Hyponatremia and Hypokalemia

 Corrected Sodium
o Corrected sodium = measured sodium + 0.016 x (serum glucose – 100)
o MUST know formula!
 SIADH-dumping of sodium by kidneys
o Diagnostic Criteria
 Serum osmolality <275, urine osmolality > 30 with no recent use of
diuretic agents
 Clinical euvolemia and absence of adrenal or thyroid insufficiency
 Thiazides and Desmopressin are notorious for causing SIADH!
 Hyponatremia Presentation
o Acute
 Onset <48 hours
 Neurologic symptoms from cerebral edema, seizure, coma, altered
mental status
o Chronic
 Developing >48 hours
 Possibly asymptomatic b/c brain has adapted, therefore mild symptoms
like N/V, loss of appetite, frequent falls and gait disturbances
 Osmotic Demyelination Syndrome
o Serum sodium concentration is corrected too fast and water rushes out of brain
back into the blood too quickly
o Causes breakdown of myelin sheath on the neurons and causes quadriplegia and
pseudobulbar palsy (inability to control facial muscles)
 Hyponatremia Goals of Therapy
o Increase plasma tonicity to control severe symptoms
o DO NOT increase serum sodium by more than 10 mEq/L/day or 0.5 mEq/L/hr to
avoid ODS some recommend no more than 6-8 mEq/L/day and 0.33mEq/L/hr
o Initial goal is a small increase in serum sodium just enough to control symptoms
Hypovolemic Euvolemic =SIADH Hypervolemic
NS until vitals stable, then Water Restriction Sodium and water restriction
maintenance fluids Demeclocycline, Urea, Loop Diuretics
Vasopressin receptor Vasopressin receptor
antagonists antagonists
 Drugs that can treat Euvolemic hypernatremia
o Demeclocycline- blocks vasopressin effects
o Urea- induces osmotic diuresis, monitor for hypernatremia if patients have lack
of access to free water
 o Vasopressin Receptor Antagonists
 Conivaptan (Vaprisol) -IV
 V1 and V2 antagonist, inhibits effect of vasopressin on kidney
 Do not use with CYP3A4 inhibitors
 Reduce dose if hepatic impairment and renal impairment
 Tolvaptan (Samsca)-PO
 Selective V2 antagonist, initiated only in hospital
 Do not use with CYP3A4 inhibitors
 Limit to 30 days of therapy to minimize liver injury risk
 Hypokalemia
o Caused by GI tract losses, intracellular shift of potassium caused by insulin, beta
2 agonists, or alkalosis, or can be lost through kidneys
o Drugs that most commonly induce hypokalemia are:
 Insulin-drives potassium into cells
 Thiazides and Loops- renal potassium loss
o Goal of Therapy
 Deficit estimated as 200-400 mEq for every 1 mEq/L reduction in plasma
K+
 Asymptomatic Hypokalemia- use PO
 Symptomatic Hypokalemia- use IV route
 10 mEq of IV potassium raises serum potassium by 0.1
 20 mEq of PO potassium raises serum potassium by 0.1
 Must have adequate magnesium to replenish potassium