Makindo Medical Notes.com

The physician must weigh up the risks of a low Na against the risks of too rapid correction. Risk groups are those with hypoxia, alcoholism or malnutrition

About

• First described 1956
• Also called osmotic demyelination syndrome

Aetiology

• Seen in those with rapid correction of hyponatraemia
• As serum Na rises water moves out of swollen CNS cells
• This appears to cause demyelination

Risks

• Commoner in malnourished alcoholics
• Also seen in cachexia and cancer patients
• Initial Na < 120 mmol/L for more than 48 hours
• Rapid rise in Na due to hypertonic saline solutions

Clinical

• Progressive quadriplegia and brainstem signs
• Delirium, Ophthalmoplegia, Bilateral pin point pupils
• Fever may be seen and can raise issues of infective cause
• Corneal reflexes usually remain
• Related to rate of correction of hyponatraemia

Differential

• Brainstem Encephalitis, Brainstem stroke
• Tetanus, Meningitis, Drug overdose
• Post ictal state, non-convulsive status

Investigations

• FBC, U&E, LFTS, Clotting: may suggest alcohol
• U&E: Na usually < 110 mol/L however if occurred pre admission the shifts in Na may not have been seen
• CSF may be done in workup: High opening pressure, raised protein, Mild elevated WCC
• MRI: demyelination of the pons in the basis pontis, central pons and tegmentum. May be bat-wing appearance on T2 pontine sequences. Occasionally can affect the thalamus, midbrain, medulla and cerebellum

Management

• Prevention is key with slow correction of serum [Na] at < 10-12 mmol/24 hrs and 18 mmol/L in the first 48 hrs. Even slower in high-risk groups such as alcoholism or malnutrition
• See Hyponatraemia and SIADH for more information
• Long term some recovery may take place following neurorehabilitation