How is diabetes insipidus managed after TBI?

• A. High-dose cortisol therapy.
• B. Hypertonic saline without fluid restriction.
• C. Insulin therapy.
• D. Desmopressin (DDAVP) with careful fluid and electrolyte management.

Answer: (D)

Central diabetes insipidus after traumatic brain injury happens when the posterior pituitary can’t release enough antidiuretic hormone, so the kidneys waste water and the patient becomes very thirsty with large volumes of dilute urine and rising or fluctuating sodium levels.

The best management is replacing the missing hormone with desmopressin (DDAVP) and carefully watching fluids and electrolytes. Desmopressin acts like ADH, prompting the kidneys to reabsorb more water, which reduces urine output, concentrates the urine, and helps bring serum sodium back toward normal. Because brain-injury patients are sensitive to shifts in fluid and sodium, this replacement is given with meticulous fluid balance and frequent monitoring of urine volume, urine osmolality, serum sodium, and overall hydration. Adjust the DDAVP dose to avoid too little urine output or too much water retention, which could cause hyponatremia.

The other options don’t fit this situation: high-dose cortisol is for adrenal failure, not DI; insulin is for glucose control, not water balance; hypertonic saline would worsen hypernatremia and fluid loss in DI and is not a standard treatment for this condition.