2.2 Brain edema Introduction Vasogenic edema Brain edema may result from a wide array of causes, which can be divided into the four principal forms listed in Table 22.214.171.124–3 Clinically, multiple forms of brain edema can occur simultaneously, and often the predominating form depends on the inciting cause as well as the time course of the disease. Whether intracellular or extracellular, edema appears mildly to moderately hypoattenuating to normal brain parenchyma on CT images and T1 hypointense and T2 hyperintense on MR images. Because edema fluid is distributed within a microenvironment of cells and macromolecules, it will also appear hyperintense on FLAIR and other pure water‐nulling sequences. Vasogenic edema occurs because of a disruption of the tight junctions of the blood–brain barrier, resulting in extravasation of high‐protein fluid into the brain. Vasogenic edema is extracellular, so it tends to preferentially accumulate in white matter, which has a sparser cellular density and therefore more potential space for fluid distribution compared to highly cellular gray matter.3 Depending on the initiating cause and volume of fluid, edema can distribute widely (Figures 2.2.2, 2.2.3). Cytotoxic edema Cytotoxic edema occurs as a result of ischemia resulting in cell membrane Na/K pump dysfunction, increased intracellular fluid volume, and cell swelling. Because of the underlying cause and the intracellular nature of this form of edema, white and gray matter may both be affected, and the distribution of edema roughly ­conforms to the geographic distribution of ischemia (Figure 2.2.1).3 In most instances, cytotoxic edema occurs in combination with vasogenic edema. Diffusion‐weighted imaging has been used to discriminate between the two forms following acute episodes of ischemia, with reduced apparent diffusion coefficient (ADC) intensity reflecting predominantly cytotoxic edema.4 Interstitial or hydrocephalic edema Interstitial edema most often occurs in association with obstructive hydrocephalus when intraventricular pressure increases, causing transependymal CSF migration into adjacent brain parenchyma. As a result, hydrostatic edema preferentially occurs within periventricular parenchyma and is extracellular (Figure 2.2.4). Unlike vasogenic edema, interstitial edema fluid is a transudate containing little in the way of cells or macromolecules.3 Osmotic edema Osmotic edema occurs rarely and is caused by reduced plasma osmolality resulting from water intoxication, hemodialysis, or metabolic disorders that reduce plasma sodium or glucose concentration. The imbalance in brain extracellular fluid osmolality and plasma osmolality results in a fluid shift to the brain leading to ­formation of extracellular edema.3 Atlas of Small Animal CT and MRI, First Edition. Erik R. Wisner and Allison L. Zwingenberger. © 2015 John Wiley & Sons, Inc. Published 2015 by John Wiley & Sons, Inc. 162 Brain Edema 163 Table 2.2.1 Distribution and causes of brain edema. Cytotoxic Vasogenic Interstitial Osmotic Distribution Intracellular gray and white matter Extracellular predominately white matter Extracellular periventricular Extracellular Cause Cell membrane Na/K pump dysfunction due to cell hypoxia from ischemia Disruption of blood–brain barrier resulting in extravasation of high‐protein fluid Increased intraventricular pressure. Usually from obstructive hydrocephalus Systemic plasma hypo‐osmolality Figure 2.2.1 Cytotoxic Edema (Canine) (a) T1, TP (b) FL, TP MR (c) T2, DP 3y FS Dachshund with right‐sided cerebellar infarction. There is a well‐circumscribed geographic region of FLAIR and T2 hyperintensity involving the right cerebellum (b,c: arrow). The T2 hyperintensity is due, in part, to intracellular cytotoxic edema resulting from cell hypoxia. The lesion distribution coincides with the tissue volume normally perfused by the right rostral cerebellar artery. Figure 2.2.2 Vasogenic Edema (Canine) CT 3y MC Basset Hound with aspergillosis involving the frontal sinus and forebrain. This ­unenhanced CT image is caudal to the primary lesion. Marked, diffuse hypoattenuation is evident involving the white matter of the right cerebral hemisphere because of the ­presence of vasogenic edema. Although edema is recognized on CT images, it may be less ­conspicuous than on corresponding MR images. (a) CT, TP 163 164 Atlas of Small Animal CT and MRI Figure 2.2.3 Vasogenic Edema (Canine) MR Adult dog of unknown age and gender with a large left frontal lobe meningioma. This image is at a level caudal to the mass. Marked, diffuse hyperintensity is evident involving the white m ­ atter of the left cerebral hemisphere, representing vasogenic edema. There is also diffuse volume expansion of the white matter associated with prominent right‐sided midline shift. (a) FL, TP Figure 2.2.4 Interstitial Edema (Canine) (a) T1+C, DP (b) T1, TP MR (c) FL, TP 6y FS Toy Poodle with a caudal fossa meningioma causing obstruction of the ventricular system (a). Images b and c are at the level of the rostral horns of the lateral ventricles. The thin, hyperintense rim surrounding the rostral horns of the lateral ventricles on the FLAIR image (c: arrowheads) represents transependymal migration of cerebrospinal fluid to the periventricular extracellular fluid space due to increased intraventricular hydrostatic pressure. References 1. Betz AL, Iannotti F, Hoff JT. Brain edema: a classification based on blood–brain barrier integrity. Cerebrovasc Brain Metab Rev. 1989;1:133–154. 2. Iencean SM. Brain edema – a new classification. Med Hypotheses. 2003;61:106–109. 164 3. Nag S, Manias JL, Stewart DJ. Pathology and new players in the pathogenesis of brain edema. Acta Neuropathol. 2009;118: 197–217. 4. Loubinoux I, Volk A, Borredon J, Guirimand S, Tiffon B, Seylaz J, et al. Spreading of vasogenic edema and cytotoxic edema assessed by quantitative diffusion and T2 magnetic resonance imaging. Stroke. 1997;28:419–426; discussion 426–417.