NP8 Nephrology

Electrolyte Disorders

Essential Med Notes 2015

Hyponatremia

hyponatremia: serum [Na+] <135 mEq/L

can be associated with hypo-osmolality (most common), iso-osmolality, or hyperosmolality
consider if it is appropriate vs. inappropriate" ADH secretion
if appropriate ADH secretion, is it real vs. effective volume loss?
Hyponatremia

Hypo-Osmolar (dilutional)
Most common cause of
hyponatremia
Excess water in relation to
sodium stores which can be
decreased, normal, or increased
Categorized by volume status
as determined by clinical
assessment

Hypervolemic
UNa<20 and FeNa >1% (renal losses)
CHF
Cirrhosis and ascites
Nephrotic syndrome
Pregnancy
UNa>20
AKI, CKD

If the urine osmolality is unknown,

assume the urine is hypo-osmolar/dilute

Iso-Osmolar
Retention in ECF of large volumes
of isotonic fluids that do not
contain sodium (e.g. mannitol)
Pseudohyponatremia lab artifact
seen with severe hyperlipidemia
or paraproteinemia (e.g. multiple
myeloma)

Euvolemic
Uosm>100
SIADH (normal UNa)
Adrenal insufficiency
Hypothyroidism
Uosm<100
Psychogenic polydipsia
Low solute - tea & toast

Hyper-Osmolar (translocational)
Extra osmoles in ECF draw
water out of cells diluting the
Na+ in ECF
Usually glucose (rarely
hypertonic mannitol)
Every 10 mmol/L increase in
blood glucose results in
3 mmol/L decrease in Na

Hypovolemic
UNa>20
Diuretics (especially thiazides)
Salt-wasting nephropathy
UNa<10 and FeNa<1% (extra-renal losses)
Diarrhea
Excessive sweating
Third spacing (e.g. peritonitis,
pancreatitis, burns)

Figure 4. Approach to hyponatremia

Signs and Symptoms

depend on degree of hyponatremia and more importantly, velocity of progression from onset
acute hyponatremia (<24-48 h) more likely to be symptomatic
chronic hyponatremia (>24-48 h) less likely to be symptomatic due to adaptation
adaptation: normalization of brain volume through loss of cellular electrolytes (within
hours) and organic osmolytes (within days)
adaptation is responsible for the risks associated with overly rapid correction
neurologic symptoms predominate (secondary to cerebral edema): headache, nausea, malaise,
lethargy, weakness, muscle cramps, anorexia, somnolence, disorientation, personality changes,
depressed reflexes, decreased LOC
Complications
seizures, coma, respiratory arrest, permanent brain damage, brainstem herniation, death
risk of brain cell shrinkage with rapid correction of hyponatremia
can develop osmotic demyelination of pontine and extrapontine neurons; may be irreversible
(e.g. central pontine myelinolysis: cranial nerve palsies, quadriplegia, decreased LOC)
Risk Factors for Osmotic Demyelination
rise in serum [Na+] with correction >8 mEq/L/d if chronic hyponatremia
associated hypokalemia
if patient with hyponatremia and hypovolemia is given large volume of isotonic fluid (ADH
is stimulated by hypovolemia; when hypovolemia is corrected, the ADH level falls suddenly
causing sudden brisk water diuresis, and therefore rapid rise in serum Na+ level)
Investigations
ECF volume status assessment (see Table 4)
serum electrolytes, glucose, Cr
serum osmolality, urine osmolality
urine Na+ (urine Na+ <10-20 mEq/L suggests volume depletion as the cause of hyponatremia)
assess for causes of SIADH (see Table 6)
TSH, free T4, and cortisol levels
consider CXR and possibly CT chest if suspect pulmonary cause of SIADH (e.g. small cell lung
cancer)
consider CT head if suspect CNS cause

Central Pontine Myelinolysis

Cranial nerve palsies
Quadriplegia
Decreased LOC

HypOnatremia = swOllen cells

HypeRnatremia = shRunken cells