SALT SYNDROMES - Stony Brook Medicine



SALT SYNDROMES

ADH:

■ Made by the supraoptic and periventricular nuclei of the hypothalamus – stored in the posterior pituitary gland

■ Acts on kidney epith cells – increases cAMP – increases water permeability in the collecting ducts so that water can leave and equilibrate with the medullary interstitium

■ Its secretion is determined by osmoreceptors in the ant hypothalamus and by baroreceptors in the vascular system (also released secondary to cardiac failure, hypoxia, stress, etc. which predominates)

■ Decreases in ~10% of plasma volume will stimulate ADH; also increases in osms of ~2%

■ Suppression of ADH occurs sec to incr plasma volume (may be mediated by Atrial Natriuretic Peptide)

■ Also acts as a vasopressor; increases glucagons release and insulin suppression

SIADH

■ Loss of nl regulatory mechanisms that control secretion of ADH that leads to free water excess and intravascular fluid overload

■ Criteria for dx:

o decr Na and serum osmolarity

o Inappropriately incr urine osm’s (usu > 250) and sodium excretion (usu >20)

o Nl circulating volume

o Nl kidney/adrenocortical/ thyroid fx

■ Causes

o CNS disorders – includes head trauma, tumors, meningitis, surgery in pit/hypothalamic area (DI -( SIADH ( DI)

o Pulmonary disorders (decr CO ( baroreceptor-mediated incr in ADH)

o Lung tumors – secrete ADH-like substance

o Chemotherapy – vincristine, cyclophosphomide augment ADH release

■ Clinical picture/lab work

o Volume overload

o Sodium < 120; osms < 240 with subsequent neurological impairment

o FENA increased

o Urine Na > 30 because body trying to expel Na

■ SIADH-like conditions

o Decreased thyroid function (lowers GFR and Na)

o Adrenal insufficiency (hyponatremic salt wasting) – cerebral salt wasting

o Decr pit fx with decr ACTH (cortisol normally suppresses ADH)

■ Therapy

o Watch VS/UOP/USG/lytes

o Fluid restriction to insensibles + output

o Seizures sec to decr Na ( give 3% NaCl (513 meq/L) corrected to a sodium of 125 (½ in first 10 minutes, ½ in 2 hrs)

■ CPM

o Too rapid a correction

o Quadriplegia, coma, death

Central DI

■ Failure of the hypothalamus or pituitary to release ADH which leads to inability to conserve water at the collecting duct which leads to polyuria and polydipsia

■ Problems arise when pt can’t meet fluid intake requirements

■ Causes:

o CNS surgery – particularly for craniopharyngioma (polyuria within hours for 2-3 days ( residual ADH released for 5-7 days ( DI

o CNS trauma/infections

o Congenital septo-optic dysplasia

o Histiocytosis X

■ Diagnosis: in at risk pts

o UOP >5 cc/kg/hr

o Urine osms 150)

■ Therapy

o If hypovolemic ( bolus with ½ NS; then replacement of uop with appropriate soln

o If Na < 165, should correct no faster than 1 meg/l/hour; if >165, should be slower

o DDAVP (nasal/sub-Q/ IV) or vasopressin as a drip—MUST WATCH UOP

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download