SIADH: Water Retention and Hyponatremia

SIADH causes excessive ADH release (often from small cell lung cancer, head injury, or certain medications), leading to water retention, concentrated urine despite normal or high volume, and dilutional hyponatremia with weight gain but no edema. Symptoms progress from headache and nausea to confusion, seizures, and coma as sodium drops below 120 mEq/L. Treatment includes fluid restriction (the primary intervention), hypertonic saline for severe symptomatic hyponatremia given slowly to avoid osmotic demyelination syndrome, and demeclocycline or vasopressin receptor antagonists (tolvaptan) for chronic cases.

Diabetes Insipidus: Water Loss and Hypernatremia

DI results from insufficient ADH (central, often from head trauma or pituitary surgery) or renal insensitivity to ADH (nephrogenic), causing massive dilute urine output (often over 5 L/day), severe thirst, dehydration, and hypernatremia. Urine specific gravity is very low (under 1.005) despite concentrated serum. Central DI is treated with desmopressin (DDAVP); nephrogenic DI is treated by addressing the underlying cause (often lithium-induced) and low-sodium, low-protein diet with thiazide diuretics paradoxically reducing urine output. Monitor strict intake and output and daily weights closely.

Comparing Fluid Management Priorities

The core distinction for treatment is opposite: SIADH requires fluid restriction to correct dilutional hyponatremia, while DI requires generous fluid replacement to correct dehydration and hypernatremia. Correcting sodium too quickly in either direction is dangerous — rapid sodium correction in chronic hyponatremia risks osmotic demyelination syndrome, while overly rapid fluid replacement in DI can cause cerebral edema. NCLEX often tests urine specific gravity trends: SIADH shows concentrated urine (high specific gravity) with dilute blood, while DI shows dilute urine (low specific gravity) with concentrated blood.