Ali Ahmed, Arif Saeed, Khan Maroosha, Khan Laiba
Internal Medicine, Fauji Foundation Hospital, Rawalpindi, PAK.
Neurology, Fauji Foundation Hospital, Rawalpindi, PAK.
Cureus. 2023 Sep 7;15(9):e44850. doi: 10.7759/cureus.44850. eCollection 2023 Sep.
Basal ganglia are highly metabolically active deep gray matter structures that are commonly affected by toxins, metabolic abnormalities, and systemic, degenerative, and vascular conditions. Basal ganglion affected by uremic encephalopathy can typically result in a "Lentiform fork sign" on T2-weighted imaging (T2WI) and a fluid-attenuated inversion recovery (FLAIR) sequence of magnetic resonance imaging (MRI). This sign represents bilateral symmetrical hyperintensities in the basal ganglia surrounded by a characteristic hyperintense rim demarcating the lentiform nucleus from surrounding structures. This finding is also reported in other conditions resulting in metabolic acidosis from any cause, e.g., diabetic ketoacidosis, organic acidemias, dialysis disequilibrium syndrome, and drugs like metformin. In an appropriate clinicopathological context, the presence of this sign helps in the accurate diagnosis of uremic encephalopathy. The peculiarity lies in the reversible nature of these lesions and their affective response to treatment. However, sometimes these lesions may not be reversible. We present the case of a 60-year-old female who presented to the ER with chief complaints of fever and altered sensorium. Laboratory workup revealed deranged renal function tests (RFTs) and leukocytosis with pyuria. MRI of the brain showed bilateral basal ganglion hyperintensities on T2WI/FLAIR images characteristic of the lentiform fork sign. Therefore, a diagnosis of uremic encephalopathy due to acute kidney injury (AKI) secondary to septic shock from urosepsis was made. The patient was managed conservatively with IV hydration and antibiotics. Remarkable clinical recovery was seen over three weeks. The patient was stable on a five-month follow-up. However, the repeat MRI did not show resolution of the lesions.
基底神经节是代谢高度活跃的深部灰质结构,通常会受到毒素、代谢异常以及全身性、退行性和血管性疾病的影响。受尿毒症性脑病影响的基底神经节在磁共振成像(MRI)的T2加权成像(T2WI)和液体衰减反转恢复(FLAIR)序列上通常会出现“豆状叉征”。该征象表现为基底神经节双侧对称性高信号,周围有特征性的高信号边缘,将豆状核与周围结构区分开来。在其他因任何原因导致代谢性酸中毒的情况下也有此发现,例如糖尿病酮症酸中毒、有机酸血症、透析失衡综合征以及二甲双胍等药物。在适当的临床病理背景下,该征象的出现有助于准确诊断尿毒症性脑病。其独特之处在于这些病变具有可逆性以及对治疗的反应。然而,有时这些病变可能不可逆转。我们报告一例60岁女性,因发热和意识改变为主诉就诊于急诊科。实验室检查显示肾功能检查结果异常以及白细胞增多伴脓尿。脑部MRI在T2WI/FLAIR图像上显示双侧基底神经节高信号,具有豆状叉征的特征。因此,诊断为因泌尿道感染导致脓毒症性休克继发急性肾损伤(AKI)引起的尿毒症性脑病。患者接受了静脉补液和抗生素的保守治疗。三周内可见明显的临床恢复。患者在五个月的随访中情况稳定。然而,复查MRI显示病变未消退。