Ionic cerebral oedema is a form of cerebral oedema usually associated with cytotoxic oedema, and represents the passage of water and sodium from capillaries into the brain parenchymal extracellular space. It is distinguished from vasogenic oedema as the blood brain barrier (BBB) remains intact and the oedema occurs as a result of cellular damage, often from ischaemia.

It is not a term most radiologists use in reports, nor are familiar with, usually preferring to use the term cytotoxic oedema to denote the combination of true cytotoxic oedema (cellular swelling) and ionic oedema. Ionic oedema is essentially the swelling caused by an imbalance of ions, specifically observed during the transition from cytotoxic oedema to vasogenic oedema.³

Nonetheless the concept of ionic oedema is useful in separating out different pathophysiological processes as these are mirrored in imaging findings. Along with cytotoxic oedema, ionic oedema forms a spectrum of pathological changes secondary to brain insult, the most advanced stage of which includes haemorrhagic transformation.

Pathology

Once cytotoxic oedema has occurred (sodium, chloride and water have moved intracellularly) and provided there is some replenishment of blood in the capillaries, a sodium (Na+) concentration gradient exists from the capillary lumen, across the endothelium and into the extracellular space. Sodium is transported into the extracellular space, drawing with it chloride (along a electrochemical gradient) and water (along an osmotic gradient) ¹. 

It is therefore ionic oedema which is responsible for the tissue swelling seen in ischaemic infarcts, not cytotoxic oedema which is merely a redistribution of water (and sodium and chloride) from the extracellular to the intracellular compartment ¹. Other common clinical settings for ionic oedema to occur include head injury and the presence of toxins such as drugs. Broadly, it can result from any cause of hypoxic brain injury.

An important note to be made is that for tissue to swell it requires the influx of fluid, and therefore requires some blood flow ¹. It has been observed that the very centre of infarct cores does not swell as much as the periphery of the infarct, or as much as infarct which is reperfused ¹. 

Radiographic features

CT

• area of uniform low attenuation change due to influx of additional water into the extracellular spaces

• in cases of ischaemia it often corresponds to the affected cerebral vascular territory

• grey-white matter junction becomes blurred i.e. there is a loss of grey-white differentiation; this is distinct from vasogenic oedema where the grey-white matter distinction becomes more pronounced

• cortical ribbon swells

MRI 

• seen as high T2 or FLAIR signal in the affected regions, usually affecting both white and grey matter

• unlike vasogenic oedema, it will usually be accompanied by restricted diffusion on diffusion weighted imaging sequences; this is due to the presence of underlying cytotoxic oedema which precedes ionic oedema in the acute and subacute phase

Treatment and prognosis

Treatment is usually of the underlying cause.