A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 24-year-old man is running a marathon (42.2 km) on a hot summer day and collapses about halfway through the run. Emergency personnel are called and find him having a seizure. As the seizure subsides, the runner exhibits confusion, dry lips and decreased skin turgor. On the way to the emergency department, he denies taking medication or having a history of seizures. He reports that he drank water, but he admits that it was probably not enough. Which of the following would be the next best step in the management of this patient?
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A
IndapamideIncorrect. Indapamide is a thiazide-like diuretic that causes hyponatremia by impairing urinary dilution — exactly the opposite of what is needed.
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B
RelcovaptanIncorrect. Relcovaptan is a selective V1a vasopressin antagonist studied for dysmenorrhea/preterm labor and is not used to correct hyponatremia.
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C
3% NaClCorrect. Acute symptomatic hyponatremia with seizures requires immediate hypertonic (3%) saline to rapidly raise serum sodium ~4–6 mEq/L and relieve cerebral edema.
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D
0.9% NaClIncorrect. 0.9% saline is roughly isotonic and will not correct hyponatremia quickly enough in an actively seizing patient; it may even worsen sodium in the setting of nonosmotic ADH release.
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E
Oral salt tabletsIncorrect. Oral salt tablets are used in chronic, mild, asymptomatic hyponatremia; they act too slowly to address acute symptomatic hyponatremia presenting with seizures.
↑ Tap an answer to reveal the reasoning
Answer: C. This marathon runner who drank water (presumably hypotonic fluid) during prolonged exertion now presents with seizure, altered mental status, and paradoxical findings of dehydration (dry lips, decreased turgor). This is exercise-associated hyponatremia, an acute, symptomatic hyponatremia caused by overconsumption of free water plus exercise-induced ADH release. Symptomatic hyponatremia with seizures is a neurologic emergency: cerebral edema can progress to herniation if not promptly corrected.
In acute symptomatic hyponatremia with seizure or coma, the immediate treatment is hypertonic (3%) saline, typically 100 mL bolus over 10 minutes (repeatable), aiming to raise serum sodium by ~4–6 mEq/L rapidly to relieve cerebral edema. Goal is no more than 8–10 mEq/L correction in 24 hours to avoid osmotic demyelination, but in acute ("<48 hour") symptomatic cases the brain has not adapted, so rapid early correction is both safe and necessary.
Normal saline (0.9%) is inappropriate — it is roughly isotonic and inadequate to raise sodium quickly in a seizing patient and may worsen hyponatremia if SIADH-like physiology is present. Indapamide (thiazide-like diuretic) causes hyponatremia. Relcovaptan is a V1a-receptor antagonist studied in dysmenorrhea, not a hyponatremia treatment (and the V2 antagonists like tolvaptan are used for chronic, not acute symptomatic, hyponatremia).
**Why each option:**
**A.** Indapamide is a thiazide-like diuretic that causes hyponatremia by impairing urinary dilution — exactly the opposite of what is needed.
**B.** Relcovaptan is a selective V1a vasopressin antagonist studied for dysmenorrhea/preterm labor and is not used to correct hyponatremia.
**C.** Correct. Acute symptomatic hyponatremia with seizures requires immediate hypertonic (3%) saline to rapidly raise serum sodium ~4–6 mEq/L and relieve cerebral edema.
**D.** 0.9% saline is roughly isotonic and will not correct hyponatremia quickly enough in an actively seizing patient; it may even worsen sodium in the setting of nonosmotic ADH release.