A serum sodium concentration >145 mmol/L.
This occurs much less commonly than hyponatraemia.
Any. Infants and elderly at greatest risk.
M = F
This is usually due to water loss in excess of sodium loss, often in combination with reduced fluid intake. Those at most risk of reduced intake include the elderly, infants and confused or unconscious patients.
· Causes of water loss include burns, sweat, hyperventilation, vomiting and diarrhoea, diabetes insipidus and hyperosmolar non-ketotic coma.
· Hypernatraemia may be iatrogenic due to osmotic diuretics which cause more water than sodium loss or excessive administration of sodium, usually in intra-venous fluids.
· A rarer cause of hypernatraemia is Conn’s syndrome or ectopic ACTH syndrome.
The normal physiological response to a rise in extracellular fluid osmolality is for water to move out of cells. Patients become thirsty and there is increased vasopressin release stimulating water reabsorption by the kidneys. Water moving out of cells causes the cells to shrink. In response to this, electrolytes are transported across the cell membrane, changing the membrane potential. Changes in the membrane potential in the brain leads to impaired neuronal function and if there is severe shrinkage, bridging veins are stretched leading to intracranial haemorrhage. Cells also begin to produce organic solutes after about 24 hours to draw fluid back into the cell.
The symptoms of hypernatraemia include thirst, nausea and vomiting. Patients may be irritable or tired, progressing to confusion and finally coma. On examination there may be features of fluid depletion including reduced skin turgor, hypotension, tachycardia, peripheral shutdown and reduced urine output. Signs of fluid over-load suggest excessive administration of salt or Conn’s syndrome. Polyuria and polydipsia suggest diabetes insipidus or hyperglycaemia. There may be neurological signs such as tremor, hyperreflexia or seizures.
Hypernatraemic encephalopathy and intracranial haemorrhage (may be cerebral, subdural or subarachnoid) may occur in severe cases. Too rapid rehydration can cause cerebral oedema as the cells cannot clear the organic solutes rapidly.
· The diagnosis is confirmed by the finding of high serum sodium on U&Es. Serum glucose and urine sodium, potassium and osmolality should also be requested. If there is raised urine osmolality, this is a sign that the kidneys are responding normally to hypernatraemia by producing low volume, high concentration urine. The underlying cause is therefore due to non-renal fluid losses.
· Conn’s syndrome or ectopic ACTH syndrome is suggested by a mild hypernatraemia, hypertension, hypokalaemia (in the absence of diuretic drugs used to treat hypertension) and a raised urinary potassium.
· CT scan of the head is indicated if there are neurological symptoms or signs, and in severe hypernatraemia to look for an underlying cause (such as head trauma) or complications such as haemorrhage.
· The aim is to gradually reduce the serum sodium concentration by no more than 0.5–1 mmol/L/h in order to avoid cerebral oedema. Urine output and plasma sodium should be monitored frequently. The under-lying cause should also be looked for and treated.
· If the patient is alert and conscious he/she should be allowed to drink freely as this is the safest way to correct hypernatraemia.
· If the patient is fluid depleted, intravenous replacement should be with 0.9% saline to restore intravascular volume. In severe hypernatraemia even 0.9% saline is less hypertonic than the plasma so this will help to correct the high sodium.
· If the patient is not fluid depleted but is unable to drink, 5% dextrose is given slowly.
· In hyperosmolar non-ketotic coma saline or half-normal saline (0.45% saline) should be used until glucose concentrations are near normal. This is to prevent worsening hyperglycaemia which can alter the osmolality further.
The mortality rate of severe hypernatraemia is as high as 60% often due to coexistent disease, and there is a high risk of permanent neurological deficit.