Absorption of irrigation fluids
Serum hyponatremia
Variably present
Stress hyperglycemia
Steroid administration
Pseudohyponatremia
Hypokalemia
Acidosis (DKA)
↑osmolality (HHNK)
Loop
bumetanide
ethacrynate
furosemide
torsemide
Potassium-sparing
amiloride hydrochloride
spironolactone
triamterene
Carbonic anhydrase inhibitors
acetazolamide
methazolamide
Osmotic
glycerin
isosorbide
urea
Pregnancy, craniopharyngioma, medications:
lithium
demeclocycline
ofloxacin
aminoglycosides
cimetidine
amphotericin
Low serum osmolality
DDAVP = desmopressin, NSAIDs = non-steroidal anti-inflammatory drugs, DKA = diabetic ketoacidosis, HHNK = hyperglycemic hyperosmolar non-ketotic coma, ATN = acute tubular necrosis, SAH = subarachnoid hemorrhage
Management: Non-specific therapy for nephrogenic DI includes administration of thiazide diuretics. Administration of a diuretic in treatment of polyuria may seem paradoxical, but the increased urinary sodium losses limit free water loss. NSAIDs may limit renal free water loss by affecting renal prostaglandins. Lithium-induced DI may be specifically antagonized by amiloride. Parathyroidectomy may be curative of nephrogenic DI caused by hyperparathyroidism. Treatment of hypercalcemia will improve DI due to increased serum calcium.
Cerebral salt wasting syndrome (CSW)
CSW may develop after traumatic brain injury, craniotomy, or subarachnoid hemorrhage. Increased sympathetic outflow and inappropriate release of natriuretic proteins may lead to polyuria. The clinical presentation has significant overlap with neurogenic DI, but the volume loss includes salt wasting rather than free water. Neurogenic DI and CSW may be distinguished by laboratory findings. Management of CSW is supportive replacement of sodium and fluid losses.[16]