Re-lowering serum sodium after overcorrection of hyponatremia

Electrolyte Disordersmedium

A 75-year-old woman with a history of hypertension and diabetes is brought to the emergency department after being found confused at home. She was in her usual state of health the previous day. She is unable to provide any history, but her children report that since her husband passed away 2 weeks ago, she has hardly eaten while consuming an increased amount of alcohol. Medications include chlorthalidone and metformin. On arrival, BP is 92/60 mm Hg and heart rate is 104/min. Skin turgor is poor. She is lethargic but answers simple questions, and there are no focal neurologic deficits. She receives 0.9% saline 2 L and potassium chloride 60 mEq over the next few hours, and urine output increases from 20 to 300 mL/h. Mental status remains unchanged. Laboratory data (on arrival, 6 hours later; reference): sodium 110, 121 mEq/L (136–145); potassium 2.9, 3.4 mEq/L (3.5–5.0); chloride 78, 93 mEq/L (98–106); glucose 154, 102 mg/dL (70–99, fasting); BUN 38, 18 mg/dL (8–20); creatinine 1.3, 0.9 mg/dL (0.5–1.1); serum osmolality 240, 263 mOsm/kg H₂O (275–295); urine sodium 11 mEq/L on arrival (varies); urine osmolality 190 mOsm/kg H₂O on arrival (varies). Which of the following is the next BEST STEP in management?

  1. A.5% dextrose IV and desmopressinCorrect
  2. B.5% dextrose IV
  3. C.No additional management
  4. D.0.9% saline IV and desmopressin

Explanation

This patient with severe hyponatremia and overcorrection should receive 5% dextrose IV and desmopressin to decrease the serum sodium back into the safe range. This patient presented with severe hyponatremia and rapidly overcorrected after receiving isotonic fluid. The etiology of her hyponatremia is uncertain, and there are several factors that may contribute to her presentation, including excessive fluid consumption in the setting of alcohol use and low solute intake. Additionally, hypotension, tachycardia, and low urine sodium concentration with an inappropriately high urine osmolality all suggest volume depletion. She takes chlorthalidone, which can also predispose to hyponatremia, although the low urine sodium indicates an absence of diuretic effect at the time of presentation. Uncontrolled diabetes is yet another consideration, although the modestly elevated serum glucose is reassuring in this regard. The duration of hyponatremia is also uncertain, despite information that she was in her usual state of health one day before presentation. Without definitive laboratory data to confirm the acute onset of hyponatremia, she should be managed as having chronic hyponatremia. In this setting, the rate of correction should not exceed 6–8 mEq/L in 24 hours to avoid osmotic demyelination (OD). This patient has several risk factors for both overcorrection and OD, including female sex, low initial plasma sodium concentration, low initial urine sodium concentration, alcohol use disorder, and hypokalemia. Volume expansion suppresses antidiuretic hormone, leading to a large, dilute urine output. The contribution of potassium supplementation to correction is equivalent to the provision of sodium, a fact that may be underappreciated by practitioners. This patient's sodium has corrected by 11 mEq/L within 6 hours, and prompt re-lowering of her serum sodium is indicated. The next best step would be to administer 5% dextrose in addition to desmopressin. If retained, 5% dextrose at a dose of 6 mL/kg would be expected to lower her serum sodium approximately by 2 mEq/L. To induce water retention, desmopressin 1–2 μg IV every 6–8 hours should be provided. Without desmopressin, it is challenging to deliver the volume of 5% dextrose required to relower the plasma sodium concentration to target. Re-lowering the serum sodium should be done promptly even if there are no new or worsened neurologic symptoms in the setting of overcorrection. The signs and symptoms of osmotic demyelination often do not appear for several days and cannot be used to guide therapy. Changing her fluids to 0.9% saline, with or without desmopressin, would not provide the water required to effectively re-lower her serum sodium concentration.

Why each option

A.
Correct. Desmopressin stops the aquaresis while 5% dextrose supplies free water, re-lowering sodium after an 11 mEq/L rise in 6 hours in a high-risk patient.
B.
Without desmopressin, ongoing dilute diuresis of 300 mL/h outpaces infused dextrose, making it difficult to re-lower sodium to a safe range.
C.
Osmotic demyelination signs appear days later, so a rise of 11 mEq/L in 6 hours in a high-risk patient requires prompt re-lowering regardless of symptoms.
D.
Saline with desmopressin halts water loss but provides no free water, so it cannot lower a sodium already raised 11 mEq/L in 6 hours.

Reference: Sterns RH, N Engl J Med 2015 (disorders of plasma sodium: causes, consequences, and correction); Verbalis JG, Am J Med 2013 (expert panel recommendations on hyponatremia)

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