High urine output with hypernatremia: distinguish AVP deficiency from osmotic diuresis, restore circulation first when depleted, replace free water, and use desmopressin with close sodium/urine monitoring.
Quantify urine output and measure serum sodium/osmolality plus urine osmolality. Very dilute urine in a hyperosmolar/hypernatremic patient suggests AVP deficiency, but hyperglycemia, mannitol, diuretics, high urea load, post-obstructive diuresis and recovery from AKI can mimic the presentation.
If intravascular volume is depleted or shock is present, restore circulation with isotonic crystalloid before attempting to replace the full free-water deficit. Hypovolemia is the immediate threat even when the sodium is high.
Once circulation is secure, replace ongoing water losses and the calculated deficit using enteral water when safe or IV dextrose-containing free water when needed. Individualize the correction rate to acuity/duration of hypernatremia and neurologic risk; avoid rapid sodium shifts.
Inpatient central DI/AVP-deficiency fluid, desmopressin and sodium-monitoring guidance.
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From urgent 'AEIOU' indication screening and modality selection to vascular access, dosing, and anticoagulation.
Structured ICU evaluation of polyuria and hypernatremia with safe diagnosis and treatment of central or nephrogenic diabetes insipidus.
ICU evaluation of hypotonic polyuria and hypernatremia with safe fluid replacement, desmopressin use, and differentiation of AVP deficiency from osmotic and nephrogenic causes.
Tonicity assessment, etiologic classification, 3% hypertonic saline bolus protocols, individualized ODS-safe correction limits, DDAVP relowering, DI diagnostics, and evidence-aware hypernatremia correction.