Hyponatremia in Emergency Medicine Treatment & Management

Hyponatremia is necessarily a hospital-based diagnosis, but patients may exhibit signs of severe neurologic dysfunction during prehospital evaluation and transport.

Address acute life-threatening conditions and initiate supportive care.

Establish reliable intravenous access and give supplemental oxygen to patients with lethargy or obtundation. In these patients, evaluate the possibility of hypoglycemia with a rapid glucose check. Administer intravenous glucose to hypoglycemic patients.

Administer standard prehospital anticonvulsant therapy to patients experiencing seizures. Seizures secondary to hyponatremia are unlikely to respond to this therapy, but it should be administered until a definitive diagnosis and therapy are available.

Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg, obtundation; fixed, unilateral, dilated pupil; decerebrate or decorticate posturing) until a more definitive therapy can be initiated.

Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.

The ED evaluation of patients with hyponatremia includes determining the cause and the chronicity of the hyponatremic state in order to direct appropriate therapy.

Acute hyponatremia is less common than chronic hyponatremia and typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).

Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.

The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.

The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.

The source of free water must be identified and eliminated.

In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.

Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient. Any further correction is potentially dangerous and must be avoided unless necessary to correct continued seizures or other severe CNS abnormality.

Chronic hyponatremia is more common than acute hyponatremia. Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia. These patients lack any history of sudden free water loading.

Chronic hyponatremia must be managed with extreme care. Treatment of chronic hyponatremia has been associated with the development of the osmotic demyelination syndrome (also known as central pontine myelinolysis) characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.

The pathophysiology of osmotic demyelination is controversial. Multiple cohort studies and 3 reviews of the literature suggest that the syndrome is caused by overly rapid correction or overcorrection of chronic hyponatremia.^[12] Some investigators note that osmotic demyelination often develops when chronic hyponatremia is complicated by hypoxia and believe that osmotic demyelination may be a form of hypoxic encephalopathy associated with hyponatremia and not a complication of therapy.^[13] Until further data are available, management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.

Symptoms of osmotic demyelination (eg, dysarthria, dysphagia, seizures, altered mental status, quadriparesis, hypotension) typically begin 1-3 days after correction of serum sodium level.

The condition is typically irreversible and often devastating. Slow, cautious correction of serum sodium level and maintenance of adequate oxygenation in these patients is important.

Patients with hypokalemia, female gender, or history of alcoholism or liver transplant seem to be particularly prone to develop osmotic demyelination.^[14] Exercise extreme caution in treating hyponatremia in these subgroups.

The risk of osmotic demyelination appears to be minimal in patients whose chronic hyponatremia is corrected at a rate not to exceed 10-12 mEq/L in the first 24 hours and not to exceed 18 mEq/L in the first 48 hours.^[12]

Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity. Further correction should proceed at an overall rate that is no greater than 10-12 mEq/L in the first 24 hours and no greater than 18 mEq/L in the first 48 hours. Anecdotal reports suggest that therapeutic relowering of the serum sodium level with hypotonic fluids and desmopressin (DDAVP) may help avert neurologic sequelae in patients whose chronic hyponatremia is inadvertently corrected too quickly.

In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination. Regardless of the therapeutic approach, serum sodium must be monitored closely and corrected no faster than 10-12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours.

Patients with hypovolemic hyponatremia have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that the serum sodium level increases slowly.

Patients with hypervolemic hyponatremia have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause. The vasopressin receptor antagonists conivaptan (Vaprisol) and tolvaptan (Samsca) are now approved for use in hospitalized patients with hypervolemic hyponatremia, though clinical experience is scant.^{[12, 15]}

Euvolemic hyponatremia implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists (eg, conivaptan, tolvaptan) show promise as effective and well-tolerated intravenous therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH.^[16]