Hyponatremia Diagnosis: Primary Polydipsia (Psychogenic Polydipsia)
This patient has hyponatremia due to primary polydipsia (excessive water intake), characterized by low serum osmolality (234 mOsm/kg), appropriately dilute urine (osmolality 97 mOsm/kg), and elevated urine sodium (41 mEq/L) indicating normal renal function with physiologic natriuresis. 1
Diagnostic Interpretation
The laboratory pattern is pathognomonic for water intoxication:
Serum sodium 120 mEq/L with serum osmolality 234 mOsm/kg confirms hypotonic hyponatremia, excluding pseudohyponatremia and hyperglycemic causes 1, 2
Urine osmolality 97 mOsm/kg (<100 mOsm/kg) indicates maximal urinary dilution and appropriate suppression of ADH, which is the key distinguishing feature 1, 3
Urine sodium 41 mEq/L (>20 mEq/L) reflects physiologic natriuresis that occurs when the kidneys excrete excess sodium to maintain volume homeostasis despite continued water intake 1, 2
This combination excludes SIADH, which would show inappropriately concentrated urine (>100-300 mOsm/kg) despite hypotonicity 1, 4. The dilute urine proves ADH is appropriately suppressed, but water intake exceeds even maximal renal excretory capacity (typically 10-15 L/day) 3.
Volume Status Assessment
The patient is likely euvolemic based on the elevated urine sodium and absence of features suggesting hypovolemia or hypervolemia 1:
- Hypovolemic hyponatremia would typically show urine sodium <30 mEq/L as the kidneys avidly retain sodium 1, 2
- Hypervolemic hyponatremia (heart failure, cirrhosis) would show edema, ascites, or jugular venous distention 1, 5
- The urine sodium >40 mEq/L with dilute urine confirms euvolemia with intact renal function 1
Differential Diagnosis Exclusions
SIADH is definitively excluded by the maximally dilute urine 1, 4:
- SIADH requires urine osmolality >100 mOsm/kg (typically >300 mOsm/kg) with inappropriately high urine sodium despite hypotonicity 1, 3
- The urine osmolality of 97 mOsm/kg proves ADH is suppressed, not elevated 4
Cerebral salt wasting is excluded because it presents with hypovolemia, not euvolemia, and occurs primarily in neurosurgical patients 1
Beer potomania could present similarly but requires a history of poor solute intake combined with beer consumption 1
Management Approach
The primary treatment is cessation of excessive water intake 1:
Immediate intervention: Stop all free water intake and implement strict fluid restriction 1, 2
For asymptomatic or mildly symptomatic patients: Fluid restriction alone with gradual correction over 24-48 hours is appropriate 1, 4
For severe symptoms (seizures, altered mental status): Administer 3% hypertonic saline with target correction of 6 mEq/L over 6 hours, not exceeding 8 mEq/L in 24 hours to prevent osmotic demyelination syndrome 1, 6
Correction rate: Limit to 8 mEq/L per 24 hours maximum 1, 4. In primary polydipsia, once water intake stops, spontaneous correction often occurs rapidly as the kidneys excrete free water 3
Critical Monitoring
Check serum sodium every 2-4 hours initially to prevent overly rapid correction, as primary polydipsia can self-correct quickly once water intake stops 1, 6
Watch for overcorrection: If sodium rises >8 mEq/L in 24 hours, consider administering D5W or desmopressin to slow correction 1
Address underlying psychiatric condition if psychogenic polydipsia is confirmed, as recurrence is common without behavioral intervention 2, 3
Common Pitfall
Do not use fluid restriction as the sole long-term treatment without addressing the underlying compulsive water drinking behavior, as patients will resume excessive intake once unsupervised 2, 3. Psychiatric evaluation and treatment are essential for preventing recurrence 3.