Hypernatremia

Hypernatraemia is a relatively rare presentation seen in clinical practice. It is defined as a [Na+] > 145mmol/L, however symptoms of hypernatremia are normally only seen when [Na+] > 160mmol/L.


Causes

There are a wide range of potential causes for hypernatraemia, which can be divided depending on fluid volume status.

Hypovolaemic Hypernatremia

  • Diuretics (common)
    • Mainly from loop diuretics
  • Dehydration / fluid restriction (common)
    • Includes diarrhoea, vomiting, burns, or excessive sweating
  • Acute tubular necrosis
    • Has an early polyuric stage
  • Hyperosmolar states
    • Includes HHS (hyperosmolar hyperglycaemic state)

Euvolemic Hypernatremia

  • Diabetes insipidus (DI), discussed below

Hypervolaemic Hypernatremia

  • Excessive hypertonic saline administration (common)
  • Steroid excess
    • Conn’s syndrome or Cushing’s syndrome

Diabetes Insipidus

Diabetes Insipidus (DI) is the disorder characterized by excessive (5-20L/day) excretion of dilute urine and an increased thirst response. It can be classified as:

  • Cranial DI is due to impaired anti-diuretic hormone (ADH) secretion from the posterior pituitary, often after pituitary surgery or head trauma
  • Nephrogenic DI is an impaired response of the renal tubules to ADH

Patients will present with symptoms of polyuria (+compensatory polydipsia). Diagnosis of DI can be confirmed by doing a water deprivation test, whereby the patient is deprived of fluids for up to eight hours (or 5% loss of body weight), following which desmopressin is given

  • Normal: Urine Osmolality >600mOsm before desmopressin test
  • Cranial DI: Urine Osmolality increases >600mOsm after desmopressin test
  • Nephrogenic DI: Urine Osmolality does not increase after desmopressin test

Clinical Features

Hypernatremia is generally asymptomatic, although mild cases can result in excessive thirst*. However, in severe cases, progression of symptoms can result in weakness, lethargy, irritability, confusion, coma and seizures.

In cases where [Na+]>200, neurological defects can appear, including ataxia, tremor, coma, and seizures.

*The rise in [Na+] results in fluid moving from the intracellular to extracellular fluid to compensate, yet also results in the direct stimulation of the thirst response.


Investigations

A metabolic panel of bloods should be taken, including serum glucose, potassium, chloride, urea, and creatinine. A blood gas will also help assess for any associated acid-base disturbance

As a general rule for serum sodium values:

  • Levels of 150-170 mmol/L usually indicate volume depletion
  • Levels >170 mmol/L are usually associated with diabetes insipidus (nephrogenic or cranial)
  • Levels >190 mmol/L are usually a result of exogenous sodium gain

Urine osmolality* can aid the diagnosis when uncertain. Any recorded hypertonic urine is seen with extra-renal fluid losses, such as vomiting or burns, isotonic urine can be seen with diuretic use, osmotic diuresis, or salt wasting, and hypotonic urine is associated with polyuria from diabetes insipidus.

*The normal kidney response to hypernatraemia is to excrete a minimal amount of urine that is maximally concentrated (urine osmolality >800 mmol/kg)

 Following this, depending on the suspected underlying causes, further investigations can be requested, which may include ADH levels and CT head to assess the pituitary gland.


Management

The aim is to replace any fluid deficit and correct the serum sodium at a suitable rate, yet depending on the underlying cause the means by which this is done can vary.

It is important not to correct the serum sodium concentration too rapidly due to the risk of cerebral oedema (the aim is to lower the serum sodium level by 10 mmol/L/day). When replacing any fluid deficits, enteral free water replacement is preferred where possible (including administration via nasogastric tube if needed)

If enteral intake is not possible, intravenous fluid choice includes 5% dextrose (most preferred), 0.9% saline* (used if evidence of volume depletion) or 0.45% saline, or Hartmann’s solution. Adjust rates and fluid compositions depending on sodium levels and fluid status accordingly.

*Remember that even 0.9% saline has a [Na+] 154, therefore will have a dilution effect for severe hypernatraemia; however, 0.9% saline and Hartmann’s solution should only be avoided in cases of hypernatraemia associated with excess free water losses or accidental or iatrogenic excess intake of sodium.

Key Points

  • Hypernatraemia is defined as [Na+] > 145mmol/L
  • Common causes include dehydration, vomiting, diarrhoea, burns, and excessive saline administration
  • Most cases are asymptomatic yet neurological defects can present in severe cases
  • Urine osmolality and fluid status can help identify an underlying cause
  • Do not correct serum sodium concentrations too rapidly, due to the risk of cerebral oedema

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