Overview
In a state of chronic low plasma sodium (hyponatraemia), water would normally move into cells (as the concentration of solutes inside cells would be higher than that of the blood and extracellular fluid) and this can cause swelling of the cells (oedema). The brain compensates for this by reducing the number of solutes within brain cells to reduce the steepness of the concentration gradient within the cells and the extracellular fluid.
If hyponatraemia is corrected too quickly, the extracellular fluid now has a higher concentration of solutes compared to the brain cells, which have not had enough time to adapt. This leads to water being drawn out of brain cells and demyelination and this describes central pontine myelinolysis (CPM).
Therefore, hyponatraemia should be corrected slowly to avoid precipitating CPM.
Risk Factors
Conditions that predisposes to hyponatraemia may be a risk factor:
- Causes of water excess (e.g. heart failure, liver cirrhosis, nephrotic syndrome, psychogenic polydipsia)
- Chronic excess alcohol consumption
- Losses of sodium (diarrhoea, burns, thiazide diuretics, loop diuretics, Addison’s disease, chronic kidney disease)
- Syndrome of inappropriate antidiuretic hormone ADH release (SIADH)
- Hyperemesis gravidarum
- Diabetic ketoacidosis
- Hypothyroidism
Presentation
Symptoms occur in two phases:
- Patients initially have symptoms (within 2 weeks) relating to the sodium imbalance which resolve as sodium is corrected:
- Encephalopathy (confusion, memory problems, personality changes)
- Seizures
- Around 3-5 days later patients have symptoms due to demyelination. These may be irreversible and include:
- Spastic quadriparesis
- Pseudobulbar palsy
- Locked-in syndrome
- Coma
Management
Overview
Treatment is mainly supportive and aimed at prevention. Sodium ion levels are corrected slowly (around 4-6 mmol/L in a 24-hour period).
