Kim D M, Lee I H, Song C J
From the Department of Radiology, Chungnam National University Hospital, Chungnam National University School of Medicine, Daejeon, Korea.
AJNR Am J Neuroradiol. 2016 Sep;37(9):1604-9. doi: 10.3174/ajnr.A4776. Epub 2016 Apr 28.
Uremic encephalopathy is a metabolic disorder in patients with renal failure. The purpose of this study was to describe the MR imaging findings of uremic encephalopathy.
This study retrospectively reviewed MR imaging findings in 10 patients with clinically proved uremic encephalopathy between May 2005 and December 2014. Parameters evaluated were lesion location and appearance; MR signal intensity of the lesions on T1WI, T2WI, and T2 fluid-attenuated inversion recovery images; the presence or absence of restricted diffusion on diffusion-weighted images and apparent diffusion coefficient maps; and the reversibility of documented signal-intensity abnormalities on follow-up MR imaging.
MR imaging abnormalities accompanying marked elevation of serum creatinine (range, 4.3-11.7 mg/dL) were evident in the 10 patients. Nine patients had a history of chronic renal failure with expansile bilateral basal ganglia lesions, and 1 patient with acute renal failure had reversible largely cortical lesions. Two of 6 patients with available arterial blood gas results had metabolic acidosis. All basal ganglia lesions showed expansile high signal intensity (lentiform fork sign) on T2WI. Varied levels of restricted diffusion and a range of signal intensities on DWI were evident and were not correlated with serum Cr levels. All cortical lesions demonstrated high signal intensity on T2WI. Four patients with follow-up MR imaging after hemodialysis showed complete resolution of all lesions.
The lentiform fork sign is reliable in the early diagnosis of uremic encephalopathy, regardless of the presence of metabolic acidosis. Cytotoxic edema and/or vasogenic edema on DWI/ADC maps may be associated with uremic encephalopathy.
尿毒症性脑病是肾衰竭患者的一种代谢紊乱疾病。本研究的目的是描述尿毒症性脑病的磁共振成像(MR)表现。
本研究回顾性分析了2005年5月至2014年12月期间10例临床确诊为尿毒症性脑病患者的MR成像表现。评估的参数包括病变位置和形态;病变在T1加权成像(T1WI)、T2加权成像(T2WI)及T2液体衰减反转恢复序列(T2 FLAIR)图像上的信号强度;扩散加权成像(DWI)及表观扩散系数图(ADC图)上是否存在扩散受限;以及随访MR成像中记录的信号强度异常的可逆性。
10例患者均出现与血清肌酐显著升高(范围为4.3 - 11.7 mg/dL)相关的MR成像异常。9例有慢性肾衰竭病史的患者出现双侧基底节区扩张性病变,1例急性肾衰竭患者有可逆性的主要累及皮质的病变。6例有动脉血气结果的患者中有2例存在代谢性酸中毒。所有基底节区病变在T2WI上均表现为扩张性高信号(豆状核叉征)。DWI上可见不同程度的扩散受限及一系列信号强度,且与血清肌酐水平无关。所有皮质病变在T2WI上均表现为高信号。4例患者在血液透析后进行随访MR成像,结果显示所有病变完全消失。
无论是否存在代谢性酸中毒,豆状核叉征在尿毒症性脑病的早期诊断中都具有可靠性。DWI/ADC图上的细胞毒性水肿和/或血管源性水肿可能与尿毒症性脑病有关。