestation in a previously normotensive client.
  • Severe preeclampsia is defined by BP ≥160/110 mmHg, platelet count <100,000 cells/mm³, creatinine >1.2 mg/dL, or urine output <30 mL/hour.
  • Warning signs of deterioration: severe persistent headache, visual disturbances (blurred vision, photophobia), epigastric or RUQ pain, and sudden facial edema.
  • HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) and eclampsia (tonic-clonic seizures) are life-threatening complications.
  • HELLP syndrome can progress to severe hemorrhagic complications, including hepatic rupture.
  • The only definitive treatment is delivery; magnesium sulfate prevents seizures and antihypertensives reduce severe hypertension.

Pathophysiology

Preeclampsia results from inadequate placental vascular development causing impaired blood flow to the fetus. Reduced oxygen and nutrient delivery triggers systemic inflammation and widespread maternal vasoconstriction, damaging target organs including the kidneys, brain, and liver. Increased capillary permeability causes fluid shifts into interstitial spaces (edema) while decreasing circulating volume.

Spectrum of Hypertensive Disorders in Pregnancy

DisorderDefinition
Gestational hypertensionHTN after 20 weeks without proteinuria or end-organ dysfunction
PreeclampsiaHTN + proteinuria or end-organ dysfunction after 20 weeks
Preeclampsia superimposed on chronic HTNPreeclampsia developing in client with preexisting hypertension
HELLP syndromeHemolysis, Elevated Liver enzymes, Low Platelets — life-threatening complication of preeclampsia
EclampsiaTonic-clonic seizures in preeclampsia without other neurologic cause

In gestational-hypertension pathways, progression to proteinuria/end-organ features can occur and requires close reassessment for evolution into preeclampsia-spectrum disease.

Risk Factors

Prior preeclampsia, preexisting hypertension, pregestational diabetes mellitus, obesity, multifetal gestation, chronic kidney disease, systemic lupus erythematosus, nulliparity, age ≥35 years, adolescent pregnancy, first-degree family history.

Nursing Assessment

NCLEX Focus

Recognize progression cues — a severe headache that is persistent and unrelenting is a red flag for cerebral edema and may precede eclampsia. Report immediately, do not wait for BP readings alone.

Mild versus severe preeclampsia criteria:

ParameterMildSevere
Blood pressure≥140/90 mmHg≥160/110 mmHg
Proteinuria (24-hour urine)300–2,000 mg/24 hr>2,000 mg/24 hr
Platelet countNormal<100,000 cells/mm³
CreatinineNormal>1.2 mg/dL
Urine output≥30 mL/hour<30 mL/hour
Headache/visual changesMild blurred visionSevere, unrelenting headache

Clinical findings to report immediately:

  • Severe or persistent headache (cerebral edema warning)
  • Visual disturbances: photophobia, blurred vision, scotomata
  • Epigastric or right upper quadrant pain (hepatic distension or rupture risk)
  • Sudden facial edema, rapid weight gain >5 lb/week
  • New dyspnea or orthopnea (pulmonary edema)
  • Decreased fetal movement
  • Postpartum clonus or hyperreflexia (deep tendon reflexes expected around 2+; new clonus/hyperreflexia suggests rising seizure risk)

Diagnostic testing: CBC (thrombocytopenia), serum creatinine and BUN, liver enzymes (AST, ALT, bilirubin), 24-hour urine protein, fetal nonstress test or biophysical profile, ultrasound for growth restriction and amniotic fluid volume.

  • In suspected HELLP overlap, trend LDH and platelet decline serially (including postpartum intervals) because laboratory deterioration may progress after delivery.

Nursing Interventions

Antihypertensive therapy (for BP ≥160/110 mmHg):

  • Oral nifedipine (calcium channel blocker) — first-line oral agent
  • IV labetalol (alpha/beta blocker) — use cautiously in clients with asthma or HR <50 bpm
  • IV hydralazine (peripheral arterial vasodilator)

Magnesium sulfate for seizure prevention (eclampsia prophylaxis):

  • Administer as IV loading dose followed by continuous infusion; continue until 24 hours postpartum
  • Assessment before each dose: respirations ≥16 breaths/minute, patellar reflexes present, urine output ≥30 mL/hour
  • Monitor serum magnesium levels; toxicity produces loss of reflexes, respiratory paralysis, cardiac arrest
  • Antidote: calcium gluconate 1 g IV — keep at bedside

Fluid management:

  • Isotonic saline infusion at approximately 80 mL/hour to maintain kidney function while avoiding volume overload
  • Clients with preeclampsia are at high risk for pulmonary edema (third-spacing)
  • Oliguria (<30 mL/hour) may indicate kidney impairment and requires provider notification

Fetal surveillance: continuous electronic fetal monitoring during intrapartum period; decreased baseline FHR variability is expected with magnesium sulfate.

Intrapartum environment and safety:

  • Reassess rising BP values promptly and report escalation without delay.
  • Minimize environmental stimulation (low lights, reduced noise/visitors) when severe-feature symptoms are present or seizure risk is rising.
  • During labor, monitor for pulmonary edema cues (crackles, wheeze, dyspnea) and worsening edema while maintaining strict I&O.

Eclampsia Emergency

Tonic-clonic seizures require: (1) call for help immediately, (2) position on left side, (3) protect airway, (4) administer magnesium sulfate as ordered, (5) monitor fetal heart rate continuously. Do not restrain the client or insert objects in the mouth.

Self-Check

  1. Which three assessment findings indicate severe preeclampsia requiring immediate hospitalization?
  2. A client receiving magnesium sulfate has a respiratory rate of 10 breaths/minute and absent patellar reflexes. What is the priority nursing action?
  3. Why is delivery the only definitive treatment for preeclampsia, and how does this affect timing decisions?

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