Internal Medicine

0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 4, 2007 21:13

Hypernatremia 753

Can be complete or partial

Treated with DDAVP

➣Nephrogenic diabetes insipidus – resistance to ADH action

Congenital – X-linked and autosomal recessive

Acquired – secondary to renal diseases, hypokalemia, hyper-

calcemia, drugs (lithium, amphotericin)

Does not respond to DDAVP

➣Diabetes insipidus secondary to vasopressinase

Seen during pregnancy or early post-partum states – uncom-

mon condition

Due to degradation of endogenous ADH (vasopressin) by pla-

cental vasopressinase

Treated with DDAVP, which is not lysed by this enzyme

management

n/a

specific therapy

■Involves judicious administration of water and hypotonic fluids

■Depends on two factors: ECF volume status and rate of development

of hypernatremia

■Correction of ECF volume depletion

➣Normal saline used until euvolemia is restored

➣Neck veins, orthostasis can be used to guide therapy if CVP mon-

itoring not available

➣Hypotonic fluids (0.45% saline, 5% dextrose) used to correct

hypernatremia once volume status is restored

■Correction of ECF volume expansion:

➣Diuretics mainstay of therapy

➣Dialysis may be needed if renal failure is advanced

■Water Replacement

➣Water replacement done orally, via NG tube or parenterally

➣Hypotonic fluids like 5% dextrose and 0.45% saline should be

used.

➣Fluid deficit should be calculated as follows:

Total body water (TBW)=current body weight×0.6

Fluid deficit=TBW (Current plasma sodium/140−1)

Ongoing losses (e.g., diarrhea) should be added to the fluid

deficit.

The rate of correction depends on the rate of development

of hypernatremia. Acute hypernatremia with symptoms