Diagnosis: Central Diabetes Insipidus
This patient has central diabetes insipidus (CDI), evidenced by hypernatremia (143 mEq/L), inappropriately low ADH (<0.8 pg/mL), and dilute urine (osmolality 220 mOsm/kg) that fails to concentrate despite elevated serum osmolality (295 mOsm/kg). 1, 2
Diagnostic Confirmation
The laboratory findings definitively establish CDI:
- Serum osmolality of 295 mOsm/kg with urine osmolality of only 220 mOsm/kg indicates the kidneys are inappropriately excreting dilute urine despite normal-to-high serum tonicity 1, 2
- Undetectable ADH (<0.8 pg/mL) in the setting of elevated serum osmolality confirms lack of ADH production/release, distinguishing this from nephrogenic DI where ADH would be elevated 1, 3
- 24-hour urine volume of 1300 mL is relatively modest but combined with low urine osmolality indicates impaired concentrating ability 2, 4
- Low 24-hour urine sodium (34 mEq/day, reference 40-220) suggests the patient may be volume depleted and compensating by retaining sodium 5
Immediate Management Plan
1. Initiate Desmopressin (DDAVP) Therapy
Start intranasal desmopressin 10 mcg once or twice daily, or oral desmopressin 0.1-0.2 mg twice daily as the primary treatment for CDI 1, 2, 3
- Desmopressin is synthetic ADH and directly replaces the deficient hormone 3
- Titrate dose based on urine output, urine osmolality, and serum sodium monitoring 2
- The goal is to reduce polyuria while avoiding hyponatremia from overtreatment 3
2. Correct Free Water Deficit
Calculate water deficit using: Water deficit = 0.6 × weight (kg) × [(Current Na/Desired Na) - 1] 6
- For this patient targeting sodium of 140 mEq/L from 143 mEq/L, the deficit is modest
- Administer D5W (5% dextrose in water) as the primary IV fluid to correct hypernatremia without adding sodium burden 6
- Never use 0.9% NaCl as it will paradoxically worsen hypernatremia by providing excessive osmotic load 6
- Correction rate must not exceed 8-10 mEq/L per day to prevent cerebral edema 6
3. Monitoring Protocol
Check serum sodium every 4-6 hours initially during correction and desmopressin initiation 6
- Monitor urine output, urine osmolality, and specific gravity to assess treatment response 1, 4
- Target urine osmolality >300 mOsm/kg and urine specific gravity >1.010 as indicators of adequate ADH replacement 4
- Assess volume status through hemodynamic monitoring, input/output measurements, and clinical examination 6
- Ensure serum osmolality changes do not exceed 3 mOsm/kg/hour 6, 7
4. Investigate Underlying Etiology
Obtain MRI of the brain with focus on the pituitary/hypothalamus to identify structural causes of CDI 1, 2
- Common causes include: pituitary surgery, head trauma, tumors (craniopharyngioma, germinoma), infiltrative diseases (sarcoidosis, histiocytosis), or idiopathic 1, 2, 3
- Review medication history for drugs that may impair ADH release 2
- The relatively modest polyuria (1300 mL/day) may indicate partial rather than complete CDI 2
Critical Pitfalls to Avoid
- Do not restrict fluids in CDI as this will worsen hypernatremia and cause severe dehydration 1, 8
- Do not use normal saline for rehydration as it contains 154 mEq/L sodium and will exacerbate hypernatremia 6
- Avoid overcorrection with desmopressin which can cause hyponatremia and water intoxication 2, 3
- Do not confuse with nephrogenic DI where desmopressin would be ineffective and ADH levels would be elevated 1, 3
- Monitor for hypokalemia as hypernatremia often coexists with potassium depletion; consider adding 20-30 mEq/L potassium to IV fluids once renal function confirmed 6
Long-Term Management
Patients with CDI require lifelong desmopressin replacement unless the underlying cause is reversible 2, 3