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Chronic hyponatraemia and risk of myelinolysis: why is it so difficult to control the change in plasma sodium?

Acute hypotonic hyponatraemia is almost always caused by excess total body water — in adults, ranging from 5 L to 10 L. The water excess causes cerebral oedema, 1 with neurological features that include headache, nausea, weakness , lethargy, confusion, disorientation, blurred vision, muscle cramps, coma and seizures. These usually appear when the plasma sodium concentration is less than 125 mmol/L, but may also occur at higher sodium concentrations when there is a sudden fall in sodium, exceeding 15 mmol/L/24 hours. 2-5 Acute hyponatraemia with cerebral oedema is a medical emergency 6 requiring intravenous hypertonic saline. 7 In contrast, chronic hyponatraemia may be well tolerated 3,8 — even with plasma sodium levels below 125 mmol/L — as the brain adapts to a lower extracellular fluid osmolality and prevents cerebral swelling by reducing intracellular fluid osmolar content. 2,4,9-11 Studies in a rat model of hyponatraemia suggest that osmolar equilibration is complete within 48 hours. 12 Thus, most clinicians distinguish acute from chronic hyponatraemia, when the latter exists for more than 48 hours. Experimentally, the process of osmotic " adaptation " is faster than the process of osmotic " de-adaptation " , with studies in chronically hyponatraemic dogs 13 and rats 12,14 revealing that rapid restoration of osmolality using hyper-tonic saline can cause dehydration of brain tissue 15 (an effect which is greater in the hyponatraemic animal than the normonatraemic one), 16 leading to central pontine myelinolysis (CPM) and extrapontine myelinolysis CPM and EPM (eg, myelinolysis within the thalamus, basal ganglia, lateral geniculate nucleus or cerebellum) are non-inflammatory demyelination disorders (in contrast to the inflammatory demyelination disorder, multiple sclerosis). They are thought to be caused by neuronal cell apoptosis, which can be triggered by acute osmotic stress in a patient with prolonged nutritional disturbance. 18,19 CPM may be asymptomatic, 20 but is usually associated with clinical features that include dysarthria, dysphagia, pseudobulbar palsy, flaccid upper limb weakness (" man-in-the-barrel " syndrome) 21 or flaccid quadriparesis with a " locked-in " syndrome. EPM may also be asymptomatic, but is usually associated with clinical features that include tremor, ataxia, dystonia, mutism, Parkinsonism and catatonia. In a post-mortem study of 58 patients with non-inflammatory demy-elination, 47% had CPM only, 31% had both CPM and EPM, and 22% had EPM only. 22 Hyponatraemia is one of the most common disorders in clinical medicine and found in up to 80% of critically ill patients, yet despite rapid …