Hypernatraemia

Hypernatraemia is a disorder of sodium homeostasis characterised by high levels of sodium (< 146 mmol/L). It's a rare condition, and much less common than hyponatraemia, due to the body's defence against hypernatraemia being very robust. Hypernatraemia due to loss of water is called dehydration.

Grading of severity

Sodium level	Severity
146 - 154	Mild
155 - 165	Moderate
> 165	Severe

Classification

Establishing the patient's fluid status and serum osmolality (tonicity) is important to determine the underlying cause. We usually distinguish between hypotonic, isotonic, and hypertonic hypernatraemia. In case of hypotonic hyponatraemia, the fluid status is essential in the evaluation.

Etiology

Hypernatraemia most frequently occurs following loss of water or a body fluid which contains less sodium and potassium than plasma, and that water or body fluid is not replaced. In most cases, thirst increases appropriately, which replaces the lost water, preventing hypernatraemia from developing. However, people who cannot feel thirst or freely drink water in response to thirst, such as elderly, infants, and comatose people, cannot properly compensate and are therefore at higher risk for developing hypernatraemia.

• Loss of certain body fluids
  • Vomiting
  • Osmotic diarrhoea
  • Infectious diarrhoea
  • Diabetes insipidus
  • Osmotic diuresis
    • Significant glucosuria
    • Mannitol
• Lesions of the hypothalamus (impairs thirst)
• Massive salt ingestion
• Excessive administration of saline
• Excessive muscle work (seizure or extreme exercise) (transient)

Hypothalamus lesions causes hypernatraemia by impairing thirst.

Excessive muscle work rapidly breaks down glucagon into smaller and more osmotically active molecules, causing rapid water movement from the extracellular to the intracellular space, causing transient (a few minutes) hypernatraemia.

Depending on whether the cause is acute or chronic, hypernatraemia can be acute or chronic as well. Hypernatraemia is acute if it has developed over 48 hours or less. Acute hypernatraemia is rare; most cases are chronic.

Pathophysiology

The body prevents elevated sodium levels by regulating thirst and anti-diuretic hormone (ADH) levels. When sodium levels increase, thirst increases, stimulating water intake, which decreases the plasma concentration of sodium. ADH decreases the loss of water in the urine, further decreasing the concentration of sodium. Thirst and ADH increases when the plasma osmolality increases beyond 280 mosmol/kg. These compensatory mechanisms are very effective, and so only a severe insult without appropriately increased water intake will cause hypernatraemia.

For loss of body fluid to cause hypernatraemia, the fluid lost must have a lower concentration of sodium plus potassium than the concentration of sodium in the plasma.

Hypernatraemia causes hypertonicity, which causes water to flow out of cells. This is most important in the brain, where the brain volume shrinks, potentially causing rupture of cerebral veins.

Clinical features

The major clinical feature of hypernatraemia is increased thirst. Other features include lethargy, muscle weakness, irritability, and seizures. Severe causes can cause coma and death.

Diagnosis and evaluation

Unlike hyponatraemia, the evaluation of hypernatraemia is relatively straightforward. The cause is usually evident from history alone. If not, the osmolality of the urine is of assistance.

In physiological cases, hypernatraemia causes an increase in ADH, which causes the urine osmolality to be increased to more than 600 mosmol/kg. If the urine osmolality is > 600, it's indicative of the hypothalamus and thirst response as well as kidney function being normal. The cause must therefore be extrarenal fluid loss or increased sodium intake.

A urine osmolality of < 600 mosmol/kg is indicative of disease of the kidney, causing the kidney to lose more water than normal, usually due to diabetes insipidus or osmotic diuresis.

A lack of thirst indicates a disorder of the hypothalamus.

Management

Mild hypernatraemia does not usually require hospitalisation, but moderate, severe, or symptomatic hypernatraemia requires hospitalisation. Sever hypernatraemia requires intensive care. For treatment of diabetes insipidus, see the corresponding article.

Regardless of severity or cause, management requires administration of isotonic or hypotonic fluids. In mild cases, administration can be oral (simply drink water). In other cases, administration of D5W (free dextrose in water, a solution with no sodium) is usually appropriate.

Rate of correction

Sodium levels must be corrected slowly to allow the body to reverse its compensatory mechanism to hypertonicity. Failure to do this will cause cerebral oedema.

The sodium level should not decrease more than (all of the following):

• 0,5 mmol/L per hour
• 10 mmol/L per the first 24 hours