Erschienen in:
01.11.2017 | Head and Neck
Severity-specific alterations in CBF, OEF and CMRO2 in cirrhotic patients with hepatic encephalopathy
verfasst von:
Gang Zheng, Hanzhang Lu, Wenkui Yu, Song Luo, Ya Liu, Wei Liu, Hui Liu, Long Wu, Lijuan Zheng, Xiang Kong, Long Jiang Zhang, Guang Ming Lu
Erschienen in:
European Radiology
|
Ausgabe 11/2017
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Abstract
Objectives
To assess how the severity of hepatic encephalopathy (HE) affects perfusion and metabolic changes in cirrhotic patients and the association between severity and liver disease and anemia.
Methods
The study groups comprised 31 healthy subjects and 33 cirrhotic patients who underwent MR examinations, and blood and neuropsychological tests. Of the cirrhotic patients, 14 were unaffected, and 11 had covert HE (CHE) and 8 overt HE (OHE). Global cerebral blood flow (CBF), oxygen extraction fraction (OEF), and metabolic rate of oxygen (CMRO2) were noninvasively measured by phase-contrast and T2-relaxation-under-spin-tagging MRI. Correlations were performed between MR measurements, hematocrits, ammonia levels, Child-Pugh scores and neuropsychological test scores.
Results
Compared with the values in healthy subjects, CBF was higher in unaffected patients, the same in CHE patients and lower in OHE patients, OEF was higher in all patients, and CMRO2 was the same in unaffected and CHE patients and lower in OHE patients. Hematocrit was negatively correlated with CBF and OEF, but not with CMRO2. Ammonia level was negatively correlated with CBF and CMRO2, and Child-Pugh score was negatively correlated with CMRO2.
Conclusions
The severity-associated alterations in cirrhotic patients indicate that homeostasis of oxygen delivery and oxidative metabolism in HE is regulated by multiple mechanisms. These physiological alterations appeared to be associated with the degree of anemia, ammonia level, and liver function.
Key Points
• CBF, OEF and CMRO2 did not change monotonically with HE progression.
• Anemia possibly contributed to CBF and OEF changes in cirrhotic patients.
• Liver dysfunction mainly contributed to changes in CMRO2 in cirrhotic patients.