Quantification of cerebral edema on diffusion tensor imaging in acute‐on‐chronic liver failure

Abstract

Cerebral edema is a major complication of acute liver failure but may also be seen in other forms of liver failure such as acute-on-chronic liver failure (ACLF) and chronic liver failure (CLF). ACLF develops in patients with previously well-compensated chronic liver disease following acute hepatitis A or E superimposed on underlying liver cirrhosis. The aim of this study was to detect the occurrence, and determine the nature, of cerebral edema in patients with the defined subset of ACLF using diffusion tensor imaging (DTI) metrics. Twenty-three patients with ACLF were studied and compared with 15 healthy controls and 15 patients with CLF. DTI metrics including fractional anisotropy (FA), mean diffusivity (MD), linear anisotropy (CL), planar anisotropy (CP), and spherical isotropy (CS) were calculated by selecting regions of interest in the white matter and deep grey matter of the brain. Significantly decreased FA and increased CS were observed in the anterior limb (ALIC) and posterior limb (PLIC) of the internal capsule and frontal white matter (P<0.05) in patients with different grades (1-4) of ACLF when compared with healthy controls. No significant changes in MD and CP were seen in any brain region. However, significantly decreased CL was observed in the PLIC, caudate nuclei and putamen. In patients with CLF, significantly decreased FA with increased CS in the ALIC and PLIC along with significantly increased MD in the ALIC and caudate nuclei were observed. The presence of significantly decreased FA and CL and increased CS along with no significant change in MD and CP suggests the presence of both intracellular and extracellular components of cerebral edema in patients with ACLF.

Acute Hepatic Encephalopathy: Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Findings, and Correlation with Plasma Ammonia Level and Clinical Outcome

“…[13][14][15][16] In fulminant AHF or ACHF, recent studies have demonstrated lower ADC values in affected locations, suggesting intramyelinic edema, intracellular edema, acute astrocytic swelling, or oligodendroglial injury. [23][24][25][26] Accordingly, studies using diffusion tensor imaging in patients with ACHF have recently demonstrated reduced mean diffusivity in affected regions with reduced fractional anisotropy compared with controls. [24][25][26] Hence, we suspect that this difference in whether ADC values are increased or decreased in such involved regions would be, in part, related to the time of symptom onset, when more recent acute or early subacute lesions would demonstrate reduced ADC values due to cytotoxic effects and chronic lesions would have elevated ADC values from chronic interstitial edema or gliosis.…”

“…[23][24][25][26] Accordingly, studies using diffusion tensor imaging in patients with ACHF have recently demonstrated reduced mean diffusivity in affected regions with reduced fractional anisotropy compared with controls. [24][25][26] Hence, we suspect that this difference in whether ADC values are increased or decreased in such involved regions would be, in part, related to the time of symptom onset, when more recent acute or early subacute lesions would demonstrate reduced ADC values due to cytotoxic effects and chronic lesions would have elevated ADC values from chronic interstitial edema or gliosis. Thus, the degree of involvement of the PLIC, thalami, and PVWM has also varied among these studies.…”

“…These differences again may relate not only to the timing of MR imaging relative to symptom onset but also to the location measured (tighter white matter tracts would have lower ADC values) and possibly to the lack of visual detection of subtle findings in these regions. [12][13][14][15][16][23][24][25][26] Future studies could use diffusion tensor imaging, MR spectroscopy, or molecular imaging to provide further insight into the mechanism of injury in acute hepatic encephalopathy, particularly by focusing on the thalami, PLIC, DBS, and PVWM. Also, a prospective evaluation of patients with acute hepatic encephalopathy via FLAIR, DWI, and ADC measurements is needed to validate our findings.…”

“…However, early studies using diffusion tensor imaging in patients with acute hepatic encephalopathy have produced varied measurements in NAWM compared with controls. [24][25][26] Notably, such findings have varied as to whether visually NAWM (and which locations) was abnormal, and the results are difficult to interpret, in part because whether such measurements were correlated with abnormalities visualized on T2WI, FLAIR, or DWI as determined by a neuroradiologist was not specified. [24][25][26] Finally, because the PLIC may normally have mildly hyperintense signal intensity on FLAIR, T2WI, and DWI, and the DBS may also have a slightly greater intensity compared with the intensity ventrally (particularly on higher field strength magnets), we could have been predisposed to "overcalling" abnormalities in those locations and thereby generating falsepositives.…”

Biexponential Analysis of Diffusion-Tensor Imaging of the Brain in Patients with Cirrhosis before and after Liver Transplantation

“…This is supported by the observation of an MD decrease in patients with acute-on-chronic liver failure. 35 Thus, a better explanation of what occurs during episodes of HE is the presence of mixed edema, 16 consisting of chronic vasogenic edema secondary to cirrhosis and superimposed acute cytotoxic edema secondary to hyperammonemic decompensation.…”