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2016 ; 17
(ä): 150-3
Nephropedia Template TP
Am J Case Rep
2016[Mar]; 17
(ä): 150-3
PMID26956638
show ga
BACKGROUND: Drug-induced hyponatremia characteristically presents with subtle
psychomotor symptoms due to its slow onset, which permits compensatory volume
adjustment to hypo-osmolality in the central nervous system. Due mainly to the
syndrome of inappropriate antidiuretic hormone secretion (SIADH), this condition
readily resolves following discontinuation of the responsible pharmacological
agent. Here, we present an unusual case of life-threatening encephalopathy due to
adverse drug-related effects, in which a rapid clinical response facilitated
emergent treatment to avert life-threatening acute cerebral edema. CASE REPORT: A
63-year-old woman with refractory depression was admitted for inpatient
psychiatric care with a normal physical examination and laboratory values,
including a serum sodium [Na+] of 144 mEq/L. She had a grand mal seizure and
became unresponsive on the fourth day of treatment with the dual serotonin and
norepinephrine reuptake inhibitor [SNRI] duloxetine while being continued on a
thiazide-containing diuretic for a hypertensive disorder. Emergent infusion of
intravenous hypertonic (3%) saline was initiated after determination of a serum
sodium [Na+] of 103 mEq/L with a urine osmolality of 314 mOsm/kg H20 and urine
[Na+] of 12 mEq/L. Correction of hyposmolality in accordance with current
guidelines resulted in progressive improvement over several days, and she
returned to her baseline mental status. CONCLUSIONS: Seizures with
life-threatening hyponatremic encephalopathy in this case likely resulted from
co-occurring SIADH and sodium depletion due to duloxetine and
hydrochlorothiazide, respectively. A rapid clinical response expedited diagnosis
and emergent treatment to reverse life-threatening acute cerebral edema and
facilitate a full recovery without neurological complications.