Hypernatremia

Exam 1, Dr. Wai

hypernatremia

• Na > 145 mEq/L

• less common

• high mortality in ICU patients (30-70%)

• impaired thirst mechanism or limited water access

hypernatremia cause

• excess Na intake or excess water loss

• increase in osmolality and serum Na causes acute water movement from the ICF to the ECF

hypernatremia clinical presentation

• decreases brain volume can cause cerebral vein rupture, leading to focal intracerebral hemorrhages and possible irreversible neurologic damage

hypernatremia correction goal

• Na < 145 mEq/L

• no more than 10-12 mEq/L/day

hypernatremia symptoms

• mild: lethargy, weakness, confusion, restlessness, irritability

• moderate: twitching

• severe: seizures, coma, death, usually acute elevation Na > 160 mEq/L

• other: postural hypotension, tachycardia, dry mucous membranes, diminished skin turgot, increased or decreases urinary output

hypernatremia labs

• serum Na > 145 mEq/L

• UNa and or UOsm may be helpful

hypernatremia risk factors

• hospitalized (iatrogenic)

• ICU

• elderly or infants

• tube feeding

• diabetic non-ketoic hyperglycemia

• GI disorders

• renal dysfunction

• diabetes insipidus

cerebral edema

• caused by improper therapy of rapid correction of hypernatremia

hypovolemic hypernatremia

• most common cause of hypernatremia

• water loss »» sodium loss

• can be from renal loss or extra renal loss

• TBW and TBNa decrease

hypovolemic hypernatremia causes

• renal- loop diuretics, osmotic diuresis (mannitol, glucose), intrinsic renal disease

• extrarenal- GI losses, cutaneous (burns, excessive sweating)

loop diuretics

most common cause of hypovolemic hypernatremia from renal loss

hypovolemic hypernatremia laboratory values

• renal- UOsm high, UNa high

• non renal- UOsm high, UNa low

hypovolemic hypernatremia clinical presentation

• orthostasis, hypotension, tachycardia, dry mucuous membranes

hypovolemic hypernatremia treatment

• 0.9% NaCL until vital signs stable, then free water replacement

hypovolemic hypernatremia treatment for rapid development (<48 hours)

• can correct rapidly

• correct as a rate of 1-2 mEq/L/hr

hypovolemic hypernatremia treatment for chronic

• slow correction to prevent cerebral edema

• vital signs unstable (low BP, tachycardia) → give 0.9% first to restore volume and stabilize patient, then switch to hypotonic fluid

• vital signs stable → start with hypotonic fluids (D5W, 0.2% NaCl, 0.45% NaCl) more hypotonic, slower the rate of infusion

hypovolemic hypernatremia treatment for chronic with unstable vital signs

give 0.9% first to restore volume and stabilize patient, then switch to hypotonic fluid

hypovolemic hypernatremia treatment for chronic with stable vital signs

• start with hypotonic fluids (D5W, 0.2% NaCl, 0.45% NaCl)

euvolemic hypernatremia

• pure water loss exceeds sodium loss (diabetes insipidus)

• extrarenal free water loss (increased insensible loss)

• decrease TBW, no effect on TBNa

euvolemic hypernatremia cause

• congenital or acquired diabetes insipidus

• nepgrogenic DI

euvolemic hypernatremia lab values

• renal UOsm low, UNa variable

• non renal- UOsm high, UNa variable

euvolemic hypernatremia clinical presentation

• depends on the severity of hypernaremia

• seizures, lethargy

euvolemic hypernatremia treatment

• treat the underlying cause of free water losses

• replace free water deficits, ongoing losses, and daily maintenance requirements

  • free acces to water or D5W

    • correct serum sodium at a rate of 0.5mEq/L/hr, maximum correction rate of 10-12 mEq/L/day

    • prevent cerebral edema development

• vasopressin

diabetes insipidus

• secrete inadequate amounts of ADH (central) or renal tubules do not respond to ADH (nephrogenic)

• clinical manifestations: polyuria, polydipsia, nocturia

polyuria, polydipsia, nocturia

• clinical manifestations of diabetes insipidus

lithium

• most common cause of nephrogenic diabetes insipidus

• incidence is 15-87%

• usually reversible rarely fatal

treatment of diabetes insipidus

• remove underlying cause if possible

• replace ADH in central DI

  • desmopressin 5-20 mcg intranasally q12-24 hr

• chronic cases- lithium induced

  • treat with amiloride

lithium mechanism

• may antagonize adenylyl cyclase and cAMP

• inhibits the opening of aquaporin channels in the renal tubules

• preventing reabsorption of water in the collecting duct

amiloride

• treatment for lithium induced diabetes insipidus

• blocks the epithelial sodium channel (ENaC), which is the primary route for lithium entry

• this decreases associated polyuria caused by lithium toxicity

desmopressin acetate, hydrochlorothiaze, amiloride

• euvolemic hypernatremia diabetes insipidus treatment

hypervolemic hypernatremia

• uncommon

• sodium gain »» water gain

• TBW goes up slightyl, TBNa goes up more

hypervolemic hypernatremia cause

• caused by addition of Na to the ECF

• Na overload

• latrogneic, hypertonic saline infusion, cushing’s syndrome, ingestion of sea water, hypertonic tube feeding, hypertonic dialysis

hypervolemic hypernatremia lab values

• UOsm high, UNa high

hypervolemic hypernatremia clinical presentation

• peripheral and pulmonary edema

• variable blood pressure

hypervolemic hypernatremia treatment

• free water and loop diuretics

• must combine because loop diuretics alone is not sufficient

• may require hemodialysis to remove volume

decrease lithium back to 200mg BID, start amiloride daily

31 yo M with bipolar returns to clinic with polydipsia and polyuria after his PCP increased lithium from 200 mg BID to 400 mg BID.

Labs: Na 154, K 4.1, Cl 115, CO2 22, BUN 16, SCr 1.1, glucose 110

What would be the best treatment option?

stop NaCl tabs, encourage free water, give Lasix

A 83 yo F has a clinic follow-up after being sent home on NaCl tabs 1 g TID from the hospital for SIADH 1 week ago. She says she’s been thirsty, retaining water, and gained 5 pounds. He labs came back with Na 149.


What would be the best treatment option?