What is the likely diagnosis and management for an adult patient with serum hyperosmolality, urine hypo-osmolality, hypernatremia, and low Antidiuretic Hormone (ADH) level?

Diagnosis: Central Diabetes Insipidus

Your laboratory findings—serum osmolality 295 mOsm/kg, urine osmolality 220 mOsm/kg, serum sodium 143 mEq/L, and ADH <0.8 pg/mL—are diagnostic of central diabetes insipidus (DI), characterized by inability to concentrate urine despite elevated serum osmolality due to inadequate ADH secretion. 1, 2

Diagnostic Interpretation

Your labs reveal a classic pattern of central DI:

• Serum osmolality 295 mOsm/kg is at the upper limit of normal (normal range 275-295 mOsm/kg), indicating mild hyperosmolality that should trigger maximal ADH release 3
• Urine osmolality 220 mOsm/kg is inappropriately dilute—a normal response would be urine osmolality >600-800 mOsm/kg when serum osmolality exceeds 290 mOsm/kg 2, 4
• ADH <0.8 pg/mL is undetectable or severely deficient when it should be elevated given your serum osmolality 1, 2
• Serum sodium 143 mEq/L is at the high-normal range, consistent with mild water deficit 3

The key diagnostic feature is the dissociation between elevated serum osmolality and inappropriately low urine osmolality with undetectable ADH, which definitively indicates central DI rather than nephrogenic DI (where ADH would be elevated) or primary polydipsia (where serum osmolality would be low-normal) 1, 2.

Distinguishing Central DI from Other Causes

Central DI is confirmed by:

• Undetectable or low ADH despite hyperosmolality 1, 2
• Urine osmolality remaining below plasma osmolality 2
• Expected dramatic response to desmopressin (>50% increase in urine osmolality) 2, 5

Nephrogenic DI would show:

• Normal or elevated ADH levels despite hyperosmolality 1, 2
• Minimal response to desmopressin (<50% increase in urine osmolality) 2

Primary polydipsia would show:

• Serum osmolality below 285 mOsm/kg from excessive water intake 2
• Normal ADH response when dehydrated 2

Management Approach

Immediate Assessment

Evaluate for underlying causes of central DI:

• Obtain brain MRI to assess for pituitary/hypothalamic pathology (tumors, infiltrative disease, trauma, surgery) 1, 5
• Review medication history for drugs affecting ADH secretion 1
• Assess for recent head trauma, neurosurgery, or CNS infections 1, 5

Pharmacological Treatment

Desmopressin (DDAVP) is the first-line treatment for central DI:

• Start with intranasal desmopressin 10 mcg once or twice daily, or oral desmopressin 0.1-0.2 mg twice daily 1, 5
• Titrate dose based on urine output, thirst, and serum sodium monitoring 5
• Goal is to reduce polyuria while avoiding hyponatremia from overtreatment 1, 5

Critical Monitoring

Monitor serum sodium and osmolality closely:

• Check serum sodium every 24-48 hours initially when starting desmopressin 5
• Risk of hyponatremia if desmopressin dose is excessive or if water intake is not adjusted 1, 5
• Target serum sodium 135-145 mEq/L and serum osmolality 275-295 mOsm/kg 3

Ensure adequate hydration access:

• Patients with DI require unrestricted access to water to prevent severe hypernatremia 1, 5
• If thirst mechanism is intact, patients will self-regulate fluid intake 1
• If thirst is impaired (adipsic DI), prescribe fixed daily fluid intake of 2-3 liters 1, 5

Common Pitfalls to Avoid

• Do not restrict fluids in central DI—this will cause severe hypernatremia and dehydration 1, 5
• Avoid over-treating with desmopressin, which can cause hyponatremia and water intoxication 1, 5
• Do not assume nephrogenic DI without measuring ADH levels or performing a desmopressin trial 2
• Do not delay brain imaging if central DI is confirmed, as underlying structural lesions require identification 1, 5

Special Considerations

Your early morning sample is ideal for diagnosis because overnight water deprivation naturally concentrates urine in healthy individuals, making the failure to concentrate (urine osmolality 220 mOsm/kg) even more diagnostic 2. The undetectable ADH with borderline-high serum osmolality confirms inadequate ADH secretion from the posterior pituitary 1, 2.