Hypernatraemia is defined as an elevated concentration of sodium in the blood, usually referenced as over 145 mmol/L. As sodium is the major osmotically active extracellular electrolyte, it is usually associated with changes in volume status.
An understanding of the normal physiology is important to aid understanding, and is discussed elsewhere (here). As sodium is the most important extracellular cation and osmotically active, it is intrinsically linked to water. Hypernatraemia represents an increased ratio of sodium in proportion to the extracellular water volume. As can be appreciated, this either means more sodium (without a change in water) or less water (without a change in sodium). It usually arises from a decrease in water i.e. some degree of dehydration. In health, this change is usually accompanied by an appropriate thirst response, and increased ADH release, maintaining homeostasis. These are particularly powerful and so often help maintain normality despite pathology. As such it can be seen that an inability to respond appropriately to thirst is a major risk for developing hypernatraemia e.g. when critically ill.
The conditions results from an increased ratio of sodium to extracellular water. A good way to consider the causes is to assess how this may arise.
Water loss in excess of sodium loss
Diabetes Insipidus - Cranial or Nephrogenic
Osmotic diuresis - hyperglycaemia, mannitol
Lower GI - diarrhoea
Upper GI - NG tube, vomiting
Decreased water intake
Hypothalamic dysfunction leading to thirst impairment
Behavioural prevention of response to thirst
No access to water
Increased sodium intake
Oral ingestion - seawater
IV - bicarbonate, hypertonic saline, antibiotics
Reduced sodium loss
This can be very varied. As with hyponatraemia, the speed of change is important, as this is what result in the osmotic gradients that cause the symptomatic fluid shifts. Slow change can be better tolerated than rapid.
CNS Relates to cerebral dehydration and is the most common source of symptoms. The symptoms are general worse with more rapid, larger changes:
Focal neurological deficits
General Signs of dehydration
Reduced skin turgor
Specific causes may have relevant presenting features e.g. polyuria in DI.
Urinary electrolytes and osmolality - may aid diagnosis of DI
Investigations may be directed as specific cause:
The management principles are:
Correct water/sodium state
Correct underlying cause
Avoid/treat complications of hypernatraemia or over-rapid correction
Ongoing fluid losses should be stopped if possible. Some causes may be more amenable to treatment than other e.g. antiemetics for vomiting.
The volume deficit should be correction. This will usually be a water deficit, but may also be a sodium deficit. Options include:
IV glucose 5%
IV balanced crystalloid
A slow correction rate is desirable in most cases to reduce the risk of cerebral oedema. A correction rate of 10 mmol/L over 24 hours is reasonable. Rapid correction may be possible in acute changes e.g. with DI
The patient’s drugs should be reviewed.
Calculating the water deficit (WD) can be useful to guide management. This is the volume of water needed to correct the hypernatraemia.
WD = TBW x ((Serum Na+/145)-1)) The total body water (TBW) will vary depending on the patient’s gender and age and can be estimated as: Lean body weight x 0.6 - men 0.5 - women/elderly men 0.45 - elderly women
When there is sodium loss in addition to water loss, the total amount will be more than this.