Hypernatraemia
Last updated 17th April 2019 - Tom Heaton
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.
As sodium is the major osmotically active extracellular electrolyte, it is usually associated with changes in volume status.
Pathophysiology
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.
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.
Aetiology
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.
A good way to consider the causes is to assess how this may arise.
- Water loss in excess of sodium loss
- Renal loss
- Diabetes Insipidus - Cranial or Nephrogenic
- Drugs
- Osmotic diuresis - hyperglycaemia, mannitol
- Renal injury
- Diabetes Insipidus - Cranial or Nephrogenic
- Skin loss
- Sweat
- Burns
- Sweat
- GI losses
- Lower GI - diarrhoea
- Fistula
- Upper GI - NG tube, vomiting
- Lower GI - diarrhoea
- Renal loss
- Decreased water intake
- Hypothalamic dysfunction leading to thirst impairment
- Behavioural prevention of response to thirst
- Sedation
- Cognitive impairment
- Sedation
- No access to water
- Hypothalamic dysfunction leading to thirst impairment
- Increased sodium intake
- Oral ingestion - seawater
- IV - bicarbonate, hypertonic saline, antibiotics
- Oral ingestion - seawater
- Reduced sodium loss
- Mineralocorticoid excess
- Hyperaldosteronism
- Cushing’s
- ACTH
- Hyperaldosteronism
- Mineralocorticoid excess
Presentation
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:
General
Signs of dehydration
Specific causes may have relevant presenting features e.g. polyuria in DI.
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:
- Thirst
- Weakness
- Lethargy
- Confusion
- Focal neurological deficits
- Coma
- Seizures
General
Signs of dehydration
- Dry mouth
- Reduced skin turgor
Specific causes may have relevant presenting features e.g. polyuria in DI.
Investigations
Bloods
Urinary electrolytes and osmolality - may aid diagnosis of DI
Investigations may be directed as specific cause:
- U&Es
- Bone profile
- Glucose
Urinary electrolytes and osmolality - may aid diagnosis of DI
Investigations may be directed as specific cause:
- Neuroimaging
- ACTH-adrenal axis
Management
The management principles are:
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:
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.
- 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:
- Oral/enteral water
- 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.
Complications
- Seizures
- Intracranial haemorrhage
- Cerebral oedema - over-rapid correction
Links & References
- Cadogan, M. Hypernatraemia. LITFL. 2017. https://lifeinthefastlane.com/investigations/hypernatraemia/
- Harding, M. Hypernatraemia. Patient.info. 2016. https://patient.info/doctor/hypernatraemia
- Sterns, R. Etiology and evaluation of hypernatremia in adults. UpToDate. 2017.
- Heaton, T. Fluid & electrolyte overview. Medical Physiology. 2019. http://www.medicalphysiology.co.uk/fluid--electrolyte-overview.html
