背景:对比剂诱导性脑病(CIE)是一种罕见的短暂性脑病,血管内使用造影剂引起的神经系统结构或功能的可逆性异常。CIE可以表现出一系列的神经系统表现,包括局灶性神经功能缺损(偏瘫,偏盲,皮质失明,失语症,和帕金森病)和全身症状(混乱,癫痫发作,和昏迷)。然而,如果不及时准确诊断和治疗,CIE可能会对患者造成不可逆转的损害,尤其是危重病人。
方法:50多岁的男性,数字减影血管造影后2小时,有进行性意识障碍,混合性失语症,双侧瞳孔缓慢的光反射,和右侧肢体无力。手术后七个小时,他变得无意识,高烧(39.5°C),癫痫发作,偏瘫,颈部僵硬度(+),和右边的巴宾斯基标志(+)。术后2h的计算机断层扫描(CT)检查结果非常混乱,导致我们误诊为蛛网膜下腔出血患者。手术后7小时再次进行脑部CT检查。与术后2h的CT相比,术后7hCT显示,左侧大脑半球蛛网膜下腔出血的表现消失,取而代之的是脑组织肿胀,脑沟消失了.结合患者的临床表现及排除蛛网膜下腔出血和脑血管栓塞后,我们诊断了病人的CI-E,并给予静脉输液以获得足够的水合作用,以及甘露醇,白蛋白脱水,呋塞米和糖皮质激素甲基强的松龙。经过17d的积极治疗,病人出院,没有后遗症。
结论:应认真对待CIE,但很容易误诊,一旦CIE被诊断出来,快速,准确的诊断和治疗是关键步骤。应密切评估是否可以使用造影剂进行后续检查,患者应充分了解相关风险。
BACKGROUND: Contrast-induced encephalopathy (CIE) is a rare transient, reversible abnormality in the structure or function of the nervous system caused by the intravascular use of contrast agents. CIE can present with a range of neurological manifestations, including focal neurological deficits (hemiplegia, hemianopia, cortical blindness, aphasia, and parkinsonism) and systemic symptoms (confusion, seizures, and coma). However, if not accurately diagnosed and treated in a timely manner, CIE can cause irreversible damage to patients, especially critically ill patients.
METHODS: A male in his 50 s, 2 h after digital subtraction angiography, had a progressive disorder of consciousness, mixed aphasia, bilateral pupillary sluggish light reflex, and right limb weakness. Seven hours after the procedure, he developed unconsciousness, high fever (39.5 °C), seizures, hemiplegia, neck stiffness (+), and right Babinski signs (+). computed tomography (CT) findings 2 h postprocedure were very confusing and led us to misdiagnose the patient with subarachnoid hemorrhage. Brain CT was performed again 7 h after the procedure. Compared with the CT 2 h after the procedure, the CT 7 h after the procedure showed that the manifestations of subarachnoid hemorrhage in the left cerebral hemisphere had disappeared and were replaced by brain tissue swelling, and the cerebral sulci had disappeared. Combined with the clinical manifestations of the patient and after the exclusion of subarachnoid hemorrhage and cerebrovascular embolism, we diagnosed the patient with CIE, and intravenous fluids were given for adequate hydration, as well as mannitol, albumin dehydration, furosemide and the glucocorticoid methylprednisolone. After 17 d of active treatment, the patient was discharged with no sequelae.
CONCLUSIONS: CIE should be taken seriously, but it is easily misdiagnosed, and once CIE is diagnosed, rapid, accurate diagnosis and treatment are critical steps. Whether a follow-up examination using a contrast agent can be performed should be closely evaluated, and the patient should be fully informed of the associated risks.