Hypernatremia

Pathophysiology

• The vast majority of hypernatremia cases seen in the ED are a result of severe volume loss.
• As in hyponatremia, the predominant effects of hypernatremia are on the central nervous system. High plasma osmolality results in a shift of water out of cells, causing decreased brain cell volume.
• The overall decrease in brain volume may lead to intracranial hemorrhage, causing further worsening neurological findings.

Diagnosis and Evaluation

• Hypernatremia is manifested clinically with progressive neurological symptoms corresponding to increasing serum osmolality. Also contributing to the serum osmolality are glucose, urea and alcohols, alcoholic ketoacidosis. Initial irritability is followed by tremulousness and ataxia, with extreme manifestations (seizure, coma) as osmolality increases.
• Consider causes of hypernatremia that may require other critical actions:

  Causes	Actions
  Severe dehydration	Volume resuscitation with NS
  Central lesion causing	DI Head CT
  Renal etiology of high sodium	Consider emergent dialysis
  Excessive sodium intake	Discontinue diet, medications containing sodium
  Lithium toxicity	Saline diuresis, consider dialysis

Laboratory/Studies

• Obtain serum electrolytes including STAT glucose, electrolytes should be followed during treatment every 1-2 h.
• Head CT is indicated for any alteration of mental status.
• A lithium level is indicated if any suspicion of its use exists.
• A Foley catheter is necessary to closely follow urine output.

ED Management

• Decreased level of consciousness (LOC) may cause airway obstruction and may require airway adjuncts and/or intubation.
• Hypovolemia and hypotension should be treated initially with normal saline (0.9%) boluses.
• Follow neurological status for deterioration—this dictates more aggressive normalization of sodium.
• Use 0.45% normal saline at approximately 50 ml/h once euvolemic for altered mental status. The rate of infusion may need to be increased or switched to free water if seizures or worsening mental status occur.
• Be mindful that overaggressive normalization of sodium, especially if it is chronic, may cause cerebral edema and death. Ideally one should not correct serum sodium faster than 0.5 meq/L/h. There is also a risk of causing pulmonary edema with rapid hypotonic fluid administration. The risk of cerebral edema is less of a concern in cases when hypernatremia develops acutely, before the brain has the opportunity to create idiogenic osmoles, hypocalcemia.
• For hypervolemic patients, one may consider the addition of loop diuretics (e.g., furosemide)
• Consider vasopressin or desmopressin if central diabetes insipidus (DI) is the suspected etiology
• Dialysis may be required if kidneys are unable to excrete sodium.