Hypernatremia is a pathophysiological condition characterized by serum sodium levels exceeding 145 mmol/L. The total body sodium content may be increased, normal, or decreased.
Classification
Concentrative Hypernatremia
This is the most common form, also referred to as hypertonic dehydration. It occurs when total body sodium is reduced, but intracellular and serum sodium concentrations are elevated. Situations include cases of pure water loss or when water loss exceeds sodium loss.
Sodium-Retentive Hypernatremia
This is less common and primarily results from reduced renal excretion of sodium and/or excessive sodium intake. Conditions associated with this type include right heart failure, nephrotic syndrome, ascites from liver cirrhosis, Cushing’s syndrome, primary hyperaldosteronism, traumatic brain injury, acute and chronic renal failure, and excessive alkali supplementation.
Idiopathic Hypernatremia
This is rare. The ability to secrete arginine vasopressin (AVP) is preserved, but the osmotic threshold for AVP release is elevated, requiring significantly hypertonic body fluid to trigger AVP secretion.
Clinical Features and Diagnosis
The clinical manifestations and diagnostic criteria for concentrative hypernatremia align with those described in the section on hypertonic dehydration.
For sodium-retentive hypernatremia, neurological and psychiatric symptoms are the main clinical features. The severity of symptoms correlates with the speed and degree of serum sodium elevation. In the early stages, symptoms are mild or absent. As the condition progresses, or in cases of acute hypernatremia, symptoms of brain cell dehydration often appear, such as confusion, agitation, irritability, convulsions, seizures, epilepsy-like episodes, coma, and even death.
Idiopathic hypernatremia typically presents with milder symptoms and is often accompanied by elevated plasma osmolality. Unlike other forms, there are no apparent signs of dehydration. Persistent hypernatremia is observed, with retained AVP secretion ability and tubular responsiveness to AVP.
Prevention and Treatment
Management involves treating the underlying cause, limiting sodium intake, and avoiding excessive sodium administration.
In the early stages, sufficient water replenishment is required to correct the hypertonic state, followed by appropriate electrolyte supplementation as needed. Rapid fluid infusion or overly rapid correction of hypertonicity can result in cerebral edema, seizures, neurological damage, and potentially death. The treatment of concentrative hypernatremia is detailed in the section on hypertonic dehydration.
For sodium-retentive hypernatremia, sodium intake reduction is advised. Dilution therapy using 5% glucose solution or encouragement of increased water consumption may also be effective. At the same time, sodium-excreting diuretics may be necessary. In these patients, extracellular fluid volume is often increased, necessitating close monitoring of cardiac and pulmonary functions to prevent overly rapid or excessive fluid infusion, which may lead to pulmonary edema. For cases unresponsive to these treatments or where the condition worsens, dialysis therapy using 8% glucose solution may be considered.
Hydrochlorothiazide and chlorpropamide can help alleviate symptoms of idiopathic hypernatremia.