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Maternal Newborn Health
문제

A nurse is caring for a client at 32 weeks gestation who is experiencing preterm labor. The client has been receiving magnesium sulfate for tocolysis for the past 8 hours. Which nursing intervention is the highest priority?

해설
Monitoring deep tendon reflexes and respiratory rate is the highest priority to detect magnesium toxicity early, which can cause respiratory depression and loss of reflexes. Other interventions are important but secondary to preventing life-threatening complications.
같은 주제 다음 문제A 28-year-old gravida 2, para 1 client at 32 weeks gestation presents to the labor and del…

심화 해설

Understanding the Clinical Scenario

This question presents a client at 32 weeks gestation in preterm labor who has been receiving a magnesium sulfate infusion for tocolysis over the past 8 hours. Magnesium sulfate is a cornerstone therapy in obstetrics, but its therapeutic window is narrow, and systemic toxicity can develop insidiously. The nurse must prioritize interventions that directly monitor for and prevent life-threatening maternal adverse effects.

Analysis of the Correct Answer (Option 2)

Monitoring deep tendon reflexes (DTRs) and respiratory rate every hour is the highest priority. This intervention serves as a direct, real-time clinical assessment of the patient’s neuromuscular and respiratory status, which are the first systems to exhibit signs of magnesium sulfate toxicity.

The pharmacodynamics of magnesium sulfate explain this prioritization. Magnesium acts as a competitive antagonist to calcium at the presynaptic nerve terminal, inhibiting the release of acetylcholine and thereby decreasing the excitability of the muscle fiber membrane [2]. Clinically, this manifests as a progressive loss of deep tendon reflexes, which is the earliest and most reliable sign of impending magnesium toxicity. A systematic review of maternal adverse effects confirms that the suppression of patellar reflexes is a critical clinical indicator used to titrate or discontinue therapy to prevent progression to more severe toxicity [1]. As serum magnesium levels continue to rise, the blockade extends to the respiratory musculature, causing respiratory depression. Therefore, a systematic, hourly assessment of DTRs and respiratory rate is not merely a monitoring task; it is a direct safety check to ensure the patient is not progressing toward respiratory arrest, a potentially fatal complication [2].

Critique of Incorrect Options

Option 1: Encourage the client to ambulate frequently to prevent blood clots.
This intervention is contraindicated and potentially dangerous. A client in active preterm labor should be on bed rest or activity restriction to minimize uterine stimulation. Furthermore, magnesium sulfate causes vasodilation and smooth muscle relaxation, which can lead to orthostatic hypotension and muscle weakness . Ambulating a patient with diminished reflexes and potential hemodynamic instability creates a significant fall risk. While thromboembolism prevention is a nursing consideration, it is addressed with non-pharmacologic methods like pneumatic compression devices or pharmacologic prophylaxis, not ambulation during an acute tocolytic episode.

Option 3: Administer calcium gluconate prophylactically every 4 hours.
Calcium gluconate is the antidote for magnesium sulfate toxicity, as it directly antagonizes the effects of magnesium at the neuromuscular junction [2]. However, it is never administered prophylactically. Its use is reserved for the emergency management of confirmed, serious toxicity, indicated by signs such as absent DTRs, a critically low respiratory rate, or cardiac conduction abnormalities. Administering it routinely would counteract the desired tocolytic and neuroprotective effects of the magnesium sulfate infusion .

Option 4: Increase fluid intake to prevent dehydration from the medication.
While magnesium sulfate is excreted renally and adequate hydration supports renal function and drug clearance, aggressive fluid intake is not the highest priority and can be harmful. Magnesium sulfate is a tocolytic, but it is not a diuretic that causes dehydration. More critically, indiscriminate fluid loading in a patient receiving intravenous magnesium sulfate, who may also be receiving antenatal corticosteroids (which can cause fluid retention), can precipitate pulmonary edema. The focus should be on strict intake and output monitoring, not on pushing fluids, to maintain a balanced fluid status and monitor renal function, which is essential for safe drug elimination [2].

Synthesis of Evidence and Clinical Judgment

The systematic review by Bain et al. underscores that maternal adverse effects from magnesium sulfate regimens are common and can be severe enough to necessitate treatment cessation, making vigilant monitoring the cornerstone of safe care [1]. The pharmacological review by Xia et al. reinforces that the clinical signs of toxicity follow a predictable, dose-dependent sequence: loss of DTRs occurs first, followed by respiratory depression, and finally cardiac arrest [2]. By mandating hourly checks of DTRs and respiratory rate, the nurse is positioned to detect toxicity at its earliest, most reversible stage, long before a life-threatening event occurs. This makes Option 2 the clear clinical priority over comfort measures, prophylactic antidote administration, or unindicated fluid loading.
References (research sources)
  • [1]
    Maternal adverse effects of different antenatal magnesium sulphate regimens for improving maternal and infant outcomes: a systematic review.Meta-analysis/systematic reviewBain ES, Middleton PF, Crowther CA. (2013) · DOI: 10.1186/1471-2393-13-195
  • [2]
    Magnesium sulfate pharmacology for maternal and critical-care indications: mechanisms, pharmacokinetics, and the therapeutic window.Research articleXia M, Ni Q, Zhu S. (2026) · DOI: 10.3389/fphar.2026.1749828

임상 시나리오

Magnesium Sulfate for Tocolysis: Priority Nursing Assessment

When caring for a client receiving magnesium sulfate for preterm labor, the highest priority is continuous monitoring for signs of toxicity. The therapeutic range is narrow, and toxicity can progress rapidly from loss of reflexes to respiratory arrest.

Hourly Monitoring Protocol
  • Deep Tendon Reflexes (DTRs): Assess patellar reflexes hourly. Loss of DTRs is the earliest sign of magnesium toxicity and indicates the need to immediately hold the infusion and notify the provider.
  • Respiratory Rate: Count for a full minute every hour. A rate less than 12 breaths per minute indicates respiratory depression, a late and critical sign of toxicity.
  • Urine Output: Monitor hourly output. Magnesium is excreted renally; output must be at least 30 mL/hour to prevent accumulation and toxicity.
  • Serum Magnesium Levels: Obtain per facility protocol (often every 6 hours). Therapeutic range is typically 4-7 mg/dL; patellar reflexes are lost around 8-12 mg/dL.
Clinical Signs of Toxicity Progression
  1. Loss of DTRs (patellar) - Earliest sign
  2. Feeling of warmth, flushing, nausea - Mild toxicity
  3. Respiratory depression (RR < 12) - Moderate to severe toxicity
  4. Decreased level of consciousness, cardiac arrhythmias, cardiac arrest - Severe, life-threatening toxicity
Critical Safety Measures
  • Antidote at Bedside: Ensure calcium gluconate (10% solution) is immediately available. Administer IV push only for confirmed severe toxicity, not prophylactically.
  • Fall Precautions: Implement due to muscle weakness and CNS depression; keep side rails up and call light within reach.
  • Fluid Balance: Monitor intake and output strictly. Avoid aggressive fluid boluses to reduce the risk of pulmonary edema.
  • Fetal Monitoring: Continuous electronic fetal monitoring is indicated, as magnesium crosses the placenta and can cause decreased fetal heart rate variability.

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