NURS 2866 - Week 4 Lab Packet 3

What are the major differences between gestational hypertension, preeclampsia, and eclampsia in terms of diagnostic criteria and severity?

Gestational hypertension = BP ≥140/90 after 20 weeks with NO proteinuria or organ damage; Preeclampsia = BP ≥140/90 after 20 weeks WITH proteinuria (≥300 mg/24 hr or ≥2+ dipstick) OR signs of end-organ damage (renal, liver, brain, hematologic, pulmonary); Eclampsia = preeclampsia PLUS new-onset seizures not explained by another condition, representing the most severe progression.

What specific risk factors increase a patient’s likelihood of developing Preeclampsia and which apply to this patient?

Risk factors include primigravida (first pregnancy), age ≥35, obesity, chronic hypertension, diabetes, kidney disease, autoimmune disorders, multiple gestation, and history/family history of preeclampsia; in this patient, primigravida status and age 35 are the key contributing risks.

Based on the SBAR data, what clinical findings confirm this patient is developing preeclampsia rather than gestational hypertension?

Elevated BP from baseline (147/93 → 150/86), 2+ proteinuria, edema severe enough to prevent ring fitting, decreased urine output, and neurologic symptoms (lethargy/irritability) confirm preeclampsia due to renal and systemic involvement.

Why is decreased urine output in this patient a concerning sign of worsening preeclampsia?

It indicates reduced renal perfusion and possible kidney involvement due to vasospasm and endothelial damage, increasing risk for fluid imbalance and magnesium toxicity.

What are the overall nursing goals when managing a patient with preeclampsia?

Prevent progression to severe preeclampsia/eclampsia, prevent seizures, maintain maternal organ perfusion, ensure adequate uteroplacental perfusion for fetal oxygenation, monitor for complications (HELLP, stroke), and prepare for possible early delivery if instability occurs.

What specific education should the nurse provide to the patient and her husband regarding warning signs and disease progression?

Immediately report severe headache, visual disturbances (blurred vision, spots), RUQ/epigastric pain (liver involvement), decreased fetal movement, decreased urine output, and worsening edema; understand need for continuous monitoring, medication (magnesium sulfate), and possibility of early delivery.

Which assessment findings in this patient are most concerning and why do they indicate worsening disease?

4+ pitting edema (significant fluid shift), decreased urine output/no void since admission (renal compromise), rising BP (worsening hypertension), and lethargy/irritability (possible CNS involvement) indicate progression toward severe preeclampsia.

What do the L/S ratio and phosphatidylglycerol (PG) values reveal about fetal lung maturity and clinical decision-making?

L/S ratio assesses surfactant production (≥2:1 indicates maturity); this patient’s L/S of 1.8 suggests borderline immature lungs; presence of PG supports lung maturity but does not fully override low L/S, meaning the fetus may still be at risk for respiratory distress if delivered early.

What are deep tendon reflexes (DTRs), how are they graded, and why are they important in preeclampsia management?

DTRs assess neurologic excitability and magnesium toxicity; grading is 0 (absent), 1+ (diminished), 2+ (normal), 3+ (brisk), 4+ (hyperactive/clonus); hyperreflexia (3+–4+) suggests CNS irritability and seizure risk, while absent reflexes indicate possible magnesium toxicity.

Why is magnesium sulfate ordered in Stage 2 and what is its primary therapeutic purpose?

Magnesium sulfate is administered to prevent seizures (eclampsia) by depressing CNS excitability and stabilizing neuronal activity.

What side effects and signs of toxicity must the nurse monitor for during magnesium sulfate therapy?

Flushing, nausea, sedation, decreased deep tendon reflexes, respiratory depression (RR <12), hypotension, and decreased urine output; severe toxicity includes absent reflexes and respiratory arrest.

What underlying pathophysiological changes in preeclampsia increase seizure risk?

Endothelial dysfunction and vasospasm decrease cerebral blood flow, leading to brain edema and increased CNS irritability, which predisposes the patient to seizures.

What seizure precautions should be implemented for this patient and why are they essential?

Padded side rails, low-stimulation environment, oxygen and suction at bedside, continuous monitoring, and fall precautions; these reduce injury risk and prepare for airway management during a seizure.

What fetal concerns arise in a patient with worsening preeclampsia?

Decreased uteroplacental perfusion leads to fetal hypoxia, abnormal fetal heart rate patterns, decreased movement, and increased risk of emergency delivery.

What is the antidote for magnesium sulfate toxicity and when should it be administered?

Calcium gluconate, given when signs of toxicity occur such as respiratory depression or absent reflexes.

What do new symptoms of headache and nausea indicate in Stage 3 of this patient’s condition?

Progression to severe preeclampsia with CNS involvement, indicating increased risk for imminent seizure (eclampsia).

What is the purpose of labetalol in this patient and how is it administered?

Labetalol lowers blood pressure to prevent complications such as stroke and organ damage; administered IV push (20 mg in this scenario).

Can magnesium sulfate and oxytocin be administered simultaneously, and what is the nursing priority when both are used?

Yes, they can be used concurrently per protocol; priority is continuous monitoring of maternal vital signs, reflexes, respirations, urine output, contraction pattern, and fetal heart rate.

Why must blood pressure not be lowered too rapidly in this patient?

Rapid reduction can decrease uteroplacental perfusion, leading to fetal hypoxia and inadequate maternal organ perfusion.

Why is delivery recommended when the mother’s condition cannot be stabilized?

The placenta is the source of preeclampsia pathophysiology; delivery removes the cause and prevents further maternal and fetal deterioration.

What must the nurse monitor closely when labor is induced with oxytocin in this patient?

Contraction frequency, duration, intensity, uterine resting tone, fetal heart rate patterns, and signs of tachysystole, while also monitoring maternal status due to concurrent magnesium therapy.

What are the major risks to the mother and fetus in severe preeclampsia?

Maternal risks include seizures, stroke, HELLP syndrome, renal failure, pulmonary edema, and hemorrhage; fetal risks include hypoxia, growth restriction, prematurity, distress, and potential fetal demise.

What are the signs of magnesium toxicity in both the mother and newborn?

Mother: respiratory depression (RR <12), absent DTRs, extreme sedation, hypotension, decreased urine output; newborn: hypotonia (floppy), respiratory depression, decreased responsiveness.

Will preeclampsia resolve after delivery and what should the nurse anticipate postpartum?

Delivery is the definitive treatment and symptoms usually improve after placental removal, but complications may persist or worsen temporarily postpartum, requiring continued monitoring for seizures and organ dysfunction.

What is the key exam-level connection between ectopic pregnancy, placental abruption, and preeclampsia?

Ectopic pregnancy leads to rupture and hemorrhage, placental abruption leads to premature placental separation and fetal hypoxia, and preeclampsia causes systemic vasospasm leading to organ damage and seizures.