A 36-year-old woman undergoes an abdominal hysterectomy for symptomatic uterine fibroids. Medical history is otherwise unremarkable, and preoperative blood cell counts, serum chemistry, and coagulation studies are normal. There are no intraoperative complications and blood loss is minimal. She receives postoperative morphine sulfate by patient-controlled analgesia and an intravenous infusion of 5% dextrose in 0.45% saline. The following day, the patient experiences increasing global headache and severe nausea and is noted to be confused. Temperature is 36.7 C (98.1 F), blood pressure is 110/70 mm Hg, pulse is 88/min, and respirations are 14/min. Twenty-four-hour urine output is 1600 mL. On physical examination, the patient is lethargic and disoriented. The abdomen is soft with mild incisional tenderness and decreased bowel sounds. Neurologic examination shows no focal weakness or sensory loss. Laboratory results are as follows:
| Serum chemistry | |
| Sodium | 119 mEq/L |
| Potassium | 3.7 mEq/L |
| Creatinine | 0.5 mg/dL |
| Glucose | 78 mg/dL |
Which of the following is the most appropriate intervention for this patient?
This patient has symptomatic hyponatremia, most likely due to the use of hypotonic intravenous fluids (ie, 0.45% saline) and to postoperative syndrome of inappropriate antidiuretic hormone (SIADH) release (which is stimulated by pain, nausea, or stress). Low serum tonicity results in the influx of water into brain cells, leading to swelling and cerebral edema. Symptoms reflect elevated intracranial pressure: mild/moderate symptoms include nausea, malaise, headache, and confusion, whereas severe symptoms include seizure, coma, and respiratory arrest. Adaptations to normalize brain volume (eg, extrusion of osmolytes from brain cells) typically take ~48 hours.
Acute hyponatremia (present for <48 hr) is poorly tolerated, and patients are at high risk of brain herniation. Therefore, patients with serum sodium of <130 mEq/L with any symptoms of elevated intracranial pressure should be treated with hypertonic 3% saline boluses to rapidly correct serum sodium. Because neural adaptations have not occurred, patients are at relatively low risk of osmotic demyelination syndrome (ODS).
Chronic hyponatremia (present for ≥48 hr) is typically better tolerated; therefore, hypertonic saline is often reserved for those with severe hyponatremia (<120 mEq/ L), severe symptoms (eg, seizure), or concurrent intracranial pathology (eg, masses, hemorrhagic stroke).
The goal of hypertonic saline infusion is to raise serum sodium levels by 4-6 mEq/L over a period of hours, which markedly reduces the risk of herniation. The maximum rate of correction is 8 mEq/L in 24 hours to prevent ODS.
(Choice A) Acute adrenal insufficiency may occur in the postoperative setting and requires rapid administration of hydrocortisone or dexamethasone. It causes nausea, weakness, confusion, and hyponatremia, but most patients also have hyperkalemia and severe hypotension.
(Choice C) Vasopressin receptor antagonists (eg, tolvaptan) may be used for patients with chronic hyponatremia due to SIADH; however, they have slower onset than hypertonic saline and are not indicated in the treatment of acute, symptomatic patients.
(Choices D and E) Patients with symptomatic hyponatremia require rapid correction of sodium levels to prevent herniation; this cannot be accomplished with isotonic solutions (eg, 0.9% saline, lactated Ringer), which slowly raise serum sodium. Additionally, the use of isotonic fluids in patients with SIADH will likely worsen hyponatremia.
Educational objective:
Hyponatremia can cause cellular swelling and cerebral edema. Symptoms reflect elevated intracranial pressure; mild/moderate symptoms include headache, nausea, and confusion, whereas severe symptoms include seizure, coma, and respiratory arrest. Acute hyponatremia (<48-hr duration) is poorly tolerated, and patients are at elevated risk of brain herniation; therefore, patients with any symptoms should receive hypertonic 3% saline.