Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L. Hyponatremia is not a sodium disorder; hyponatremia is a water disorder. Edelman discovered that serum sodium concentration does not depend on total body sodium but on the ratio of total body solutes (e.g., total body sodium and total body potassium) to total body water. Hyponatremia represents an imbalance in this ratio where total body water is more than total body solutes.
Most hyponatremia is either hypertonic, normotonic, or hypotonic in origin.
Physiologic stimuli that cause vasopressin release combined with fluid intake can result in hyponatremia. Additionally, reduced thyroid function or adrenal insufficiency may contribute to an increased release of vasopressin. Physiologic stimuli for vasopressin release include loss of intravascular volume (hypovolemic hyponatremia) and the loss of effective intravascular volume (hypervolemic hyponatremia).
Causes of Hypovolemic Hyponatremia
Causes of Hypervolemic Hyponatremia
Causes of Euvolemic Hyponatremia
Nonosmotic, pathologic vasopressin release may occur in the setting of normal volume status, as with euvolemic hyponatremia.
Causes of euvolemic hyponatremia include:
Many drugs cause hyponatremia and the most common include:
Hyponatremia is the most common electrolyte disorder with a prevalence of 20% to 35% in hospitalized patients. Hyponatremia, even mild (125 mEq/L to 135 mEq/L) has been associated with increased mortality and morbidity in the form of attention deficits, gait disturbances, falls, fractures, and osteoporosis.
Hypertonic hyponatremia (plasma tonicity of greater than 285 mOsm/kg)
Isotonic hyponatremia (plasma tonicity between 270 and 285 mOsm/kg)
Hypotonic hyponatremia (plasma tonicity of less than 270 mOsm/kg)
Hypotonic hyponatremia represents an excess of free water. This excess free water can be caused by two mechanisms:
There are three mechanisms involved in the inability of kidneys to excrete water:
1. High ADH activity: High ADH can be caused by three different mechanisms:
2. Low glomerular filtration rate (GFR): a low glomerular filtration rate would impair kidney's ability to get rid of water. Typical examples are Acute kidney injury (AKI), chronic kidney disease (CKD), and end-stage renal disease (ESRD).
3. Low solute intake: Patients on a regular diet consume 600 to 900 mOsm of solute per day. Solutes are defined as substances that are freely filtered by the glomeruli but have relative or absolute difficulty in being reabsorbed by the tubules in relationship to water. The main solutes are urea (which comes from the metabolism of proteins) and electrolytes (e.g., salt). Carbohydrates do not contribute to solute load. In steady state conditions, solute intake is equal to urine solute load. Therefore, it is expected that these patients also excrete 600 to 900 mOsm of solute in the urine. Urine volume, and hence water excretion, is dependent on the urine solute load. The more solute one needs to excrete, the larger the urine volume one needs to produce. The less solute one needs to excrete, the smaller the urine volume one needs to produce. Patients who eat a low amount of solute per day (e.g., 200 mOsm/day), on steady state conditions, will also excrete a low amount of solute in the urine and therefore they will do it in a smaller volume of urine. This decreased urine volume will limit the capacity of the kidneys to excrete water. Typical examples of this are beer potomania and tea-and-toast diet.
Important elements of the history and physical include:
Step 1: Plasma osmolality.
Step 2: Urine osmolality
Step 3: Urine Sodium
Treatment of hyponatremia is based on the severity of symptoms:
The goal of correction:
Risk factors for osmotic demyelination syndrome (ODS):
Limits of correction:
Overcorrection of hyponatremia: