Management of overcorrection of hypotonic hyponatremia
For overcorrection that exceeds the 4-6meq/24hrs, would want to give pt 5% dextrose in water especially if digressing significantly bc will continue to diurese an d lose free water
Tetracyclic abc used to treat SIADH once fluid restriction has failed. Works by making collecting tubules less responsive to ADH->induces diabetes insipidus
Management of asymptomatic hyponatremia
Fluid restriction. In absence of neurologic findings->most likely chronic thus rapid corrections not indicated. . For vol up conditions such as cirrhosis would fluid restrict when serum Na <120.
-Hypertonic saline (3%) only indicated in presence of neurologic sxsor if serum Na <130 mimed preceding liver transplant
-Conivaptan blocks V2, V1a receptors which can i dec blood pressure and inc risk of vatical bleeding in its with cirrhosis->contraindicated in cirrhotics.
-Demeclocyline used to treat SIADH
Osmotic demyelination syndrome
Correction of acute hyponatremia that exceeds 10meq within first 24hrs and 18 meQ within first 48hrs. Clinical features: progressive quadriparesis, speech and swallowing disorders, coma, locked-n syndrome
develops over 72hrs or more.. Less likely to have symptomatic cerebral edema.
Chronic hypotonicity stimulates extrusion of ntracellular solutes and leads to reduction in cel vol toward normal.
-can often have superimposed acute hyponaremia 2/2 illness
Symptoms of hyponatremia
Can initially present with nonspecific sxs such as nausea, fatigue & headache. Cerebral edema occurs in its in whom serum Na levels dec by more than 10meq over 1-3 days. . As cerebral edema worsens sxs progress to obtundation, seizures, coma, hypoxia and respiratory arrest.
Onset of hypotonicity in less than 24hs. RFs: postop admin of hypotnonic fluid, thiazide diuretics or ecstasy or over hydration assoc with extreme exercise & polydipsia.
Cerebral Salt wasting
syndrome of hypotonic hyponatremia that may complicate subarachnoid hemorrhage or neurosurgery. Of net. Also increased levels of BNP can result in kidney sodium wasting and hypovolemic hyponatremia.
Caused by marked hyperglycemia or exogenously administered solutes such as mannitol or sucrose. Hyperglycemia causes translocation of water from intracellular to the E F compartment which results in dec in serum Na levee by approx 1.6meq/L for every 100mg/dL inc in plasma glucose above 100.
lab artifact seen with hyperglobulinemia or severe hyperlipidemia * Measured osmolality is nl but there is still increased osmolol gap not accounted for by high glucose , BUN or other solutes (mannitol etc)
normal serum osm
275-295 mosm/Kg H2)
Evaluation of hyponatremia
1. Check plasma osmolality. if pseudohyponatremia is suspected, serum osm. will be nl. (also elevated levels of cholesterol, TG, protein gap)
2. Check Uosm. If Uosm <100 & UNa < 20 then the issue is primary polydipsia and low solute intake.
-If Uosm>100 then look at volume status.
3. Once volume status is assessed will use UNa.
-If pt has true vol depletion and UNa<20 then most likely 2/ vomiting/diarrhea/burns
- if pt is volume up but UNa <20 then likely 2/2 chronic heart failure/cirrhosis/nephrosis.
-Euvolemic & UNa>40 then likely SIADH (once exclude thyroid issues and mineral corticoid def)
Most common form of hypnatremia. Measured plasma osmolality is usually low but may be nl or increased in presence of high BUN, flu or etch