Cerebral diffusion tensor imaging and in vivo proton magnetic resonance spectroscopy in patients with fulminant hepatic failure.

BACKGROUND AND AIM: Cerebral edema is a major complication in patients with fulminant hepatic failure (FHF). The aim of this study was to evaluate the metabolite alterations and cerebral edema in patients with FHF using in vivo proton magnetic resonance spectroscopy (MRS) and diffusion tensor imaging, and to look for its reversibility in survivors. METHODS: Ten FHF patients along with 10 controls were studied. Five of the 10 patients who recovered had a repeat imaging after three weeks. N-acetylaspartate, choline (Cho), glutamine (Gln), glutamine/glutamate (Glx), and myoinositol ratios were calculated with respect to creatine (Cr). Mean diffusivity (MD) and fractional anisotropy (FA) were calculated in different brain regions. RESULTS: Patients exhibited significantly increased Gln/Cr and Glx/Cr, and reduced Cho/Cr ratios, compared to controls. In the follow-up study, all metabolite ratios were normalized except Glx/Cr. Significantly decreased Cho/Cr were observed in deceased patients compared to controls. In patients, significantly decreased MD and FA values were observed in most topographical locations of the brain compared to controls. MD and FA values showed insignificant increase in the follow-up study compared to their first study. CONCLUSIONS: We conclude that the Cho/Cr ratio appears to be an in vivo marker of prognosis in FHF. Decreased MD values suggest predominant cytotoxic edema may be present. Persistence of imaging and MRS abnormalities at three weeks' clinical recovery suggests that metabolic recovery may take longer than clinical recovery in FHF patients.

Measurement of cytotoxic and interstitial components of cerebral edema in acute hepatic failure by diffusion tensor imaging.

PURPOSE: To use diffusion tensor imaging (DTI) metrics for measuring cytotoxic and interstitial components of cerebral edema (CE) in acute hepatic failure (AHF) patients. CE is a major complication in patients with AHF. MATERIALS AND METHODS: DTI was performed in 20 patients with AHF and 15 controls. Ten patients underwent repeat imaging after recovery from encephalopathy. Various regions of interest (ROIs) were drawn in the white and deep gray matter of the brain for the quantitation of fractional anisotropy (FA), mean diffusivity (MD), spherical isotropy (CS), linear anisotropy (CL), and planar anisotropy (CP) values. RESULTS: Significantly decreased MD values were observed in most brain ROIs in patients compared to controls. Significantly decreased FA, CL with increased CS values was also observed. In survivors with normal clinical profile after 3 weeks, a significant increase in MD and FA values were associated with decreased CS values in some regions compared to baseline study; however, it was still significantly changed compared to controls. CONCLUSION: Decreased MD and increased CS associated with decreased FA represent cytotoxic and interstitial components of CE, respectively. Incomplete normalization of these metrics in survivors after 3 weeks clinical recovery may be due to incomplete metabolic recovery.