Essentials of Diagnosis
Hyponatremia develops when water intake exceeds water losses.
Most cases of hyponatremia are caused by impaired water excretion due to excess antidiuretic hormone (ADH).
The reason for excess ADH can be determined by a clinical assessment of extracellular volume status and measurement of urine chemistries.
Hyponatremia frequently occurs in hospitalized patients because acute illnesses often promote antidiuretic hormone (ADH) secretion. Outside the hospital, hyponatremia can be a side effect of medications, most notably thiazide diuretics and antidepressants, and it is a common problem among alcoholics, particularly heavy beer drinkers. Identifying the cause of persistent hyponatremia is important, because it can be an indication of serious, unsuspected underlying illnesses, such as adrenal insufficiency and small cell lung cancer. Hyponatremia can also develop in patients with heart failure and hepatic cirrhosis, and its appearance portends a bad prognosis. Chronic hyponatremia, even when mild, causes impaired cognition, gait disturbances, osteoporosis, falls and fractures. Very low serum sodium concentrations can result in serious neurological complications, either from hyponatremia itself, or from overzealous efforts to correct it.
Excretion of dilute urine is the normal defense against hyponatremia (Figure 3–1). On a typical Western diet with normal kidneys, adults can match 18 L of daily water intake with 18 L (750 mL/h) of maximally dilute urine (urine osmolality 50 mOsm/kg). Psychotic patients can develop acute water intoxication within several hours, despite a normal ability to excrete water, if they drink more than 1 L/h. More often, patients with hyponatremia have impaired water excretion and become hyponatremic on more modest water intakes; in most cases, the reason is too much antidiuretic hormone (ADH), a hormone released from the posterior pituitary that promotes water reabsorption by the kidney. The presence of ADH is reflected by urine that is not maximally dilute (urine osmolality >100 mOsm/kg) and is, rather, sometimes very concentrated (up to a maximum urine osmolality of 1200 mOsm/kg).
ADH levels should normally be low when the serum sodium concentration falls, but an inadequate circulating volume (due to volume depletion, heart failure, or hepatic cirrhosis), can stimulate ADH secretion despite low serum sodium levels; in such cases, the kidney avidly reabsorbs sodium. ADH-mediated hyponatremia with a normal circulation is considered “inappropriate.” Because sodium excretion is controlled by effective intravascular volume, and not the serum sodium concentration or ADH, the syndrome of inappropriate ADH secretion (SIADH) is characterized by sodium excretion that equals or exceeds sodium intake.
In some cases, impaired water excretion is persistent, so that patients are always at risk of hyponatremia, unless their water intake is restricted or the effect of ADH is thwarted. In other cases, impaired water excretion is reversible, so that hyponatremia may correct itself through excretion ...