MON-434 - Severe Euvolemic Hyponatremia as the Initial Presentation of Hypothyroidism

Overt hypothyroidism typically presents with systemic symptoms such as fatigue, weight gain, constipation, and cold intolerance. Severe hypo-osmolar hyponatremia as the primary clue to hypothyroidism, especially in the absence of classic clinical features, is uncommon and can be overlooked during routine inpatient evaluation. We present a case in which incidentally discovered, persistent euvolemic hyponatremia prompted endocrine evaluation and revealed previously unrecognized hypothyroidism.

An 83-year-old woman with type 2 diabetes mellitus and knee osteoarthritis presented to the emergency department with progressively worsening knee pain. Imaging supported osteoarthritis as the etiology. Her knee pain improved and resolved by the following day with conservative management. While in the emergency room, she was incidentally found to have severe hyponatremia (serum sodium 121 mmol/L) and was admitted for evaluation and management. She denied diarrhea, vomiting, decreased oral intake, polydipsia, or use of medications commonly associated with hyponatremia. She reported an urgent care visit two months earlier with sodium 123 mmol/L, for which she was advised to increase oral intake and salt consumption but did not establish follow-up care.

On admission, she appeared euvolemic without edema or ascites and without clinical signs suggestive of hypothyroidism or adrenal insufficiency. Serum osmolality was 271 mOsm/kg. Urinalysis was unremarkable with a specific gravity of 1.008. Urine sodium was 112 mmol/L and urine osmolality was 309 mOsm/kg, indicating inappropriately concentrated urine in the setting of hypo-osmolar hyponatremia. Serum glucose was 120 mg/dL; creatinine was at baseline (1.0 mg/dL); liver enzymes and other electrolytes were within normal limits. CBC showed normocytic anemia (hemoglobin 10.1 g/dL). After 500 mL of intravenous normal saline, serum sodium remained 121 mmol/L. Given unclear etiology of her euvolemic hypo-osmolar hyponatremia, further evaluation was pursued and revealed hypothyroidism (TSH 16.2 µIU/mL; free T4 0.28 ng/dL). Morning cortisol level was adequate (7.5ug/dL). Levothyroxine 50 µg daily was initiated, and serum sodium improved steadily to 126 mmol/L by discharge. She was advised to follow up with primary care for levothyroxine titration and continued monitoring of sodium.

This case is notable for an uncommon presentation of overt hypothyroidism identified through chronic, severe euvolemic hypo-osmolar hyponatremia that was refractory to isotonic saline but improved after levothyroxine initiation. Severe hypothyroidism can cause refractory dilutional hyponatremia via non-osmotic ADH release and reduced free-water clearance (↓GFR/renal perfusion). Thyroid function testing should remain part of the evaluation of persistent euvolemic hyponatremia to identify a reversible endocrine cause and prevent recurrence.

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