Hypernatraemia is defined as a serum sodium concentration > 145 mmol/L.
Hypernatraemia is commonly encountered in clinical practice. Normal serum sodium concentration is 135-145 mmol/L. Elevations above 145 mmol/L are consistent with hypernatraemia.
Hypernatraemia should be considered a problem with total body water (TBW), rather than a problem with sodium homeostasis. There is typically a fall in TBW relative to sodium with failure of normal adaptive mechanisms including thirst and anti-diuretic hormone (ADH).
When the differentiation between acute and chronic is unknown, patients should always be assumed to have chronic hypernatraemia due to the risk of cerebral oedema on correcting sodium too rapidly.
Hypernatraemia is a common electrolyte abnormality.
Elderly patients and children are most at risk of hypernatraemia. The overall prevalence varies depending on the study. It is roughly seen in 1% of hospital admissions through A&E, although the condition tends to develop in more patients during an inpatient admission.
In the majority of cases, hypernatraemia results from water depletion.
Sodium is one of the main determinants of effective osmolality within the extracellular fluid. Osmolality is the concentration of a solute dissolved in a solution. Effective osmolality or ‘tonicity’ is essentially the effective osmotic pressure gradient. In other words, tonicity governs the transcellular distribution of water.
Normal plasma osmolality is approximately 275-295 mOsm/L. It can be estimated using the formula 2Na + urea + glucose. Therefore, hypernatraemia, by definition, causes a state of hyperosmolality.
The relationship between unbound plasma sodium and body electrolytes and water can be represented in the following equation:
Plasma Na = Total body (Na + K) / Total body water (TBW)
Based on this equation, we can see that hypernatraemia may develop due to a loss of free water (TBW), gain of sodium, or a combination of both.
TBW can be regulated to alter the plasma sodium concentration. There are two predominant mechanisms:
At an osmolality > 280 mOsm/L, both the ADH system and thirst may be stimulated leading to an increase in free water (via drinking or renal reabsorption). This maintains serum sodium at a normal level.
ADH, also known as vasopressin, is synthesised in magnocellular neurons in areas of the hypothalamus (supraoptic and paraventricular nuclei). It is transported via axons to the posterior pituitary where it may be released after activation of osmoreceptors at an osmolality > 280 mOsm/L. In the kidneys, it promotes the insertion of aquaporins into the collecting ducts of nephrons that allows the free absorption of water in the absence of sodium. ADH may also be released in response to hypovolaemia (i.e. decreased in arterial blood volume).
The rise in plasma osmolality activates osmoreceptors within the hypothalamus that stimulate our thirst mechanism. Thirst is such a powerful mechanism for maintaining normal osmolality that even with extreme urine outputs seen in diabetes insipidus (> 10 L/day) hypernatraemia will not develop if the patient can continue to drink. Therefore, sustained hypernatraemia will usually only occur when the thirst mechanism is impaired or water is not available.
The predominant cause of hypernatraemia is unreplaced water losses.
There are three main mechanisms that lead to hypernatraemia:
Most commonly seen in the elderly presenting with a concurrent illness such as urinary tract infection or gastroenteritis. Typically seen in patients with dementia due to the reliance on others for maintaining oral intake.
There are three major systems through which water is lost:
Diabetes insipidus is caused by a decreased release or increased resistance to anti-diuretic hormone:
The clinical consequence of an inadequate ADH response is polyuria (increased urine) and polydipsia (increased thirst). If the thirst mechanism remains functioning (will be in most cases) and the patient can continue to drink, then hypernatraemia should not develop.
Any compromise in the thirst mechanism or ability of the patient to drink (e.g. peri-operatively) can lead to a dramatic loss of free water and rise in plasma sodium concentration.
NOTE: a form of diabetes insipidus known as adipsic diabetes insipidus occurs when both the ADH and thirst mechanism are impaired. This leads to dangerous, recurrent episodes of hypernatraemia. May be congenital or acquired (e.g. sarcoidosis).
The primary symptom of hypernatraemia is usually pronounced thirst.
The clinical features can often indicate the underlying cause. It is important to exclude polyuria, which may be suggestive of diabetes insipidus.
The diagnosis of hypernatraemia is based on a laboratory sample of plasma sodium > 145 mmol/L.
The diagnosis of hypernatraemia is easily made from a urea and electrolyte (U&E) blood sample. Further investigations depend on the suspected underlying cause (e.g. chest x-ray or urine culture if infection suspected).
Urinary sodium is a useful marker of TBW. A urinary sodium < 10 mEq/L is suggestive of volume depletion and overactivation of the renin-angiotensin aldosterone system (RAAS).
Urine osmolality is useful at differentiating suspected cases. It should be used in context of the urinary sodium and volume status of the patient (e.g. hypovolaemia, euvolaemia, hypervolaemia).
A series of routine blood tests help determine the cause.
The principal treatment of hypernatraemia involves restoration of total body water and treating the underlying cause.
The goal is to provide fluid replacement but to reduce serum sodium concentration by no more than 10 mmol/L in a 24-hour period. More rapid correction can lead to rapid shifts of water intracellularly. In the brain, this can lead to major neurological injury from cerebral oedema.
The amount of fluid needed to replace the fluid deficit and carefully reduce serum sodium can be estimated using different formulas.
*Correction factors: Children and men (0.6), women and elderly men (0.5), elderly women (0.45)
Formula 2 is based on the infusion of 1L of fluid that may have a variable content of sodium:
An elderly male is 70 kg and found to have a serum sodium concentration of 161 mmol/L
Two scenarios are listed below. In one he is prescribed a litre of a balanced crystalloid and the other a litre of 5% dextrose.
The aim is to reduce serum sodium by no more than 10 mmol/L within 24 hours:
Additional litres of fluid can be added to these regimens to account for fluid losses.
The above formulas are good for guiding fluid management in patients with hypernatraemia, but one size does not fit all. Compounding factors may be present such as marked hyperglycaemia or hypervolaemic hypernatraemia.
Usually, a combination of crystalloids are used to help restore water depletion while not over correcting the serum sodium. It is vital that serum sodium is checked regularly and the patients fluid balance frequently assessed. This allows clinicians to adapt management to changes in serum sodium and fluid status.
The management of diabetes insipidus depends on whether it is central or nephrogenic. It is a complex condition and should always be managed based on advice of the endocrinology team.
General management principles:
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