The authors emphasize the role of magnetic resonance imaging (MRI) and present some new therapeutic approaches, the effectiveness of which cannot yet be conclusively determined (1). Even though MRI has led to a deepening of the pathophysiological understanding of these syndromes, I would argue that neither MRI nor “the considerable progress achieved by modern intensive care medicine” has led to a decisive advancement.
Osmotic demyelination syndromes can be prevented by avoiding too rapid changes in serum osmolality (<1 mosmol/h, corresponding to 0.5 mmol/L sodium/h if only changes in sodium concentration are considered). However, diseases are not themselves the cause of osmotic demyelination syndromes, as all changes in serum osmolality resulting from diseases are slow (with the exception of rapid-onset central diabetes insipidus, with increased sodium). Rather, inadequate therapy causes demyelination syndromes. With the goal of quickly correcting hyponatremia, the brain tissue is exposed to osmotic stress.
Careful planning of the infusion therapy and tightly controlled monitoring of the osmotically active substances, followed by an adequate adjustment of the infusion therapy, can prevent rapid fluctuations in osmolality and thus prevent demyelination syndromes. It is important to consider the cause of the electrolyte imbalance. In this light, it is also necessary to determine whether hypovolemia, normovolemia, or hypervolemic hyponatremia is present. For this, the technical requirements (point-of-care devices, to determine sodium and potassium levels, among other things) and knowledge (osmolality should not change by more than 1 mosmol/h) are well-known and widely available. If osmotic demyelination syndromes nevertheless occur, it is due to inadequate care during therapy. Work overload of doctors may be one of the causes.
|1.||Lambeck J, Hieber M, Dreßing A, Niesen WD: Central pontine myelinolysis and osmotic demyelination syndrome. Dtsch Arztebl Int 2019; 116: 600–6 VOLLTEXT|