Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (1097 page)

   Defect in thirst (hypodipsia)—forced water intake returns serum osmolality to normal

   Hypernatremia with overhydration—iatrogenic or accidental (e.g., infants given feedings with high sodium concentrations or given NaHCO
₃
for respiratory distress or cardiopulmonary arrest)

   Alcohol ingestion, which is the most common cause of hyperosmolar state and of coexisting coma and hyperosmolar state

Decreased In

   Hyponatremia with hypovolemia (urine sodium is usually >20 mmol/L)

   Adrenal insufficiency (e.g., salt-losing form of CAH, congenital adrenal hypoplasia, hemorrhage into adrenals, inadequate replacement of corticosteroids, inappropriate tapering of steroids)

   Renal losses (e.g., osmotic diuresis; proximal RTA; salt-losing nephropathies, usually tubulointerstitial diseases such as GU tract obstruction; pyelonephritis; medullary cystic disease; polycystic kidneys)

   GI tract loss (e.g., vomiting, diarrhea)

   Other losses (e.g., burns, peritonitis, pancreatitis)

   Hyponatremia with normal volume or hypervolemia (dilutional syndromes)

   CHF, cirrhosis, nephrotic syndrome

   SIADH

   Limitations

Variations in the urine osmolality play a central role in the regulation of the plasma osmolality and Na+ concentration. This response is mediated by osmoreceptors in the hypothalamus that influence both thirst and the secretion of ADH.

The relationship between serum and urine osmolality and the clinical significance of laboratory values are shown in Table 16.60.

(1.86 × serum Na) + (serum glucose ÷ 18) + (BUN ÷ 28) + 9(in mg / dL)

or

in SI units: = (1.86 × serum Na) + serum glucose (mmol/L) + BUN (mmol/L) + 9

   More simply: NA
⁺
+ K
⁺
+ (BUN ÷ 28) + (glucose ÷ 18). Because K
⁺
is relatively small, and BUN has no influence on water distribution, the formula can be simplified to 2Na
⁺
+ (glucose ÷ 18).