Ionic cerebral edema
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At the time the article was created Frank Gaillard had no recorded disclosures.View Frank Gaillard's current disclosures
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Ionic cerebral edema is a form of cerebral edema usually associated with cytotoxic edema, and represents the passage of water and sodium from capillaries into the brain parenchymal extracellular space. It is distinguished from vasogenic edema as the blood brain barrier (BBB) remains intact and the edema occurs as a result of cellular damage, often from ischemia.
It is not a term most radiologists use in reports, nor are familiar with, usually preferring to use the term cytotoxic edema to denote the combination of true cytotoxic edema (cellular swelling) and ionic edema. Ionic edema is essentially the swelling caused by an imbalance of ions, specifically observed during the transition from cytotoxic edema to vasogenic edema.3
Nonetheless the concept of ionic edema is useful in separating out different pathophysiological processes as these are mirrored in imaging findings. Along with cytotoxic edema, ionic edema forms a spectrum of pathological changes secondary to brain insult, the most advanced stage of which includes hemorrhagic transformation.
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Once cytotoxic edema 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 edema which is responsible for the tissue swelling seen in ischemic infarcts, not cytotoxic edema 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 edema 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 center of infarct cores does not swell as much as the periphery of the infarct, or as much as infarct which is reperfused 1.
area of uniform low attenuation change due to influx of additional water into the extracellular spaces
in cases of ischemia 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 edema where the grey-white matter distinction becomes more pronounced
cortical ribbon swells
seen as high T2 or FLAIR signal in the affected regions, usually affecting both white and grey matter
unlike vasogenic edema, it will usually be accompanied by restricted diffusion on diffusion weighted imaging sequences; this is due to the presence of underlying cytotoxic edema which precedes ionic edema in the acute and subacute phase
Treatment and prognosis
Treatment is usually of the underlying cause.
- 1. Simard JM, Kent TA, Chen M et-al. Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications. Lancet Neurol. 2007;6 (3): 258-68. doi:10.1016/S1474-4422(07)70055-8 - Free text at pubmed - Pubmed citation
- 2. Jesse A Stokum, Volodymyr Gerzanich, J Marc Simard. Molecular pathophysiology of cerebral edema:. (2015) Journal of Cerebral Blood Flow & Metabolism. 36 (3): 513-38. doi:10.1177/0271678X15617172 - Pubmed
- 3.Obenaus A, Badaut J. Role of the non‐invasive imaging techniques in monitoring and understanding the evolution of brain edema. Journal of Neuroscience Research. 2022 May;100(5):1191-200