most cases are caused by excessive water intake (oral or iv) and subsequent retention of water, particularly at risk are those with impaired ability to suppress ADH secretion, or if they have primary polydipsia which overwhelms the renal ability to excrete water (max. amount normal people can excrete is ~10L/day)
patients with chronic levels of 120mEq/L or higher are generally asymptomatic although may have subtle neurologic impairments, increased anxiety and increased falls risk
chronic hyponatraemia in mice alters monoaminergic signaling in the amygdala, with reduced levels of serotonin and dopamine, which results in increased anxiety.1) The amygdala is a brain region critical for processing fear and emotion
severe neurologic symptoms are most likely to occur with acute hyponatraemia (occurring in less than 24hrs before cerebral protective processes are in place), and with severe hyponatraemia with levels below 125 mmol/L and are most likely to occur due to acute events such as:
extreme exercise with mainly water intake and persistent ADH secretion
diuretics:
Thiazide diuretics in particular may cause hyponatraemia, esp. soon after starting Rx due to:
direct reduction in renal distal tubular NaCl reabsorption with impaired water excretion due to increased ADH actions resulting in urinary sodium + potassium concentrations exceeding plasma concentrations
primary adrenal insufficiency (Addisonian crisis) with aldosterone deficiency
as aldosterone secretion usually is unaffected, a low BP and muscle spasms do not usually occur in constrat to primary adrenal insufficiency where there is alos low aldosterone levels
caused by low ACTH which may be due to either:
pituitary pathology
prolonged exogenous glucorticoid use
pregnancy tends to reset the osmostat so serum sodium tends to be 5 mmol/L lower
may be due to excessive water intake overwhelming renal water excretion capabilities:
maximally dilute urine has an osmolality of < 100 mmol/kg, if it is higher than this in a euvolaemic patient with hyponatraemia then it suggests there is either syndrome of inappropriate ADH secretion (SIADH) or something preventing maximum dilution such as diuretic Rx contributing to the problem
eg. drinking excessive water in heat stress with high salt losses from perspiration, etc
hyponatraemia with normal serum osmolality
pseudohyponatraemia due to high lipid or protein levels:
marked elevations in serum lipids or proteins result in a reduction in the fraction of serum that is water and an artificially low serum sodium concentration
usually lipids and proteins account for ~7% of plasma volume, thus actual sodium concentration in the water component is actually higher than measured by the lab (actual = measured / fraction water in plasma)
decreasing the fraction water of plasma by having more lipids or proteins will decrease the measured sodium concentration but actual water concentration of sodium will be the same.
advanced renal failure:
advanced renal failure can impair free water excretion and serum osmolality may be normal or high due to high blood urea levels
note that urea is an ineffective osmole as it can freely cross cell membranes and thus effective serum osmolality is often low once the urea component is subtracted from measured levels.
low protein diets:
normal diets result in 600-900 mosmol of solute (mainly sodium, potassium and urea) excreted renally per day
minimum urine osmolarity is ~60mosmol/kg urine
thus low protein diets such as tea and toast only, have reduced water excretion capability due to decreased solute excretion
beer contains minimal sodium, potassium or protein and suppresses muscle breakdown thus further reducing urea production, resulting in solute excretions of only 250 mosmol/day and maximum urine output of only 4L/day.