Polyuria -

Polyuria in the ICU

🔴 WHY POLYURIA IN ICU IS NOT BENIGN

In ICU, polyuria is never “just kidneys working”. It may signal:

DEFINITION (ICU-RELEVANT)

STEP 1: CONFIRM IT IS TRUE POLYURIA

Exclude pseudo-polyuria

Measure hourly UOP and confirm sustained output

STEP 2: RAPID PHYSIOLOGIC CLASSIFICATION— Is the urine WATER or SOLUTE?

STEP 3: LAB TRIAD THAT DEFINES EVERYTHING

Send STAT:

🔵 A. WATER DIURESIS (Dilute Urine)

Category	Cause	Mechanism	Urine Osmolality	Serum Sodium Trend	ICU Clues
WATER DIURESIS	Central Diabetes Insipidus	↓ ADH secretion	Very low (<300, often <150)	↑ Hypernatremia	TBI, SAH, post neurosurgery, hypoxic brain injury, brain death
	Nephrogenic Diabetes Insipidus	Renal resistance to ADH	Low (<300)	↑ Hypernatremia	Lithium, amphotericin B, hypercalcemia, hypokalemia, CKD recovery
	Primary Polydipsia	Excess water intake	Low (<300)	↓ Hyponatremia	Rare in ICU, psychiatric history

BRAIN DEATH NOTE (EXAM FAVORITE)

🟠 B. SOLUTE DIURESIS (Concentrated or Iso-osmolar Urine)

Category	Cause	Mechanism	Urine Osmolality	Serum Sodium
SOLUTE DIURESIS	Hyperglycemia	Glucose osmotic effect	High (>300 mOsm/kg)	Normal or ↓
	Mannitol therapy	Exogenous osmotic agent	High (>300)	Variable
	High urea load	Protein catabolism / GI bleed	High (>300)	Variable
	Contrast-induced diuresis	Tubular osmotic effect	High (>300)	Usually normal
RENAL / STRUCTURAL	Post-obstructive diuresis	Tubular concentrating defect + osmotic washout	Variable (often >300 initially)	↓ or normal
	Polyuric phase of AKI (ATN recovery)	Tubular dysfunction	Variable	Often normal
IATROGENIC CAUSES	Loop diuretics	Na-K-2Cl inhibition	Variable	Usually normal
	Thiazide diuretics	Distal Na⁺ blockade	Variable	Usually ↓
	Acetazolamide	Bicarbonate diuresis	Variable	↓
NEURO-CRITICAL CARE CAUSES	Cerebral salt wasting	Renal sodium wasting → water loss	High (>300)	↓ Hyponatremia
	Brain death	Severe central diabetes insipidus	Very low (<150)	Markedly ↑
ENDOCRINE CAUSES	Adrenal insufficiency	Mineralocorticoid deficiency → salt wasting	Variable	↓ Hyponatremia
	Hypercalcemia	ADH resistance + natriuresis	Low to variable	Normal or ↑
	Hypokalemia	Impaired tubular concentration	Low to variable	Often ↑
MISCELLANEOUS ICU CAUSES	Refeeding syndrome	Electrolyte shifts impair tubular function	Variable	Variable
	Cold diuresis	Central volume expansion from vasoconstriction	Low to variable	Usually normal
	Fluid mobilization phase	Reabsorption of third-space fluid,48–96 hours after resuscitation	Variable	Normal

MANAGEMENT PRINCIPLES (DO NOT DO GUESS WORK)

General Rules

Condition-Specific Treatment