Hypernatremia

Essentials of Diagnosis

• Serum sodium > 145 mEq/L (> 145 mmol/L)

• Increased thirst and water intake are the main defense against hypernatremia

• Urine osmolality helps differentiate renal from nonrenal water loss

General Considerations

• Develops when there is a relative loss of water (compared to sodium) that is inadequately compensated for by water ingestion

• The primary responses to hypernatremia are stimulation of thirst (to increase water intake) and increased secretion of ADH (to minimize water loss in the urine)

• Nearly impossible to develop hypernatremia in the context of an intact thirst mechanism with appropriate access to water

• Cells in the hypothalamus sense minimal changes in serum osmolarity, triggering the thirst mechanism, and subsequent intake of water

• All patients with hypernatremia have hyperosmolality, unlike hyponatremic patients who can have a low, normal, or high serum osmolality

• Rarely, excess sodium intake contributes to hypernatremia when it is associated with an increase in extracellular volume

• With dehydration, orthostatic hypotension and oliguria are typical findings

• Because water shifts from the cells to the intravascular space to protect volume status, symptoms may be delayed

• Lethargy, irritability, and weakness are early signs

• In severe hypernatremia (sodium > 160 mEq/L), symptoms include

  • Hyperthermia

  • Delirium

  • Seizures

  • Coma

• Symptoms in older adults may not be specific

Laboratory Tests

• Urine volume, osmolarity and the osmole excretion rate

• Determine whether the patient with hypernatremia is oliguric (urine flow < 0.5 mL/min) or nonoliguric (urine flow > 0.5 mL/min)

• Elevated levels of copeptin suggest presence of vasopressin and therefore excludes a diagnosis of central diabetes insipidus

• In general, treatment involves inducing a positive water balance by the administration of hypotonic fluids

  • Can be accomplished either through the GI tract with oral intake or boluses via a feeding tube or intravenously (or a combination of both)

  • Because it can be difficult to correct large water deficits via the GI tract alone, the most common strategy is infusion of 5% dextrose in water (distilled water is contraindicated due to the development of hemolysis)

  • For chronic hypernatremia, fluid replacement should include correcting the free water deficit based on total body water (TBW) (Table 21–1) in the formula below and adding maintenance fluid from ongoing water loss via urinary output and insensible losses (estimated at 500–1000 mL daily but they can vary significantly)

    

• Although there appears to be little risk in the rapid correction of hypernatremia, caution should be exercised when infusing large amount of 5% dextrose in water due to the theoretical risk of cerebral edema because of the osmotic brain adaptation that occurs with chronic hypernatremia

• In patients who are concurrently volume depleted, priority should be to restore euvolemia via the administration of isotonic fluids

When to Refer

• Patients with refractory or unexplained hypernatremia should be referred to a nephrologist for consultation

When to Admit

• Patients with symptomatic hypernatremia require hospitalization for evaluation and treatment

• Significant comorbidities or concomitant acute illnesses, especially if contributing to hypernatremia, may necessitate hospitalization