Hypernatraemia is a relatively rare presentation seen in clinical practice. It is serum sodium > 145mmol/L, however symptoms of hypernatraemia are normally only seen when [Na+] > 160mmol/L.
However, hypernatraemia in surgical patients also has impacts on peri-operative outcomes, with even mild hypernatraemia associated with increased morbidity and mortality rates. A cohort study of over 20,000 patients with pre-operative hypernatraemia demonstrated higher 30-day mortality rates than the control patients (5.2% vs 1.3%).
There are a wide range of potential causes for hypernatraemia, which can be divided depending on fluid volume status.
- Diuretics (common)
- Mainly from loop diuretics
- Dehydration / fluid restriction (common)
- Includes diarrhoea, vomiting, burns, or febrile illness
- Acute tubular necrosis
- Due to the early polyuric stage
- Hyperosmolar states
- Includes HHS (hyperosmolar hyperglycaemic state)
- Diabetes insipidus (DI)
- Excessive hypertonic saline administration (common)
- Steroid excess
- Conn’s syndrome or Cushing’s syndrome
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, seizures and coma.
In cases where [Na+]>180, neurological defects can appear, including ataxia, tremor, coma, and seizures.
Taking a thorough clinical history is the most important tool in evaluating the cause of hypernatraemia. A metabolic panel of bloods should be taken, including serum glucose, potassium, chloride, urea, and creatinine. A venous blood gas will also help assess for any associated acid-base disturbance
Urine osmolality can aid the diagnosis when uncertain; hypernatraemia stimulates hypothalamic ADH release which leads to concentration of urine:
- If both hypothalamic and renal function are intact, the urine osmolality in the presence of hypernatraemia should be above 600mOsmol/kg, this is typically seen in extra-renal causes of hypernatraemia
- If the urinary osmolality is less than 600mOsmol/kg despite hypernatraemia, it may indicate an ADH or renal dependent mechanism, such as osmotic diuresis or diabetes insipidus
Diabetes Insipidus (DI) is the disorder characterised by excessive excretion of dilute urine (5-20L/day) and an increased thirst response. It can be classified as:
- Cranial DI– impaired anti-diuretic hormone secretion from the posterior pituitary
- Often occurs after pituitary surgery or following head trauma
- Nephrogenic DI– impaired response of the renal tubules to anti-diuretic hormone
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
The aim is to replace any fluid deficit and correct the serum sodium at a suitable rate. Depending on the underlying cause, and whether the hypernatraemia is acute (<48 hours) or chronic, 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 (in chronic hypernatraemia, 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 Hartmann’s solution. Adjust rates and fluid compositions depending on sodium levels and fluid status accordingly.
- Hypernatraemia is defined as a serum sodium > 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
- Even mild hypernatraemia may be associated with an increased risk of morbidity and mortality
- Do not correct serum sodium concentrations too rapidly, due to the risk of cerebral oedema