Emergent Care / Stabilization:
Establish intravenous (IV) access. If the patient is actively seizing, administer a bolus of 150 mL of hypertonic (3%) saline.

Diagnosis Overview: 
Hyponatremia is an abnormally low serum sodium concentration (serum Na+ < 134 mmol/L). It is often asymptomatic, although acute onset (developed in less than 48 hours) may cause nausea, vomiting, headache, stupor, coma, and seizures, as well as other signs of cerebral edema (ie, increased intracranial pressure, impaired cerebral circulation). Symptoms more common in patients with chronic hyponatremia include fatigue, lethargy, hyporeflexia, edema, decreased skin turgor, headache, confusion, irritability / agitation, and muscle twitching; these symptoms may also be present in acute hyponatremia. Elderly individuals with hyponatremia may additionally present with gait deficits, falls, and fractures.

Management is predicated on an understanding of the specific etiology and duration of the patient's hyponatremia and severity of presentation. While hyponatremia can be life-threatening in severe cases and requires rapid correction in select situations, overly rapid correction of long-standing hyponatremia can cause osmotic demyelination syndrome (previously central pontine myelinolysis), a devastating neurologic consequence.

Hyponatremia may be caused by low levels of serum sodium, increased intravascular volume, or both. True hyponatremia is marked by concurrent hypotonicity with a serum osmolality of < 280 mOsm/kg. Serum Na+ < 134 mmol/L with normal or elevated serum osmolarity suggests pseudohyponatremia (hyperparaproteinemia, hyperlipidemia) or the presence of an osmotically active substance such as mannitol or glucose in the serum. True hyponatremia occurs in patients with normal renal water excretion (measured by urine osmolarity), such as in primary polydipsia (or in infants being fed diluted formula or in patients receiving excessive tap water enemas); a reset osmostat (Type C syndrome of inappropriate antidiuretic hormone [SIADH]); or impaired water excretion, which may be due to endocrinological abnormalities such as hypothyroidism or adrenal insufficiency, which should be excluded.

Evaluation of the renal excretion of sodium is necessary for proper diagnosis and management. Low levels of urine excretion (< 20 mmol/L) indicate hypovolemia or intravascular depletion states despite total body volume overload, as is seen in congestive heart failure (CHF), cirrhosis, and nephrotic syndrome. Inappropriately high rates of urinary sodium excretion (> 40 mmol/L despite serum hyponatremia) indicate SIADH, which can be due to medications or renal salt wasting. Selective serotonin reuptake inhibitors (SSRIs), anticonvulsants, alcohol, and opioids are frequently implicated in inappropriate antidiuretic hormone levels. Intracranial injury can lead to cerebral salt wasting, which causes hyponatremia, intravascular volume depletion, and a concentrated urine with natriuresis. Diuretics are another frequent cause of drug-induced hyponatremia due to their effects on intravascular volume, or the aldosterone system, or due to sodium retention in the kidneys.

Hyponatremia is common in elderly individuals due to decreased glomerular filtration rate (GFR), intrarenal prostaglandin production, and percentage total body water content, as well as high sensitivity to osmotic stimuli resulting in greater frequency of SIADH. Older individuals are also more likely to be on a greater number of drugs with the propensity to induce hyponatremia, such as thiazides and antidepressants.